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Title: Text book of veterinary medicine, Volume 4 (of 5)
Author: James Law
Release date: September 8, 2024 [eBook #74391]
Language: English
Original publication: Ithaca: Published by the author, 1902
Credits: Richard Tonsing and the Online Distributed Proofreading Team at https://www.pgdp.net (This file was produced from images generously made available by The Internet Archive)
*** START OF THE PROJECT GUTENBERG EBOOK TEXT BOOK OF VETERINARY MEDICINE, VOLUME 4 (OF 5) ***
TEXT BOOK
OF
VETERINARY MEDICINE
BY
JAMES LAW, F.R.C.V.S.
Director of the New York State Veterinary College Cornell University,
Ithaca, N. Y.
VOL. IV.
INFECTIOUS DISEASES.
ITHACA
PUBLISHED BY THE AUTHOR
1902
Copyright by
JAMES LAW
1902.
PRESS OF
ANDRUS & CHURCH
ITHACA, N. Y.
VETERINARY MEDICINE.
PYÆMIA AND SEPTICÆMIA.
Multiplicity of Septicæmias. Pyæmia and Septicæmia, distinction
between. Multiple secondary abscesses in pyæmia; no secondary
abscesses in uncomplicated septicæmia. Septico-pyæmia. _Pyæmia._
Causes: bacteria, deep wound infection, susceptibility, debility,
shock, illness, narcotic ptomaines, partial immunization, complexity
of infection, mutual decomposition of toxins, dose, lesions of intima
of blood vessels, thrombosis, embolism, action of microbes on
hæmatoblasts and blood globules, viscidity of cells, adhesion to
endothelium, coagula, solution of clot, escape of microbes. Lesions:
wound, abscess, thrombus, emboli, infarction, abscesses, ulceration,
endocarditis. Spleen. Blood coagulates. Symptoms: rigor, hyperthermia
with remissions, pulse weak, soft, rapid, perspiration, diarrhœa,
sweet breath, fæces, urine acid, dulness, prostration, mucosæ dusky or
yellow, blood shows leucocytosis, hæmolysis, cardiac murmur,
arthritis, stupor, coma, palsy, dry, puffy sore, source of infection.
Prognosis grave. Prevention: largely surgical, antisepsis, asepsis,
excision of infected vein. Treatment: antiseptics, locally and
internally, stimulants, tonics, nourishment. _Septicæmia_: microbes,
toxins, septic intoxication, septic infection, fermentation fever,
sapræmic fever. Lesions: blood dark, incoagulable, spleen
enlarged—gorged, petechiæ, cloudy swellings, coagulation necrosis,
organs as if parboiled, congested glands, kidneys. Symptoms: chill
slight, hyperthermia without marked remissions, weak, rapid pulse,
hurried breathing, anorexia, emesis, yellow mucosæ, nervous
disorder—dulness, apathy, stupor, paraplegia. Value of precursory
conditions. Prognosis grave. Prevention, Treatment: remove source of
poison, antiseptics, drainage, internal antisepsis, strychnia,
quinine, iron chloride, stimulants, supporting, easily digestible
food, sponging.
At first introduced to indicate the supposed results of pus and septic
material respectively in the blood, these terms have come to represent
the clinical phenomena which come from the introduction into a
susceptible system of pyogenic and necrogenic microbes and their toxic
products. Gradually different affections, which would have been included
under the same general terms, came to be identified under specific
names, and a number of these will be described as individual
diseases—strangles, mouse and rabbit septicæmias, metritis, phlebitis,
omphalitis, rouget, barbone, chicken cholera, septicæmia hæmorrhagica,
etc.—yet a certain number have been left to be referred to under the
generic terms, though respectively due to different microbes.
_Distinctions between Pyæmia and Septicæmia._ _Pyæmia_ is a morbid
condition characterized by the formation in different organs of multiple
metastatic abscesses, dependent on the transference, in the blood
stream, of infected clots, or particles containing pus microbes, and
their arrest at distant points, so as to cause foci of suppuration
commencing with the intima of the vessels.
_Septicæmia_ indicates a general infection often by the same microbes,
but showing its results in enlargement and blood engorgement of the
spleen and lymph glands and necrotic foci of the liver, kidneys and
other organs, but without the formation of multiple abscesses. The
presence of the microbes in the different organs affected, shows that it
is not due to the diffusion of the toxic chemical products alone, as at
one time supposed, and the lack of abscesses appears to be due to the
absence of clots or of modified and adhesive leucocytes or hæmatoblasts,
which adhering to the epithelium of the vessels predispose to
suppuration.
The two conditions are, however, often combined, constituting what is
known as _septico-pyæmia_.
As in the occurrence of other infecting diseases, the condition of
varying susceptibility must be taken into account, one individual, or
one species resisting an inoculation which would be deadly to another.
=Pyæmia.= _Causes._ The causation microbes are most commonly
staphylococcus pyogenes aureus, or albus, the streptococcus pyogenes,
and less frequently bacillus pyocyaneus, bacterium coli commune, and
probably any pus producing microbe. Many conditions must however be
accepted as contributing to the general infection.
Inoculation on a mere abrasion or surface sore is not to be dreaded so
much as if the virus is lodged _subcutaneously or in a deep wound_. The
ready escape of the toxic products, the active leucocytosis which takes
place in the granulations, and the action of the oxygen of the air are
more or less protective in the exposed sores.
The native _susceptibility of the subject_,—horse, ox,—conduces to the
disease, while the insusceptibility,—bird—tends to obviate it.
The _debility of the system or of individual tissues attacked_, lowers
the resistant power, and especially that of leucocytosis, and thus
favors survival and encrease of the microbes and their chemical
products. Thus the _shock_ succeeding a serious operation, the general
depression attendant upon severe illness, or the poisoning by
narcotizing ptomaines and toxins, may easily become the extra weight
which causes the system to succumb. On the contrary, pre-existing or
long standing disease, with consequent general debility appears at times
to prove to some extent a protective factor, the previous exposure to
the invading germ having educated the leucocytes to resist the toxins
and to produce the defensive sera which neutralize the latter or keep
the invading microbes in check. A measure of immunization has been
secured.
The resulting immunization cannot be looked on as very perfect, nor
permanent, as a specially strong inoculation by a virulent microbe, or
large dose, or different conditions of life, will entirely overcome it,
and the pyæmic fever appears. Yet in chronic cases of secondary
abscesses from a deep source of infection, the resistance is often such
as to ward off febrile pyæmia. In a horse with primary abscess situated
deeply under the humerus, free evacuation and healing of the wound,
have, in my experience, been followed by the formation of abscesses in
distant points for a period of seven years, but without any marked
febrile reaction.
The _complex nature of the infection_ appears at times to overcome the
vital resistance more effectively than will the presence of even a
potent microbe alone. Some of the worst cases follow on a wound, the
seat of complex infection, and even saprophytes are to be dreaded in
this connection. This may operate in various ways, either by mutual
combinations or decompositions of the toxic products of associated germs
producing more deleterious products, or by the individual action of one
ptomain or toxin on leucocytes, hæmatoblasts, sera, or tissue, laying it
more open to the attacks of those of another microbe which by itself
would have been comparatively harmless.
Koch’s experiments showed that the _attack is violent in ratio with the
size of the dose_: one-thousandth part of a drop of pyæmic blood was
harmless to the rabbit, while one tenth of a drop killed in one hundred
and twenty-five hours, and a syringe full in forty hours.
In ordinary cases of pyæmia the occurrence of internal _phlebitis_ or
_arteritis_ with the inevitable thrombosis is an important step in
causation. Any inflammation of the inner coat of the vessel leads
promptly to the formation of a coagulation of the contained blood, and
blocking of the lumen. Beginning on the diseased or abraded surface, the
clot forms backward along the line from which the blood normally comes
(proximal in the arteries; distal, in the veins), until it reaches the
next considerable colateral branch. The clot is firmly adherent to the
intima except at the free end, which is conical and projects into the
blood current.
If small portions are detached from the thrombus and washed on in the
blood stream they become arrested when they reach a vessel too small to
admit them, it may be a smaller artery, or it may be a capillary, and
always in the line of the circulation,—from the systemic circulation to
the lungs, or from the lungs to the system at large. This is =embolism=.
Wherever arrested, the contact of the leucocytes and hæmatoblasts with
the inner coat of the vessel, leads to metabolic changes and firm
adhesion, and the pus microbes in the clot determine suppuration and
abscess.
Eberth and Schimmelbusch have shown that the hæmatoblasts, even more
than the other blood elements, when acted on by the pus microbes become
viscous and stick not only to each other, but to any floating body, and
to the inner serous coat of the vessel, particularly when the latter has
been abraded or injured. This clumping together of the hæmatoblasts
forms white clots which block the smaller vessels, but in the viscous
condition they further the coagulation of the fibrine, and again when
they come in contact with the intima, instead of passing through, or
moving on, they remain adherent and start the formation of thrombi. This
is above all common in given tissues, and the medulla of bone has in
this respect a bad preëminence, so that acute suppurative osteomyelitis,
is a familiar lesion and is liable to become chronic, and determine
distant abscesses and general infection long after.
The thrombus thus formed is an infective coagulum, tending to constant
encrease, as the clot is a favorable culture-field for the microbes, and
the tendency is to coagulate more and more of the adjacent blood. It
tends further to disintegration, as the action of the microbes and their
toxins on the leucocytes, transforms these into pus cells, inducing
softening of the mass, and the washing on of individual infective pus
cells and minute portions of the clot to form infective centres and
abscesses at distant parts.
If the pathogenesis of the invading microbe is weak and the resistance
of the leucocytes potent, such clots may remain circumscribed or may
even be absorbed, but in the opposite conditions with potent and
numerous microbes and abundant and effective toxins, the disposition is
not only to a continuance of infection, but to an acute febrile pyæmia.
Pyæmia does not supervene at once upon a trauma as may septicæmia, but
only after a variable number of days, (3 to 8), a peculiarity which is
explained by the temporary protection of the clot. By the constant
accretions on its exterior, of the new layers of hæmatoblasts and
fibrin, the microbes are at first imprisoned, and it is only when
softening has taken place, or when the coagulum has extended into the
free flowing current passing into a colateral trunk, that the infection
is liable to be washed on in dangerous amount.
The mere presence of pus microbes or their toxins in the blood, does not
determine pyæmia: a modification of the intima of the vessels leading to
local infections with thrombosis or embolism and abscess is an essential
condition. This lesion of the vessels may be a trauma, as from bruise,
puncture, operation, ligature, or it may be the extension of a disease
process as in arteritis, phlebitis, atheroma, the growth of a tumor from
adjacent tissues, or parasitism. The seat of the secondary abscess
depends primarily on the location of the original suppurating centre. As
such centres are most commonly in the systemic circulation
(osteomyelitis, omphalitis, wounds, traumas) the lungs are most commonly
attacked, the pulmonary capillaries acting as a sieve and arresting the
floating infective coagula. When the primary infection comes from the
chylo-poietic viscera, the liver is likely to show the first crop of
secondary abscesses. When, on the other hand, the primary abscess is in
the lungs, the great flow of blood through the kidney renders it
especially subject to secondary suppurating foci, though these may form
in any part of the body.
_Lesions._ Pyæmia may result from a wound or abscess in connection with
which will usually be found a vein containing a thrombus more or less
softened or liquefied. If from a deep seated injury or from
osteomyelitis, the same condition is met with. The thrombus and
circulating blood furnish abundance of the infective microbes, and at
distant points, in the complimentary circulation, most commonly in the
lungs the arteries are found to be the seats of _embolism_ from arrested
clots. The arrest always takes place where the vessels are diminished by
bifurcation, or the giving off of a considerable colateral trunk, and
the appearances will depend on the duration of the embolism. If quite
recent, a wedge-shaped mass of tissue supplied by the vessel is ischæmic
and pale, its blood passing on into the veins without further arterial
supply; if later, this tissue forms an _infarct_ being gorged with deep
red or black blood which has filtered in from adjacent anostomosing
capillaries and distended those of the exsanguine area. This area
becomes of a deep red or black color, consolidated by an exudate of
lymph, and rapidly invaded by suppuration. The microbes determine
suppuration and softening, first in the clot and intima, and next in the
outer coats of the vessel and the surrounding exudate, so that an
abscess of variable size may result. Abscesses are usually smaller and
more numerous in the acute forms of the disease, and larger and less
numerous in the more chronic.
Ulcerative endocarditis with coagula on the valves is not uncommon. The
spleen is often the seat of small abscesses in the centre of solid
exudates, with in many cases softening and enlargement of the organ. The
blood tends to retain its normal bright red color, and clots firmly,
contrary to the usual condition in septicæmia.
_Symptoms._ The formation of emboli and secondary abscess is usually
marked by a violent rigor, lasting from a few minutes to an hour and
which may be repeated at irregular intervals, serving, in some measure,
to distinguish pyæmia from septicæmia. The temperature rises with the
rigor, (102° to 105°) but shows marked remissions especially in the
morning, when it may not exceed the normal, and rising again with the
recurrence of chill or staring coat. The pulse is usually encreased in
frequency even during the remissions and is soft and compressible.
Remissions may be attended by profuse perspirations or even, in the
advanced stages, by fœtid diarrhœa. The breath has a peculiar sweetish
or mawkish odor. Blood passed with the fæces may indicate intestinal
abscess, and albumen or pus in the acid urine, bespeaks suppurating foci
in the kidney. The cloudy mucus from the pelvis of the kidney in the
horse must not be mistaken for this. Cough or dyspnœa will indicate
abscess of the lungs, and intercostal tenderness, pleurisy.
The buccal mucosa may be dry and cracked, and the tongue coated. From
the first the animal is dull, and prostrate, and the visible mucosæ
become dusky brown or even yellowish from the liberated hæmatin. Blood
abstracted, will show the microörganism, an excess of leucocytes and
diminution of the red globules. The poison determines hæmolysis. A
cardiac murmur, usually with the first sound, betrays endocarditis. This
is especially characteristic of chronic pyæmia. Again multiple
suppurating arthritis may appear. Stupor, coma or paralysis will
indicate cerebral or meningeal lesions.
In pyæmia following trauma there is drying up of the pus which becomes
serous or bloody, a puffy condition of the granulations, and the
evidence of a thrombus in one or more veins leading out from the wound.
In other cases the occurrence of pyæmic symptoms, consequent on
parturition, metritis, omphalitis, bone-abscess or osteomyelitis, on
suppurating internal inflammations, ulcerative endocarditis, or
infective fevers like strangles, influenza, contagious pneumonia, cattle
plague, distemper, rouget, hog cholera, etc., serves to identify the
disease.
The _prognosis_ of pyæmia is always grave, and death may be expected in
six to fourteen days in acute cases. Chronic forms last much longer.
_Prevention_ is the great object in regard to surgical cases, and this
means the prevention of suppuration in the wound. As far as possible,
however, this is to be sought by asepsis, or the use of weak non-caustic
antiseptics only, as cauterized tissues form favorable culture media,
when the action of the antiseptic is spent, there being no longer any
living and resistant leucocytes present. The early excision of veins,
the seat of thrombosis, has proven successful.
In purely medical cases, the seat of the primary suppuration is not
always obvious and one is thrown back on medical treatment which is
rarely satisfactory in severe cases.
_Treatment._ When accessible even the secondary abscesses may be opened,
washed out with a weak antiseptic (3 per cent. carbolic acid solution),
and covered with antiseptic dressing. Antipyretics are worse than
useless, because of the resulting depression of the vital powers, and
the reduction of the natural powers of resistance. Calomel in small and
repeated doses tends to assist in elimination, and to counteract
complications through sepsis of the contents of the bowels. Quinine and
chloride of iron continued in large doses have been especially relied on
as antiseptic tonics. Liberal feeding, if the appetite will admit, is
all important, to tide the patient over the period of depression. In the
chronic cases tepid bathing is of great value (Senn). Senn has great
confidence in the stimulating and supporting action of alcoholic
liquors—beer, ale, porter and even whisky, and in human beings
accustomed to the daily use of these beverages they are more imperative
than in the lower animals.
=Septicæmia.= The micro-organisms causing septicæmia are the same as
those of pyæmia, but they differ somewhat in activity, and act upon a
system with a modified susceptibility, and above all one void of lesions
in the internal membrane of the vascular system. The symptoms can be
developed by the introduction of the ptomaines and toxins alone, which
hypothetical condition has been named _septic-intoxication_. In case of
excessive doses of septic material, death occurs so early as to indicate
simple narcosis. If, as is usually the case, the microbes also gain
access to the blood and multiply there, the condition has been known as
_septic infection_. In any prolonged case of septicæmia, the tendency is
to the formation of suppurating foci (_septico-pyæmia_), so that the two
affections may be looked upon as probably the same, with modifications
of the earlier phenomena.
In connection with septicæmia must be mentioned the _fermentation fever_
of Bergmann, (_aseptic_ or _resorption fever_) which follows on
extensive wounds, even if aseptic, on the intravenous injection of the
blood of healthy animals or even of fine foreign particles (charcoal,
flour), of a normal salt solution, or of well water, or of pancreatin,
pepsin or trypsin. It has been attributed to the introduction and
metabolism of fibrine and other elements, but manifestly arises also
from the solution of blood globules, (hæmolysis). It comes on within a
few hours after a severe operation or other cause and lasts from one to
three days, terminating in recovery, unless complicated by some
intercurrent infection.
The _sapræmic fever_, of Mathews Duncan (sapros—putrid, haima—blood) may
also be named in this connection. It is associated with one or more of
the common saprophytes (Bacillus saprogenes 1–2 and 3 of Rosenbach,
Proteus Vulgaris, Proteus Zenkeri, Proteus mirable, etc.) These are
propagated with difficulty in the blood, but grow readily in pus or
necrotic tissue from which their toxic products can pass into the blood.
Again the observations of Brieger and Maas, Ruine, Vaughan, Bourget and
others show that the isolated toxins from putrefactive fermentation of
animal matters, apart from the living bacteria are capable of producing
the characteristic symptoms of septicæmia.
It is now generally concluded that the septicæmic phenomena can be
produced by the introduction of such poisons, whether they are the
product of septic fermentations outside the animal poisoned, or of
fermentation in dead matter in the economy of such animal.
_Lesions._ In _fermentation fever_ no tissue lesions are known. In
_septicæmia_ gross lesions are usually lacking unless the case has been
prolonged to allow of secondary abscesses (septico-pyæmia). The blood
however is dark and coagulates feebly if at all. The spleen is enlarged,
softened, dark in color and gorged with blood. There are petechial
hæmorrhages into the serosæ and mucosæ, and the solid organs; cloudy
swelling of internal organs from coagulation necrosis; a parboiled
appearance of heart, liver, kidneys and voluntary muscles; congestion of
the lymph glands and usually the presence of the specific microbes in
the blood and local lesions. The kidneys are always congested, and their
epithelia granular and swollen, and there may be exudation between the
glomeruli and their capsules.
_Symptoms._ Septic intoxication or septic infection may be ushered in by
a staring coat or slight chill, but it rarely shows a violent rigor,
such as inaugurates pyæmia. There is a rapid rise of temperature (102°
to 104°), which persists for three to seven days without the marked
remissions of pyæmia; weak, compressible pulse; great muscular debility;
hurried, shallow breathing, usually without cough; anorexia; emesis in
vomiting animals; dusky or yellow mucosæ from dissolved hæmoglobin;
scanty, high colored urine, rarely albuminous; dulness, sometimes
nervous twitching, delirium, apathy, stupor or paraplegia; and either
constipation or, later, diarrhœa. When such symptoms supervene on a
gangrenous sore, septic abscess or fistula, retained placenta, blood
clot in the uterus or elsewhere, suppurating tubercle, or other morbid
product, gangrenous lung or other internal organ, purulent pericarditis,
pleuritis or peritonitis, or any febrile affection which is complicated
by necrosis, septicæmia is to be suspected. “Septicæmia should always be
suspected during the course of any disorder the lesions of which afford
an opportunity for the growth and development of septic microörganisms,
when the symptoms of that disorder depart from the usual type and an
elevated temperature continues beyond the usual duration.” (Atkinson).
“The final diagnosis of septic infection must be based on the existence
of an infection atrium, through which pus microbes have entered the
tissues, and from which they have reached the general circulation.”
(Senn).
_Prognosis_ is always grave. A slight infection, overcome by the
leucocytes or a simple septic intoxication may get well in two or three
days, but an _acute progressive septic infection_ will usually prove
fatal in from one to seven days.
_Prevention_ does not differ from that recommended for pyæmia.
_Treatment_ is virtually hopeless unless it can secure the removal of
the necrotic tissue or fermenting material from which the poison is
derived. When the poisoning is due to the absorption of septic products
only, with little or no introduction of microbes (septic intoxication)
the removal of their source of supply may bring about a speedy and
permanent improvement. The removal of a putrid placenta, or liquid from
the womb, followed by irrigation with an antiseptic lotion, the
evacuation of a putrid abscess, empyema, or ascites, followed by a
similar disinfection, or indeed the extirpation of a sloughing and
putrid mass of any kind may be followed by a lowering of temperature
within a few hours, and a steady improvement in the general symptoms.
The antiseptic agents employed must be sufficiently potent, and
persistently applied to render the surface sterile and yet not so
caustic as to destroy more tissue to become a future culture medium for
the septic microbes. Mercuric chloride (1:2000), aluminium acetate
(1:100), powdered iodoform, or aristol will often serve a good purpose,
to be followed, when necessary, by efficient drainage and a covering of
antiseptic gauze. When the primary source of infection is in the
intestinal canal, calomel, naphthalin or B. napthol may be tried.
For the weak heart strychnine is the most safe and reliable agent.
Quinia in large doses acts as an antipyretic, without the attendant
dangers of the coal tar products. It may be advantageously combined with
tincture of chloride of iron.
Ammoniacal and alcoholic stimulants are largely resorted to to tide the
patient over the period of depression, and nourishing and easily
digested food should be given so far as the stomach can make use of it.
Skim milk, eggs, and beef tea may be given even to the herbivorous
patient.
The thirst should be met by plenty of pure water to favor elimination of
the toxins, and the surface frequently sponged with tepid water, not
only on the ground of cleanliness and disinfection, but also as
calculated to lower the febrile temperature.
MALIGNANT ŒDEMA.
_Definition._ Causes. Bacillus septicæmiæ gangrenosa, anærobic, rarely
in living blood. Source of germ in soils. Pathogenic to man and
domestic animals except cattle. First attack immunizes. Infects deep
wound, exudates, dropsical and gangrenous parts, womb, intestine,
debilitated parts, large dose intravenously. Lesions and symptoms:
excess of exudate, boggy swelling, watery discharge, fœtid gas
bubbles, œdema of lungs and bowels. Complex infection. Minimum
dose—abscess. Diagnosis: from black quarter and anthrax. Treatment:
free incisions, hydrogen peroxide. Prevention: disinfection of skin
and wounds. Immunity.
_Definition._ An acute bacteridian disease of domestic and wild mammals,
and of man, manifested by doughy, painful and often crepitating swelling
in the vicinity of the affected part, and proving fatal in many cases in
twenty-four to forty-eight hours.
_Cause._ The essential cause is the bacillus of malignant œdema, the
septic vibrio of Pasteur, bacillus septicus gangrenæ of Arloing, the
bacillus of septicæmia gangrenosa of others.
_Morphology._ This is a staff-shaped microbe 3–4 μ. long by 1 μ. broad,
often united in chains of three or more to form long flexuous filaments.
They are furnished with numerous flagella by which they are rendered
very actively motile. The movements are tardy or simply flexuous in the
filaments. Spores form in the isolated bacilli (not in the filaments) in
suitable culture media and at a temperature of from 20° to 38° C. They
occupy a place near the centre of the bacilli, not the ends as in the
bacillus of emphysematous anthrax. The bacilli are anærobic and die
quickly in air, but the spores are unaffected by oxygen. The spores are
similarly resistant to most disinfectants. They will grow readily in
ordinary culture media if oxygen is excluded, for example under an
atmosphere of hydrogen, nitrogen or carbon dioxide, and liquefy
gelatine. Even the oxygen present in the circulating blood is highly
inimical to them, so that they are rarely found in the blood during
life, but rapidly invade both it and the tissues after death, and the
suspension of respiration. In peptonised and glucosed gelatine the
colonies are characterized as globules of liquefaction usually combined
with gas. The germ is widely distributed in soils in general and not
confined to limited areas like the bacilli of anthrax and black quarter.
_Animals susceptible._ The bacillus attacks man, horse, ass, goat,
sheep, pig, mouse, Guinea pig, rabbit, white rat, cat, dog, chicken,
pigeon, and duck. The mature ox is immune, but calves suffer. Dogs are
often immune having already suffered from the disease. A first attack
gives immunity from a second.
_Infection Channels._ Inoculation on an abrasion of the skin or surface
sore is not usually infecting, the oxygen of the air destroying the
germ. If, however, it is inserted deeply in the connective tissue,
subcutem, it grows readily in a susceptible animal. Hence the danger of
infection in deep wounds the recesses of which are not exposed to the
air, and in such it becomes a most redoubtable surgical complication. If
such wounds are the seat of active inflammation, with abundant exudate
and more or less exclusion of the air-bearing blood, and in cases of
blood stasis the field is specially inviting to the bacillus.
The debility of the injured tissue is a further invitation to the
attack. Chauveau injected 4 to 5cc. of virulent liquid of malignant
œdema into the veins of a ram and then practised bistournage, with the
result that an invasion of malignant œdema of the scrotum and tunica
vaginalis followed immediately. Pure cultures may be harmless, whilst an
admixture of proteus vulgaris or micrococcus prodigiosus renders them
most deadly (Penzo). Granulating wounds are even less favorable to
invasion than simple abrasions. In these the bacillus cannot enter at
once into the lymph channels and is exposed to destruction by the
combined influence of the air and leucocytes.
Wounds in dropsical or gangrenous parts are equally favorable, to the
development of the bacillus. Under such conditions the tissues are
wanting in oxygen and resemble the condition of the entire body after
death, when the bacillus of malignant œdema quickly penetrates its whole
substance. Petri has traced the infection through the genital passages
of newly delivered rabbits, producing a fatal metro-peritonitis and
cutaneous œdema. A similar invasion may take place in other susceptible
parturient animals. Lustig in a certain number of cases satisfied
himself that he had traced the invasion through the intestine of the
living horse. Invasion by the lungs, even by spores, is usually rendered
impossible by reason of the presence of the inspired air.
A large dose of the virus is most likely to effect a successful
invasion, since the toxins tend to debilitate and lower the defensive
powers of the tissues and leucocytes. The effect of the toxins is shown
under injections into the arteries, veins or trachea. A certain amount
of hyperthermia follows, but there is rarely any colonization and
reproduction of the bacillus in the connective tissue. In dogs and
rabbits large doses given in this way induce short inspiration and
broken or double expirations. In fatal doses death is preceded by
extreme dyspnœa and convulsions. (Rodet and Courmont).
_Lesions and Symptoms._ The tissues where invasion occurs, become the
seat of an abundant œdematous exudation, which feels boggy and painful
and may even crepitate when pressed or manipulated. In case of an open
wound, there is a profuse liquid discharge of a yellowish watery or
serous aspect, and bubbles of gas or froth having a somewhat fœtid odor.
The center of the swelling may become soft and flaccid while the
peripheral parts where the disease is advancing are tense and resistant.
In fatal cases the mucosæ of the small intestine and lungs are usually
the seats of œdema in which the bacillus is found. The bacilli may also
be found in the liver. It is noticeable that gross lesions of the spleen
and kidneys are usually absent, in marked contrast with anthrax. The
microbes found in the tissues may be in the form of bacilli, micrococci
(spores, or m. prodigiosus), and sometimes filaments.
Inoculation with a minimum dose usually results in local abscess only.
_Diagnosis._ From _emphysematous anthrax_, with which malignant œdema is
most likely to be confounded, it is to be distinguished by its
appearance anywhere outside the black quarter areas, by the immunity of
cattle which are so obnoxious to emphysematous anthrax, by the
susceptibility of man, who does not contract black quarter, by the
formation of the spore near the middle of the bacillus in place of at
one end, by its resistance to the action of ordinary disinfectants, and
by the greater tendency to form filaments.
From _anthrax_ it is differentiated by its appearance outside the
anthrax localities, by the absence of the bacillus from the blood and
from the surface layers of the skin, by the normal size of the spleen,
and by the active motility of the bacillus. It cannot be cultivated like
anthrax in the free air or on the surface of culture media, and unlike
anthrax bacillus, its cultures produce bubbles or gas.
_Treatment._ This is essentially surgical and consists in free incisions
to admit air freely to all parts of the œdematous tissue, perfect
drainage and a liberal use of peroxide of hydrogen. Other disinfectants
may be employed but are much less promising. The free disinfection of
the adjacent skin is an important element in treatment.
_Prevention._ This consists essentially in the thorough disinfection of
all accidental and surgical wounds, the careful cleansing and antisepsis
of the skin before an operation, the exclusion of earth, manure, or
water from driven wells or fountains, from all wounds, and above all the
exclusion of proteus vulgaris, and micrococcus prodigiosus.
_Immunity_ may be secured by a first, non-fatal attack of the disease.
INFECTIOUS FEVERS OF SWINE.
One name for several affections. Differentiation, swine erysipelas,
hog cholera and swine plague. Complex infections. Effects of large,
medium and small doses, of more or less potent germ, of greater or
less susceptibility.
Until comparatively recent years the various infectious fevers of swine
have been confounded and described as a single disease, the name varying
in the different countries in which they were observed. In America it
was _Hog Cholera_; in England, _Swine Fever_; in France, _Rouget_; and
in Germany, _Schweineseuche_. A closer study showed a marked tendency to
a particular class of lesions in different epizoötics, and
bacteriological research associated plagues in given localities with
different microbes, so that progress has been made in differentiating
one from another to a certain extent.
The first clear distinction was made in setting aside the swine
erysipelas (rouget, rothlauf,) from the rest as distinguished at once by
its small, delicate bacillus, differing notably from the others in its
staining and cultural peculiarities, as well as in the predominance of
the cutaneous lesions.
What remains after eliminating erysipelas, constitutes a group having so
much in common that attempts at further differentiation have led to much
disputation, and not even to-day is there such accord in different
countries as the writer of a text-book would find desirable. One class
of pathologists claims but one common disease with many varieties under
different conditions, just as the term _septicæmia_ or _blood poisoning_
has been made to designate a whole class of local and general
infections, irrespective of the particular microbes that cause them.
Others with greater precision give the disease a name according to the
causation by one particular microörganism, or by another, which may be
closely related to it in many respects, but which in successive subjects
and outbreaks, maintains its own individual characteristics as regards
morphology, cultural and staining habits, pathogenesis, etc. The
question has been rendered all the more trying, by the occasional
association in the same animal system, or in the same outbreak of two
distinct varieties of microörganisms, in place of one, giving rise of
course to modifications in the symptoms, lesions, progress, mortality,
etc.
Apart from the microörganism the whole class tends to show a close
family relationship in their pathological phenomena shown under
different conditions :
1st. Under a large dose, or specially virulent germ, in a particularly
susceptible animal, all tend to a manifestation of an acute septicæmia,
with generally diffused petechiæ of the skin, mucosæ, serosæ and
internal organs, blood extravasations, and an early high mortality.
2d. Under a smaller dose, or a less potent germ, or in a less
susceptible animal the tendency is to necrotic processes in the seat of
inoculation or the point of election of local lesions. Necrotic ulcers
are especially common in cases that survive one, two or three weeks, or
that develop in a subacute or chronic form.
3d. With a minimum dose of a germ of little potency, and in a very
resistant subject even the necrotic lesions may be absent, and there may
be suppuration only or ulceration of serosæ and joints.
The question of the primary identity, or disparity of the whole class of
germs, causing the septicæmic swine plagues, may be practically ignored
in this work; it is important rather with our present knowledge to note
the diseases associated with particular germs, or varieties of germs,
and to describe these as far as possible as independent affections. This
is as permissible as it is to describe smallpox, sheeppox, and cowpox as
distinct affections, no matter what may be the truth or falsity as to
their alleged original identity.
_Rouget_ in Europe and _Hog Cholera_ and _Swine Plague_, as the best
established types in the United States deserve primary mention, to be
followed by references to additional types which have been found to be
associated with other distinct microörganisms.
ROUGET, ROTHLAUF. RED FEVER OF SWINE. SWINE ERYSIPELAS.
Definition. Comparative immunity of sucking pigs. Disease unknown in
America. Causes: Bacillus erysipelatos suis, mature age, infection
through yards, buildings, troughs, dust, mice, rabbits, pigeons, men,
dogs, vermin, birds, butcher’s and kitchen scraps, swill, hot weather,
damp seasons, close pens, movement of swine, stockyards, fairs, public
conveyances, public highways. Symptoms: incubation three days, chill,
violet mucosæ, hyperthermia, recumbency under litter, muscular
weakness especially behind, inappetence, thirst, costiveness, later
diarrhœa, tenderness to touch, lymph glands swollen, red, blue, violet
or black discoloration of skin, cutaneous swelling and pitting.
Course: death in 12 hours to 6 days, or convalescence prompt.
Mortality 20 to 80 per cent. Lesions: congestion of capillary vessel,
blood extravasations, petechiæ, affecting cutis and subcutaneous fat,
lymph glands congested, discolored; lungs engorged; spleen enlarged,
liver and kidneys congested, petechiæ general, blood little altered.
Bacillus 1.5 μ, anærobic, easily destroyed in pens, in pork.
Pathogenesis: swine, rabbits, mice, rats, pigeons and sparrows suffer.
Rabbit germ less fatal to pigs. Immunization, advantages and
drawbacks. Technique.
_Definition._ A microbian disease of swine manifested by high fever,
great prostration and muscular weakness, a violet tint of the visible
mucosæ, red or violet discoloration of the skin in spots and patches or
universally, enlarged lymph glands, encreased size of the spleen, and
general congestion of the capillary plexus.
Contrary to the habit of hog cholera and swine plague, rouget attacks
mature swine mainly, the sucking pig showing a remarkable power of
resistance. It does not appear whether this is due to the animal (milk)
diet or to the absence of infection from feeding in the trough used by
the adult animals. Up to the present this disease has not been
recognized in America.
_Causes._ The one essential cause of rouget is the presence of the
bacillus. The other conditions are either such as predispose the animal
to receive it, for example, mature age: or they are such as favor
diffusion of the poison, such as the introduction of an infected animal,
the feeding of the healthy from the same manger with the infected, the
introduction into the manger of the feet or snout which have become
soiled with the infected manure or urine, the distribution of the
infection in dust, the introduction of the bacillus in the bodies of
mice, rabbits, or pigeons, or on the feet of those animals, of men,
dogs, birds, and vermin. We may add the distribution of infection in
dried butcher’s scraps used in pig feeding, and in uncooked scraps from
the kitchen or in hotel swill.
It has been noted that the highest mortality prevails in hot summer
weather, in damp seasons, and in narrow, confined, badly ventilated
pens. Under such circumstances the introduction of a diseased pig will
lead to the infection of most of the others in a few hours. Infection is
quite as prompt through public pens in stock yards and fairs, and in
public conveyances (cars, stock wagons, steamboats, ferry boats, etc.)
and public highways.
_Symptoms._ After a period of incubation of three days or more the
subject is seized with shivering, the limbs are hot and cold
alternately, respiration and heart beats are accelerated, the mucous
membranes assume a dark violet tint and the rectal temperature rises to
104° to 108° F. From the first the pig tends to bury itself under the
litter, and refuses to move unless absolutely forced to do so, and then
only with painful grunts, swaying and staggering limbs (especially the
hind ones), and straight drooping tail. There is inappetence, but thirst
remains, and the bowels are at first costive, the manure being covered
with a film of mucous or even streaks of blood; later they become
relaxed and diarrhœa becomes often a prominent symptom. The pig seems to
suffer and often squeals when handled, and he may give a weak, dry
cough. The external inguinal glands may often be felt perceptibly
enlarged. The red discoloration of the skin appears early and extends
and deepens to the end in fatal cases. It may be of a bright red, or of
a bluish red, violet or black. The first indications appear as spots, by
preference around the roots of the ears, on the breast and abdomen,
inside the arms and thighs, and in the perineum. These isolated spots
run together into great patches, which extend over the whole ventral
aspect of the body, and may cover the entire dorsal aspect as well. In
some instances the skin is swollen and retains an impression made by the
finger.
_Course._ The disease may reach a fatal termination in twelve hours:
more commonly it endures for forty-eight hours, and at times it will
last for four, five or six days. In the most rapidly fatal cases, the
violet discoloration of the skin may be absent or only a little marked,
while in the protracted cases it acquires its greatest extensions and
its darkest shades. In the protracted cases too the prostration becomes
extreme, the animal may find it impossible to raise himself on his hind
limbs, the diarrhœa becomes profuse, liquid and fœtid, the respiration
labored, cyanosis sets in and the temperature is reduced below the
normal standard.
In case of recovery, convalescence is usually prompt and complete,
differing in this from cases of swine plague and hog cholera. The more
favorable issue in rouget probably depends on the comparative integrity
of the intestinal mucosa and mesenteric glands, which are subject to
slow healing lesions in swine plague and hog cholera. Slow convalescence
is however not uncommon, yet in such cases, the concurrent, speedy and
complete recoveries in other animals in the same herd serve to identify
the disease as rouget.
_Mortality._ The mortality among grown hogs averages eighty per cent.
_Morbid Anatomy._ The most prominent lesion is the general congestion of
the capillary blood vessels, and the numerous minute extravasations or
petechiæ. The skin shows in the red patches a general dilatation of the
capillaries which have become at the same time elongated and tortuous,
with minute, often microscopic, ruptures and extravasations at frequent
intervals. This usually extends to the whole thickness of the cutis, and
to a considerable depth in the subcutaneous fat. Where swelling occurred
or pitting on pressure, a serous infiltration of the tissues is found.
The lymph glands are uniformly enlarged and discolored, of a dark red,
almost black, color, the congestion and extravasation being extreme in
the cortical substance, while the medullary is paler, soft and cellular.
The lungs are usually gorged with black blood suggesting death by
asphyxia. In tardy cases there may, though rarely, be centres of
broncho-pneumonia. The spleen is enlarged, with dark color and uneven
surface from rounded swellings, and is filled by a soft black, bloody
pulp. The liver is congested, the kidneys congested, enlarged and
petechiated, and the gastric and intestinal mucosa congested and
thickened, with desquamating epithelium, and swollen solitary and
agminated glands, the degree of alteration usually bearing a ratio to
the duration of the disease. The serosæ are usually extensively
petechiated and serous effusions occur into the serous cavities. The
muscular substance of the heart and the endocardium are also the seats
of petechial extravasations. Unless in some protracted cases the blood
appears to be unaltered as regards its power of taking up oxygen, or
coagulating.
_Bacillus of Rouget._ The germ of this disease is found in small numbers
only, in the blood and vascular tissues, but very abundantly in the
lymph glands, the spleen, the kidneys, and the red marrow of the bone.
It is also present in enormous quantities in the urine and the bowel
dejections, the former (urine) offering a ready means of diagnosing the
disease microscopically.
The bacillus is 1µ to 1.5µ long by 0.1µ to 0.15µ broad, is nonmotile,
and stains readily even in Gram’s solution. They occur either solitary
or in pairs tending to unite at an angle. In old artificial cultures
chains of considerable length may be formed. In the blood the bacillus
is usually found in the leucocytes, as many as 20 or more being often
present in a single cell. In the lymph networks of organs they also
invade the leucocytes but are found in free masses as well. The bacillus
is anærobic, but facultative ærobic, its preference being manifestly for
the absence of oxygen. It is non-liquefying. In gelatine cultures no
development takes place on the surface, but along the line of puncture a
delicate cloud-like branching growth takes place which extends
horizontally in parallel masses from the central puncture. This
resembles but is not quite so delicate as that formed by the bacillus of
mouse septicæmia with which it is supposed to be identical. It grows
scantily on the surface of nutrient agar or blood serum, but not at all
on bouillon, in the bottom of which, however, it forms a slight grayish
white deposit. It does not grow on potato. The bacillus sometimes shows
refrangent granules which have been supposed to be spores, but this idea
appears to be negatived by the ease with which its vitality is destroyed
by heat and disinfectants. The thermal death point is 68° C. (137° F.)
maintained for 10 minutes (Sternberg). Boulton found that it was killed
in 2 hours by mercuric chloride (1:10000), by carbolic acid solution
(1:100), and by sulphate of copper solution (1:100).
It is killed by desiccation, by quick lime and by chloride of lime. At a
temperature of 18° to 27° F. it perished in 13 days. In salted pork it
lost vitality in one month.
_Pathogenesis._ The bacillus is pathogenic to swine, rabbits, white
mice, house mice, white rats, pigeons and sparrows. Field mice, guinea
pigs and chickens are immune.
Mice and pigeons take the disease most certainly, and die in three days
to five, the whole body swarming with bacilli. Rabbits take the disease
less certainly or rapidly, inoculation in the ear causing first an
erysipelatoid inflammation and recovery with immunity often takes place.
_Immunization._ When inoculated continuously from rabbit to rabbit it
encreases its potency for that animal, which it comes to kill in 24 to
48 hours, but in the same ratio it loses its virulence for swine upon
which it can then be inoculated without danger to their life.
It was on this basis that Pasteur and Thuillier established in 1883,
their preventive inoculation for rouget. The method has been most
extensively employed in Europe, and where intelligently employed has
prevented this disease. From the laboratory at Buda-Pest alone, there
was sent out in one year material for 249,816 swine.
The objections to the method are: the danger of mistaking hog cholera
and swine plague respectively for rouget, as the rouget mitigated germ
would be in no sense protective against these; and the danger of
spreading the germs of rouget in fresh localities and thus introducing a
new plague instead of controlling and preventing an old one. In the
Baden experiments 5.4 per cent. of inoculated pigs died, and of 118
unprotected pigs exposed to them 62 per cent. contracted the disease and
one died. In France and Hungary, on the other hand, 1 to 1.45 per cent.
died of the operation, instead of 20 per cent. when the disease was
contracted in the ordinary way.
It is held that the danger lies largely in the inoculation of very young
pigs, and Nocard advises to operate only on those of four months and
upward.
The danger of spreading the germ by inoculation may be the more easily
guarded against, considering that it is very destructible by
disinfectant agents (heat, dryness, cold, chloride of lime, quick lime),
and that it does not readily survive in a locality, where it cannot find
a constant succession of victims. Yet the practice ought to be confined
to herds exposed to infection, and under special precautions, as regards
the exposure of other herds.
The _technique_ of the Pasteurian inoculation is to inject, subcutem, on
the inside of the thigh, 0.1cc. of the weaker preparation (premier
vaccin), and twelve days after a similar dose of the stronger one
(deuxieme vaccin).
This produces a mild attack of the disease from which the great majority
recover, and though they still react somewhat to a second and third
inoculation yet the disease so produced is rarely fatal.
CHOLERA SUIS; HOG CHOLERA.
Definition, Synonyms, History, Losses. Bacillus choleræ suis, 1.2–2μ.,
ærobic, biology, table of germs; accessory causes, roaming pigs,
railways, car litter and manure, boats, trucks, loading banks, chutes,
runways, stockyards, pens, fairs, watershed, butchers, dealers, etc.,
wagons, dogs, birds, vermin, insects, offal of abattoirs, butcher’s
and kitchen scraps, unburied carcasses of dead hogs, convalescent and
immune hogs, susceptibility, parasites and infection atria, putrid
food, infection from ground carried into feeding trough by snout and
feet, large herds, rapid carriage of swine for long distances.
Lesions: hæmorrhagic spots and petechiæ on skin, mucosæ and serosæ,
circumscribed capillary congestions, congestion of spleen, lymph
glands, stomach, intestines, necrotic processes. Button-like ulcers on
intestinal mucosæ. Incubation, 6 to 14 days. Symptoms: fulminant
cases. Acute Cases: dulness, anorexia, recumbency on belly, weakness,
paresis behind, thirst, tenderness of skin and abdomen, hyperthermia,
easily blown, blush on skin, dark red spots and patches, enlarged
inguinal glands, cutaneous exudate—greasy or drying black, bowels
costive, later pultaceous and finally diarrhœaic, petechiæ on mucosæ,
emaciation. Chronic Cases: symptoms more slight, but great loss of
condition. Diagnosis: from swine erysipelas, swine plague, Widal test,
table of differential symptoms. Prevention: expense of extinction
prevents effective measures; removal of accessory causes, comfort,
air, light, food, salt, powdered soaps, mouldy bread, cotton seed,
space, green food, precautions against introduction of bacillus,
special shipping provisions for fat hogs, exclusion of stock hogs from
infected localities, precautions by purchasers. Immunization,
Disinfection. Certificates. Extinction in herds and districts.
Treatment: chronic cases, food, antiseptic medication, antithermics
stimulants, tonics. Serum therapy, method, merits, demerits.
_Definition._ A contagious bacteridian disease of swine, acute or
subacute, and characterized by hyperthermia and other febrile
disorders,—congestion, exudation, ecchymosis and necrotic ulceration of
the intestinal mucosa and of that of the stomach and of other parts,—by
a profuse foul, liquid diarrhœa, by enlargement of the lymph glands with
congestion and blood extravasation,—by effaceable blotches, and petechiæ
(ineffaceable) of the skin, snout and visible mucosæ, with a tendency to
necrotic changes—less frequently by pulmonary congestions, and
degeneration,—and by a high mortality.
_Synonyms._ The earlier designations were mostly drawn from the red or
black discoloration of the skin and mucosæ and applied indiscriminately
to the other forms of hæmorrhagic septicæmia which we now differentiate
as erysipelas (rouget, Rothlauf) and swine plague. They included
_measles_, _erysipelas_, _scarlatina_, _red soldier_, _purples_, _blue
sickness_, _carbuncular fever_, etc. Others basing their nomenclature on
the prominent intestinal lesions, etc., designated it _typhoid fever_,
_pig typhoid_, _typhus_, _carbuncular gastro-enteritis_,
_pneumo-enteritis_, and _diphtheria_. Even in Europe while the _pig
erysipelas_ (_rouget_, _Rothlauf_) is now recognized as a distinct
disease there is no clear distinction made between _hog cholera_ and
_swine plague_. In England we find these more or less confounded under
the names of _swine fever_, _swine plague_ and _hog cholera_, and on the
continent of Europe under those of _schweineseuche_ and _schweinepest_,
or _pneumo-enteritis infectieuses_. Differences in different epizoötics
or outbreaks are recognized, and the field is left open for the future
identification of different forms of this common group of swine fevers,
but the existence of constant bacteriological distinctions are not
always insisted on, as we do in the United States in the case of the two
great leading types _swine plague_ and _hog cholera_.
_History._ Definite history of this disease may be said to begin with
the discovery and demonstration of the actively motile hog cholera
bacillus by the U. S. Bureau of Animal Industry in 1885. Yet in the
history of animal plagues, even in early times, deadly epizoötics are
described which undoubtedly represented one or other of the contagious
affections of modern times. Among the more definite may be named a
destructive gastro-enteritis (magen seuche) in Germany in 1817, a
pleuro-pneumonia in France and Bavaria in 1821, a cholera with blotching
of the skin (morbus niger) in Ireland, and an erysipelas in pigs in
France and Switzerland in 1836, and in Ohio in 1833, there was a fatal
affection afterward recognized as hog cholera. Writers conjecture that
it was imported into America from Europe in improved pigs, and from one
European country to another in the same way, but we have no absolute
proof of times and shipments and their immediate effects, so that these
theories are but more or less reasonable deductions from the familiar
extensions of the disease in more recent cases. Under the great
commercial activity of the latter half of the 19th century, the active
movements of animals by canal, steamboat and rail, and the massing
together in one market of many animals drawn from widely different
sources, hog cholera has made extraordinary extensions on both sides of
the Atlantic, until Friedberger and Fröhner pronounce the schweineseuche
and schweinepest the most widely disseminated and dangerous of swine
epizoötics, and Dr. Salmon estimates the losses in the United States at
$10,000,000 to $25,000,000, per annum.
_Bacteriology._ Prior to 1885 bacteria had been found in the different
outbreaks of contagious fevers in swine, and the bacillus of swine
erysipelas had been demonstrated in 1882, but it was only two years
later (1884) that the motile bacillus choleræ suis was first described
by Klein, and in 1885 that Salmon and Smith demonstrated it as the
essential cause of the disease, together with its biological and
cultural peculiarities.
It is a short bacillus, 1.2 to 2μ × 0.5 to 0.8μ, but varying
considerably in size according to the stage of its growth and the genera
of animal or culture medium in which it is grown. It has rounded ends
and is usually in pairs connected by an invisible band. It stains
promptly in all the aqueous aniline colors, but loses the stain in a
solution of iodine (Gram’s). Prolonged exposure of artificial cultures
produces an uniform stain, while a transient exposure, and especially of
bacilli obtained from the tissues, stains them most deeply at the ends
(polar) and periphery, while the centre remains somewhat clear. This is
less marked than in the bacillus of swine plague, yet serves to show the
relation between this microbe and the colon group.
It is _ærobic_ (facultative anærobic), non-liquefying, and, in fluids,
very actively motile, the movements lasting for months in preserved
specimens (Smith). It grows luxuriantly in various culture media, and
especially in alkaline ones, at the room temperature, and most actively
at 85° to 100° F. It may grow as low as 60° to 70° F. and as high as
104°. (Swine plague bacillus grows at 55.4°).
On _peptonized gelatine_ the surface colonies are usually round and
flattened, those in its substance globular and smaller, and those at the
bottom expanded next the glass and rising in the center into the
gelatine like a knob. At 48 hours they appear as opaque whitish points
and slowly increase to ½ to 2 mm. They may be brown by transmitted
light, the depth of color increasing with age. On _agar_ the colonies
are grayish, shining and translucent and may reach the size of 4 to 6
mm. On _potato_ (alkaline) a straw yellow film is formed, darkening with
growth. In _bouillon_ a turbidity appears in 24 hours, and in 1 or 2
weeks a precipitate and surface film.
The bacillus is usually larger in the gelatine and smaller in the
bouillon than it is in the tissues. It seems to produce neither phenol
nor indol.
Its behavior with sugars is significant. It ferments glucose producing
acid and gas; does not ferment saccharose nor lactose, but turns the
saccharose solution alkaline (no gas). In bouillon containing muscle
glucose, it may without additional glucose form a little gas. The swine
plague bacillus ferments saccharose producing acids but no gas: it
ferments neither glucose nor lactose but turns the former acid.
Milk is neither coagulated nor soured by the hog cholera bacillus, but
in 3 to 4 weeks it undergoes a change, becoming saponified.
Cultures have no special nor offensive odor. Some varieties in close
tubes may cause a faint acid odor.
Oxygen is not essential to the success of a culture. The colonies form
as promptly and as large in the depths of gelatine, or in a vacuum, as
if in free air.
The following table will serve to show differences between the hog
cholera bacilli, and related pathogenic microbes:
=Hog Cholera.= =McFadyean’s.= =Swine Plague.=
B. Choleræ Suis Swine Fever B. B. Pestis Suis
1.2 to 2μ × 5 to 0.8μ 2 to 2μ × 0.6μ 0.8 to 1.5μ × 0.6 to
0.8μ
Ends rounded Ends rounded Ends rounded
Involution forms Involution forms
Actively motile in Actively motile Nonmotile
liquids
Flagella No Flagella
Stains throughout, Polar or uniform faint From fresh organs polar
lighter in center stain stain, from old
cultures uniform
Bleaches in Gram’s (I) Bleaches in Gram’s (I) Bleaches in Gram’s (I)
Solu Solu Solu
Ærobic (Fac. Anærobic) Ærobic Ærobic, (Fac. Anærobic)
Vigorous growth in Slight growth in Weak growth in alkaline
alkaline nutrient alkaline nutrient nutrient fluids
fluids fluids
Active growth on potato No growth on potato On potato at 37° C. a
yellowish, becoming slight, thin gray,
darker waxy layer
On gelatine, small, On gelatine light On gelatine feeble
round brownish bluish colonies growth or none
colonies shading off
insensibly at edges
Nonliquefying Nonliquefying Nonliquefying
On agar conical On agar slight, On agar, grayish
colonies, grayish, transparent, almost translucent, or
white, semi- invisible growth brown, knobbed,
translucent shining waving edges
In milk grows freely, Grows in milk, no clot Grows in milk, no acid,
no acid, no clot: no clot
Saponifies in 3 or 4
weeks
Forms no indol in Forms no indol in
pancreatic bouillon pancreatic bouillon
Ferments glucose, Does not ferment
forming acid and gas glucose, forms acid,
no gas
Lactose not fermented Lactose not fermented
Saccharose not Saccharose fermented,
fermented; forms acid, no gas
alkalinity; no gas
Thermal death point Thermal death point 58° Thermal death point
(moist) 58° C. in 15 C. in 10 minutes (moist) 58° C. in 7
minutes minutes
Desiccated it dies Dies quickly, if dried Dies in 3 days if dried
according to bulk in at body temperature
7 to 49 days
Dies in water in 3 to 4 Dies in water in 10 to
months 15 days
Dies in soil in 2 to 3 Dies in soil in 4 to 6
months days
Pathogenic to swine, Pathogenic to swine and Pathogenic to swine,
rabbits, guinea pigs, rabbits hens, pigeons,
mice, pigeons pheasants, sparrows,
mice, rabbits,
cattle, deer,
guineapigs, etc.
Guinea pigs immune
=Swine Erysipelas.= =B. Coli Commune.= =Typhoid Fever.=
B. of S. Erysipelas B. Typhi Abdominalis
1 to 1.5µ × 0.1 to 0.2µ 2 to 3µ × 0.4 to 0.6µ 1 to 3µ × 0.6 to 0.8µ
Ends rounded Ends rounded Ends rounded
Involution forms Involution forms
Nonmotile in liquids Nonmotile or very Motile
slightly so
No flagella No flagella Flagella
Stains readily and Stains uniformly or Stains uniformly
uniformly polar (points clear)
Stains in Gram’s (1) Bleaches in Gram’s
Solu
Anærobic (F. Ærobic) Ærobic (F. Anærobic) Ærobic (F. Anærobic)
Active growth in common Grows well in usual Grows well in usual
nutrient liquids at nutrient liquids, nutrient liquids
37° C. even if acid
Usually no growth on Yellowish thick white Grows on potato;
potato; variable growth on potato transparent
glistening surface
In gelatine In gelatine amber On gelatine clear
stab-culture delicate colonies, becoming colonies with
feathery branching brown; may be bubbles radiating and
growth of gas encircling lines
Nonliquefying Nonliquefying Nonliquefying
Grows in milk; Acidifies and clots Acidifies milk growing
acidifies, often milk in 8 to 10 days freely
coagulates it
Thermal death point Thermal death point Thermal death point
(moist) 58° C. in 10 (moist) 60° C. in 10 (moist) 56° C. in 10
minutes minutes minutes
Loses virulence rapidly
when dried
Dies in water in 18 to
20 days
Lives and even Lives and grows in
multiplies in rich fæces
soils, manure, etc.
Loses virulence slowly
in light and air
Pathogenic to swine,
pigeons, sparrows,
rabbits, white and
house mice, white
rats
Guinea pigs, field mice
and hens immune
=Hog Cholera.= =McFadyean’s.= =Swine Plague.=
Hen or pigeon has Hen or pigeon dies in
slough where 48 hours, after
inoculated, diarrhœa, drowsiness, drooping
ruffled plumage, wings, sunken head,
somnolence ruffled plumage,
liquid stools, soft
black comb and
wattles, prostration
Rabbits getting 0.1cc. Rabbits getting 0.5 to Rabbits getting 0.01cc.
virulent culture 1cc. culture subcutem culture subcutem die
subcutem die in 5 to had tumor like walnut in 16 to 20 hours,
7 days with enlarged but recovered with inflamed serosæ
spleen and necrotic and lung; Petechiæ
liver foci
Weaker culture kills in Weak cultures kill in 4
10 to 20 days with to 10 days, with
enlarged spleen, or inflamed serosæ and
recovery ensues suppuration
Guinea pigs die in 7 to Not pathogenic to Guinea pigs die in 1 to
12 days Guinea-pig 4 days
Swine inoculated Swine inoculated have
subcutem have often local lesions only,
local lesions and only exceptionally
bacilli, also in fatal
lymph glands, only
exceptionally fatal
Ingestion of virulent Ingestion of 30cc. by Ingestion of virulent
cultures by fasting pigs proved always cultures by pigs is
pig causes bowel fatal usually harmless
lesions and death
Intravenous inoculation Intravenous inoculation
in pig causes causes septicæmia and
septicæmic lesions death in 1 or 2 days
and death, or chronic
diseases and typical
bowel ulcers
Intrapulmonary
infection causes
pleuro-pneumonia
Swine erysipelas kills inoculated pigeon in 3 to 8 days, and rabbit in
4 to 8 days.
_Accessory Causes._ These are especially those conditions which favor
the transmission of the germ from animal to animal. They include the
reprehensible habit of allowing swine to run at large so that herd
mingles with herd; the freedom to wander along the lines of railroad by
which hogs are carried, and where the infected excretions fall on the
ground; the scattering of infected litter or manure from a car or boat;
the use of the same cars, boats or trucks for the conveyance of infected
and sound pigs in succession, without intermediate disinfection; the use
of the same loading banks, chutes, runways, yards, pens and feeding and
watering troughs by strange pigs from all sources in succession, without
constant disinfection; the purchase of stock swine at public markets;
the return of swine from public fairs and exhibitions; the feeding and
watering of pigs on the line of streams that have drained pig pens or
pastures higher up; the use for pigs of premises that have harbored
infected ones at an earlier (even distant) date; the supply of food or
litter from barns where pigs have recently died; the admission to the
pens or yards of butchers, dealers or others who are likely to carry
infection on their persons; the admission even of wagons, dogs or other
animals, including birds, tame and wild, which are liable to carry
infection. Of all birds the buzzard is the most to be shunned as having
presumably just come from infected carrion, but barnyard fowl and small
birds that feed from the same trough with the pig are to be feared as
well. The same remark applies to rats and mice, squirrels, skunks,
woodchucks and rabbits which may easily carry the infection on their
paws. If the infection is near, flies and other insects, in the warm
season, will convey it for some distance from herd to herd. A common
cause is the feeding of swine about abattoirs where they devour the
offal and waste in a raw condition. Another is the feeding of boarding
house, hotel or other kitchen slops, raw, or without the most exhaustive
precautions in the way of cooking. Many outbreaks can be traced in this
way to the consumption by the animals of the products of infected swine.
Some indeed are fostered by the utter neglect of the parties in charge
of an infected herd, in leaving the infected carcasses exposed so that
they are eaten by wandering hogs, or portions are carried away by
buzzards, carrion crows, dogs and other animals. In some cases a strong
wind will carry the infection on dust, straw or other light object into
sound herds at a distance. The introduction into a hitherto healthy herd
of an apparently sound pig may be the occasion of a deadly outbreak. The
strange new pig may have already had the disease, and in a condition of
immunity, may without hurt to itself, carry the germ which becomes so
fatal to the susceptible.
This susceptibility is one of the most important factors. It may be
inherent in a given family or strain of blood. It may be enhanced by a
constitutional weakness, engendered by too close breeding, by breeding
from the young and immature, or from the old and worn out. It may be
favored by a general debility from starvation, faulty or injudicious
feeding, as exclusive feeding on corn (maize), an unbalanced ration,
feeding cotton seed, irregular feeding, etc. It may result from
parasitism, as round worms in the lungs, bowels, muscles, fat, kidneys
or liver, from trichinosis, from cysticerci, echinococci, or from
distomatosis. These not only lessen the force of constitutional and
phagocytic resistance, but they also in many cases open the way for the
entrance of the microbe by the wounds which they inflict. Perhaps
nothing operates more effectively in this way than the attacks of other
pathogenic microbes. The treatment of the domestic hog is often such
that it would almost appear as if it were designed to destroy health and
vitality. He is used to clear up the soiled and spoiled provender which
has been rejected by other animals. Decayed vegetables and flesh of all
kinds, which is no longer fit for other use, is supposed to be good for
him and is furnished raw. Worse still, this is conveyed in barrels that
are never washed, but are sent for each new supply reeking with
abominations which render them a nuisance on the highway. It is left
standing till wanted in these barrels, or in still larger receptacles,
which are never emptied nor cleaned, but are allowed in the hottest
weather, to continue a hotbed of the foulest fermentations. On a smaller
scale the kitchen swill barrel becomes a similar centre of
decomposition. Even at the creamery and cheese factory the surplus or
waste products often remain in a common tank breeding larvæ, toxins and
ptomaines, before they are fed to the hogs. In the hog pen, or yard,
corn in the ear is thrown on the ground, already filthy with the solid
and liquid excretions and is eaten with the rotting, if not infecting,
filth in which it has been rolled. From grubbing in this filth with his
snout, the pig plunges the latter in the liquid food in his trough and
too often he gets his feet into the food as well, and further charges it
with the injurious ferments. Again the kitchen swill is liable to
contain various inorganic poisons and notably the carbonates and
bicarbonates of potash and soda which are used to excess in the form of
_powdered soaps_ and, as shown by experiment, are deadly poisons to
pigs.
The gastro-intestinal disorders caused by these poisons; (it may be
botulism from stale or decomposing flesh, fish or fowl, the poisoning by
mouldy bread or musty grain, or meal, or by the toxins of the many and
varied saprophytic fermentations), often prove as deadly as outbreaks of
genuine hog cholera, and are habitually mistaken for them. They do not,
however, as a rule extend beyond the particular herd which has been
exposed to the faulty management, and introduce no risk of a general
spreading infection. The careless owner suffers and adjacent herds
escape, unless exposed to similar causes. But if the hog cholera germ is
present these pave the way for its destructive advance and tend to
enhance the mortality. It may even be that the combination of the two
factors is a condition of the eruption of a severe attack. The faulty
feeding or food or poison by itself could be resisted, and the
comparatively non-virulent hog cholera bacillus might have been
resisted, but with the weakened system and digestive apparatus, the
microbe finds a specially inviting field in which it can multiply
destructively, and where it can gather a virulence which will enable it
to invade and sweep away herd after herd in a deadly epizoötic.
I may add, as a prominent factor in the great modern extensions of hog
cholera, the habitual aggregation of swine in large herds. This with the
rapid steam transit of modern times, and the great aggregations of hogs
in one common market, probably contributes more than anything else to
the extraordinary diffusion of the infection. By accident, purchase or
otherwise, a large herd becomes infected, and the owner, knowing that
delay is ruin, at once ships the apparently healthy animals to market;
these infect anything they or their excretions come in contact with; if
sold in smaller lots they carry infection into every locality where they
go, and along the route; if sold for slaughter, they still diffuse
infection through the herds that receive their butcher and kitchen
trimmings.
Finally other domestic animals may bring in an infection which becomes
manifested by symptoms similar to those of hog cholera, and which if
really different, yet serves to pave the way for such an outbreak.
Galtier’s remarkable experience with a _pneumo-enteritis_ in sheep,
introduced into five separate flocks by infected pigs from the same
market, is significant in this respect. It is further significant that
the hog cholera bacillus is a very protean microbe. Th. Smith, to whom
we owe more than to any one else the identification of the germ, gives
seven varieties, which showed well-marked distinctions in their
morphology, in their modes of growth on culture media, in the amount of
gas they respectively produced in a glucose bouillon, or in their
pathogenesis for rabbits. One of these modified germs which has largely
parted with its virulence for pigs and some other animals, may under
specially favorable conditions, resume its former potency and proceed on
a new career of infection.
_Lesions in the Acute or Septicæmic Form._ The skin and subcutaneous fat
are the seats of diffuse blotches or spots of a deep red varying from
dark purple to light red, confined it may be to the inner sides of the
arms and thighs the belly, the ears, eyelids, and muzzle, or it may be
all but uniformly diffused over the body. When pressed so as to expel
the blood, the greater part of the surface may be momentarily whitened,
but red points remain representing the minute extravasations. Under the
microscope the red points show tortuous and enlarged capillaries with
here and there a rupture and minute clot. The visible mucosæ may show
similar petechiæ, as may also the serosæ of the chest, cranium and
abdomen. In the latter blood extravasations are liable to be more
extensive. The spleen and lymph glands (particularly those of the bowels
and omentum, the sublumbar and subdorsal regions) are usually enlarged,
gorged with blood and softened. Many of the lymph glands may escape, and
in others the congestion is largely confined to the cortical portion.
The lungs may show petechiæ and even extensive hæmorrhages into their
substance. The kidneys may show petechiæ in the glomeruli, the medullary
substance, the papillæ or the pelvic mucosa, or there may be larger
circumscribed hæmorrhages.
The stomach in its greater curvature especially is usually deeply
congested and petechiated, with small submucous extravasations, and
these conditions are liable to be still more marked in the small
intestines and especially in the large, which may have a dark red or
port wine hue. Blood may be present in clots among the contents.
Necrotic ulcers are absent.
_Lesions in the Protracted and Chronic Forms._ The lesions of the skin
are usually less extensive than in the acute type, and may be almost
entirely absent. The lymph glands are enlarged and congested, though the
discoloration may be largely confined to the cortical layer. The spleen
is as a rule normal in size. The liver is firm, but it may show
softening of the secreting acini and encrease of the fibrous framework.
Petechiæ or circumscribed hæmorrhages may or may not be present on or
under the serosæ or in the tissues.
The characteristic lesions belong to the gastric-intestinal organs.
Congestions and ulcers may be found on the gastric mucosa, on that of
the small intestine, and rectum, but they are above all common on the
ileocæcal valve, cæcum and first half of the colon. In the earlier
stages of these lesions the mucosa and submucosa are the seat of a
congestion and exudation, but later the round button-like ulcer usually
stands out prominently with its necrotic centre dirty white, brown or
black, and composed of superposed layers, the whole resting on a
congested and thickened submucosa. This contains small round and giant
cells and may show considerable encrease in connective tissue. The
ulcers may be seated on the agminated or solitary glands but do not show
the same predilection for these parts which is seen in typhoid fever.
_Incubation._ This varies according to the dose and susceptibility from
two or three to as many as thirty days. With the short incubation the
disease tends to assume its most acute and deadly type, while the
prolonged incubation bespeaks a milder form. During ordinary outbreaks
from six to fourteen days represent the average interval between
exposure and the onset of active symptoms. During the extreme heats of
summer and the excessive cold of midwinter in our northern states
incubation tends to be shortened.
_Symptoms in Fulminant Type._ In violent outbreaks some pigs are found
dead without observed preliminary symptoms, and have been set down as
fulminant examples of the disease. When these occur during very hot
weather, in open yards or fields, there is reason to believe that
insolation, acting on a system rendered specially susceptible by the
toxic fever, has much to do with the early death. Though seldom observed
during life, it has been said that such cases, show extreme dulness,
prostration, stupor, weakness, unsteady gait, thirst, hyperthermia,
persistent recumbency, and at times red blotching of the skin and even
convulsions.
_Symptoms in Acute Type._ In contrast with erysipelas these may advance
slowly and insidiously, there is a lack of the customary life and
vivacity, the tail droops, appetite is impaired, the pig creeps under
the litter and lies there, preferably on its belly, a great part of its
time, there may even be tremors suggestive of slight chill, when moved
it shows weakness, may stagger, or it may have difficulty in rising on
its hind limbs and there is encreased thirst and heat of the skin. Even
in the absence of shivering or chill, the skin is usually tender to the
touch, calling out plaintive grunting or squealing, and the same is
often true of manipulation of the belly. The temperature is raised, yet
this must be compared with the previous temperature under the conditions
in which the pig has been kept. That may have been anywhere from 100° F.
in a confined, cold, draughty pen, to 104° F. in a warm, dry pen and
with plenty of exercise. In hog cholera it may rise 1° to 3°. The
patient is breathless under exertion, the circulation is accelerated and
the mucosæ congested.
Sooner or later, (usually by the second or third day) the skin shows an
erythematous blush, especially on the ears, breast, belly and inner
sides of the thighs and forearms, in greater part effaceable by pressure
but promptly reappearing and complicated by darker spots of
extravasation which retain their color under pressure. The blush may
appear in spots of ⅒ to ⅓ inch in diameter, or it may cover the region,
or indeed the whole body uniformly. At first of a brighter red it tends
to pass in succession through the different shades of purple and violet.
Appetite becomes more and more impaired, and in exceptional cases
vomiting may occur, but often the pig will drink liquid food to the
last. A marked symptom is the enlargement of the inguinal lymph glands,
which may even be tender. An early symptom is watering of the eyes, and
later a muco-purulent exudate may form, and drying, gum the lids
together. An abundant exudate appears on the skin as the disease
advances, most abundantly about the eyelids, roots of the ears, axillæ
and groins, but often covering the whole body, forming a foul greasy
inunction, and later a black scaly covering.
The bowels may be costive at first, with fæces, firm, moulded, and
covered with mucous, and this may continue to the end. In most cases,
however, about the second or third day they become soft, pultaceous and
finally liquid, profuse, fœtid, and mixed with abundance of mucous or
even blood. The color varies, they may be whitish, yellowish (on maize
diet), red, or black (on swill).
Petechiæ usually form on the mucosæ and small sloughs and ulcers may be
found on the lips, tongue or elsewhere on the buccal mucosa.
A cough may be present but is by no means a marked symptom.
Emaciation advances with great rapidity, the patient arches the back,
tucks up the abdomen, moves weakly and unsteadily or is unable to rise,
and dies in one or several weeks, it may be quietly or in a state of
coma, but usually without convulsions.
_Symptoms in Subacute and Chronic Forms._ In this type the disease may
be obscure, and even overlooked, so that infected animals carry the
microörganism into fresh herds, without rousing a suspicion as to its
true source. In other cases, after a slow and progressive development,
it takes on such a distinct pathognomonic character that its diagnosis
becomes more easy.
In the slightest cases there may be only a capricious or irregular
appetite, drooping tail, enlarged inguinal glands, and a progressive
emaciation, with loss of life and strength and occasional irregularity
of the bowels. The greasy exudation on the skin and black scaly
encrustation is not uncommon. Such patients usually survive but they are
liable to prove unthrifty and unprofitable.
In other cases the pig becomes dull and listless, leaves its fellows,
creeps and lies much under the litter, has impaired or irregular
appetite, some costiveness followed by a fœtid diarrhœa, abdominal
tenderness, enlarged inguinal glands, progressive emaciation, arched
loins, hollow flanks, skin exudation, and oftentimes in the end
erythematous eruption with petechiæ and black scaly exudate on the skin.
It is in these protracted cases especially that the formation and
detachment of the necrotic intestinal sloughs take place and these may
pass in the fæces as flattened rounded masses or more extensive plaques.
Necrotic ulcers are also liable to show on the buccal mucous membrane or
skin. The patient may finally die of colliquative diarrhœa, of
exhaustion and marasmus, in a state of coma as in the more acute cases.
The mortality may be high and the survivors are liable to prove
unthrifty and unprofitable.
_Diagnosis._ With a group of plagues in swine bearing a strong family
resemblance, and maintained by microörganisms, which, though maintaining
distinct characters, yet show so much in common that it seems not
impossible that they may have been originally derived from a common
ancestor, and in face of the not infrequent complication of two of these
microbes in one patient, it becomes a task of great difficulty to
diagnose at once the particular outbreak that is met with in the field.
In some outbreaks, however, the differential features are clear enough
to allow the veterinarian to pronounce at once on the true nature of the
disease. In others he must withhold his diagnosis until he can put it to
the test of microscopic examination, bacteriological culture, the Widal
test, or inoculation.
_Hog Cholera_ may be decided upon, when upon wholesome food, in healthy
environment, without any change of food, and in six to fourteen days
after the introduction of pigs from outside, or the arrival of strange
pigs in the near vicinity, or higher up on the watershed, sickness
appears tardily, taking one or two daily, with or without a sudden
hyperthermia, petechiæ on nose, eyes, belly, axilla, or groin, a general
soreness of the skin and abdomen, stiffness or weakness, hiding much
under the litter, enlargement of the lymph glands, costiveness with dark
red rectum and glazed dung, followed by a profuse, watery, fœtid,
bloody, black or yellow diarrhœa, and death mostly after one or two
weeks or more. The absence of cough, and the presence of ulcers bearing
necrotic sloughs on the lips, mouth or skin, and above all the presence
of the button-like necrotic ulcers on the mucosæ of the cæcum, colon or
ileum may be accepted as conclusive evidence on this point. So also its
prompt fatality to rodents, but not to pigeons.
Swine erysipelas has a much shorter incubation, more rapid and violent
onset, deeper, darker congestion of visible mucosæ, more extensive
petechiæ of skin, mucosæ, serosæ, and tissues generally, a comparative
absence of inflammatory and necrotic lesions of bowels, a very early and
high mortality in swine, rabbits and pigeons, and a harmlessness toward
the inoculated Guinea pig.
_Swine plague_ also shows a shorter incubation, a speedy elevation of
temperature, more mucous congestion, less indication of abdominal
tenderness or of diarrhœa, more cough, dyspnœa, wheezing and objective
symptoms of pulmonary consolidation, less congestion or engorgement of
the spleen, or ulceration of the bowels, and finally is very much more
fatal to pigeons, and spares neither rabbits nor Guinea pigs.
_Widal test._ The cessation of movements and the agglutination of the
bacilli of hog cholera, noted by Dawson, is a valuable test, but as in
the case of typhoid fever in man is not to be implicitly relied on in
all cases. Some of the forms of bacillus coli commune and other allied
microbes act in a similar way. It necessitates the maintenance of fresh
(24 hours) active, artificial, agar cultures of the hog cholera bacillus
and is thus virtually reserved for the bacteriological laboratory. A
drop of blood is drawn from the suspected pig smeared very thinly on the
cover glass and about 10 times the amount of sterile water added. Then
the smallest possible addition of the agar culture of the bacillus is
made. Immediately, or in ½ hour the bacilli cease their active motility
and mass together in clumps in which they can be seen individually clear
and distinct but absolutely still and crossing each other in all
directions forming a kind of network. A few isolated bacilli remaining
in the intervals between the clumps and even showing a slight motility
are not to be considered as invalidating the reaction.
The table on the next page will serve to place in contrast the
differential phenomena of the diseases caused by bacilli of hog cholera,
swine plague and swine erysipelas in uncomplicated infections.
_Prevention._ As in all other contagious diseases, effective preventive
measures imply the destruction of the pathogenic germ and all sanitary
measures should aim at the early and final extinction of this organism
and its subsequent exclusion from the country. This, however, entails an
outlay and governmental control which it seems idle to expect in the
very near future so that palliative measures, and those looking toward
success over limited areas must still be resorted to. It should be here
distinctly stated, however, that the extinction of a plague, though
often the most expensive at the start, is in the end by far the most
economical resort.
_Removal of accessory causes._ The _health_ and _vigor_ of the animal
exposed is not without its influence in case of attempted invasion by a
virus of diminished potency.
DIFFERENTIAL SYMPTOMS AND PHENOMENA.
=Hog Cholera.= =Swine Plague.= =Rouget.=
Incubation 6 days + Incubation 1 day to + Incubation 1 day
Mucosæ not necessarily Mucosæ congested Mucosæ deeply
congested congested, dark red,
violet
Petechiæ on snout, Petechiæ on snout, Petechiæ extensive
eyes, mouth, etc. eyes, mouth, etc.
Necrotic ulcers on Necrotic ulcers rare Necrotic ulcers less
snout, mouth, skin, frequent
etc.
Furred tongue, vomiting Vomiting less likely Vomiting not uncommon
common
Temperature high in Temperature high in Temperature very high,
acute cases (104° to acute cases 107° to 109°
108°)
Lies on belly mostly, May lie on side May lie on side
abdomen hot, tender
Moves stiffly, feebly, Stiff but less so, Stiff, weak, paraplegic
unsteadily with Paretic.
grunting, may be
paraplegic
Bowels 1st costive, Diarrhœa less marked, Diarrhœa usually sets
fæces molded, glazed; may be entirely in
2d or 3d day, or absent
before death,
diarrhœa, profuse,
watery, fœtid,
bloody, black on
slops,—yellow on corn
(maize)
Everted anus dark red Anus may not be deep Anus may be less red,
red, less everted less everted
Cough often present, Cough, hard, frequent; Cough absent, save in
hurried breathing wheezing breathing. latter stages with
Auscultation and pulmonary
percussion may show consolidation
lung consolidation
toward lower border.
May bleed from nose
Spleen slightly Spleen usually little Spleen enlarged, soft,
enlarged altered grumous
When death is deferred Necrotic, button-like Necrotic ulcers on
1 to 2 weeks, ulcers on cæcum bowels rare
necrotic button-like rarely marked
ulcers on ilio-cæcal
valve, cæcum, colon,
or ileum
Lobar pneumonia Lobar or lobular Pulmonary and enteric
uncommon pneumonia a marked inflammation rare
lesion
Kills rabbits (5 to 7 Kills rabbits (1 to 12 Kills pigeon (3 to 8
days) and Guinea pigs days), Guinea pigs (1 days), rabbit (4 to 8
(7 to 12 days). to 4 days), pigeon days), Guinea pig
Pigeons sicken but (48 hours) resists
survive
Blood serum of hog
cholera patient
causes agglutination
of bacilli in
cultures; (not
constant, occurs with
other bacilli)
_Dry, warm beds_ with plenty of _air_ and _light_ are essential to
vigorous health and the usual damp, filthy, dark pens are depressors of
the vital forces and virtually invitations to hog cholera as to other
diseases. The close packing of swine under manure or under rotten piles
of straw where they often suffocate each other is to be carefully
guarded against. It is a sufficient commentary on this to say that for
every kilogramme of its body weight, the horse consumes daily 13,272
grammes oxygen, the cow, 11,040 grammes, and the pig, 29,698 grammes.
This is in perfect keeping with the high normal temperature maintained
by the latter animal. In the interest of health the pig requires twice
the breathing space for every 100 lbs. of his weight that is demanded by
either ox or horse. What violence is done to this demand of nature in
the daily treatment of the hog!
_Fresh, sound, wholesome food_ is no less a _desideratum_. Yet the
omnivorous pig is condemned to become the scavenger for the kitchen, the
stable, the feeding pen, the slaughter house, the creamery, the sugar
works, the brewery and even the rendering works. Whatever is considered
unfit for human use is thrown into a swill barrel, and as this is never
emptied it becomes the field of endless decompositions with the
production of the most varied toxins, ptomaines and enzymes. Many of
these chemical toxic products cause gastro-intestinal inflammation with
vomiting, bloody diarrhœa and tenesmus, and derangement of the nervous
and other functions as manifested in weakness, staggering, dulness,
stupor, etc. Death may follow in a few hours and the cases are set down
as acute forms of hog cholera, rather than the simple poisoning that
they are. All the same they pave the way for the attack of hog cholera
if its germ is present even in a form of little potency. All such foods
should, on the contrary, be fed fresh and after boiling.
_Salt_ in excess, the _brine of salt meats or fish_ (containing toxins),
the _powdered soaps_ used in kitchens and added to swill, _mouldy bread,
cotton seed meal_ fed in any considerable proportion in the food, and
even an exclusive diet of _corn_ (maize), must be guarded against.
The crowding of many pigs in a small yard where they root continually
in each others’ droppings and their own, should be avoided. Individual
pens, or pens holding two or three only and kept clean are to be
preferred, and still more a wide grassy range where they may escape
from their own filth. The long feeding trough should be discarded in
favor of one into which the pig can introduce his nose only. The nose
itself will introduce filth ferments, but, where there are not
specific-plague-germs, it is the quantity that tells and the exclusion
of the foul feet is an important consideration. To these various
poisonous products of saprophytic ferments it often happens that the
older swine have by continuous exposure, acquired a comparative
immunity, while the young growing pigs perish in large numbers.
Feeding pigs in confinement, without green or animal food is very liable
to induce costiveness and indigestion which pave the way for the inroad
of the hog-cholera germ. A certain allowance of green food, slops, and,
above all, a variety of food constituting a well-balanced ration are
always desirable.
Again, the constitution of the pig is often material. On the continent
of Europe it is the high bred English pigs that suffer most, and in all
cases a lack of the rugged vigor attained through an active, open air
life lays the system more open to a violent attack. Too close breeding
must be similarly avoided, together with breeding from the immature, the
weak and the debilitated. In this connection it is important to rid the
herd of parasitisms which not only weaken the system and lessen the
power of resistance, but by the bites or the inflammation induced, open
channels for the introduction of the hog-cholera bacillus.
_Prevent the Introduction of the Bacillus._ The above precautions are
important in obviating infection and favoring a milder type of the
disease when the germ has been introduced, but they are but palliatives
at best, and will not hinder the development of a plague in the presence
of an active and potent virus. Adopted alone they are worse than useless
as a means of extinction of the germ: they tend to preserve it. The
exclusion of the hog-cholera germ is the one essential thing in
prevention and whatever comes short of this must have at best but a
partial effect.
Avoid pens, pastures or streams that drain swine enclosures higher up.
Discard all provender or litter that has come in contact with other pigs
or their products. Allow no visitors to the herd such as butchers,
dealers, drovers, that have habitually come in contact with other herds.
Exclude as far as possible domestic animals (dogs, sheep, cattle, fowls,
pigeons), and even vehicles coming from places where hogs are kept. Wild
animals such as buzzards, and other carrion feeders, must be especially
guarded against. Wild rabbits and hares (jack rabbits), skunks, wood
chucks, minks, rats and mice should be exterminated. Small birds and
flies are difficult to deal with but the latter may be destroyed by
acids, copperas, or sulphites on the manure and the former may even be
exterminated when hog-cholera exists in the vicinity.
Sows should not be sent from herd to herd for service or otherwise, and
any swine that have been hired out, or sent to an exhibition, and all
that are acquired in any manner, should, on arrival, be excluded from
the herd and held in quarantine, well apart for three or four weeks, and
finally washed with carbolic acid soap before they are admitted.
The pestilential prevalence of hog cholera and other swine plagues
to-day is largely the result of the great industrial and commercial
activity of modern times. In America the disease was comparatively
unknown until after 1830, and in Europe even later. But with the advent
of steamboat and railroad, the few pigs raised in separate pens, or
secluded localities, and killed and cured near by, gave place to the
large herds, sent when fattened to great markets where pigs were
collected from distances of many hundreds of miles, the stock animals
and the fat occupied in succession the same boats, cars and yards, and,
as a matter of course, the virulent germs were concentrated and diffused
through the infected places and things. We cannot go back to the
antiquated safer methods, but it would be possible to so regulate our
commerce, that the evil could be reduced to a minimum. Separate cars,
loading banks, chutes, alleyways, and yards can be reserved for fat
swine going to immediate slaughter and no animal having passed through
any of these should be allowed to be taken out for stock purposes,
unless it has been passed through a rigid quarantine. The places and
things used for such fat swine should be disinfected at intervals, and
the manure and offal should be disinfected, or exposed to a boiling
temperature for a sufficient length of time before removal from the
premises. Stock swine on their part should be shipped only on a
certificate of the complete immunity of the herd and locality from which
they come from swine epizoötics, and of the roads or vehicles by which
they reached the shipping point. They should be debarred from all yards,
loading banks and cars or boats used for fat hogs, and admitted only to
such as have just passed through a thorough disinfection. They should be
sent directly to their destination, or if to a market, for purposes of
sale, it should be well apart from that used for fat swine, and the
loading banks, chutes and yards should be entirely distinct and should
be thoroughly disinfected on every occasion after use. The millions now
lost yearly from swine epizoötics might well warrant the inconvenience
and expense entailed by such precautions. Heavy penalties should be
imposed on those shipping pigs from infected localities, on those making
false certificate, and on all who in any way violate the law.
Independently of State or local authorities the stock owner can do much
to protect himself. He can make a number of pens large enough to hold 2
or 3 pigs each, safely fenced off from one another and so constructed
that no drainage can take place from pen to pen. Then in winter in the
absence of flies, and with rats, mice, and birds excluded the
opportunity for the extension of infection from pen to pen can be kept
at its minimum. All pigs must be kept apart from the manure heap, and in
summer the manure must be so treated as to destroy the larvæ of flies.
All food and water that might convey infection must be guarded against.
Then if one pig is attacked it will only be necessary to destroy it and
its two fellows in the same pen, and even if those in adjacent pens are
killed or quarantined the loss will be a trifle as compared to the ruin
of the whole herd, as usually happens. Prompt disinfection of the pens
and manure is imperative, and the same would apply to the person and
clothes of the attendant, and to all stable utensils.
_Immunization_ by injection of _sterilized products_ of the bacillus,
has not proved satisfactory. In 1880 I applied this to two pigs, causing
a transient fever, after recovery from which, the subjects resisted
exposure to infected pens and pigs, and even virulent inoculations. But
they failed to thrive well. Later experiments by Drs. Salmon and
DeSchweinitz respectively, also proved unsatisfactory. The latter
separated and injected the enzymes, but lost 50 per cent of his cases,
the survivors proving immune, with the drawback of troublesome local
lesions. The enzymes obtained from cultures in milk could be used safely
on guinea pigs in the dose of 0.01 grams and in some cases even up to
0.04 securing immunity. But the great risk of an overdose, the frequent
local lesions, and the subsequent unthrift, have prevented the adoption
of the method.
_Disinfection._ The experiments of the Bureau of Animal Industry show
that, apart from freezing, _four months in the soil_, serves to render
the bacillus harmless.
From .75 to 1 per cent of quick lime added to soil in the form of lime
water, destroyed the virulence in 11 days.
Lime can be employed as a thick whitewash on pens, fences, yards, etc.,
the precaution being taken to see that it is newly burned, caustic and
applied in sufficient amount. Lime that has been kept absorbs carbon
dioxide and loses its disinfectant property. If ¼lb freshly made
chloride of lime is added to each gallon of the caustic lime white wash
the certainty of success is insured. Lime water has the advantage of
being applicable to grassy surfaces, without proving hurtful to the
vegetation. For buildings and yards it furnishes a ready means of
estimating the thoroughness of the application.
_Sulphuric acid_ (1:100 or 1¼ oz. to 1 gallon) makes a good disinfectant
for buildings and yards. Like lime this can be used freely without fear
of poisoning the animals.
_Carbolic Acid_, 5 per cent, can be used with great safety. The Bureau
of Animal Industry advises the combination of this with sulphuric acid,
which adds greatly to its solubility.
_Formalin_ may be employed, diluted one to forty of the solution (1 per
cent of the gas) in buildings and on woodwork generally. It may also be
applied in the form of gas by heating the solution in closed rooms. Like
carbolic acid it is especially applicable to cars, boats, and other
vehicles.
_Corrosive Sublimate_ (1:500) makes a convenient and cheap disinfectant,
with the drawback that it is poisonous, and destructive to metals.
_Mercuric Iodide_ though more potent is also more expensive. Blue stone
(2:100) and zinc chloride (10:100) are also effective but poisonous.
The failure to _stamp out_ hog cholera in England and America has been
largely chargeable on the appointment of laymen to do the work of the
expert, and no less so on the attempt to deal with the disease in hogs
in transit or in the market rather than in the farm where they have been
raised or kept. Let the fat and stock markets be kept rigidly apart,
together with the means of conveyance to and from these, and let no
stock swine start for a market or destination without a certificate of
the soundness of the locality from which they came, and the purity of
the means of transit, and we shall have taken a long step toward the
final extinction of the pest.
State limits and rights stand in the way of successful work, but this
can be partly met by a frontier supervision by national officials, and
should be further, by a prompt and hearty coöperation of the sanitary
officers of the two states involved. When it becomes possible to trace
infecting hogs, back to the infected place in another commonwealth, and
punish the offender who shipped them, we shall be within sight of a
satisfactory control or extinction of hog cholera.
_Extinction of Hog Cholera in Herds and Districts._ As in all deadly
plagues this should be a recognized governmental function to be carried
out at public expense. It is a question of political economy and its
neglect is subversive of prosperity not in Agriculture alone but in all
public industries whose workers must subsist on the fruits of the soil.
The $10,000,000 lost yearly by the farming community, is a dead loss,
not to agriculture alone, but to the prosperity of the nation, the
markets of which would be revived and improved by such a yearly sum
expended.
The existence of the disease at any point should be reported by the
stockowner or guardian, under penalty in case of failure. When the
nature of the outbreak has been certified by the expert, the district
should be scheduled, and the herd appraised, slaughtered and all
products disposed of in such a way as to prevent any escape of
infection. The carcasses may be burned, buried deeply, or boiled and
rendered. The buildings, yards, utensils, fences, manure, cesspools, and
infected fields should be thoroughly disinfected, or secluded from all
animals for a year. The owners of the herd should be indemnified
according to appraisment, and not to exceed ¾ths of the actual market
value, provision being made that no award shall be made if the herd
sickened within a fortnight after their arrival from another State, or
in case the owner, has concealed the existence of the illness, or has
otherwise deliberately or carelessly contributed to its spread.
Many minor rules and restrictions will be required to fit the general
measures to individual cases and local conditions, and these require the
direct supervision of an expert, and not of a mere business manager or
layman.
_Therapeutic Treatment._ With state, county or municipal measures for
the extinction of hog cholera, treatment is to be condemned, as
calculated to encrease and spread the infection. But until the states
can be educated out of the past wasteful system, into economical
measures of extinction, the swine breeders are entitled to whatever
salvage they can secure through therapeutics. For acute cases there is
no hope. For the _chronic_ a clean, dry, comfortable pen, well
disinfected, and a moderate diet of varied and laxative food are
essential. Wheat, bran or middlings, with corn, oat, barley or linseed
meal may be allowed in form of a mash. A little green vegetable food may
be added. Medicinal agents may be used to meet special indications, but
when a whole herd must be treated at once, antiseptics and febrifuges
have apparently proved the most generally helpful. The Bureau of Animal
Industry especially recommends the following: Wood charcoal, sulphur,
sodium sulphate and antimony sulphide, of each 1 lb.; sodium chloride,
bicarbonate and hyposulphite, of each 2 lbs.; mix thoroughly and add to
each feed in ratio with the size of the patient. In suitable cases, this
is said to improve the appetite and contribute much to convalescence.
Modifications will readily suggest themselves to meet individual
conditions and different stages of the disease—antithermics, eliminants,
calmatives. stimulants, tonics, etc.
_Serum Therapy._ This has been especially exploited and advocated in
America by De Schweinitz of the Bureau of Animal Industry, and Dr.
Peters of Lincoln, Neb. In Europe, Perroncito has prepared an antitoxin.
The serum is produced in the body of the cow or other animal which is
inoculated repeatedly with gradually encreasing doses of living hog
cholera cultures and with solutions of the bacilli and their products,
for a period of eight months, or until no reaction takes place from
large doses, and the blood serum added to cultures of hog cholera
bacilli causes agglutination of the latter. The serum is further tested
as to its power of preserving Guinea pigs inoculated with a lethal dose
of live hog cholera cultures. After separation from the blood the serum
is concentrated until it reaches a standard at which 10cc. proves
curative to a pig of 40 to 60 lbs. weight.
It proves most successful in animals in which the subacute or chronic
form of the disease has just begun. One injection only was given to each
animal. Of 1923 cases treated (1897–8) 30 per cent. died, and 70 per
cent. recovered. Of 3197 in abandoned herds (checks), 81.24 per cent.
were lost. (De Schweinitz.)
One drawback was found in the short period of immunity secured, the
susceptibility reappearing as soon as the antitoxin had been eliminated
from the body. This was met in part by using sterilized cultures
(toxins) along with the serum.
Another desideratum was a speedy means of distinguishing in field work
between hog cholera and swine plague, as the antitoxin of the one was
not protective against the other. To meet this, serum was obtained from
an animal immunized to both diseases, or a mixture was made of the sera
of two animals respectively made resistant to the two affections.
De Schweinitz was very optimistic in the matter, claiming that the serum
is absolutely harmless, can be used on pigs freely, and will cost but 15
cents for each animal. He estimated that of the $15,000,000 per annum
lost by Hog Cholera and Swine Plague in Iowa alone, $11,000,000 can be
saved at a comparatively small cost.
The method is scientifically sound in availing of the defensive products
of the immunized system for imparting to the animal attacked, the power
of vital resistance, and after allowing for enthusiasm, for the
inevitable mistakes, when used on a large scale, of other deadly swine
diseases for hog cholera, for the many accidents incident to its
application by operators who are not specially trained like the employés
of the Bureau, for its demand for acute and deadly outbreaks, as well as
for chronic and mild ones, and taking into account that in other hands
it has not fully borne out the promise made for it; yet it seems to have
some measure of merit, and where no systematic attempt is made by the
authorities for the extinction of the disease and its germ, it is an
available resort for the owner of herds.
The fundamental objection is that it entails the preservation, encrease
and spread of the poison, and like all temporizing measures, stands as a
barrier to the complete extinction of the plague. Giving such a very
transient protection, its repetition may be demanded in a few months or
a year, and proceeding on the ground that the pest must continue for all
time, the apparent economy of the process will prove, in the long run,
but a permanent and grievous tax.
The soundest and only truly economical course in dealing with this and
other deadly infections of swine is the radical extinction of the germ.
When the people can be educated up to this we shall see the dawn of a
brilliant future for our animal industries. Until then we must be
satisfied to fall back upon, and make the best use of the temporizing
measures now in vogue or that may hereafter be devised. Even if it
should be shown that hog cholera is at long intervals developed from a
‘sport’ of the usually harmless bacillus coli commune, the fact remains
that its great extensions and the resulting fatality are due to the
contagion alone, so that extinction remains the true watchword of
success and economy.
SWINE PLAGUE: SEPTICÆMIA HÆMORRHAGICA SUIS.
Definition. Synonym. Bacillus pestis suis, 0.8–1.5μ, nonmotile.
Pathogenesis. Accessory causes, as in hog cholera: less vitality than
in virus of hog cholera, bacillus in apparently healthy, deadly to
birds and rodents. Lesions: like as in hæmorrhagic septicæmia, lungs
suffer more than bowels, lymph glands swollen hæmorrhagic, liver and
spleen may seem almost normal, bowels slightly congested, marked
emaciation. Symptoms: Acute cases like hog cholera, shorter
incubation—1 day, troubled breathing when driven, cough, congested
petechiated skin, hyperthermia, costiveness followed by diarrhœa.
Diagnosis: constancy and predominance of lung lesions and symptoms,
nonmotile bacillus with polar staining, not gasogenic with glucose,
very fatal to birds and rodents. Prevention: as in hog cholera.
Immunization. Treatment: as in hog cholera dangerous. Serum-therapy.
_Definition._ A contagious bacteridian disease of swine, acute or
subacute, characterized by a short incubation, hyperthermia, marked
congestion of the mucosæ, petechiæ and circumscribed blood
extravasations in the skin, subcutis, mucosæ, submucosæ, and tissues,
swelling, congestion and petechiation of the lymph glands, and a marked
tendency to inflammatory localization in the lungs.
_Synonyms._ Th. Smith identifies this affection with the
“Schweineseuche” of Germany.
_Bacteriology. The bacillus of Swine Plague_ (_B. Pestis Suis_) has
already been described in the differential table of allied bacteria
given under hog cholera. It is a short rod, with rounded ends, 0.8 to
1.5μ. × 0.6 to 0.8μ, staining readily in aqueous basic aniline colors
and bleaching in Gram’s iodine solution. The staining is distinctly
polar, the colored portions being more or less crescentic with the
concave or straight border turned inward toward the central clear space.
It is destitute of flagella and distinctly nonmotile unlike the very
active bacillus of hog cholera. It further differs in its growth on
potato which is slight, gray and waxy. On gelatine, too, it gives a
feeble growth (or none) unlike the brownish colonies of the bacillus of
hog cholera. It fails to liquefy gelatin. On agar the growth is more
active, being grayish, translucent or brown. Those forming under the
surface are like flat horizontal discs with a small microscopic
elevation or knob in the center. It grows in milk producing little or no
acid and no clot. It produces gas with none of the sugars—glucose,
lactose, saccharose—in contrast with the gas production in glucose by
the hog cholera bacillus. It shows much less vitality and hardihood than
the hog cholera bacillus, growing but feebly between 65° and 70° F., and
most actively at 97° to 100° F.; dying in 7 minutes at a temperature of
58° (moist); dying in 3 days when dried, in 4 to 6 days in the soil, in
10 to 15 days in water and instantly in 0.04 per cent solution of lime
water.
_Pathogenesis._ It is pathogenic to swine, hens, pigeons, pheasants,
sparrow, mice, guinea pigs, rabbits, cattle, deer, etc., showing not
only a wider range than the hog cholera bacillus, but a more deadly
action outside the genus suis. Inoculated birds die in 2 days, rabbits
in 16 to 20 hours and guineapigs in 1 to 4 days.
_Accessory Causes._ These agree in the main with those of hog cholera
already described so that it is needless to repeat them here. The
principal distinctions depend on the lesser vitality of the swine plague
bacillus outside of the animal body, and its wider range of pathogenesis
outside the genus suis. Infecting materials that have been thoroughly
dry for a week may be considered harmless, also that which has been more
than two weeks in water, and that which has been more than a week in the
soil. If, therefore, the buildings have been thoroughly disinfected, the
simple disuse of yards and pastures for a fortnight, and of ponds of
water for three weeks may suffice. In the case of hog cholera it may be
necessary to abandon such places for 5 months or for the season.
Abandonment by swine is, however, insufficient: all susceptible animals,
wild and tame, (see pathogenesis) must be excluded as any one of these
may maintain the infection. The preservation of recovered swine on the
premises, or the early return of the immune may become a means of
preserving the bacillus for the next susceptible pigs that may be
introduced. The bacillus of swine plague may be found on the air
passages of swine and other animals that are not themselves, at the
time, susceptible to the disease, and these animals accordingly become
the occasions of what have been thought to be spontaneous outbreaks, and
of invasions of fresh herds after the introduction of healthy pigs which
have been thought to be beyond suspicion. The danger of the
communication of the germ by wild birds and rodents would be enormous,
but for the fact that it is so much more deadly to these animals than
the microbe of hog cholera, that few survive to maintain the infection.
Yet the rule ought to be, to exclude from the fields or premises
occupied by new or susceptible pigs, all animals, that may by any
possibility become the means of introducing the infection so recently
prevalent. Though so easily destroyed when outside the living body, the
microbe of swine plague can be carried by the apparently healthy living
animal and we must rigidly exclude the possibility of this occurring.
_Lesions._ _Acute_ and _rapidly fatal cases_ of swine plague furnish
lesions indicative of a hæmorrhagic septicæmia. The abundance of
petechiæ on the skin, mucosæ, serosæ, and tissues generally, with
circumscribed hæmorrhages, congestions, inflammations and exudations,
agree in the main with what is observed in the acute examples of hog
cholera. If the congestive or inflammatory lesions, concentrate in the
lungs rather than the bowels it assists in the diagnosis of swine
plague. The swelling and blood engorgement of the lymph glands are
nearly alike in the more acute types of the two diseases. The spleen is
less constantly enlarged than in hog cholera or swine erysipelas. In the
_subacute_ and _chronic forms_ the lesions may be almost entirely
confined to the enlarged and congested or hæmorrhagic lymph glands.
Usually, however, the lungs are the seat of lobular or lobar pneumonia,
affecting by preference the lower portions of the anterior and median
lobes, and sometimes also the posterior lobe. The pleuræ are often
involved, showing arborescent congestion, thickening, exudate, false
membranes and hydrothorax. The exudate may at times fill up the
interlobular connective tissue, even before the pulmonary tissue is
materially involved suggesting a local infection starting at the pleural
surface. The hepatised lobule has a general red color varying in depth
at different points, and showing lighter yellowish or grayish spots
representing the purulent air sacs and terminal bronchia, and necrotic
foci. On section the bronchia often yield pus, while the pulmonary
tissue oozes a bloody liquid rich in small lymphoid cells.
The liver and spleen may be all but normal, though in a number of cases
they may be congested and softened. The stomach and bowels may be
virtually sound, or they may show extensive congestion, petechiation and
thickening of the mucosa at different points, with, in some cases
ulcers, but these latter are mostly excavated and rarely assume the
projecting, button-like, laminated form which is so characteristic of
chronic hog cholera. Emaciation is a marked feature as in hog-cholera.
_Symptoms._ In the most acute type these may not differ from those of
similar cases of hog-cholera. If there has been any opportunity of
estimating the incubation it will be found to have been shorter, the
skin and mucosæ have a darker red blush, showing first on the ears,
breast, belly and inner sides of the thighs and forearms, the lymph
glands are enlarged, and there is cough and dyspnœa if the patient is
roused to exertion. The presence of petechiæ on the skin and of a very
high temperature (107° to 109°) is to be specially noted. There are
great prostration and dulness, complete anorexia, hiding under the
litter, indisposition to rise, often weakness, staggering, paresis or
even paraplegia, somnolence, and death in coma or convulsions.
In the _subacute_ and _protracted_ cases, there is the short incubation
(1 day), followed by hyperthermia, drooping tail, hiding under the
litter, flushed eyes, nose and mouth, impaired appetite, arched loins,
hollow flanks, retracted abdomen, cough easily roused by driving, and
signs of consolidated lungs in their lower parts (crepitation,
suppressed murmur, abdominal or heart sounds etc.). After a day or two
the skin becomes flushed and together with the visible mucosæ the seat
of petechiæ. The superficial lymph glands are enlarged. The bowels are
usually confined but as the disease advances diarrhœa may set in. There
is rapid loss of condition, and the patient may die as the result of
exhaustion, toxin poisoning, colliquative diarrhœa, or other condition.
_Diagnosis during life_ is based largely on the shorter incubation, the
greater reddening of the visible mucosæ, the comparative absence of
abdominal tenderness, and offensive diarrhœa, and the constancy of the
cough and other symptoms of broncho-pneumonia.
_Post-mortem._ It is marked by the constancy and predominance of the
lung lesions, and the comparative absence of ulceration of the ileum,
cæcum and colon, and especially of the projecting, laminated,
button-like, necrotic sloughs.
The morphology of the bacillus, its habit of polar staining, its lack of
automatic movements, its comparatively poor growth in alkaline bouillon,
on potato, gelatine and agar, its inability to ferment glucose with the
production of gas, its rapidly fatal action on hens and pigeons as well
as on rabbits and guinea pigs serve to distinguish it from the microbe
of hog cholera. (See table p. 38).
_Prevention._ In this connection the reader is referred to the
precautions, given under hog cholera, against conditions, hereditary,
hygienic, climatic, dietetic, parasitic, etc., which lay the system more
open to microbian invasion. In the matter of exclusion of the bacillus,
the swine plague germ is less difficult to deal with, because it is so
much more easily destroyed. Disinfect the buildings, and all
contaminated objects as advised under hog cholera, clean yards, and shut
up these and pastures or runs, and all infected water for one month. In
case of public market yards and alleys, and railway loading banks,
chutes, and cars, a thorough cleansing and disinfection may warrant that
they may be put to use again immediately. No animals that occupied the
yards before disinfection should be allowed to mingle with the new
stock, as they at times carry the microbe, though themselves apparently
healthy and immune. All regulations as to railway and boat transit,
recommended under hog cholera, are equally applicable to swine plague.
The possibility of protecting private herds, by keeping them in special
pens, holding two or three each, is also the same for swine plague.
_Immunization_ is somewhat more promising than in hog cholera.
Metchinkoff and Th. Smith working independently found a fair measure of
success in inoculating rabbits and guinea pigs with three to five small
injections of sterilized bouillon cultures, agar cultures or blood,
intravenously, intraabdominally or hypodermically. But as applied to
swine it has not proved satisfactory, and the irregularity of the
results and the tendency to induce unthriftiness have caused it to be
abandoned.
_Treatment._ The therapeutics of swine plague like that of hog cholera
is essentially unsatisfactory. Benefit might be derived in individual
cases from a careful and judicious use of drugs to meet the special
indications, but with the comparatively low value of the individual
animal, the certainty of the multiplication of the deadly poison by the
preservation of the diseased, and the extreme danger of its diffusion
and extension, treatment is anything but commendable.
_Serum-therapy_ has been advocated for years by De Schweinitz, and under
the auspices of the Bureau of Animal Industry it has been given a wide
trial, but it has not met with the full success that was at first
claimed for it. The serum is prepared in a similar way to that of hog
cholera and is similarly employed. It is open to the same class of
objections, and though when skillfully employed it will reduce the
mortality, it does not yet seem to have reached the point at which it
can be recommended as a profitable investment. Like all temporizing
measures it draws attention from the sounder and more economical measure
of extinction and is indirectly a means of the perpetuation and even the
diffusion of the infection. So long as extinction cannot be secured,
this is a less valuable alternative for the adoption of owners of high
priced hogs.
MODIFIED AND COMPLEX FEVERS OF SWINE.
Double infections. Varieties of bacillus choleræ suis, and bacillus
suis pestis. McFadyean’s swine fever bacillus. Marseilles swine plague
bacillus.
We accept fully the duality of the Hog Cholera and Swine Plague, though
this duality has been hotly contested on both sides of the Atlantic.
Many of the best observers in Europe now support this position. These
include Selander, Bang and Jensen who are familiar with the _svinpest_
(hog cholera) of Scandinavia; Kitt, Friedberger and Fröhner who are
familiar with the _Schweineseuche_ (swine plague) of Germany; Raccugla,
Canova and others in Southern Europe; and Lignieres and others in France
who have studied the hog cholera and _pasturellose porcine_ (swine
plague).
But the conceded duality of these two diseases as they occur in typical
examples in swine, does not account for all the infectious fevers of
swine, in which these microbes or others closely allied to them may
figure. Salmon, Smith and their coadjutors describe double infections in
the same system, in which both the bacillus choleræ suis and the
bacillus pestis suis figure, and in which there result a combination of
symptoms and lesions, that together represent both of these germs. It
may be that one or other of these germs in a given outbreak, shows a
predominance in potency so that the symptoms are more characteristic of
it than of its companion; it may be that the more potent germ kills the
victim, quickly by an acute septicæmia and gross lesions that would
apply almost as well to one germ as to the other; or it may be that both
act moderately and the attack is protracted with resulting lesions in
both lungs and bowels that respectively suggest the plague and the
cholera.
Then as regards varieties in the individual germ. Th. Smith recognizes
this as a frequent condition and describes no less than seven different
types of bacillus choleræ suis which he had studied and which varied in
morphology, cultural qualities and virulence. Lignieres found that the
virulence especially of bacillus suis pestis is very easily affected by
successive passages through the bodies of small experimental animals. We
ought not to be surprised then if we find in different epizoötics, in
different countries and even in the same, bacilli which for the time at
least show characteristics different from those to which we have been
accustomed. These give us varying phases of septicæmia which however
come together in one great class. Two of these types which have been
placed on record may be here named. For others see septicæmia
hæmorrhagica of cattle and sheep.
=McFadyean’s Swine Fever Bacillus.= The characters of this microbe found
constantly by McFadyean in swine fever, approximates closely to the hog
cholera germ in morphology and motility and in its deadly action when
eaten, while it approaches toward the swine plague germ in its cultural
habits on potato, gelatine and agar, and in alkaline culture liquids,
and finally it differs from both in the absence of pathogenesis to
Guinea pigs and in its very moderate action on rabbits. The symptoms and
lesions of the _swine fever_ of Great Britain are those of the _hog
cholera_ of America rather than of swine plague.
=Marseilles Swine Plague Bacillus.= This microbe was found by Rietsch
and Jobert in a febrile epizoötic of swine at Marseilles, and was
studied by Caneva and Bunzl-Federn separately. The latter identified it
with the bacillus of ferret septicæmia, as described by Eberth and
Schimmelbusch. It was longer and thicker than the hog cholera bacillus,
twice as long as broad, actively motile, with flagella, and differed
from bacillus choleræ suis, in its polar staining, its free growth in
acid media, in acidifying and coagulating milk, and in its forming both
indol and phenol in peptonized bouillon.
In this case the source of the disease was in importations from Africa
(Fouquet), and it spread widely in Southern France for nine months. It
proved almost constantly fatal, in from four days to two or three weeks.
The symptoms were weakness especially in the hind limbs, with more or
less fever, constipation often followed by diarrhœa, an infrequent
cough, and red blotches on the skin. In chronic cases ulcers formed in
the mouth and intestines especially the cæcum and colon. Appetite was
often retained to the end. The young, under a year old, were the chief
sufferers. It made 20,000 victims in several months in the province of
Bouches-du-Rhone.
SEPTICÆMIA HÆMORRHAGICA OF BOVINE ANIMALS.
Synonyms. Definition. Historic notes. Resemblance to black quarter.
Bacteriology; saprophytic cocco-bacillus, nonmotile, ærobic, related
to microbe of swine plague, chicken cholera, and rabbit septicæmia.
Pathogenic to deer, buffalo, cattle, horses, swine, rabbits, rats,
mice, goats, and sheep. Variability. Vitality: great in soil, dies in
6 to 20 days when dried, and quickly in antiseptics, resistant to
heat. Accessory causes: rise of soil water in winter or in spring,
drying of marshes in summer, wet, rich, swampy, mucky soils; youth,
gregariousness, carnivorous habit, insects, vermin, wild animals and
birds, epizoa, entozoa, wire fences, wounds of all kinds, hard, woody
provender; inoculations in wounds the most fatal. Symptoms:
superficial with hyperthermia, functional disorder; muscular tremors;
violet mucosæ; segregation; swelling in intermaxillary space, tongue,
throat, neck, dewlap, or elsewhere, not pitting on pressure. Petechiæ.
Death in six hours to four days; thoracic form kills in four to eight
days; abdominal form with colics, and bloody often frothy fœtid fæces.
Chronic forms usually pulmonary. Lesions: straw-colored exudations
subcutem or intramuscular; blood extravasations; in lungs resembles
lung plague; on bowels blood effusions, and exudates; softened,
blood-stained lymph glands. Spleen usually normal in size. Blood
black. Petechiæ extensive. Chronic lesions. Bacillus in exudate, blood
and bronchial mucus. Diagnosis: from anthrax, black quarter, lung
plague, rinderpest, and malignant œdema. Mortality 50 to 80 per cent.
Prevention: isolate and kill affected; destroy or disinfect carcasses
and infected things and places, feeding and drinking troughs and
manure. Close and drain infected fields. Immunization, by three
inoculations with cultures made at a high temperature (86° to 90°) in
free air; or with virus that has been grown in pigeon. In case of
deer, drive a few days into a noninfecting enclosure, and then on to a
sound range. Treatment.
_Synonyms._ Wild—und Rinderseuche (Bollinger), Buffalo Disease, Barbone
(Oreste and Armanni), Cornstalk Disease (Billings, Moore), Sporadic
Pneumonia (Smith), Pneumo-enteritis (Galtier.)
_Definition._ An acute bacteridian disease of domestic and wild
herbivora and swine, characterized by sudden onset, rapid and fatal
course, marked hyperthermia, accelerated breathing and pulse, and
extensive gelatinoid or sanguineous extravasation in the intermaxillary
space, tongue, skin, subcutaneous or intermuscular connective tissue,
lungs, pleura, pericardium or intestine.
_Historic Notes._ It is almost certain that in earlier times this
affection was often mistaken for gloss-anthrax, blackquarter, or even
lung plague. Metaxa, in 1816 in Italy, manifestly describes it. Oreste
and Armanni, in 1882 and 1887, traced Italian cases to the microbe. In
1854 it destroyed many cattle and deer in England (Veterinarian). In
1878 Bollinger records its great fatality among the deer, wild boars,
cattle and horses in and near the royal parks at Munich, and for a
number of years after in Bavaria. Friedberger records its presence in
Schlüchtern, Prussia, in 1885–6, Condamine in Cochin China in 1868, and
Guillbeau and Hess in Switzerland in 1894. In America, what appears to
be the same affection is noted as corn-fodder disease in Nebraska
(Billings), as Wildseuche in Tennessee (Norgaard), and as hæmorrhagica
septicæmia in Minnesota (Reynolds). I have repeatedly met with the
affection in New York in cows arriving from the west, and in the
indigenous cattle on wet, mucky, undrained land in spring, about the
period of the melting snows.
_Bacteriology._ The essential cause of the disease is a saprophytic
cocco-bacillus, ovoid, with rounded ends, about 1μ long by 0.3 to 0.6μ
broad, but showing involution forms and a variable size. It is nonmotile
(Kitt claims motility), ærobic (facultative anærobic), takes a polar
stain with clear centre in aniline colors, bleaches in Gram’s (1)
solution, shows neither spores nor flagella, grows readily in bouillon,
on gelatine, (a bluish transparent layer without liquefying), serum at
98° F., milk (without acidifying or coagulating), and alkaline potato
(not on the acid). The cultures have a peculiar odor and yield no indol.
The microbe shows a very close relationship with those of swine plague,
chicken cholera and rabbit septicæmia, but it sometimes differs in
showing little or no pathogenesis for the Guinea-pig.
_Animals susceptible._ It is pathogenic to deer, buffalo, cattle,
horses, swine, rabbits, rats, mice, and to a lesser extent to goats and
sheep.
The _pathogenesis_ varies with the immediate source of the microbe. When
obtained from cattle a drop of blood kills rabbits in twelve to twenty
hours, with intense hæmorrhagic laryngitis and tracheitis. Guinea pigs
die in forty to eighty hours. When obtained from the buffalo it killed
horse, ox, or pig in twenty to forty-eight hours. That obtained from
barbone (buffalo) appears to be more potent than that from septicæmia
hæmorrhagica (cattle).
_Vitality of the microbe._ Simple drying destroys virulence in six to
twenty-two days. Virulence is retained for nine days in putrid flesh. It
is preserved, and the microbe multiplies in soil or water containing
organic matter and nitrates. It is easily destroyed by ordinary
antiseptics 1:5000 of mercuric chloride destroying its vitality in one
minute (Hueppe). On the contrary it shows a great resistance to changes
of temperature. It grows in the soil at 55° to 60° F. (Hueppe), and in
old cultures may resist for an hour a temperature of 175° to 195°
(Oreste and Armanni).
_Accessory Causes._ These are such conditions as favor transmission of,
or receptivity to the microbe. In Southern France the disease is most
common in the winter months, probably because the soil water rises then;
on the Roman marshes on the other hand, it prevails especially from May
to October, when the water is lowest and most impure. In New York I have
seen it especially at the breaking up of the winter frosts, when the
water, pent up in the rich organic soils, is suddenly released. It is
pre-eminently the disease of wet soils, rich in the debris of
decomposing organic matter, of the rich prairies and bottom lands of the
Mississippi Valley, of springy, swampy or mucky soils elsewhere, of the
Pontine marshes at Rome, of the Delta of the Nile, of the rich virgin
soils in Asia. Youth has the greatest receptivity, the older animals
having probably acquired immunity through an earlier attack. The animals
that live in herds infect each other by contact, fighting, licking,
etc., others are affected by eating the vegetation or drinking the water
soiled by the diseased, wild boars by eating the carcasses, and all
animals by the attacks of biting or blood-sucking insects which have
just come from the diseased. It is claimed that the infection is carried
by men and animals, and by the sale in villages of the flesh of infected
animals. Dogs, wolves, foxes, and other carnivorous animals and birds
will also carry the infection for long distances. Finally, it will
travel to a greater or lesser distance with running water.
The entrance of the microbe by wounds must always be counted on, and
explains the casual inoculations, by bites of dogs, insects, worms, by
barbed wire fences, by wounds with horns, tusks, or feet, by nails,
etc., and in winter by hard, woody aliment scratching the lips, mouth,
fauces or pharynx. Shedding of teeth, diseased teeth or gums, and
everything that causes abrasion of the alimentary mucosa must be
admitted into the list of causes. Infected traumatisms of any kind, like
intratracheal and intravenous inoculations usually prove fatal, while
infection by ingestion is not necessarily so. The pathogenic potency
appears to be impaired in the stomach or intestines.
_Symptoms._ These vary widely according to the subject, the seat of
infection and the violence of the attack. They may be classed under
three principal heads: _superficial_, _thoracic_ and _intestinal_, and
in addition into _acute_ and _chronic_ cases.
In the _superficial_, _external_ or _cutaneous form_ there is usually a
sudden onset with high fever (104° to 107° F.), accelerated pulse, (70
to 90), and breathing (24 to 50), anorexia, suspended rumination,
muscular tremors or shivering, staring coat, dry, hot muzzle, burning of
ears, horns and hoofs, suppression of milk, and more or less stringy
salivation. The visible mucosæ are of a deep red or violet tinge, and
the patient will often remain apart by himself when the herd has moved
elsewhere. Soon there develops a tense, hard, hot, painful swelling of
the intermaxillary space, tongue, throat, neck, dewlap or elsewhere,
amounting to perhaps six inches in thickness, extremely resistant and
not usually indented on pressure with the finger. The breathing becomes
stertorous and deglutition difficult or impossible. The mouth is hot and
filled with tenacious saliva, and the tongue may hang pendant while on
its borders and lower surface are projections of the mucosa swollen by
infiltration, yellowish and semi-transparent, or blood-stained. At other
points petechiæ are more or less abundant.
Death may take place from pharyngeal obstruction or closure, or as the
disease advances, there may be indications of implication of the
viscera, of the chest or abdomen: encreasingly difficult breathing, a
mucous or suffocative cough, colicy pains, tenesmus, and the passage of
moulded glazed fæces, of pseudo-membranous casts, or of profuse liquid
stools. The animal may move the hind feet uneasily, lie down and rise
alternately, may remain persistently recumbent until death, or he may
stand up until he falls to perish of asphyxia. Death may occur in six
hours, or may be delayed four days.
In the _thoracic form_ the extreme hyperthermia is complicated by early
lesions in the lungs, while the muscular or cutaneous ones are omitted
or deferred. So long as the lesions are confined to the chest, they are
betrayed by hurried and even oppressed breathing or dyspnœa, a frequent,
moist, suffocative cough, persistent standing to favor respiration, and
there are the percussion and auscultation indications of consolidated
lungs or hydrothorax. The mucosæ are usually of a darker red, than in
the external form, cyanotic indeed, and the peculiar asphyxial position,
with legs apart, head extended, dilated nostrils and open mouth may be
very significant. These symptoms are likely to be modified or
supplemented before death, by those caused by intestinal or renal
disorder. In the thoracic form in young animals death by suffocation may
occur in a few hours, but more commonly the disease progresses slowly
and a fatal result is not reached until the fourth day or even the
eighth. This form is common in the deer, and less so in cattle.
In the _intestinal_ or _abdominal form_ the usual sudden onset and high
fever, are complicated by inappetence, tympany, rumbling of the bowels,
uneasy movements of the hind feet, perhaps twisting of the tail, looking
at the flanks, and even lying down and rising. There is frequent,
violent straining with the passage of fæces at first glazed, later
streaked with blood, or mixed with pseudo-membranous casts, and very
soon soft, watery, frothy and fœtid. These are usually black or reddish
black from contained blood.
The urine may also be blood-stained.
Before death, complications on the lungs or skin will often come in to
assist in diagnosis.
In the _chronic_ and _subacute types_ the lesions are often concentrated
on the lungs, and there are a moderate fever cough, hurried breathing
under exertion, dulness on percussion over limited pulmonary areas,
blowing sounds, mucous râles, crepitations and more or less
muco-purulent expectoration. These phenomena are all the more
significant if complicated by digestive disorders, costiveness, fœtid
mucous diarrhœa, tympany, or by the eruption of the superficial
swellings.
_Lesions._ The swellings on or _under the skin_ or among the _muscles_
show extensive straw-colored exudations, colored at points with blood,
with enlargement, infiltration and staining of the adjacent lymph
glands. On the chest walls the sero-sanguineous exudate may extend from
the root of the lungs, through the intercostal spaces to the skin in the
breast, the axilla and behind. The tongue is often enormously swollen
and black, charged with extensive blood extravasations in addition to
the yellowish exudate. Along its sides and on its lower surface, the
mucosa stands out in projecting masses of yellowish infiltration, which
may show equally on the fauces, pharynx, larynx, trachea and bronchi.
In the _lungs_ the pleuræ and subpleural and interlobular tissue are
extensively infiltrated and thickened by a profuse yellowish serous or
sero-sanguineous exudate, so that the appearance may closely resemble
that of lung plague. The lung tissue is consolidated, hepatized and dark
red, with at some points emphysema. The pleural sac is usually filled by
a serous or bloody effusion (2 to 25 quarts) and there is often
extensive implication of the pericardium. The tracheo-bronchial mucosa
and bronchial glands show extensive infiltration and thickening.
In the _abdomen_ are found extensive infiltrations and blood
extravasations in the mucosa and submucosa of the stomachs and
intestines, softening and shedding of the epithelium, infiltrations of
the peritoneum, diaphragm, and sublumbar adipose tissue, and softening
and degeneration of the liver and kidneys. The intestinal gastric and
mesenteric glands are usually infiltrated, softened and blood-stained.
Engorgement of the spleen is exceptional.
The _blood_ is very black but not usually materially changed in
consistency nor coagulability. Petechiation of the different serosæ and
other tissues is a prominent feature.
In _chronic cases_ the lesions are mostly shown in the lungs and lymph
glands. The lungs show circumscribed lobular islets of congestion,
induration or caseation, offering a suggestion of tubercle, which is all
the more deceptive when cretifaction has set in. The caseous centres may
vary in size from a pea to a walnut, and some may have ruptured to form
a vomica discharging into a bronchium. Bronchia leading to affected
lobules are blocked with muco-purulent matter, yellowish, thick and
tenacious, and their mucosa is thickened and puckered. The enlarged
lymph glands are especially those of the bronchia, trachea, mediastinum,
bowels, mesentery and sublumbar region.
The bacillus is present in the exudate but is especially abundant in the
blood, and in the chronic cases in the bronchial mucous.
_Diagnosis._ From _anthrax_ (gloss-anthrax) this affection is easily
distinguished by the absence from the blood and exudates of the large,
square ended anthrax bacillus, by the absence of enlargement and blood
engorgement of the spleen, and of the softness and diffluence of the
blood clot which characterize anthrax. Swine which are with difficulty
inoculated with anthrax are very susceptible to hæmorrhagic septicæmia.
Sheep which are very receptive to anthrax are somewhat refractory to the
disease now in hand. Pigeons resist anthrax but readily contract
septicæmia hæmorrhagica.
From _black quarter_ it is readily distinguished by the absence of
emphysema and crepitation and of a secondary cooling in the external
swellings, by the presence of the germ in abundance in the blood, by its
smaller size, its bipolar staining, and its lack of motility and of
spores. Inoculation with black quarter bacillus kills the guinea pig,
but spares the pigeon.
From _lung plague_ it is distinguished by the suddenness of its attack
and rapidity of its progress to a fatal issue; by the usual coincidence
of skin and bowel lesions, while the lung plague affects the chest only;
by its communicability to pigs, sheep, pigeons, and even horses, which
are all immune from lung plague; and by the usual absence of lung
lesions of different ages, which are so characteristic of lung plague.
The abundance in the blood of the cocco-bacillus with bipolar staining
in hæmorrhagic septicæmia is characteristic. _Lung plague_ spreads
slowly to exposed cattle, but spares all other domestic animals.
From _Rinderpest_ it is differentiated by the history of its advent, by
the presence of the surface œdematous swellings, by the absence of the
whitish epithelial concretions on the mouth or vulva, and of the deep
dark portwine discolorations of the mucosæ of the mouth, rectum and
vulva, and by the fact of its inoculability on domestic animals
generally. Rinderpest spreads rapidly to all exposed ruminants, but
spares pigs, rabbits, Guinea pigs, horses and birds.
From _malignant œdema_ it differs in its inoculability on the surface in
place of subcutaneously only, in the presence of the cocco-bacillus in
the blood during life, whereas in malignant œdema the germ is confined
to the local lesion, in the absence of crepitation, which may be present
in the swelling of œdema, in the greater facility with which cultures
can be made of the septicæmic cocco-bacillus and in the absence of gas
production in such cultures. The malignant œdema comes from a single
accidental deep inoculation from almost any rich soil, and is not a
malady spreading widely and generally on given limited damp, rich lands
which have become infected. Finally the cocco-bacillus of septicæmia
hæmorrhagica is found singly in the blood or exudate, whereas the
microbes of malignant œdema may be found in form of sporeless filaments
intermingled with the bacilli.
_Mortality._ The hæmorrhagic septicæmia of cattle cuts off from 50 to 80
per cent. of the animals attacked.
_Prevention._ The first consideration is to isolate and kill all the
affected animals, to destroy the carcasses by burning or boiling and to
burn or disinfect all objects that may have become contaminated. The
buildings, yards, and fences, must be disinfected, and as the bacillus
is very resistant a solution of corrosive sublimate and sodium chloride,
a drachm of each to the gallon of water may be freely used after
thorough cleansing. Or a whitewash containing ¼ lb. chloride of lime to
each gallon may be substituted. Feeding and drinking troughs may be
burned. Manure may be freely treated with sulphuric acid. Infected
fields should be closed for years and if possible drained.
_Immunization_ of buffalo and sheep has been secured by making cultures
of the microbe in free air at 86° to 90° F. and inoculating the animals
with the weakened virus, on three successive occasions with intervals of
several days. It induces a transient fever, with no serious phenomena
(Oreste and Armanni). A second available method is to pass the virus
through the system of the pigeon and inoculate with the pigeon’s blood,
on three successive occasions, the animals to be protected. It is
manifestly impossible to put such immunizing methods in force on wild
deer, and for these probably the best course is to drive them from the
infected range, to an uninfected one, having retained them for a few
days interval in a confined area, to allow of any already infected
animals developing the disease. A similar avoidance of waters running
from the infected tract is imperative.
_Treatment_, has been unsuccessful. Friedberger failed with hypodermic
injection of carbolic acid, and internal administration of salicylic
acid. Gal gave subcutem 5 per cent. solution of creolin, and doses of 1½
oz. of the same agent by the mouth. Five buffaloes out of seventeen
recovered. Friedberger suggests deep incisions of the swellings so as to
admit the air, and treatment of the wounds with strong antiseptics.
SEPTICÆMIA HÆMORRHAGICA OF THE SHEEP: LOMBRIZ.
Synonyms. Definition. Geographical distribution, Argentina, France,
etc. Causes: bacillus; intravenously, etc., youth, verminous
affections, low condition. Bacteriology: ovoid bacillus with polar
stain, bleached by Gram’s solution, ærobic, nonmotile. Symptoms:
Chronic form in summer, diarrhœa, arched back, stiffness, emaciation,
flattened wool, segregation, impaired or depraved appetite, shedding
wool, anæmic skin, dependent dropsies, sunken eyes, weak small pulse,
temperature variable—elevated, nasal and buccal discharge, weakness,
paresis, dulness, torpor, lung symptoms, arthritis. Diagnosis: from
distomatosis and strongylosis. Acute form with high fever,
constitutional disorder, colics, diarrhœa, death in 24 to 36 hours,
subacute form. Lesions: black blood, congestions, and general
petechiæ. Lungs, liver, kidneys and spleen, congested, swollen.
Subacute cases have lighter blood, and lesions. Chronic cases anæmic,
blood diffluent, lymph glands enlarged, congested; connective tissues
and serous cavities dropsical, gastric, intestinal and hepatic worms,
spleen shrunken. Mortality: great in acute, less in chronic.
Prevention: segregation, exclusion of all sheep from unknown or
suspected flocks, antiseptic dip and quarantine for new purchases,
expose a few as a test; cleanliness, disinfectants, avoid watershed
from infected lands, wide range, outdoor life, generous diet, remove
weak, emaciated, anæmic. Immunization. Treatment.
_Synonyms._ Pasteurellosis Ovina. Infectious Pneumo-Enteritis.
_Definition._ An infectious febrile affection of the sheep, chronic or
acute, characterized by dulness, stiffness, or paresis, anorexia,
thirst, disorder of the breathing and digestive organs, black diffluent
blood, petechiæ, reddish effusions in the serosæ or connective tissue,
and congestive or inflammatory lesions of the lungs, liver, kidneys and
intestines. The presence of a cocco-bacillus (diplococcus,
strepto-cocco-bacillus, pasteurellosa) in the lesions is especially
characteristic.
_Geographical Distribution._ Though Lignieres first demonstrated this as
a bacteridian disease in the Argentine Republic, he was, after his
return, able to identify the same affection in the flocks of almost
every department of France, in newly imported English Lincolns and
German Merinos, so that there can be little doubt that the malady exists
in all or nearly all countries engaged in sheep husbandry, though it has
been usually attributed to parasitisms of the lungs, liver or alimentary
canal alone.
_Causes._ The essential cause is manifestly the bacillus, which
Lignieres has isolated, cultivated in vitro, and successfully inoculated
intravenously in the sheep, which he also infected by feeding the pure
cultures. Intravenously it proved fatal to Guinea pig, rabbit, pigeon,
chicken, rat, mouse, horse, ass and ox. Yet many other accessory causes
must be admitted as operating in different cases.
_Youth_ shows the greatest susceptibility whether the victim be mammal
or bird. So marked is this influence that the principle sufferers are
lambs just weaned or yearlings. Yet mature animals, that are debilitated
from any cause, also fall victims. The measure of immunity usually
noticed in mature sheep may well be attributed to a previous mild and
non-fatal attack of the bacillus.
_Verminous affections_ are undoubtedly predisposing causes, hence, the
common practice of attributing the malady to the worms alone. This again
in part explains the susceptibility of the young which so often harbor
worms to a dangerous extent. It seems to matter less what worms are
present than, that they are in sufficient numbers to greatly deteriorate
the health. It is noticeable, however, that those worms that make
breaches in the mucosæ, have been noted as infesting the victims of this
malady. In the stomach worms sent from Argentina, Railliet identified
Strongylus Contortus, S. circumcentus, and S. instabilis and in the
duodenum S. filicollis and S. Curticei. These, like the distomata often
found in the liver, are blood suckers and not only render the animal
anæmic, but make numerous perforations to act as infection-atria. The
various lung worms, encysting themselves in the air sacs and determining
local congestions may act in the same way, opening channels for the
entrance of the microbe.
_Low condition_ or a _low tone_ of health from any cause predisposes.
Old, worn out animals, ewes in lamb, or those just lambed, sheep that
have been shut up and denied proper exercise in winter, those on poor
feeding and perhaps nursing twins, those that have suffered from any
debilitating disease of any kind are especially obnoxious to a dangerous
attack.
_Microbiology._ The microbe, which Lignieres found in the pulmonary
lesions, is one of the colon group of pathogenic bacteria that have been
classed together as _pasteurella_. It usually appears as a very minute
ovoid bacillus which stains promptly and deeply at the poles in fuchsine
or gentian violet, leaving a clear median part, so that it seems a
_diplococcus_. It bleaches readily in Gram’s solution. Its form varies
in different culture media sometimes showing long _bacilli_, and
sometimes _streptococco-bacilli_, but the usual and characteristic
appearance is that of a _cocco-bacillus_, and to this it constantly
returns. The microbe is ærobic and nonmotile (the slow zig-zag motion
sometimes seen does not seem to be automatic). In peptonised bouillon it
produces opacity in 18 hours, or in simple bouillon in 24 to 48 hours,
the best temperature being 100° F. Gelatine plate cultures are slow
because of the compulsory low temperature, yet in 36 to 48 hours it
forms pale blue, translucent, round colonies the size of a pin head. It
never liquefies. In coagulated blood serum it forms only a thin
transparent pellicle hardly visible, and there is no growth on potato.
_Symptoms: Chronic Form._ In Argentina, Lignieres observed the disease
especially during the hot summer months (December to May), and after
weaning in the lambs. This may be from the marked change of food, from
the greater activity of microbian life at this season, from the
exhausting effect of the heat, or from a combination of two or more of
these conditions. It appears alike in the sheepfold, and on the open
prairie. In considerable flocks the symptoms may be at first overlooked,
so that the death of several sheep may be the first thing to draw
attention. Then a certain number are found to scour, arch the back, walk
stiffly, lose condition, and have the wool flattened and devoid of yolk
(_clapped_ wool). The sheep may be dull, lagging behind its fellows, or
lying apart by itself, ruminating infrequently and for shorter periods
than natural, and there may be inappetence, or depraved appetite (eating
earth), though some eat well to the end. Irregular and at intervals
capricious appetite is a frequent condition. When caught and examined,
the wool is easily torn out, the muscles are soft and wasted, (the leg
muscles may have practically disappeared), the bones stand out at all
points, the skin is pale, thin, bloodless and devoid of its subcutaneous
fat, (paper skin), there may be œdemas along the ventral aspect of the
body, pitting on pressure, and between the branches of the lower jaw
(poked), the eyes are sunken, the conjunctiva may be puffy and
œdematous, but like the muzzle and mouth they are pale and anæmic and
the pulse is small, though the excitement may have roused cardiac
palpitations. The temperature varies from time to time often reaching
105° or 106° F. There is liable to be a muco-purulent discharge from
nose and mouth especially noticeable during drinking. As the disease
advances the subject becomes weak, paretic, dull and stupid, it remains
down without interest enough to seek food, though still eating if it is
brought to it. The head is usually rested on the flank, and the animal
often lies so for days in a state of semi-stupor without disposition or
ability to rise, paretic or paraplegic. Auscultation may sometimes
detect a mucous râle or crepitus, and percussion a flatness of sound
over some part of the lung. Chronic arthritis is an occasional symptom.
_Diagnosis._ The symptoms closely resemble those of distomatosis or
strongylosis, and the disease is often complicated with one or more of
these, so that it may become difficult to judge how much is due to the
microbian infection and how much to the helminthiasis. The presence,
continuously or intermittently, of the hyperthermia is almost
pathognomonic of the operation of the microbe.
_Acute Form._ This has been particularly observed in the ewe just after
lambing, when the system is especially susceptible to microbian
invasion, and little able to cope with it. There are hot ears, nose and
feet, temperature of 104° to 106° F., accelerated pulse and breathing,
anorexia, ardent thirst, deeply congested mucosæ, colicy pains, pawing
the ground, frothy or bloody diarrhœa, arched back, pendent head, ears
and eyelids, muscular trembling, albuminous urine, plaintive cries, dark
red vaginal discharge, muco-purulent or glairy nasal discharge, and
death in 24 to 36 hours. Such animals may be in fair condition or even
fat, no time having been allowed for emaciation.
In other cases death may be delayed for three or four weeks, with the
same general symptoms, only less marked. In such cases, pregnant ewes
are likely to abort, and the lambs are born dead, or prove weak and
listless, and die when a few days old. Some have too little energy to
suck; others suck heartily but perish all the same on the second or
third day, after diarrhœa, thirst, hyperthermia, prostration, and
stupor.
_Lesions._ These vary according to the type. In the _rapidly fatal
cases_ there is dark colored blood, with congestion of the serous and
mucous membranes, which, together with the skin and often the solid
tissues, are covered with petechiæ, and even circumscribed hæmorrhages.
The lungs, liver, kidneys, spleen, and many of the lymph glands are
congested and swollen, seeming at times of a black hue as if
blood-saturated. The lesions, indeed, indicate an acute septicæmia.
In _cases that have survived three or four weeks_, the morbid changes
are slighter, the blood is brighter in tint, and the congestions less
deep in color, ecchymoses may be especially confined to the heart,
abomasum and small intestines, which may also show hæmorrhages.
Enlargement and congestion of the lymph glands are the rule, while
pulmonary consolidation and gastro-intestinal mucous inflammations are
frequently found. As in the more acute types the urine is albuminous.
In _chronic cases_ the anæmia is prominent. The clot is soft, relatively
small, elastic and black, the serum is relatively very abundant and
pale. The red globules are greatly reduced in numbers, and there are a
number of giant cells which stain deeply as in chlorosis. The lymph
glands are usually enlarged, softened and slightly congested but rarely
the seat of blood extravasation. The tissues generally are pallid, soft
and shrunken. There is a marked absence of subcutaneous and
intermuscular fat, while the connective tissue is more or less
infiltrated with a transparent, watery lymph. The serous cavities
usually contain more than the normal amount of fluid, transparent or
straw-colored, and with few globules or granules. Congestions and even
shreds of false membrane are sometimes present on the serosa. In some
cases the lungs and bronchia are the seat of inflammatory exudates,
causing nodular consolidations of from one-half to one inch in diameter.
Not unfrequently the lungs show strongylosis as the fourth stomach shows
strongylus contortus, the small intestines strongylus filicollis, tæniae
(expansa, fimbriata, etc.), the large intestines æsophagostoma
Columbiana, and tricocephalus affinis, and the gall ducts distoma
hepaticum and distoma lanceolatum. In these chronic cases the spleen is
usually shrunken, and the liver firm, sometimes even cirrhotic.
_Mortality._ The acute cases are usually fatal. Those that assume a
chronic form, if free from local lesions in important organs, well-fed,
and, above all, kept in the open air, and changed to a different
pasture, tend largely to recovery.
_Prevention._ The propagation of the infection from animal to animal is
slow and somewhat uncertain, and when introduced by the purchase of a
new ram or other animal, it may take a considerable time to affect the
stock extensively, but for this reason, and because an apparently sound
sheep may harbor the germ, it is difficult to oppose it successfully by
segregation. All the same, it is desirable to take all possible
precautions against its advent, and among these, the exclusion of
strange sheep from noninfected pastures and flocks. When the time comes
to make an outcross from the home strain, the ram must be selected not
only for his pedigree and individual qualities, but no less for the
soundness of the flock from which he is taken. If the lambs of that
flock have been decimated by disease, the best blue blood, and most
faultless form should not tempt the flockmaster. He should be rejected
in favor of one taken from a flock that is above suspicion. It matters
little if it can be plausibly argued that the mortality came from worms
of the lungs, liver, or digestive organs; these in themselves may soon
ruin any flock, but they, too, often coexist with the microbe of
infectious septicæmia, and, when this is the case, they prepare the
system and open a way for its invasion.
New purchases should not only be selected from apparently sound and
guaranteed stock, but they should be passed through an antiseptic dip on
arrival, and then if possible quarantined in a special enclosure until
they shall have proved their freedom from infection. A valuable ram may
be placed with some lambs or yearlings in close quarters to ascertain
whether he has brought the infecting matter with him. If all escape
after some months the presumption is that he is sound. Perfect
cleanliness of the fold should be maintained, and disinfectants may be
freely used in it.
The water supplies should be watched, rejecting streams that have
drained sheep-pastures where there have been marked losses of lambs and
ewes. Water from deep wells without any surface leakage is to be
preferred.
When new stock (ram, ewes, lambs) are of necessity mixed with the sound
herd, a wide range, an open air life, and abundant dietary must be
secured. The system that is full of strength and vigor can better resist
the microbe and even throw it off entirely, whereas the weak, confined
subject succumbs. For the same reason, the weak, emaciated and
debilitated subjects should be at once separated from the sound flock,
and kept in a special enclosure, in the open air, on a rich diet. Should
they harbor worms, this seclusion is even more imperative. (See
parasites of lungs, liver, stomach and bowels).
Lignieres advocates immunization by serum prepared on the Pasteur
method, but, as he has not divulged the exact technique of its
preparation, it is impossible as yet, to give this an unqualified
endorsement. It has this in its favor that the mature sheep, in full
vigor of middle life, though in an infected area, usually resist the
infection, while the young, old, debilitated and verminous suffer.
Opposed to it are these considerations that are recognized by Lignieres
himself;—1st, The acquired immunity is not perfect, as shown by
occasional relapses in sheep that have survived a first attack; 2d, The
serum inoculation is not only useless, but dangerous in animals that
already harbor the germ; I may, add 3d, Any acquired parasitism or
debilitating disease may tend to break down the immunity and prostrate
the system under the infection. Lignieres advises that the serum
treatment should be restricted to the new born lambs in infected herds,
or herds in infected areas. The first three or four weeks after birth
are to be preferred for the operation, though failing this it may still
be ventured on, up to a few days before weaning. The longer it is
delayed the greater the danger of a preëxisting infection, and of
untoward results from the new access of infecting material, on the back
of an infection which varies so extremely in its pathogenic potency.
Even among the new born lambs, Lignieres would restrict the serum
therapy to the strong, robust and healthy, and, if they survive the
resulting fever, would repeat the _treatment_ after the hyperthermia has
ceased. No satisfactory treatment of the disease has been made. An open
air life, a generous diet, and a course of iron, and bitters will,
however, be of use in serving to improve health, digestion and vigor, to
solicit a better production of red globules, and to enable the patient
to survive the period of anæmia, prostration and debility. Antiseptics
like quinia, the sulphites and the iodides might be used as adjuncts.
PNEUMO-ENTERITIS IN SHEEP: HÆMORRHAGIC SEPTICÆMIA: SWINE PLAGUE.
Historic note. Microbiology: ovoid bacterium, motile, with polar
stain, non-liquefying, chains, grows freely on culture media.
Pathogenic to sheep, goats, dogs, hens, rodents, calf, ass. Views of
Lignieres, Lienaux, and Conte. Symptoms: Acute form in young;
hyperthermia, rapid pulse, troubled breathing, dulness, prostration,
sopor, anorexia, congested petechiated mucosæ, offensive diarrhœa,
emaciation, wheezing, cough, râles, crepitus, percussion flatness,
abortion. Death in 6 hours to 3 days. Subacute form in mature:
symptoms moderate, recoveries the rule. Lesions: fœtid carcass, blood
staining of skin and organs, exudates, petechiæ, swollen congested
lymph glands, peritoneal exudate, congested liver and spleen,
gastro-enteritis, pleural effusion, lobular and peribronchial
exudates, caseation, congested womb, placenta and brain, bacterium in
lesions. Prevention: isolation, disinfection, secretions, manure,
drainage, exclude tame and wild animals. Disinfectants.
Among the different forms of hæmorrhagic septicæmia in sheep, that
observed by Galtier in 1889 in Basses Alpes, and later elsewhere in
southern and western France and in Algiers, must be specially noted. It
seems to be the same affection studied later by Lienaux, Conte, Besnoit
and Cuillé and which prevailed from Tarn in the south of France, to
Vendée in the west, and Somme in the north.
_Microbiology._ The pathogenic factor found in the lesions was an ovoid
bacterium, a little larger than that of fowl cholera, motile,
non-liquefying, with polar staining, and often showing in short chains
of two or three joined end to end. It grows easily and abundantly in all
common culture media, even on potato which fails to propagate the
cocco-bacillus of Lignieres. This, with its ready transmission from
swine to sheep and _vice versa_, apparently serves to differentiate it
from the cocco-bacillus, and the disease from the hæmorrhagic septicæmia
of Lignieres.
_Pathogenesis._ In Galtier’s first observations in Basses Alpes four
separate flocks were infected by pigs brought all from one market, and
placed in or by the pens of the sheep where they sickened and one in
seven died in a few days. Then the mortality began among the sheep and
ranged as follows: 1st flock lost 10 in 37: 2d flock 16 in 25: 3d flock
8 in 20: 4th flock 12 in 22. On one farm 10 sheep were sent to a
neighbor’s just before the arrival of the sick pigs and escaped, and on
another a second flock kept in outlying pens well apart from the home
flock kept perfectly sound.
With cultures of the microbe in vitro, he successfully inoculated sheep,
goats, dogs, chickens, Guinea pigs, rabbits, and, finally, a calf and an
ass. The cultures were inoculated in different cases; intravenously,
into the trachea, pleura, lung, and subcutaneous connective tissue, and
one goat was infected by ingestion.
Lignieres claims that Galtier must have worked with a complex infection
in which his (Lignieres’) cocco-bacillus was an essential constituent.
The evidence of this is, however, lacking, and we must recognize that
Galtier made cultures which showed the close relationship of his
organisms to swine plague, and their lack of complete identity with
those of the Lombriz.
Lienaux and Conte had pathogenic results in a limited number of animals
only (rabbit, mouse, Guinea pig) illustrating the familiar truth of the
variability in the pathogenesis of different specimens of septicæmic
bacteria of the colon group.
_Symptoms._ 1. _Acute Form._ There is a sudden marked rise of
temperature, often to 107° F., with acceleration of pulse and
respiration. Sometimes death follows so early as to prevent the
observation of other symptoms. If otherwise there supervene marked
dulness, prostration, somnolence, anorexia, suspension of rumination,
and more or less tympany of the rumen. The patient is found lying down,
apart from the flock, indisposed to rise, with deep red, congested,
arborescent conjunctiva and other mucous membranes, and petechial spots
on these and on the white portions of the skin. The fæces, at first
moderately firm and moulded in pellets, marked here and there with lines
of mucus, or even blood, become on the second or third day soft,
pultaceous, or watery and highly offensive. Parallel with this,
emaciation advances with rapid strides. Breathing becomes more hurried,
wheezing or snuffling, with a muco-serous, often bloody discharge from
the nose, and an infrequent cough. Careful auscultation and percussion
will often reveal the blowing or mucous râles, the crepitation or
flatness on percussion of broncho-pneumonia. As the disease advances the
petechiæ on skin and mucosæ extend, and extensive deep violet areas show
especially on the inner sides of the arms and thighs, on the under
surface of the tail, on the perineum and under the belly. Abortion is a
common result, the lambs coming dead.
Death may occur in six hours, more commonly in two or three days, or
even longer, the temperature going down to below normal in the last
stages. In case of recovery, convalescence is slow, the animal remaining
emaciated and weak, with lung lesions and persistent cough for a length
of time. These poor imperfectly recovered animals continue to harbor the
microbe and transmit it. Lesions of the liver and other organs, the
result of this disease, are found in sheep that have survived the
affection and are afterward killed for mutton.
_Symptoms: 2. Subacute and Chronic Form._ This is seen in mature sheep
of two or three years, that have been infected when in the full vigor of
life and health, during an open air life and by a limited dose of the
virus. The temperature is less elevated, the circulatory and respiratory
functions less disturbed, the dulness and prostration only moderate, the
interruption of feeding and rumination transient and tympany slight.
Cough and nasal discharge are however present and rather persistent,
diarrhœa may be manifested, and marked emaciation occurs. There may be
congestion of the mucosæ, but petechiæ and extensive bloody
discoloration of the mucous membranes or skin are rarely seen. Abortion
is not uncommon.
Recoveries are the rule in this type of the disease, though in some
cases it will be delayed for weeks and may even then be imperfect.
_Lesions._ In the acute types of the disease decomposition advances
rapidly after death, and the carcass from the first exhales a peculiarly
heavy odor. The skin is discolored, the nasal mucosa is the seat of a
muco-purulent or sanguinolent discharge, the anus is soiled with liquid
fæces, the subcutaneous connective tissue marked by red arborescence and
blood-stained areas, or by a gelatinoid exudation, the muscles at times
deeply colored and petechiated, the lymph glands, especially the
bronchial and mesenteric, are enlarged and congested of a deep red—the
color being highest in the cortical zone. In some old standing cases
these may have softened and acquired a grayish hue. They are rich in the
specific bacterium.
The peritoneum is congested, petechiated, thickened, and more or less
covered with thin false membranes, and it contains from a pint to three
quarts of a sero-sanguinolent liquid which coagulates loosely on
exposure. The liver is congested, with points of blood extravasation,
and zones of degeneration (fibroid, fatty or necrotic), and sometimes
abscess. The congestion extends to the spleen and pancreas. The abomasum
and intestines are the seat of mucous gastro-enteritis. The mucous folds
of the pyloric sac of the stomach are congested, reddened and
petechiated, the small intestine has tracts and patches of congestion,
thickening and softening, Peyers’ patches and the solitary glands are
enlarged, and ulcers may be present on large or small intestines.
Effusion is usually found in the pleura, clear, grayish or bloody, with
flocculi and false membranes, and further branching redness of the
serosa. The mediastinum may be thickened by exudate especially around
the glands, œsophagus and blood vessels. The lung shows lobular,
interlobular and peribronchial exudates approaching at times to the
appearances shown in lung plague, along with the atelectasis, emphysema
and, in prolonged cases, caseation.
Less constant are congestions and petechiæ of the pericardium, heart,
kidneys, vesical mucosa, testicles, ovaries or womb. The blood is dark
and forms a loose coagulum. In case of abortion the umbilical cord is
infiltrated and the placental membranes ecchymotic. The brain and spinal
cord and their membranes are sometimes congested and infiltrated and a
serous effusion exists in the arachnoid.
The bacterium is found more or less abundantly in each of the morbid
lesions.
_Prevention._ Absolute seclusion of the sick and of all their products
is the prime essential. The general distribution of the lesions
throughout the body and the uniform presence of the bacterium in the
lesions indicate that no part of the body and no secretion can be
considered as free from infection. All parts of the body, all
expectoration, saliva, fæces, urine, milk even must be withheld from all
other animals, at least until they have been thoroughly cooked or
disinfected. Manure must be burned, or buried deeply in quicklime.
Contaminated pens, yards, wallows, streams and fields must be abandoned
or thoroughly disinfected.
Galtier found that the virus remained active for six days in putrefying
organic matter at 39° to 75° F.; in 25 days in water, at room
temperature; the refuse litter, fodder, manure, and drainage matter from
the infected place must be carefully guarded against. The virus steadily
loses in force in such media, but remains infecting to animals injected
with it. The most active disinfectants may be used on the pens and yards
(copperas 5%, sulphuric acid 2% solution, or mercuric chloride .2%)
while the contaminated fields should be abandoned for the season. All
droppings may be treated with sulphuric acid (2%), creolin, lysol,
phenic acid or copper sulphate. The susceptibility of practically all
the animals of the farm, demands the exclusion of these, while that of
rodents, renders necessary the further exclusion of wild mammals; and we
may add birds, wild and tame, and if possible flies. The plowing of the
contaminated soil will do much to obviate danger, yet the sheep folds
and pastures should be separated by a considerable distance from any
place where infected animals and objects have been. If drinking troughs
for sound animals have been used by the sick or suspected they should be
emptied and washed with a disinfectant (sulphuric acid 2:100).
ULCERATIVE (ERYSIPELATOID) INFECTION OF THE LIMBS IN CATTLE AND SHEEP.
New York outbreaks. Causes: wounds by sharp pebbles, streptococci,
pure cultures, inoculations. Symptoms: swelling on lower limbs,
abscesses, implicating tendons, bones, joints, and under hoof.
Prevention: avoid septic or frosted mud, irritants, etc., disinfect
surface, keep dry and clean, open abscesses, use disinfectants,
separate infected.
This affection was seen in several herds in Oneida Co., N. Y., in the
Spring of 1897. The geological formation of the region was a calcareous
rock with a surface soil thickly impregnated with pebbles and small flat
shaly masses. Sheep suffered in Western New York.
_Causes._ In Oneida, the subjects were dairy cows, which in the early
spring, when the frost went out of the ground, had to wade through
chilly soft mud reaching to the knees or above, and mixed with small
stones with sharp edges, and with semiliquid manurial products. The
abrasions made by these stones furnished convenient infection atria for
septic microbes in the manure. In the pus obtained from the ulcers were
found in abundance the bacillus coli commune, and a long streptococcus
representing on an average from 20 to 40 cocci in a chain. Dr. Moore
made pure cultures of these and produced the same symptoms in a cow by
injecting the streptococcus subcutaneously in the back of the pastern,
and in another animal by simply abrading the surface and rubbing on the
streptococcus culture. As the inflammation, suppuration, and resulting
ulcers implicated not only the skin but also the subcutaneous connective
tissue, the affection had many of the characters of erysipelas.
_Symptoms._ The affection commenced by swelling in the region of the
fetlock, pastern, metacarpus or metatarsus, and exceptionally, the
forearm or tibial region, and advanced to a tense swelling, which pitted
on pressure, and the formation of centres of suppuration, which burst
and discharged. If the exposure to the septic mud were continued the
sores ulcerated and extended both in the skin and subcutaneous
connective tissue, but when the dry weather came and the mud
disappeared, the tendency was to spontaneous recovery. In some instances
ulceration extended beneath the hoof threatening its evulsion, and in
other cases it extended deeply to the tendons and ligaments.
_Treatment._ The main object should be prevention, to be secured by
protecting the stock against contact with septic mud, and especially
such as is near the freezing point and intermixed with such sharp stones
and pebbles as would wound the surface and open channels for infection.
When infection has taken place we should seek to limit it by lotions of
an antiseptic character. Bandages soaked in a solution of hyposulphite
of sodium, 1 dr. to the ounce will often succeed. A more potent
application is iodized phenol, prepared as follows: tincture of iodine 2
drs., carbolic acid crystals 4 drs., glycerine 1 oz., alcohol 1 oz.,
water 8 ozs. When applied on a bandage this may be diluted with water to
make 1 pint. For circumscribed application to forming sores the
undiluted iodized phenol, made of one part each of iodine and carbolic
acid crystals, may be applied twice a day with a glass rod. Other
favorite applications are a lotion of lead and laudanum; a saturated
solution of boric acid; ninety-five per cent. alcohol; a mixture of
creolin 1 part, iodoform 4 parts, and lanolin 10 parts; ichthyol and
collodion; ichthyol and vaseline; or iodol, iodoform, salicylic acid or
resorcin as dusting powders.
Internally, tincture of muriate of iron 3 drms. every three hours helps
to keep the affection in check.
GANGRENOUS INFECTION OF THE CORONET. HORSE. POTCHETCHOUI.
Seen on rich, damp lands. Symptoms: lameness, small areas of
congestion, erection of hairs, vesiculation, pustulation, gangrene as
deep as tendons, depilation, desquamation, fistulæ, slough of hoof,
early fever, impaired appetite, recovery in 14 to 21 days in most
cases. Staphylococcus and streptococcus. Prevention: segregation,
different attendants, avoidance of infecting land while damp, smear
limbs with antiseptics. Treatment: antiseptic bandages.
Under this name Sotsevich describes an infectious disease of the horse,
which prevails in the Don province, and especially on rich, low, damp
lands. Before the appearance of any local lesion, the horse goes very
lame on one limb. Afterward there appears, usually on the coronet or
pastern, an area on which the hairs stand erect, with elevation of the
epidermis and the formation of vesicles as large as barley corns, filled
with a yellowish white liquid and later with pus. Gangrene follows,
extending from the skin to the subcutaneous connective tissue,
aponeurosis and tendons, and forming large sores, one to two inches in
diameter and discharging an abundant yellow, fœtid pus. The adjacent
skin takes on a yellow tint and sheds its hair and epidermis. The
disease may extend into the interphalangean joints or under the hoof,
leading to offensive fistulæ or evulsion of the hoof. If it extends to
the higher parts of the limb it becomes less destructive.
At the onset there is some fever (101° F.), dulness and inappetence, but
these gradually subside, and in favorable cases complete recovery has
taken place in two or three weeks.
Bacteriological investigation has detected in the contents of the
vesicles, staphylococcus pyogenes aureus, and streptococcus pyogenes.
_Prevention_ is largely secured by a rigid separation of the diseased
from the healthy. Other obvious precautions would be to exclude those
dressing the sores from handling other horses until after thorough
disinfection of the hands, and to keep the sound animals, during wet
seasons, from the damp infecting soils, or when they must work on these,
to smear the lower parts of the limbs with antiseptic ointments (tar,
carbolic, iodine, mercuric, etc., etc.)
_Treatment_ with sublimate bandages proves very satisfactory, yet any
comparatively non-irritating antiseptic lotion may be used.
STRANGLES, INFECTIOUS RHINO-ADENITIS.
Synonyms. Definition. Historic notes. Bacteriology: streptococcus
coryzæ contagiosæ equi in pus, chains of 3 and upward, free cocci,
arthrospores, clumps, ærobic, growing freely in serum, or glycerined
bouillon; pathogenic to horse and white mouse; relation to other
streptococci; clinical evidence; accessory causes, youth, primary
susceptibility, dentition, training, impure stable air, grain ration,
excitement, sudation, fatigue, chill, change of climate, trading,
crowding, sea voyage, catarrh of air passages. Infecting products,
pus, ingesta, blood, manure, fodder, litter, water, secretion of
mucosa of healthy. Wounds, castration, mangers, racks, troughs,
buckets, poles, shafts, harness, halters, twitches, blankets, rubbers,
combs, brushes, men, etc. Pathology: infection of lymphatics, through
inhalation, sore, ingestion, congenital, milk; congestion of nasal
mucosa, epithelial degeneration and desquamation, discharge little
viscid, corded lymphatics rare, submaxillary swelling rarely small or
nodular, pus creamy, indolent cases, pharyngeal, thoracic, buccal,
gastro-intestinal, hepatic, pancreatic, splenic, muscular, arthritic,
cutaneous, nervous. Forms: mild, malignant, regular, irregular.
Incubation 3 to 5 days. General symptoms: hyperthermia, dulness,
apathy, costiveness. Specific symptoms: nasal, congestion, sneezing,
purulent discharge; epiphora, submaxillary phlegmon; pharyngeal and
laryngeal; parotidean; pulmonary; abdominal, hepatic, pancreatic,
splenic, perirenal, cutaneous, genital, nervous, septicæmic.
Diagnosis, from catarrh, glanders. Prognosis, favorable, apart from
malignancy. Prevention: exclude strange equine animals; avoid public
stables, yards, drinking troughs and buckets; also manure, stable
utensils, hay, fodder, litter, or watershed from infected places;
disinfect cars, wagons, etc. Seclude inmates of infected stable, yard,
park, etc., temporarily close public drinking and feeding places, make
sale or exposure of infected animal penal; temporarily close dealers’
stables; sale with general guarantee only. Disinfection. Immunization;
inoculation from mild case. Treatment: hygienic, antipyretic,
eliminating, antiseptic, surgical, tonic, antisuppurant.
_Synonyms._ Distemper; Coryza Contagiosa Equorum; Gourme (Fr.); Druse
(Ger.); Cimurro (Ital.).
_Definition._ An infective, streptococcic, febrile disease of solipeds,
usually manifested by a catarrhal inflammation of the upper air
passages, and phlegmon of the adjacent lymph glands, or less frequently
by phlegmonous inflammation of lymph glands elsewhere or of the skin.
_Historic Notes._ Strangles was fairly indicated in the writings of the
ancient Greek veterinarians, and was clearly described and attributed to
contagion by Solleysel in 1664. It was so evidently infectious that it
was experimentally inoculated by Lafosse in 1790, by Viborg, in 1802,
and later, by Erdelyi (1813) and Toggia (1823) and others. Rivolta, in
1873, found a streptococcus in the pus of its abscesses, and to this the
contagion was definitely assigned by Baruchello (1887), Schütz, Sand and
Jensen (1888). Priority in this demonstration is accorded to Schütz.
_Bacteriology._ The _streptococcus coryzæ contagiosæ Equi_
(Streptococcus rhino-adenitis or S. equi) is easily found in the pus of
gland abscesses sometimes in pure cultures (impure in the nasal
discharge), stains readily in aniline colors and in Gram’s solution so
that it stands out clearly among the pus cells. The decolorizing agent
must be weak (not muriatic acid) and applied only for a very short time.
Beside the chain forms, there are isolated, oval cocci, some of which,
larger than others and more elongated, have been held to be arthrospores
or mother cells. The number of elements articulated in a chain varies
from two to four and upward. The chains are straight or sinuous, and may
be grouped in bundles, radiating masses, or clumps like staphylococci.
They are ærobic (facultative anærobic), grow freely as transparent
droplets on blood serum at 99° F., and in glycerine bouillon, and less
vigorously on agar and gelatine. On agar the colonies reach the size of
a pin head in two days with projecting alæ, and on gelatine in three to
five days, and then dry and shrink. Multiplication takes place by
transverse division, and at such a time the organism may seem to be a
chain of diplococci.
_Pathogenesis._ Inoculation of cultures on a susceptible horse produces
the unquestionable phenomena of strangles, and solipeds alone take the
disease casually. In white mice it produces abscess in the seat of
puncture and in the adjacent lymph glands. If the action is delayed the
abscess may be in lung, spleen, kidneys, liver, or other distant organ.
Rabbits, Guinea pigs, pigeons, pigs and cattle are immune unless large
doses are employed. Intravenously large doses kill the lamb.
The _identity_ of the microbe with other streptococci of animals and man
has been claimed. Arloing alleges that, by culture of the microbe in the
blood or peritoneum of the live rabbit, he exalted the virulence, and
obtained in succession a streptococcus capable of producing
_erysipelas_; _gangrenous erysipelas_; _suppurating_, _sloughing
erysipelas_; _pseudo-membranous peritonitis_; _metastatic abscesses_;
and _fulminant septic peritonitis_. Hill, Jensen and Sand, and
Lignieres, as the result of cultures and inoculations claim that
strangles streptococcus is identical with that of contagious pneumonia.
Courmont, on the other hand, as the result of his cultures and
inoculations, concludes that the microbe of strangles and that of
erysipelas are independent organisms.
The clinical evidence is decidedly against the theory of identity. In
epizoötics of strangles we meet with a constant succession of cases of
strangles and in districts into which contagious pneumonia has never
been introduced, no single case of that disease ever comes in to break
the monotony of the sequence and to start a series of cases of the
latter affection. Conversely, in an outbreak of contagious pneumonia in
a locality heretofore free from strangles, strangles do not develop.
Again, no matter how prevalent nor how constant strangles may be in a
locality, and how habitually men have their wounded hands covered with
the pus of the abscesses, no epidemic of erysipelas is entailed in man.
Strangles spreads with remarkable rapidity through a stable, but not to
the often more than equally exposed human attendants, nor to any animal
apart from the genus equus. The absence of strangles from Iceland
(Jonsson) endorses that view.
As a practical question of sanitary science, we occupy a sound position
in differentiating the germs of strangles and contagious pneumonia, and
further that of erysipelas of man, as a wise health officer would
differentiate the microbes of cowpox and smallpox. Whatever may be true
or false as to their primary identity, or as to the transition of one to
the other in successive inoculations on animals of other genera, they
are essentially diverse pathogenically as we meet with them in practice,
and our measures may be safely based on this practical diversity.
_Accessory Causes._ _Youth_ strongly predisposes, most cases occurring
between two and five years, and seventy per cent. before five years. It
may, however, appear at any age, being congenital in some cases (Nocard,
etc.), in others appearing a few weeks after birth, and in still others
at over twenty years, if the subjects have not contracted it earlier.
_Dentition_ which is active in these early years, induces congestion
about the head and general constitutional disturbance, which make the
system more receptive.
_Training_ or _breaking_ is another reason for the predisposition in the
young. The first experience of the _hot, impure, infected air_ of the
stable, the unwonted _grain feeding_, the _excitements_ and
_perspirations_ attendant on the first handling all contribute to
temporary loss of resistance.
_Fatigue_ like other weakening conditions lays the system open to
attack.
_Chill_ is a most efficient cause, hence the disease often prevails most
extensively in spring and autumn, at the time of changing the coat, and
of passing from stable to field and the converse. Joly relates that in
Russia where large numbers die of strangles through imperfect stabling
in winter, immunity is sought through a milder first attack, brought on
in the milder autumn weather by turning the young animals into a deep
pool for half an hour and then exposing them freely to cold winds and
giving cold water to drink. The omnipresent germ takes occasion to
attack the cold debilitated system.
Any _change of latitude_ or of locality acts in the same way. Riquet
even alleges that this will bring about a second and even a third
attack. It is common, he says, for newly bought young horses to have the
disease at Hamburg, and after recovery to have a second attack at
Hanover and finally a third one after they join the regiments in France.
A similar exhaustion of immunity has been repeatedly noticed in the case
of canine distemper.
_Horse trading_ and the _stabling of large numbers_ together is
naturally the most fruitful of infection and hence strangles is a
virtual plague in dealers’ studs. The buildings in such cases are
reinfected at short intervals with virulent types of the streptococcus,
and fresh susceptible animals are being constantly introduced to keep it
up. Riquet says that in Northern Germany dealers avoid this largely by
traveling their purchases in bands of 100 or 150 head, from ten to
twelve miles a day, feeding sparingly, and turning them like sheep into
an open park at night regardless of the weather. Much of the advantage
is doubtless from the avoidance of stable infection and the warm
relaxing air of indoors.
_A sea voyage_ especially favors infection and a single victim placed on
board will speedily contaminate all susceptible animals present.
Finally the predisposing influence of _catarrh of the air-passages_ must
not be overlooked. The inflamed mucosa furnishes a most inviting
infection entrance.
_Infecting products._ The streptococcus abounds in the local phlegmons
and abscesses, in the exudate of the submaxillary, pharyngeal or other
glandular swellings, in the pustular eruption on the skin, and in the
catarrhal discharge from the air passages. It further exists in the
alimentary canal, in the ingesta and in the blood to a limited extent.
In the bowels of an immunized animal it may remain virulent for months.
Thus it comes that the manure is a source of infection, and that soiled
fodder, litter and water may prove dangerous. The infected soil can not
only harbor but can multiply the microbe, keeping it in readiness to
attack any receptive horse. On his part the horse that is immune and in
vigorous health may carry the infection for months and transmit it to
his less resistant fellow.
While the streptococcus is usually found in the blood, in limited
numbers only, its presence there implies its general diffusion and
especially in the lymph plexuses and glands. Hence, the danger of
operations on the subjects of strangles, the weakened tissues of the
wound forming a most inviting field of growth. Castrations, occurring as
they do mostly in the growing animal, are especially to be guarded
against, and I may cite the case, familiar to many, in which seven
cryptorchids died with phlegmon in the seat of the wound, the first one
operated on having had strangles.
The nasal and buccal discharges are especially liable to convey the
infection through mangers, racks, fodders, drinking troughs and pails,
harness, poles and shafts, halters, twitches and the like. Infection
through blankets, brushes, rubbers, and the clothes and hands of
attendants, dealers, veterinarians and others, is not to be overlooked.
_Pathology._ The streptococcus shows a special disposition to enter and
advance along the lines of the lymphatic circulation. The paucity of the
germ in the blood and its abundance in the lymph plexuses, vessels and
glands show that its election is preëminently for the lymphatic system.
Then the ordinary primary lesions in and around the upper part of the
air passage (nose, pharynx, submaxillary, parotidean and pharyngeal
lymph glands) bespeak infection by inhalation, rather than with the
ingesta. Primary solitary lesions on or near stomach or intestine are
almost unknown; nearly all such being secondary. Next to inhalation, the
most prominent channel of entrance is through castration and other
wounds. Abrasions and sores of skin diseases must rank after wounds as
entrance channels. Transmission by copulation the microbe being lodged
on the genital mucosa is well established, also transmission from mother
to fœtus through the placenta, and from dam to offspring through the
milk.
In the most familiar type of the disease the nasal mucosa is red,
congested and somewhat thickened with exudate, and the epithelium is
softened and desquamating. As the result of this desquamation there may
be slight abrasions or raw sores but these do not show indications of
the irregular outline, excavations, or progressive extensions that
characterize the ulcers of glanders. The surface is usually plentifully
covered with a muco-purulent material with less disposition to
adhesiveness than in glanders. It is rare to see any exudate into, and
thickening of the walls of the lymphatics running from the nostrils
toward the submaxillary glands. The predominance of the streptococcus
in, and the entire absence of the glanders bacillus from the discharge
and inflamed mucosa are conclusive. In the regular cases in which the
submaxillary lymph glands are implicated, both right and left are
usually involved, though not to the same degree, the exudate fills not
only the gland tissue, but a large amount of the surrounding connective
tissue as well, there is a great accumulation of lymphoid cells, and
more or less extensive pus cavities, containing usually a white, creamy
product. In the early stages the glands may be hard and nodular, as in
glanders, but this condition is very transient, so that the rule is to
find an extensive surrounding exudation filling up the whole
intermaxillary space, and having a great abundance of small round cells
with double or triple nuclei. In the older cases there is usually the
open abscess, and if the case is an indolent one there may be extensive
organization of the exudate with formation of dense, fibrous tissue. In
some instances the nasal sinuses are filled with muco-pus.
When lesions extend farther implicating the pharynx and larynx, the
mucosa of these parts shows the same redness, congestion, cloudy
swelling and desquamation with, in some instances, small, submucous
abscesses, and in others extensive infiltration of the submucosa with
lymph so as to narrow or even close the lumen of the larynx. The
guttural pouches may be filled with pus though this is far from
constant. The pharyngeal lymph glands, are nearly always involved and
often the lymph gland in the parotid so that a general infiltration of
the surrounding parts is met with.
If the chest is implicated there is congestion of the bronchial mucosa,
engorgement of the smaller bronchia, air sacs and cells with pus,
collapse, carnification or congestion of lobules, in some cases
pulmonary abscess, and, finally, swelling and not infrequently abscess
of the bronchial glands. Pleurisy is a not uncommon accompaniment,
appearing it may be as a simple extension, from the lung, or, in the
worst forms, from rupture of mediastinal or glandular abscesses into the
cavity and severe infection of the entire pleural walls. The pericardium
is exceptionally involved and coagula on the tricuspid valves have been
met with (Zschokke).
Circumscribed phlegmonous exudates and small abscesses are sometimes
found in the mouth (tongue, soft palate, cheeks) and less frequently in
the œsophagus.
The stomach may show congestions, petechiæ, circumscribed hæmorrhages,
ulcers, and abscesses of the gland tissue or submucosa. Rupture of the
walls may follow abscess (Cadeac).
The intestines may show congestions, colorless or hæmorrhagic exudate,
and suppurations in the agminated or solitary glands, or submucosa. The
intestinal, mesenteric and sublumbar lymph glands may be the centres of
abscesses of varying sizes.
Abscesses may also be found in the liver, pancreas, spleen, of variable
size and usually as secondary formations.
The muscles and intermuscular tissue may be the seat of more or less
extensive exudation, and abscess, and the bones may be congested and
swollen especially in their epiphysis. This may extend to suppuration or
necrosis.
The synovial membranes of joints and the tendinous sheaths are not
infrequently inflamed causing distension and even suppuration.
Congestions of the skin are sometimes met with developing as multiple
papules or hard nodules which advance to the formation of pustules or
small abscesses. These often appear especially where the skin is thin
and delicate as around the lips, nose and eyes, close to the anus or
vulva, in the perineum, sheath or mammæ, inside the thighs or elbow.
They may be of all dimensions from a millet seed upward, and may merge
into or become complicated by the extensive engorgements of petechial
fever.
Finally lesions of the nerve centres are to be looked for in the
protracted or irregular types of the disease. There may be simple
congestion, or serous effusion, intraventricular or subarachnoid, or
finally abscess in the brain, spinal cord or meninges.
_Forms of Strangles._ The types of strangles vary, special forms
characterizing given epizoötics or seasons, or at other times as
individual deviations from the current type. Division has been made into
two groups—_mild_ and _malignant_, or again into _regular_ and
_irregular_, under each of which come several varieties. Many of these
varieties consist simply in a difference in the seat of the principle
lesions, which start in lymph glands or tissues at a distance from the
nasal mucosa, or they depend on secondary foci of infection supervening
on the primary disease in the head.
_Incubation._ In inoculated cases this lasts from three to five days, in
those due to simple exposure it may appear to extend over eight days.
_General Symptoms._ In nearly all cases alike there is a marked
constitutional disturbance the temperature often rising at once to 104°
to 106° F., and oscillating on successive days between this and 102°;
the pulse is usually normal at first and the breathing is either
slightly accelerated or may be made so under slight exertion. There is
more or less dulness, or at least a lack of the vivacity of youth, the
head is somewhat pendent, the eyes may be semiclosed, the patient may be
tardy or even stiff in his movements and the appetite may be diminished
or capricious, oats being rejected by some and hay or grass by others.
The bowels are somewhat confined, the stools consisting of a few small,
hard, balls covered with mucus.
_Specific Symptoms in the Mild Form._ In the vast majority of cases the
local symptoms are concentrated on the mucosæ of nose and mouth, and the
submaxillary lymph glands. Along with the general febrile phenomena,
there appear redness and often mottled congestion of the nasal mucosa,
which not infrequently extends to the mouth and eyes, as well. Heat of
the mouth, the collection of a more or less tenacious mucus, and even
uneasy movements of the jaw may be seen. The nasal mucosa, at first dry,
is soon the seat of a watery exudation, passing into a cloudy sticky
material, and finally a thick, opaque, muco-purulent flow. This may
become colored of a variety of tints, dirty white from inhaled dust,
brownish or yellowish from exuded blood, or greenish from food
materials. The discharge is usually profuse in the young and may be
scanty in the old. Most commonly it flows from both nostrils alike,
though exceptionally it is unilateral. In this it differs from glanders
which is more often unilateral though at times bilateral. Small
abrasions and sores may appear in connection with the softening and
shedding of the epithelium, but these are not ragged, irregular and
spreading as in glanders. Sneezing or snorting is an inevitable symptom.
Epiphora is usually present. Exudations into the nasal sinuses are to be
recognized by heat of the forehead and flat sound on percussion.
Very early in the attack a swelling is noticed in the intermaxillary
space, which may be at first confined to the nodules of the lymph
glands, thus forming distinct, rounded, hard swellings, but they are
early covered by a diffuse exudation into the surrounding connective
tissue, that completely envelopes and obscures the form of the swollen
glands, and forms a more or less uniformly rounded, pasty swelling,
extending to the median line of the intermaxillary space, or filling the
whole space from one maxilla to the other and projecting downward below
their level. This early, diffuse, pasty, evenly rounded swelling, hot
and tender, is distinctive of strangles, and usually exclusive of
glanders.
Another characteristic of the strangles swelling is its steady, and
usually speedy, advance to suppuration and abscess. It becomes hard,
tense, and resistant, then, in the centre, or at various points of the
surface, small areas of circumscribed softening can be detected, and
soon show distinct fluctuation. Two or more of these may coalesce or
they may form several distinct abscesses, which may early point, burst
and discharge, when the remainder of the exudate softens and degenerates
into pus, and the cavity closes by granulation. In some cases after the
formation of the swelling it disappears by resolution, the exudate
becoming liquefied and absorbed. In glanders the nodular, insensible,
swelling tends to persist without extensive pasty exudation or
suppuration.
Cases of _strangles catarrh_ in which the submaxillary lesions are
omitted, are quite common. These occur during the regular strangles
epizoötic, and protect against a second attack.
_Symptoms of Pharyngeal and Laryngeal Strangles._ Extension of the
morbid process from nose to pharynx is exceedingly common. When
concentrated on the pharynx there are extension of the head forward with
elevation of the nose, swelling of the throat laterally or downward,
uneasy movements of the jaws, salivation, difficulty of swallowing,
return of ingested liquids through the nose, gulping, and a loose
suffocative cough. The swelling of the throat tends to attain to large
dimensions, and may threaten suffocation by interfering with the
breathing. This is still further aggravated if the laryngeal mucosa is
the seat of exudate. The breathing may become loud and stertorous, the
mucosæ of a dark leaden hue and the animal dull and stupid from the
venous condition of the circulating blood.
Abscesses forming on the lateral parts of the throat usually make their
way to the surface though this may be below the level of the parotid. If
from the parotidean lymph gland, one of the ducts may be opened thus
forming a salivary fistula. If from the retro- (supra-) pharyngeal
glands the rupture into the pharynx is more likely to take place, but in
some cases the investing sac, meeting with equal resistance in all
directions, fails to undergo degeneration and softening at any one
particular point, and the contents remain pent up indefinitely. If the
liquid is absorbed a cheesy or putty like mass may be the final outcome,
with chronic cough, some stertor in breathing and it may be difficulty
in swallowing.
If the guttural pouches should be involved, there is deafness,
parotidean swelling, which may eventuate in a fluctuating swelling at
the lower border of the parotid, and a free discharge when the head is
lowered, which is likely to last after general recovery. (See Guttural
Pouches, pus in).
Laryngeal paralysis and roaring often follow laryngitis in strangles.
_Pulmonary Symptoms in Strangles._ _Tracheitis_ and _bronchitis_ are
forms of extension of strangles from the upper air passages, and
_pneumonia_ follows of virtual necessity. In many cases these are
primarily dependent on the descent into the lungs of the infecting
discharges, complicated in many cases by the inhalation of food
materials. There are the usual symptoms of broncho-pneumonia
complicating those of strangles and the percussion and auscultation
signs usually imply circumscribed areas of congestion and consolidation
with intervening areas of pervious lung. There may be at such points the
blowing or mucous râles of bronchitis, the sibilant sounds of emphysema,
the crepitation of congestion and the abnormal clearness of sounds
carried from distant organs through the consolidated lung. On percussion
there may be the non-resonance of the consolidated areas, and the excess
of resonance over emphysematous portions or open gas-filled vomicæ. In
these last cases there may be an amphoric sound on auscultation and a
crack-pot sound on percussion. These pulmonary lesions are often fatal,
or the recovery is slow on account of a succession of lobular
congestions and abscesses.
_Abdominal Symptoms in Strangles._ The abdominal lesions in strangles
are usually secondary, the infection reaching the part through the
blood, or by the lymphatics from a castration or other wound, or from
infection by coitus. The phlegmon and abscess may be in the mucosa,
especially in the agminated or solitary glands, in the adjacent lymph
glands at the connection with the mesentery and in those of the
mesentery itself. The animal is dull, listless, with dry, staring coat,
tympany and slight colicy pains after eating, costiveness, retracted,
tender abdomen, insensible loins, and groaning when rising, when walking
down a steep incline, or turning in a very narrow circle. These symptoms
following an apparent or partial recovery from strangles are
significant, and rectal examination may detect a hard, tender mass
connected with the bowel or mesentery.
If rupture takes place into the peritoneum there is general infective
inflammation of that structure with sudden access of fever, marked
prostration and an early death. In more favorable cases its adhesion to
the bowel or to the abdominal wall opens the way for rupture into the
gut or externally and there may be a slow healing of the cavity by
granulation. It may be a month or two before such an abscess opens and
for a length of time thereafter the health is poor, and the animal
lacking in condition and endurance.
When the abscess is formed in the _liver_ there is high fever with
shivering fits, irregularity of the bowels (bound up or loose), dusky or
yellowish hue of the visible mucosæ, anorexia, followed by peritoneal
infection or pyæmia (secondary abscesses).
Abscess of the _pancreas_ or _spleen_ is even less definite in symptoms.
These may terminate in rupture and peritonitis, or the splenic abscess
may become chronic and indolent and in a measure harmless.
_Perirenal Abscess_ is betrayed by specially sensitive loins, stiffness
and groaning in rising or in turning sharply on himself, drooping of the
back under a load, and by albuminous urine. In a small animal the part
may be reached and the tenderness ellicited by handling.
_Cutaneous Symptoms in Strangles._ Though by no means a common form,
strangles sometimes attacks the skin, more particularly that of the
face, head and neck, appearing in the form of pustules or small
abscesses, or it may be of a rounded nodular elevation, which may
disappear without forming either vesicle or pustule. The points of
election are around the lips, nose and eyes, upon the mucosa inside the
lips, along the line of the facial lymphatics running toward the
submaxillary gland, and at points where there is special friction, as
under the halter, collar, saddle, crupper, in the hollow of the heel,
under the tail, on the perineum, in the groin and axilla. They may
extend more or less up the limbs, or around the point of primary attack
attended by more or less engorgement. When this engorgement has reached
extensive dimensions and is mixed with sanguineous extravasation it is
considered as having merged into petechial fever.
_Symptoms of Coital Infection._ From four to seven days after copulation
there appear fever, dullness, stiffness, anorexia, swelling and heat of
the lips of the vulva, a yellowish opaque discharge from its lower
commissure, a deep dark red blush of the mucosa, with points of distinct
infiltration and thickening, developing into vesicles and pustules. The
perineum, the groin and mammæ often show an extension of the congestion
and eruption. In exceptional cases deep abscesses form and Letard
records a fatal case with extensive suppuration among the muscles of the
hind limbs and the haunch, inside the pelvis and along the line of the
aorta.
_Symptoms of Nervous Lesions._ The lesions of the brain and spinal cord
are usually secondary and often appear when the less dangerous
superficial manifestations, are tardy and indolent, when the exudates
are indurated and indisposed to soften. There may be violent delirium,
pushing of the head against the wall, movements of the limbs as if
walking or trotting, roaring, plunging, striking with fore or hind feet,
trismus or other muscular spasms. More frequently there is great
dulness, prostration, debility, vertigo, drowsiness, amaurosis,
paraplegia, general paralysis, coma. If the lesion is in the spinal cord
the spastic or paralytic symptoms are likely to be confined to the hind
parts.
_Fulminant or Septicæmic Form._ Bigoteau describes a rapidly fatal,
septicæmic form, with sudden onset, anorexia, extreme prostration,
uncertain stumbling gait, a deep blue color and ecchymosis of the
visible mucosæ, violent heart action, pulse weak and small, hurried
breathing (45 per minute) temperature 102° to 106° F., often inability
to rise and death from asphyxia in from two to five days.
_Diagnosis._ In mild and regular cases this is easy. The attack in rapid
succession of all the young, and still susceptible horses in a stable or
locality, and the uniform coincidence of a profuse nasal catarrh, and
the formation between the branches of the lower jaw, of a diffuse, hot,
painful swelling rapidly advancing to suppuration and discharge are
virtually conclusive. Simple catarrhs even if infective and attacking
all young horses do not cause phlegmon of the submaxillary lymph glands
as occurs in the great majority of cases of strangles. Glanders which is
attended by both nasal discharge and submaxillary swelling, is slower in
its onset, usually with little or no fever, has usually a more adhesive
discharge, ragged, unhealthy ulcers on the nasal mucosa with a
disposition to extend, often it shows cord-like thickening of the
lymphatics on the side of the face, and the submaxillary swelling is
smaller, made up of a number of small, hard, insensible rounded nodules
which show virtually no tendency to suppurate. (See diagnosis of
glanders). In cases of doubt it may be advisable to inoculate a
Guinea-pig and a white mouse. The Guinea-pig resists a small dose, while
the mouse forms abscess in the seat of inoculation in the dependent
lymph glands. The Guinea-pig is very susceptible to glanders, and the
white mouse immune. Or mallein may be used.
_Prognosis._ The mild type of strangles almost invariably terminates
favorably. In the irregular types with internal abscess the prospect is
grave in ratio with the size and multiplicity of the foci and the vital
importance of the organ invaded. In 15,421 cases collected by
Friedberger and Fröhner, and representing the total in a series of
outbreaks, but 3 per cent proved fatal. Much, however, depends on the
special potency of the germ. Horses contracting this in a particular
year or from a given stable in the same year convey the disease to
others in a malignant form, while others that contracted it in another
year or a different stable infect with the mild form only.
_Prevention._ In the older countries horsemen too often accept strangles
as inevitable. They expect that all horses will have it sooner or later,
and it is not worth while to guard against it. The too absolute doctrine
of the identity of the germ with the microbe of erysipelas, puerperal
fever, contagious pneumonia, influenza, of the suppurations of the limbs
and feet in sheep and cattle, and other streptococcic infections seems
to corroborate this view. But on the other hand the absence of strangles
from given countries like Iceland where erysipelas and its coadjutors
are common, its absence from secluded breeding farms and districts in
America, though prevailing all around them, the rapidity of its spread
when introduced in a sick colt, and the entire failure to extend in the
same way from an erysipelatous man to susceptible young horses with
which he comes in contact show that preventive measures may be
successfully applied for its restriction and extinction. The conceded
family resemblance of the microbes and the experimental production, by
their inoculation, of lesions showing many points of similitude leave
them still sufficiently distinct in their pathogenesis to warrant
measures for the suppression of the variety which produces strangles.
_Precautions for the private owner._ During the existence of strangles
in the district, _exclude strange horses, asses or mules_ from the farm
or stable. Keep young susceptible horses from _public stables or yards_
(livery, feeding, training, fair, market, and above all, dealers’ and
sale stables) and even from _public drinking troughs_ and _buckets_ used
in common. Provide against their contact with _manure_ from strange or
infected stables, or with _pastures_, _fields_ and _wagons_ on which
this has been put, also against the use around the stable or on fodder
of _forks_ or _other implements_ that have been used for such manure.
Avoid _hay_ or other _fodder_ or _litter_ from a strange barn or one
that is open to any suspicion of infection. Avoid _running water_ that
has drained land, stables, or yards where strange horses have been, or
those open to suspicion. In shipping by car or other _public conveyance_
disinfect the latter before the animal is loaded. If a _second hand
wagon, shafts, pole, harness, blanket_ or other object is brought on the
place or used, disinfect the same before using.
_Measures for Sanitary Police._ Make it _compulsory to report_, under
penalty for failure, all cases of strangles, or of horses with nasal
discharge, or submaxillary swelling. Forbid removal from the stable, or
secluded enclosure, of all horses, etc., suffering in this way or which
have been pronounced by the official veterinarian to have strangles.
Provide for _exclusion of all other solipeds_ from such _stables_, or
from _contact_ or _dangerous proximity_ to animals held in them, also
from _infected yards, parks, cars, boats, etc. Close public drinking
troughs_ during an epizoötic; let each owner use his own bucket.
Circumstances may demand closure of public feeding stables as well.
_Forbid_, under penalty, _sale_, _exposure_ or _movement_ on any _public
highway_ or _unfenced place_ of any infected (diseased or exposed)
soliped. Enjoin _certificate of sanitary conditions of stable and stud_
with each animal sold. _Close dealers’ stables_, or forbid any sale from
them until all infection has ceased and the buildings have been
thoroughly disinfected. Compel thorough _disinfection of stables, yards,
cars, boats and other public conveyances_ that may be open to reasonable
suspicion of infection.
_Immunization._ An attack renders the subject immune, but this may be
early overcome by marked change of location, and exposure to a virus of
greater intensity or modified quality. Besides the crude and reckless
Russian method already referred to, direct inoculation of the virulent
products has been often resorted to from the time of Gohier onward, in
the different countries of Europe. By selecting the matter from the
abscesses or nasal discharge of a mild epizoötic, and preserving the
inoculated subjects in clean, dry, pure aired stables, on nourishing
diet, and under the best conditions of hygiene, a fair measure of
immunity was conferred with absolutely no loss. The same as after casual
cases, second attacks will sometimes be shown, but even in severe
outbreaks, of a less violent type. The pus from the abscess, or the
preceding exudate in the swelling may be simply rubbed on the nasal
mucosa, or injected subcutem in another part of the body. In many cases
there follows merely a local cellulitis, while in others the general
infection leads to the nasal discharge, with or without the submaxillary
abscess.
This method is open to the individual owner where no concerted effort is
made to _stamp out_ the infection. When, however, police measures for
suppression are in force, it must be strictly prohibited, or adopted
only under official control, and with absolute seclusion and thorough
disinfection.
_Treatment._ In mild regular cases hygienic measures only are demanded.
Cleanliness, dry stalls, pure air, warmth (a sunny exposure if
available), nourishing, easily digested food, (grass, green corn stalks,
bran mashes, roots, carrots, turnips, apples, potatoes, ensilage,
scalded oats or hay) and pure water, or linseed tea, grooming and, in
cold weather, blanketing may suffice. Rest is indispensable, though
exercise may be allowed in a sheltered or sunny field or yard in fine
weather.
Castrations and all other surgical operations are forbidden.
For costiveness or tardy action of the bowels 1, 2 or 3 ozs. of sulphate
of soda may be allowed daily in the drinking water.
To soothe the inflamed air-passages it is well to steam them with the
vapor of hot water to which has been added an antiseptic such as oil of
tar, tar, phenic acid, or creolin. This may be placed in a bucket, and a
bag with its bottom cut so as to form a tube drawn over the bucket and
nose of the horse. It may be continued an hour or more at a time, or a
nasal douche of creolin (1:100) may be employed. In case of tardy
softening of the submaxillary swelling it may be assiduously fomented,
or covered with a linseed meal or other poultice to which a little
antiseptic (carbolic acid, creolin) has been added. It may be applied on
a cotton hood having holes for eyes and ears and furnished with ends to
tie back of the ears and down the middle of the face. If still indolent
the swelling may be rubbed with soap liniment or smeared with soft soap,
or finally a cantharides blister may be applied.
As soon as any indication of softening or fluctuation is detected a free
incision should be made to allow the exit of the pus. This further tends
to hasten the liquefaction and removal of the adjacent exudate. If the
pus lies near to the surface, with little more than skin to penetrate,
it may be freely incised with one thrust of the knife, but if there is
intervening glandular or other tissue, the skin only should be first
incised, and the connective tissue bored through with the finger nail,
or the point of a sterilized director, or of closed scissors. In this
way the important vessels, nerves and salivary ducts are pushed aside
and troublesome bleeding and saliva fistula alike avoided.
Fever usually subsides on the opening of the abscess, but if it fails to
do so, or if it reappears from slight absorption of septic matters it
may be desirable to favor elimination by small doses of sodium
bicarbonate, ammonium chloride, or potassium nitrate. In extreme cases a
few doses of acetanilid may be given, or full doses of quinia.
When the discharge from nose or abscess threatens to persist, such
agents as sulphur, yellow or black sulphide of antimony, are given with
bitters, but a more prompt effect can usually be had from injections of
weak solutions of creolin, cresyl, lysol, etc. When the cough is
troublesome it may be quieted by belladonna, or, in case of weakness of
the heart, by digitalis.
The various complications require treatment appropriate to their nature.
Collections of pus in the nasal sinuses may demand trephining and
antiseptic injections. Swellings about the throat threatening asphyxia
and which cannot be relieved by evacuation of pus may necessitate
tracheotomy until suppuration occurs. The cutaneous pustules and
abscesses are dealt with by pricking the collections and washing daily
or oftener with astringent antiseptics (phenic acid and alum).
Bronchitis and broncho-pneumonia may be benefited by sinapisms applied
to the sides of the chest, the internal administration of potassium
iodide, ammonium chloride, sodium hyposulphite, terpene or terpinol; or
by inhalation of weak sulphur fumes, or tar vapor.
For abscesses in the bronchial or mesenteric glands, the brain, spinal
cord, or other internal organ, little can usually be done but to sustain
the patient and await the course of events. If the abscess can be
accurately located it may be aspirated and then injected with an
antiseptic; if in the encephalon, trephining may be resorted to; death
is certain in such a case in the absence of treatment.
During convalescence it is very important to avoid overexertion and
chill, which are very liable to bring on petechial fever. Also, to feed
nourishing food, give pure air and water, and to see that no suspension
of action of bowels, or kidneys threatens to shut up toxins and waste
products in the system. _Apropos_ of impure water Williams quotes the
case of a foul stream near Bradford, England, on the banks of which
every case of strangles did badly.
CONTAGIOUS PNEUMONIA IN THE HORSE.
Synonyms. Definition. Historic notes. Accessory causes: youth, native
susceptibility, inclement weather, exposed stables, nasal and
bronchial catarrh, sores as infection atria, lack of stable hygiene,
crowding, underfeeding, overwork, excitement, exhaustion, infection
from stables, etc., convalescents; doctrine of recrudescence.
Bacteriology: streptococcus pneumoniæ contagiosæ equi: pathogenic to
mice, rabbits, and Guinea pigs. Cocco-bacillus of Lignieres in early
lesions. Lesions: bilateral, multiple foci, congestion, consolidation,
purulent, necrotic, infarction, sequestra in purulent sacs, pleuritic
effusion; enlarged, congested liver with centres of degeneration and
necrosis. Congested spleen, kidneys, lymph glands and
gastro-intestinal mucosa. Yellow mucosæ, mahogany colored muscles.
Incubation, 3 to 10 days. Symptoms: staring coat, early extreme
hyperthermia, accelerated pulse and breathing, cough, icteric mucosæ,
anorexia, dulness, defervescence in 3 to 5 days; convalescence in 10
days; or prostration, swollen eyelids, trembling or interrupted
labored breathing, cough, nasal flow yellow, multiple centres of
percussion flatness, crepitation, râles; urine scanty, yellow or
reddish, albuminous, acid, alkalinity as a symptom; throat symptoms,
inhalation bronchitis, cardiac phenomena, swelling of legs, stupor,
trembling, staggering, vertigo, paresis. Course: duration 2 to 3
weeks, defervescence. Fatal cases, toxin poisoning. Diagnosis: by age,
history, tardy infection, prostration usually less than in influenza.
Prognosis: gravity depends on violence of attack, susceptibility,
hygiene, treatment. Mortality 1 to 20 per cent. Permanent lesions from
sequestra, adhesions, cardiac, hepatic, nervous or arthritic disease.
Treatment: pure air, sunshine, comfort, hygiene, pure water, rest,
cold rectal injections, damp compresses, hot bath, diaphoretics,
expectorants, alkaline diuretics, antipyretics, heart stimulants,
derivatives, antiseptics, nerve sedatives, tonics. Prevention: early
removal, disinfection, quarantine new horses, disinfection of public
and sale yards and stables, certificates. Immunization: by a mild
attack; serum-therapy.
_Synonyms._ Ataxic or Adynamic Pneumonia; Stable or Hospital Pneumonia;
Pleuro-Pneumonia Contagiosa Equorum; Contagious Pleuro-Pneumonia;
Bilious Pneumonia; Edematous Pneumonia; Brustseuche.
_Definition._ An infectious adynamic type of pneumonia occurring in
horses, asses and mules, characterized by marked hyperthermia; by
infiltration of lung tissue, often bloody, infarcted or caseated and
usually circumscribed; by a deep yellow discoloration of the visible
mucosa and other white tissues; and by complicating lesions of the
pleura, heart, pericardium, liver, bowels, or kidneys.
_Historic Notes._ This affection was formerly confounded with equine
influenza, and it was only in the second third of the nineteenth century
that the differentiation was attempted. S. Prangé describes this as a
special epizoötic disease in the French hussars in 1841, Leconturier in
Belgium in 1845, Seidamgrotzky in Germany in 1882 (strongly emphasizing
the contagion), and Dieckerhoff in Berlin in 1883. The latter showed
that horses, recovered and immune from influenza, still contracted
brustseuche and perished. This distinction was fully corroborated by
Lustig, Cagnat (1884), Brun, Delamotte (1886), Jolly, Benjamin,
Leclainche, Trasbot, and others. The presence of a particulate, living,
self-multiplying cause (microbe) was recognized as the essential
condition of the disease (as we still recognize the necessity for such
an organism to explain rabies) though the micro-organism itself was as
yet undiscovered.
At the same time many concurrent factors had to be considered as
accessory in different cases.
_Accessory Causes._ _Young horses_ often show a greater susceptibility
than older animals, mainly because they retain all the unimpaired
susceptibility of the colt, while old horses have already passed through
the disease and become immune. On the other hand, in the absence of
acquired immunity, the older, _worn out and debilitated animals_ are the
most susceptible and tend to have the disease in its worst form.
_Susceptibility_ and _immunity_ are therefore more important factors
than mere age. Immunity usually lasts for several years, or throughout
life, yet in some animals, or under given conditions, it is overcome
much earlier. _Inclemency of the weather_, or special exposure of any
kind, as in severe rainstorms, or working with the feet and legs in
water, may become the occasion of an attack. Exposure to cold _northwest
storms_ (America, Atlantic Slope), or northeast (Europe), _standing
without blanket_ in a temperature at zero, confinement in _draughts of
cold air_ between doors or windows, without clothing and after severe
exercise, weaken the whole system and increase susceptibility. The
presence of a _nasal or bronchial catarrh_, or of another debilitating
disease may act in the same way. The weakened tissues seem to invite the
entrance of the germ. Palat, Boiteux and Trasbot found that horses with
_local sores_ or _suppurations_ fell readier victims than
others;—perhaps the germs entered by the traumas; perhaps the tone of
the whole system was lowered, so that the resistance was lessened.
_Close_, _foul air_, _bad ventilation_, _imperfect sewerage_, and
_overcrowded stables_ not only contribute strongly to infection but tend
to aggravate the cases. _Underfeeding_ and _overwork_ act in the same
way and in this connection may be named the _excitement_ and
_exhaustion_ attendant on a _long journey by rail_. This, like the foul,
crowded stable, furnishes many more opportunities for infection and
reinfection, so that the invasion of the exposed animal system is all
but certain. Infection clings to the _loading banks_, _yards_, _feeding
stables_, _mangers_, _troughs_, _buckets_, _cars_, _litter_, and
_manure_, so that young horses shipped from the west to the Atlantic
Coast States, very frequently come down with contagious pneumonia, and
contaminate the stables in which they are placed. Peters suggests that
the germ is preserved in the _soil water_, so that after apparent
subsidence it may be again brought to the surface in time of rains or
freshets, to start a new epizoötic. _Convalescent horses_ may carry the
germ for weeks, on the mucosa or in sequestra in the lungs, and
contaminate horses with which they come in contact.
It is remarkable that the contagious pneumonia is far less diffusible on
the air than influenza, so that it is much more constantly the result of
direct contact of a sound, with an infected animal, or with a place or
thing that the sick animal has contaminated. It therefore spreads much
less rapidly, remains confined to individual stables for a length of
time, and in the absence of active interchange of horses tends to die
out of its own accord. As the infection is not generally and speedily
acquired, so immunity fails to become general, and the infection tends
to fix itself permanently in places where many strange horses
congregate, (market stables, sale stables, livery stables, etc.), and
the constant influx of fresh animals keeps the flame burning by
accessions of fresh fuel. In such cases it is manifest that the germ
outside the animal body either rests in a dry condition, or lives as a
saprophyte in earth or organic matter, and often loses much of its
virulence. Under such circumstances animals that would prove readily
susceptible to a virulent germ, prove nonreceptive to this resting germ,
until under some special devitalizing influence, like exposure,
exhaustion or local disease, it finds its opportunity and the weakened
system succumbs. Then, acquiring new force through its life in the
debilitated system, it starts on a recrudescence, and an epizoötic is
mistakenly supposed to have started without a preëxisting microbian
cause.
Cadeac even advocates the theory that the same germ possessed of greater
or lesser virulence, is always present in ordinary stables and horses,
and habitually causes in exposed or debilitated animals an ordinary
fibrinous pneumonia with no perceptible tendency to transmission by
contagion; that, in other cases when a considerable number of horses
have their defensive powers impaired, it gains a wide extension; and,
that in some such cases, the germ that has been living as a
comparatively harmless saprophyte, suddenly acquires an unwonted
potency, and breaking down the barrier of partial immunity, attacks
exposed animals on a large scale and irrespective of weather
perturbations, or debilitated conditions. He quotes from Trasbot
instances that seem to support this hypothesis, which is not at all in
disaccord with the habits of bacterial life, yet we require a solid
basis in bacteriological experiment to make it unassailable.
_Bacteriology._ Siedamgrotzky (1882) found in the hæmorrhagic centres in
the affected lung and in the pleural exudate _micrococci_. Dieckerhoff
(1882) and Mendelsohn (1883) found in the pleural exudate streptococci.
Chain cocci were also found by Peterlein (1884), Perroncito (1885),
Delamotte and Chantemesse (1888), and Mosselman and Lienaux (1893).
Schütz (1887) found a diplococcus which he studied very fully and this
is corroborated by Lustig’s ovoid bacterium, by Cadeac’s micrococcus and
diplococcus. In Dr. V. A. Moore’s cultures at the N. Y. S. Veterinary
College cocci were found constantly in pure culture, sometimes as a
diplococcus, but under slightly altered conditions the streptococcus
form predominated. As the difference between two, and three or more
cocci in chain form is merely a question of early or late separation of
cocci which multiply in line, the apparent discrepancies in the above
observations do not imply any real difference in the microbe.
Inoculated in pure cultures the Schütz diplococcus killed mice in 24 to
48 hours with enhanced virulence of the germ. In the _rabbit_,
_subcutem_, it usually killed in 24 to 48 hours, but some survived;
_intravenously_ or _intratrachealy_ it killed more certainly and
speedily and in either case with pleural, pericardial and even
peritoneal lesions. In the _Guinea-pig_, _subcutem_, it caused extensive
effusion, and death in two to six days with chest lesions. In the _dog_
it caused hyperthermia, but no marked lesion and no mortality. In the
_horse_ there were no infectious resultant lesions. A pure culture
thrown into the lung tissue of an old horse at the N. Y. S. V. College,
determined an extended pleuritic adhesion and lung hepatization. The age
of this subject was opposed to any marked susceptibility. The apparent
immunity of the horse in Schutze’s cases might depend on the
insusceptibility of the animals selected during or after an epizoötic,
or on the absence of the predisposing causes so strongly insisted on by
Cadeac.
Rats, chickens and pigs proved immune.
On peptonized gelatin at 98° F., and less rapidly at ordinary
temperature, it grew as white, opaque, colonies which gradually extended
and united in many cases. The gelatin was not liquefied. In peptonized
bouillon it produces turbidity for one or two days, after which the
microbe precipitates leaving the liquid clear. The reaction is
unchanged.
It lost virulence rapidly when kept in artificial culture or at a
temperature of 122° F., and was killed by a temperature of 150° F. Yet
it survived drying at moderate temperatures. Cadeac found that the dried
expectoration or blood, diffused in the inspired air produced pneumonia
with certainty in solipeds. Schütz and Fiedaler injected pure cultures
into the lung, and in other cases into the trachea, thereby inducing
pneumonia. Twenty grammes of the culture injected into the trachea
raised the temperature 2° or 3°, but this lessened on repetition and
after four or five treatments the subject proved immune.
Lignieres (1897) discovered his _cocco-bacillus_ in the exudation in the
tissues in the early stages of contagious pneumonia, from which it
disappears, giving place to other bacteria, and usually streptococcus,
as the disease reaches its maximum. (See Equine Influenza for
description). His theory is that the cocco-bacillus, which is slightly
smaller than the bacillus of chicken cholera, and appears like a
diplococcus when stained, and which may not be found after the first
eight days of infectious pneumonia, is the starting point of disease, in
this and influenza, making the system very receptive of the
streptococcus of strangles and of other bacteria, the identity of which
determines the nature of the malady. The diplococcus or streptococcus of
Schütz in his opinion is none other than the strangles streptococcus
which finding a congenial home in the animal invaded by his
cocco-bacillus, pervades the system and determines the pathological
phenomena of contagious pneumonia.
There are certain obstacles to the unreserved acceptance of Lignieres’
conclusions, among the chief of which is the absence of evidence that
horses, successfully inoculated with his cocco-bacillus in pure
cultures, can infect others standing near them with the same rapidity
and certainty, as does the casual case of influenza, or even of
contagious pneumonia. The same holds true of the supposed identity of
the streptococcus and that of strangles. Abscesses containing
streptococci, were formed in the seats of inoculation with Schütz’s
organism, but there is no evidence that the horses suffering from such
abscess affected susceptible horses standing beside them, as do ordinary
cases of strangles. The cocco-bacillus may be a concurrent cause of
contagious pneumonia, but we need more proof to show that it is the
essential cause, even as we need proof of the absolute identity of the
streptococcus of strangles and brustseuche.
_Lesions._ The pneumonia is far more likely to be double than in the
fibrinous form, and the area invaded, in its ratio with the high
intensity of the fever, is usually less. The consolidations are
especially common near the lower borders of the anterior parts of the
lungs. There may, however, be a number of centres in each lung, to be
accounted for by the inhalation of the germ and the starting of the
morbid process at the various points on which it falls. This, like the
double character of pneumonia is therefor in keeping with the contagious
origin. Each centre of condensation shows a small area, hepatized,
purulent or necrotic, with a surrounding zone of dark bluish red
congestion. The consolidated areas are less dry and granular than in
fibrinous pneumonia, seeming to be largely infiltrated with a still
liquid exudate and dark blood, and thus tend to a greater tenacity, and
less friability. Black areas of infarction form in the lung, the
thrombosis of the arteries, cutting off the free normal circulation and
the isolated portion fills up with dark blood globules and forms a
sequestrum. In the inflammatory and still living parts the color is
lighter with, it may be, some straw colored exudate, and always an
active leucocytosis, as in other inflamed parts. When infiltration is
located near the root of the lung, it is usually attached to the primary
bronchi, or larger bronchia and may extend into the upper portion or
almost the entire substance of the lung.
Simple abscess is rare, yet purulent sacs containing the gangrenous
masses or sequestra are common.
Pleuritic areas are common over the congested and hepatized foci, yet as
these are usually circumscribed in extent, an excessive hydrothorax is
exceptional. Yet the pleuritic effusion may at times become abundant.
Friedberger and Fröhner say seven gallons or more. It may become
purulent or even septic, exhaling an offensive odor. Adhesions and
fringes on the pleura are frequent.
The _heart and pericardium_ may be affected, the first showing the
pallid, soft, or parboiled appearance of high fever, with at times fatty
degeneration or petechiæ, and the latter congestion, exudation,
thickening, false membranes and liquid effusion.
The enlargement of the _congested liver_ is a marked feature. It
frequently attains the weight of 30 pounds. It may ooze dark blood
freely from the cut surface, has usually a yellowish tinge, and shows
points of fatty degeneration or even of commencing necrosis. The spleen
is like the liver, charged with blood, and shows an increase of pulp and
even petechiæ or circumscribed hæmorrhages.
The _kidneys_ are congested, friable and petechiated.
The _bronchial lymph glands_ and less constantly the mediastinal and
abdominal ones, are congested, pink to dark red and somewhat enlarged.
The gastric and intestinal mucosa may be congested, thickened,
hæmorrhagic or ulcerated.
The white tissues generally tend to an icteric hue, and the muscles
assume a mahogany aspect.
_Incubation_ appears to be longer than in equine influenza, varying in
different cases from 3 to 10 days.
_Symptoms._ These vary greatly in different cases, _mild_ and _severe_.
Some, in the same stable with the severe cases, simply refuse food, are
a little sluggish in work, cough, have hyperthermia (104° to 106° F.),
respirations 20–25, pulse 60, with conjunctiva only moderately yellow, a
slightly yellowish discharge from the nose, and no observable lung
consolidation. The temperature descends to normal in three to five days,
the symptoms generally abate, and the animal may be convalescent in
eight or ten days.
In the more _severe cases_ there may be seen a shivering fit, or it may
pass unobserved. Then the first morbid phenomenon is usually a rapid and
extreme elevation of temperature which may reach 104° or 106° F. in a
few hours. With this there is great impairment or complete loss of
appetite, and a loss of life and energy. In some cases the depression,
stupor and muscular weakness suggest influenza but this is not the rule.
Still more rare is infiltration of the eyelids and free watering of the
eyes, yet in the absence of this, drooping of the upper eyelids is not
uncommon. The respiration may be accelerated and short, from 20 to 30
per minute, and the pulse, which is usually small and weak in spite of
the fever, may rise to 50 or 70 per minute. The breathing may be
trembling or distinctly interrupted in the course of inhalation or
exhalation, short and with no interval between inspiration and
expiration. Cough may or may not be a marked feature, heard at long
intervals only in some cases and frequent and painful in others. It is
liable to be dry and husky rather than hard, loose or gurgling. The eye
and to a less extent the nasal and buccal mucosa tend to show a
yellowish shade, and this may even at an early stage show a distinct
brownish orange, or even a dark mahogany hue. Yet dropsy of the lids or
even epiphora are uncommon. A yellowish discharge from the nose is an
almost constant feature and this may dry up into a yellow crust on the
floor of the anterior nares and adjacent skin. The percussion and
auscultatory indications of lung consolidation are rarely obtainable
before the end of the second or third day and when at all extensive can
usually be detected on both sides. Trasbot considers the double
pneumonia as almost pathognomonic of contagious pneumonia. When confined
mainly to the lower parts of the lungs and occurring in isolated areas,
with lung tissue still pervious to air in the intervals, it comes more
nearly to being so. Crepitation round the border of consolidated areas,
is a more marked feature than in equal consolidations in influenza. It
often becomes inaudible again as the disease advances. Blowing murmurs,
coarse mucous râles, heart and intestinal sounds can often be heard with
unusual clearness, in unusual situations, when an area of consolidated
lung is immediately beneath. A transient dry friction sound of
commencing pleurisy is sometimes detected over a tender intercostal
area, but soon giving place to the uniform quiet of effusion rising to a
given horizontal level. Later still there may be the creaking sound of
organizing false membranes in process of being stretched, and which is
so often confounded with crepitation. The indications of pneumothorax
(tympanitic resonance, and metallic tinkling), are rare. In advanced
stages there may be tympanitic sound from the cavities of abscesses or
the sacs containing sequestra.
The urine is always scanty and high colored and may at times prove red
and hæmorrhagic. Albuminuria is usually present when the disease is at
its height. The same is true of uric acid, which replaces the hippuric
acid, in cases of high fever and complete abstinence so that the
products are drawn from the disintegrating tissues alone. The returning
appetite, and the restoration of a neutral or alkaline condition of the
urine, therefore tend to occur simultaneously, and to mark improvement.
Great tenderness of the throat, protrusion of the nose, and difficulty
of swallowing mark the localization of the lesions on the pharynx and
larynx. It is liable to be accompanied by the introduction of exudation
and food materials into the larynx and trachea with the occurrence of
inhalation bronchitis and pulmonary gangrene.
Symptoms of pericarditis, endocarditis and myocarditis, are especially
common in the more severe types of the disease. With soft, weak or
imperceptible pulse and tumultuous heart beats they may be suspected,
and further indications are a transient friction sound, synchronous with
the beat of the heart, intermissions, murmurs with first or second heart
sound, and an increasingly low, distant, or muffled heart beat, as
pericardial fluid accumulates. As in the case of troubles with the
kidneys or liver, stocking of the legs, or dropsical swellings elsewhere
may appear.
Exceptionally, acute nervous symptoms may appear, due to functional
derangements caused by circulation of the toxins and metabolic products,
or even to congestion or inflammation of the brain or its membranes.
This may occur at the outset of the disease indicating the election of
the nerve centres for the colonization of the microbe, and advancing to
a rapidly fatal issue (Friedberger and Fröhner). It may set in with
hepatization (Rey), or it may coincide with pulmonary gangrene (Cadeac).
There may be merely dulness, prostration, or stupor; or trembling,
unsteady gait, or falling; there may be rolling of the eyes, or
amaurosis, or vertigo occurring intermittently; or there may be
epileptic attacks or paraplegia.
_Course._ In moderate cases the disease may last from two to three
weeks, and in well conditioned horses, with strong constitutions, tends
to recovery. On the third to the eighth day all the symptoms appear
better, appetite, expression, alertness, breathing, pulsation and
temperature. The temperature which has been a degree, or more, higher in
the afternoon than in the morning, remains about the same from morning
to night, or is even slightly lowered; it is lower still next morning
and in two or three days may have reached 101°, still rising a little in
the afternoon. The pulmonary exudate is usually quickly absorbed though
less so than in favorable cases of influenza. Convalescence may be
completed by the end of the third or fourth week.
In _violent_ and _fatal cases_ the general symptoms tend to encrease in
violence, though the temperature may descend to 103°, and in the final
collapse to 100° or lower. In a mare presented at the college clinic
after three weeks illness and treatment elsewhere, prostration was
extreme, the head rested in the manger, the nose discharged a fetid,
glairy, frothy liquid, with grumous, bloody debris; breath offensive;
pulse 92, almost imperceptible; respirations 30, very labored; nostrils
widely dilated, flapping; temperature in vagina 103.6°, anus was open
with constant ingress and egress of air, and a watery glairy, frothy
discharge; extensive dropsy under the sternum; percussion and
auscultation indicated consolidation of lungs from the lower border up,
crepitation, creaking, and loud clucking bronchial sound. The mare
survived for forty-eight hours, the temperature descending to 100.5° in
the morning and rising to 102° and upward in the afternoon. At the
necropsy the right lung was consolidated throughout, the left had
pervious areas anteriorly and posteriorly; there were large areas of
infarction, necrosis, with encystment, caseation, and lobular and
perilobular exudation and hepatization.
Liver, enlarged, tense in its capsule, but soft and friable on its cut
surface, with areas of softening and necrosis. Both kidneys congested,
with pale zones of necrosis; right enlarged. Beside the substernal
exudate, there was extensive hæmorrhagic exudate between the serratus
magnus and ribs. The blood, very dark, brightened on exposure to air.
_Diagnosis_: This may be based mainly on the prevalence of the disease
in the district, or the fact that the victim has come from a long
railway journey with risks of exposure, or has stood by a horse just
arrived; on the prompt loss of appetite and sudden and extreme rise of
temperature, without notable lung lesions; on the deep brownish yellow
discoloration of the visible mucosæ, especially that of the eye, and on
the yellow discharge from the nose, the tardiness with which successive
cases follow each other comparatively to influenza, and the absence in
large measure of the early extreme prostration of that affection. (See
table under _influenza_).
_Prognosis_ varies with the progress of an epizoötic, and the youth and
susceptibility of the animal together with the favorable or unfavorable
conditions of life. The death rate is usually high at the outset when
the more susceptible animals are attacked, and for the same reason, in
the young that have not been previously exposed. Old and debilitated
animals with broken down constitutions suffer severely, and bad hygiene
contributes much to the mortality. The deaths vary from one to twenty
per cent. But short of death, permanent injury follows in a number of
cases. Encysted sequestra remain in the lungs for months and when
liquefied and absorbed, leave fibroid masses in place of healthy lung
tissue. The fibrous organization of peribronchial exudates, impairs
respiration, and the same is true of the fibrous development of false
membrane. Thus the horse is left permanently _broken-winded_ or
_short-winded_, or from interference with the recurrent laryngeal nerve,
laryngeal hemiplegia (roaring) ensues. In still other cases permanent
adhesions of the pericardium, or insufficiency of the cardiac valves, or
disease and distortion of joints or tendons, or nervous, hepatic or
renal degenerations destroy or seriously impair the value.
_Treatment._ Hygienic measures are of prime importance in treatment. A
dry, clean box stall with pure air, and genial warmth (60°–70° F.)—in
warm summer weather outdoor air—must be secured. In cold weather a sunny
outlook, and clothing—blanket, bandages, and it may be a hood—to
counteract any sensation of chill. Tepid drinks, pure water changed
often, linseed tea, barley water, are of importance in allaying thirst,
lowering temperature and favoring elimination. Absolute rest is all
essential. Keeping at work after the onset of the disease is nearly
equivalent to signing the patient’s death warrant.
The high temperature at the outset of the disease seems to demand
antipyretics, and in times past, in Southern Europe especially, bleeding
was a constant resort. But even under favorable conditions this does not
lower the temperature more than 1.5° F., and the resulting debility is
such that it has been long discarded in Germany, England and America. In
cases of acute extensive pulmonary congestion it is helpful in relieving
the vascular tension on the lungs and allowing the tissues to better
reassert their natural functions, in antagonism with invading microbes
and their poisons, but even this action is transient, and when it saves
life it is probably only by tiding over safely a very transient and
urgent danger.
The same decline of temperature can usually be secured by injections of
cool water into the rectum, and with the added advantage that this
relaxes the bowels, and removes dried irritant masses from the rectum
and floating colon.
As in other pneumonias the application of cold to the skin is liable to
bring on a chill unless the temperature is very high. A safer and hardly
less effective method is to apply around the chest a thin blanket or
sheet wrung out of tepid water and cover it closely with dry blankets
holding these close to the skin by elastic circingles. No part of the
damp compress must be allowed to remain exposed to the air under pain of
causing chill. Damp cotton wool applied next the skin tends to maintain
its contact by its own elasticity, so that it requires less care in the
elastic dry covering. This moist warmth draws a free circulation of
blood to the skin, so that it is cooled and sent back internally to cool
the burning fever, without sensation of chill. The abstraction of this
large mass of blood to the skin, acts like bleeding in diminishing the
blood tension in the chest and allowing the resumption of the normal
vaso-motor and nutritive functions without the dangers of venesection.
The soothing action on the skin, soothes by sympathy the infected and
inflamed tissues.
A steam or hot air bath may serve a similar purpose. Conjoined with an
aloetic laxative and aconite, I have seen this reduce the temperature
from 104.5° F. to 102.7° F. at the next taking 18 hours later. It only
once again reached 103° F. in the subsequent course of the disease.
To secure diaphoresis, warm mashes or gruels may be freely used.
Alcoholic drinks have been freely used (the weaker wines 1 to 2 qts.,
sherry, brandy, whisky ½ to 1 pint), camphorated spirit (2–3 drs.)
subcutem, ipecacuan (1 oz.), tartar emetic (2 drs.), liquor of acetate
of ammonia (4 ozs.), pilocarpin (2 grs. subcutem). If the alcoholic
liquors produce a free circulation and glow in the skin, better still if
diaphoresis, they are useful antithermics, but, if they fail in this,
they may do harm by reducing the vital activities of the leucocytes, and
their power of resistance. Trasbot has had uniformly unfortunate results
with alcohol in large doses. The same objection attaches to tartar
emetic and other depressant diaphoretics, though valuable if free
diaphoresis is secured.
Constipation may be met by cold water injections, calomel (½ to 1 dr.),
pilocarpin (3 grs.), eserine (1½ gr.), sodium sulphate or other agent
graduated to requirement.
An expectorant and alkaline diuretic action may be obtained from
potassium iodide (1–2 drs.), ammonium chloride (2 drs.), or ammonium
acetate. These not only liquefy the exudate, and facilitate
expectoration, but secure elimination of toxins, ptomaines and waste
products from the blood and system. The iodide is besides somewhat
antiseptic.
In the early stages especially medicinal antithermic agents may be
called for: acetanilid (2–3 drs.), phenacetin (2–4 drs.), sulphate of
thallin (2–3 drs.), sodium salicylate (½ oz.) or in the weaker cases,
caffein—natrium salicylate (1 dr.) or quinine sulphate (2–3 drs.)
Acetanilid will sometimes relieve dullness, and materially improve the
general condition.
In weak conditions of the heart we may resort to digitalis (10–15 grs.),
strychnia sulphate (2 grs.), strophanthus tincture (3 to 4 drs.),
caffein, or alcohol. Care must be taken not to overstimulate and exhaust
a weak and intermittent heart.
Derivatives are often of material value from the first, in mild cases or
to succeed damp compresses in the more violent ones. One of the best and
most convenient is essential oil of mustard and alcohol (1:12 or 20).
This may be rubbed on the surface and like mustard itself, covered with
stout paper to prevent evaporation. In the absence of this, soap
liniment, or even tincture of cantharides may be used.
The use of antiseptics has been tried with variable results. While it is
impracticable to saturate the system, safely, with sufficient antiseptic
to destroy the microbes in the blood and tissues, yet when the balance
of force between the microbian attack and systemic defence shows little
variation either way a slight increase on the side of the patient may
serve to give it the preponderance, and to restrict the increase of the
microbes and their products. Above all when the center of morbid
activity is largely on and near the bronchial mucosa, antiseptic
inhalations serve to hold them somewhat in check and to moderate the
amount of both microbes and toxins that enter the system at this point.
For this purpose camphor, oil of turpentine, or oil of tar volatilized
from hot water may be inhaled in a close room. Or we may use carbolic
acid, terpene, terpinol, creolin lysol, thymol, eucalyptol, or oil of
cinnamon. The fumes of burning sulphur diffused in the air of the room
and just short of that concentration that will cause cough, suffering
and headache, is an excellent resort. The sulphites, bisulphites or
hyposulphites may be given by the mouth.
When there are indications of encephalitis cold to the head and the
internal exhibition of bromides, iodides, and acetanilid may be resorted
to.
During convalescence nourishing and easily digestible food may be given,
and iron, strychnia, quinia and common salt may be employed. In
protracted or chronic cases with fœtid breath and indications of
sequestra or opened vomica in the lungs these may be continued along
with one or more of the disinfectants referred to above.
_Prevention._ This is much more promising than in equine influenza. The
extension of incubation to three days and the indisposition of the
infection to spread beyond the stable into which it has been brought, or
the near vicinity of the diseased animal, gives us a great relative
advantage. The early, extreme rise of temperature of the infected horses
gives the opportunity of removing these horses to a special stable or
shed, where they can have special attendants, and the stable drainage
and manure can be kept apart, and disinfected, or spread and plowed
under by oxen. The infected stable should be emptied, the soiled hay,
litter and manure burned, and the walls, partitions, floors, ceilings,
and above all the mangers and racks must be thoroughly disinfected. Lime
wash with chloride of lime or mercuric chloride will suffice. The
gutters should be cleaned, washed and drenched with mercuric chloride,
followed by the whitewash. If there is rotten wood work or
filth-saturated soil these must be effectually treated. In many stables
it will be impossible to do all this thoroughly, yet closing the empty
building tightly, and filling it with chlorine gas, or even sulphur
fumes, concentrated until they extinguish the burning sulphur, and
keeping shut up for twenty-four hours will usually suffice. Washing with
a solution of formalin (1:40 or 1 per cent of formaldehyde), or even the
evaporation of this agent by heat in the closed building is very
effective, with the serious drawback that it is very irritating to the
lungs. It can however be conveniently used for the sterilization of
harness, stable implements, halters, and all movable objects in the
building.
Strange horses, such as new purchases, should be placed in quarantine
for one week in a separate stable, and not hitched up with sound horses.
If they show evidence of recent illness this may be extended to six
weeks.
For horses that have been shipped long distances, and stopped for rest
or feeding in public stables or yards, a similar quarantine is
essential. This might be obviated if a system of thorough disinfection
of such stables, yards and cars, could be enforced, between any two
successive lots of horses, and if the latter were accompanied by
certificates of the absence of contagious pneumonia and all other
infectious diseases from the localities from which they were shipped and
through which they had come. Such certificates should be made by
veterinary officials in the employ of the government, which would thus
become responsible for their genuineness.
In view of the frequent persistence of this malady in a given stable for
a great length of time, successive animals being attacked at long
intervals, and where isolation was impracticable, Beckmann rubbed the
nasal discharges of the sick on the nasal mucosa of the unaffected,
producing the disease almost invariably in a mild form. The infected
animals were placed in the best hygienic conditions, the duration of the
infection was shortened, and the horses being rendered immune, the
stable was then disinfected with a satisfactory result.
Schütz, Hill, Pilz and a number of others have sought artificial
immunity, by the injection of blood serum from a horse that has recently
recovered from the malady. The results were very contradictory. In some
cases the disease came to a sudden end. In other stables no new cases
appeared either in those treated with serum or in those left without
treatment. In other experiments, new cases occurred among those treated
with the serum;—in Weishaupt’s cases after a lapse of one or two months.
This is exactly what might be expected. If the horse supplying the blood
serum had really recovered, and if the microbes (streptococci) had
disappeared from the blood, the latter would of necessity retain little
of the toxins, but much more of the antitoxins, the active production of
which would be continued by the stimulated leucocytes. These antitoxins
would neutralize the toxins, in case of invasion and prevent that from
reaching the maximum of intensity that it would otherwise have reached,
but would be powerless to stimulate the leucocytes of the inoculated
animal into the habit of themselves producing antitoxins. This would act
rather as a curative than a prophylactic agent, and its value would be
spent as soon as the injected antitoxins were eliminated from the
system.
The true line of inquiry would have been, whether injection of the
toxins, which acting on the leucocytes would have stimulated these to
the habit of producing antitoxins in large amount, might not be expected
to give an immunity as lasting as that which follows on a casual attack
of the disease. Lignieres appears to have approximated to this, in his
experiments on mice and rabbits. In horses suffering from contagious
pneumonia it lowered the temperature, but did not materially affect the
result of the attack. If we adhere to Lignieres’ own theory of causation
by cocco-bacillus and later by streptococcus or some other complicating
infection, we can scarcely hope that the toxins of the streptococcus or
other complicating microbe will immunize against the cocco-bacillus or
mutually against each other. If complete protection is aimed at, the
toxins of his cocco-bacillus, and of Schütz’s streptococcus, and of any
other possible microbe which may produce a secondary complication, ought
to be employed.
At the date of this writing no satisfactory sero-therapy for this
disease has been worked out and publicly demonstrated.
INFECTIOUS STABLE BRONCHITIS. SCALMA.
_Definition._ An infectious inflammation, of the upper air passages and
bronchia, attended by high fever, special nervous irritability and a
protracted convalescence.
Dieckerhoff gave the name _scalma_ (rogue) to outbreaks in given stables
of an infection, showing the high temperature of brustseuche, (104° to
107° F.) a similar incubation (6 to 7 days), a correspondingly tardy
extension from animal to animal, and duration of the disease. The
apparent differences are in the absence of the profound dulness, the
yellowness of the mucosæ, and the yellow or rusty nasal discharge, in
the ready response to the voice or touch, the disposition to bite or
kick, the spasms of the larynx and sudden dyspnœa, in certain cases, and
the paroxysmal cough in others. Apart from these transient respiratory
troubles the pulse and breathing are unaffected, relatively to the
elevation of temperature. Sometimes the jaws are kept in constant
motion, from nervousness or pharyngeal trouble.
In the absence of any conclusive bacteriological investigation, it may
be surmised that this is a form of brustseuche which has not advanced to
the same grade of destruction of red globules and prostration of the
nerve centres, the latter showing only an excited and irritable
condition.
_Treatment_ and _prevention_ do not differ materially from what is
required in contagious pneumonia. The irritable cough may be soothed by
inhalations of warm water vapor, with alcohol, camphor, eucalyptol, or
opium, or electuaries of bromides, belladonna or stramonium, and local
derivatives to the throat.
Most cases are mild and recover in a week, the cough lasting for two
weeks more.
OTHER INFECTIOUS PNEUMONIAS OF THE HORSE.
Claims have been made for infections by a variety of other germs which
it would be difficult or unreasonable to deny. In given conditions of
the horse’s lung it may succumb to the attacks of pathogenic
microörganisms which at other times or under other conditions would be
practically harmless. Thus the round ended bacillus of Friedländer is
claimed by Jacquot and others to cause one form of pneumonia in the
horse as it does in man (Vol. 1 p. 216). Again Galtier and Violet have
claimed a form of pneumonia transmitted through musty or spoilt fodders
and attacking the bowels as well as the lungs (pneumo-enteritis). Two
micro-organisms are accused, a diplococcus and streptococcus, which is
strongly suggestive of the now familiar germ of brustseuche.
EQUINE INFLUENZA. ADYNAMIC CATARRHAL FEVER OF SOLIPEDS.
Synonyms. Definition. Historic notes. Equine influenza of 1872–3; its
indication of infection. Other evidence: through stables, cars,
manure, clothes, coition, inoculation. Bacteriology: streptococci;
diplococci; cocco-bacillus, latter pathogenic to rodents, dog, cat,
sheep, pig, ox, ass, pigeon, chicken. Inoculations on horse. Present
in early stages only. Uncertainty. Accessory causes: chill, electric
tension, high barometer, impure air, overwork, poor feeding, season,
youth, primary susceptibility, acquired immunity. Incubation 1 to 3
days. Symptoms: Forms: sudden attack, anorexia, profound prostration,
weakness, hyperthermia, epiphora, brownish red conjunctiva, pulse,
heart beats, catarrhal symptoms, thoracic, pulmonary, pleuritic,
cardiac, digestive, urinary, diarrhœal, ophthalmic, nervous,
rheumatoid; complications, abortion, laminitis, strangles, contagious
pneumonia, cerebro-spinal meningitis, etc. Lesions: inflammation of
mucosæ of nose and air passages with blood unaffected; in severe
attacks, with heart clots, or later with blood black, diffluent, red
globules crenated or dissolved, without viscidity or rouleaux, reddish
serum, and hæmatoidin in masses, acid reaction, petechiæ; congestion
of mouth, stomach, small intestines or large,—ulcers, tumid follicles,
peritoneal effusion, enlarged congested mesenteric glands; liver as if
parboiled, with petechiæ and necrosis; spleen large and gorged;
kidneys infiltrated, mottled, petechiated, swollen; may be meningeal
or ophthalmic congestion; pulmonary lesions, pleural effusions,
adhesions, infiltrations, consolidations, infarctions, sequestra.
Diagnosis: sudden attack, great numbers attacked, marked prostration,
conjunctivitis, great hyperthermia, digestive disorder, evidence of
infection. Table comparing croupous and contagious pneumonia and
influenza. Prognosis. Mortality low,—high in some epizoötics, in
horses kept at work, under bad hygiene. Treatment: good diet and
hygiene, rest, shelter, stimulating diuretics and diaphoretics,
venesection, antipyretics, alkaline eliminants, inhalants—water
medicated, derivatives, collyria, guarded laxatives, antiseptics,
cardiac stimulants, nerve sedatives, tonics, transfusion of blood,
normal salt solution,—technique. Prevention: quarantine difficult, yet
possible; examples, applicability to countries, to districts, lines of
restriction.
_Synonyms._ Epizoötic Catarrh; Catarrhal Fever; Nervous
Fever; Epizoötic; Rheumatic Catarrh; Cocotte; Gastro-enteric
Epizoötic; Gastro-entero-nephro-hepatitis; Gastro-Conjunctivitis;
Gastro-Hepato-meningitis; Entero-pneumo-carditis; Pink eye; Epizoötic
Cellulitis; Typhose; Typhoid Fever; Blitz Catarrh; LaGrippe; Septicæmia
Hæmorrhagica etc.
_Definition._ An infectious fever of solipeds, of a specially low or
adynamic type, and with a tendency to localization on the respiratory or
gastro-intestinal mucosa, on the eyes, lungs, pleura, heart, liver,
kidneys, subcutaneous connective tissue, joints, fascia, or nervous
system.
This disease was long confounded with the _influenza_ of man and while
compelled for the identification of the affection, to retain this name
in combination with the qualification _equine_, yet we would prefer to
discard it entirely as conveying the idea that the illness is caused by
Pfeiffer’s bacillus, which it is not. The term _typhoid fever_ which is
in common use in France, has been selected to convey the impression of
its two prominent features of _hyperthermia_ and _stupor_. But it is
open to the same objection for it has been long applied to a specific
disease in man having its own bacillus which is not present in the
_equine influenza_. _Septicæmia Hæmorrhagica_ which has been adopted
more lately, however correct it may be as indicating the tendency of the
local lesions has a generic meaning rather than a specific one, and
requires much more qualification to correctly designate the disease. The
term _adynamic catarrhal fever of solipeds_ has this recommendation,
that it expresses the prostration and debility which is such a marked
feature of the disease, its great tendency to become localized on mucous
surfaces, and the genus of animals that prove its victims. A better
designation is still desirable and may perhaps be reached, when the
pathogenic microbe shall be demonstrated beyond question.
_Historic Notes._ Among catarrhal fevers and epizoötics of early times
it is impossible to distinguish this from widespread nasal and bronchial
catarrhs, and from contagious pneumonia (brustseuche), yet when the
epizoötic attained a sudden and wide extension without any direct
climatic cause, the presumption is in favor of the disease now before
us. Hints are obtained from Titus Livius of a Sicilian equine epizoötic
of this kind 412 B. C. This is corroborated by an account by Hippocrates
of a similar outbreak in Greece. Later, Virgil (Georgics), Columella,
Absyrtus and Vegetius give similar hints. In 1299 in Seville horses
suffered with drooping head, watery eyes, beating flanks and anorexia
and 1000 died (Laurentius Rusius). The horses of the French Army in
Germany suffered severely in 1648 (Solleysel), horses in England in 1688
(Short, Rutty), again in 1693 (Webster, Short, Foster) and again in 1699
(Webster). In 1712 horses suffered extensively in Europe (Lancisi,
Kanold) and in 1727–8 in England and Ireland (Rutty), in 1732–3
(Arbuthnot, Gibson) and again in 1736–7 (Short). Other such equine
epizoötics are recorded for Europe in 1729 (Löw), for Ireland in 1746
and 1750–1 (Rutty, Osmer), for Europe and the British Isles in 1760
(Bieset, Rutty, Webster), and again in 1762 (Rutty, Webster) and 1767
(Forster), also in America (Webster), in Europe in 1776 (Fothergill
etc.), in Europe and Asia in 1780–2 (Gluge), in England in 1798
(Wilkinson, White), in Europe and England in 1814–15 (Heusinger,
Wilkinson, Youatt), in England in 1819, 1823 (Field) and 1827 (Brown),
in Europe in 1833 (Prinz, Wilkinson, Hayes, Spooner), 1834 (Hensinger),
1835–6 (Prinz, Friedberger), 1840, 1846, 1851, 1852, 1862, 1870, 1873,
1881, 1883, 1890, 1891, 1892 (Friedberger).
In the United States as in Europe the affection has in the main
smoldered in the large cities in ordinary years, to break out without
obvious cause, in given years into an advancing epizoötic which sweeps
the whole continent. Such were the great outbreaks in Europe in 1881 to
1883, and in America in 1872–3, and 1900 to 1901. The great
recrudescence of the disease in North America in 1872–3 was so
remarkable in its progress and limitations that it seems desirable to
recal its more prominent historic features. The unquestionable
demonstration of the microbe of the affection may make such a record
superfluous, but until then, and so long as books are published which
attribute the disease to the environment, or to the soil, it is not
altogether unnecessary.
PROGRESS OF EQUINE INFLUENZA OF 1872–3.
_Last week of September, 1872._ Toronto, _Ontario_; (30th) and
neighborhood.
_First 2 Weeks of October._ Barrie, Collingwood, Owen Sound, Guelph,
_Ont._; St. John, _N. B._ (13th); Niagara Falls, (11th), _N. Y._;
Montreal (8), Ottawa (12th), Stratford, Brantford, London, _Can._;
Buffalo, _N. Y._ (14th); Detroit, _Mich._ (13th).
_Third Week in October._ Goodrich, Kingston, (19th), _Ont._; Rochester
(18th), Syracuse, Lockport, Canandaigua, Geneva, Albany, (19th),
Ogdensburg, (21st), New York, (21st) _N. Y._; Bangor, _Me._; Port Huron,
_Mich._
_After Third Week in October._ Quebec, (28th) _Can._; Utica, (29th),
Watertown, Oswego, Schenectady, Saratoga Springs, Poughkeepsie (28th),
Elmira, Binghamton, (28th), Jamestown, Ithaca, (31st), Port Jervis
(29th), Nyack, _N. Y._, (30th); Revere, (22d); Springfield, (23d),
Worcester, (27th), Fall River, New Bedford, _Mass._; Waterbury, (27th),
Norwich, (23d), New Haven, Hartford, _Conn._; Providence, (23d),
Newport, _R. I._; Burlington, (26th), St. Albans, _Vt._; Concord,
Nashua, Portsmouth, (23d), _N. H._; Bath, (28th), Portland, _Me._;
Philadelphia, (26th), Harrisburg, Lancaster, York, Erie, Corry,
Titusville, (28th), Pittsburg, (29th), _Pa._; Baltimore, (25th), _Md._;
Washington, _D. C._, (28th); Norfolk, (31st), Richmond, _Va._;
Cleveland, _O._; Chicago, (29th) _Ill._
_First Week of November._ Kingston, _N. Y._, (1st); Rutland, _Vt._,
(3d); Meadville, (2d), Pottsville, Williamsport, (6th), Reading, Easton,
Bethlehem, _Pa._; Trenton, _N. J._, (2d); Wilmington, _Del._, (6th);
Jackson, _Mich._, (7th); Milwaukee, _Wis._; Raleigh, _N. C._;
Charleston, _S. C._, (4th).
_Second Week in November._ Scranton, _Pa._, (13th); Lynchburg, _Va._,
(11th); Wheeling, (13th), Parkersburg, _W. Va._; Dayton, Sandusky,
Toledo, _O._; Adrian, Kalamazoo, (9th), Grand Haven, _Mich._ (8th);
Davenport, _Ia._, (14th); Janesville, Green Bay, _Wis._; Louisville,
_Ky._, (9th); Wilmington, _N. C._, (12th); Columbia, _S.C._; Savannah,
_Ga._
_Third Week in November._ Steubenville, (15th), Columbus, (16th),
Zanesville, (16th), Springfield, _O._; Indianapolis, (17th), Fort Wayne,
Lafayette, Evansville, (21st), _Ind._; Bloomington, Galena, (21st),
_Ill._; Dubuque, Iowa City, _Ia._; Madison, Fond du Lac, _Wis._; St.
Paul, _Minn._; Memphis, Nashville, Chatanooga, _Tenn._; Augusta,
Atlanta, _Ga._; Helena, Fort Smith, _Ark._; Havana, _Cuba_, (20th).
_In November after third Week._ Terre Haute, Madison, _Ind._; Peoria,
Galesburg, _Ill._; Keokuk, Muscatine, Des Moines, _Ia._; Paducah, _Ky._;
Knoxville, _Tenn._; Charlotte, New Berne, _N.C._; Macon, Rome, Columbus,
_Ga._; Jacksonville, Lake City, _Fla._; Mobile, Montgomery, Selma,
_Ala._; Natchez, Vicksburg, _Miss._; New Orleans, (25th), _La._;
Galveston, (29th), Houston, (28th), _Tex._; Little Rock, _Ark._
_First week in December._ Cairo, _Ill._; Lincoln, Omaha, Nebraska City,
_Neb._; Yankton, (5th), Vermilion, _Dak._; Tallahassee, _Fla._; Camden,
_Ark._; St. Louis, Kansas City, _Mo._
_Second Week in December._ Quincy, _Ill._ (8th); Shreveport, _La._;
Hanibal, _Mo._; Fort Scott, Lawrence, Leavenworth, Topeka, _Kan._
_December after the Second Week._ Denver, Central City, _Col._;
Cienfuegos, _Cuba_.
_January 1873._ San Antonio (3d) _Tex._; Cheyenne, _Wyo._; Cimarron,
(1st week), Elizabeth City (2d week), Alberquerque (4th week), _N. M._;
Salt Lake City, (2d week), Corrinne (3d week), _Utah_; Santiago, _Cuba_.
_February._ Brownsville (3d week) _Tex._; Winnemucca, _Nev._; Monterey
(1st week), _Mex._
_March._ Prescott (1st week), Tucson (2d week), Yuma (4th week) _Ariz._;
Boise City, (3d week), _Ida._; Helena (4th week) _Mont._; Virginia City,
(1st week), _Nev._; Carson City, _Nev._, Santa Barbara, Visalia, _Cal._;
Guaymas, Mazatlau, Manzanillo, _Mex._
_April._ San Diego (1st week), Mariposa, Stockton, San José, Oakland,
Sacramento, Marysville and Shasta (2d week), San Francisco, Vallejo,
Nevada City and Weaverville (3d week), and Lava Beds, _Cal._ (4th week);
Baker City (2d week), Jacksonville, _Ore._ (4th week); Walla Walla,
_Wash._ (4th week); Acapulco (1st week), _Mex._
_May._ Eugene City, (3d week), Dallas and Portland, _Ore._ (4th week);
Olympia, _Wash._
_June._ Seattle, _Wash._ (3d week).
_July._ Guatemala City, Guatemala (2d week), Victoria, _B. C._
_August._ La Union, _San Salvador_ (1st).
Among the deductions from this record are:
1. The affection advanced gradually from Toronto over the whole
continent of North America, where horses are kept, taking full ten
months to accomplish this. Nothing checked its advance, over lowland and
highland, swamp and arid land, in summer as in winter, with a
temperature at 0° or at 100° F., in country pasture or in city street or
stable, idle or overworked, on all kinds of soils and geological
formations, under all successive conditions of meteoric and terrestrial
electricity, in all conditions of the air—pure, impure, dense, light,
moist and dry. No one condition of the environment operating on the
animal system, can be conceived of that could advance as this disease
did from place to place in regular sequence for this length of time.
2d. The rapidity of its progress was manifestly subordinate to the
activity of the movement of the equine races from points already
infected. Its most rapid advance was along the lines of railway while
the back districts shut out from railway traffic were much later in
being invaded. The larger cities situated on the through railroad routes
suffered earlier than the smaller places on the same lines. The outbreak
was several days earlier in Montreal than in the nearer and smaller
cities of Kingston, Ottawa, Belleville, Port Hope, Peterboro, Stratford,
Brantford, Guelph, London and Owen Sound. The important port of St.
John, N. B., suffered two weeks earlier than Quebec. Along the N. Y.
Central and Erie Railways etc., Boston and New York suffered nearly a
week earlier than Utica, Poughkeepsie, Binghampton, Elmira, and
Jamestown, while the smaller places like Kingston, Nyack, Ithaca, etc.,
were later still. In Baltimore the disease was seen a day earlier than
in Philadelphia, and in these cities and Washington over a fortnight
before it was seen in Scranton, Pa. So it was almost everywhere and in
these large cities the outbreak could in nearly every case be traced to
horses just arrived from a pre-existing centre of infection. In Detroit,
Syracuse and Chicago it spread first in stables that had just received
Canadian horses, in Ithaca in one which had received horses from an
infected centre in Northern New York and in Pittsburgh and Washington in
stables that had just admitted horses from infected New York.
3d. It advanced with much greater rapidity eastward than westward, being
in the line of greatest horse traffic, the animals being mainly raised
and fitted in the West and shipped in large numbers to the great cities
near the Atlantic seaboard.
4th. In the absence of this active railway traffic In horses, the
advance was most rapid through other lines. In Pa., in a number of
valleys opening to the south, the disease reversed its general
direction, and extended northward up these valleys. In Lehigh Co., Pa.,
it followed the course of the canal, being carried by horses and mules
employed on the towpath. In Davidson and Sumner Cos., Tenn., it followed
the track of a circus which came through an infected locality. It
reached the Pacific coast at Santa Barbara (not at the railway terminus
at San Francisco) having followed a mule stage route in the absence of
an active, westward progress of horses by rail.
5th. The affection failed to overstep any serious gap over which there
was no movement of equine animals. It prevailed in Victoria, B. C., in
July, but, owing to a strict quarantine on horses and mules, it failed
to reach Vancouver Island. It ravaged New Brunswick and Nova Scotia in
November but failed to reach Prince Edward Island which was then ice
bound and shut off from all traffic with the mainland. It ravaged Cuba
to which it was brought by American horses landed at Havana, but no
other West Indian island was attacked. Its southward course was finally
arrested at Central America, where horses are few and horse traffic
nearly unknown.
Every fact in connection with its eruption and progress agrees perfectly
with the hypothesis of transmission by contagion alone, and taken
altogether the history excludes all other causes from being anything
more than accessory. Before the days of modern bacteriology we had ample
proof that glanders, rabies, sheeppox, lung plague, and Rinderpest were
due to contagion alone as an essential cause, and so now we have the
same evidence concerning equine influenza.
_Other testimonies to Contagion._ Trasbot says the virulence is “almost
equal to that of Rinderpest or aphthous fever,” and adds “all
practitioners have become assured that the bringing of an affected
animal into a stable constantly introduces the malady to the others.”
Cadeac says “the diseased or infected animals are the main channel of
propagation of the malady” and again the disease is “essentially
infectious.” Friedberger and Fröhner are more definite—“influenza which
is as highly infectious as any other disease can be produced only by
infection.” Cadeac implies nearly as much in saying: “in all the
epizoötics that have invaded Paris, the disease has been carried into
the four quarters of France by horses bought in this city. In most
regiments the malady shows itself after the arrival of horses from
remounts where it was prevailing. At Sibourne it is through horses from
St. Jean d’Angely. At Lyons it is by a horse from Cæn. At Bourges the
source was not traced but it spread from the garrison to the whole
surrounding country. The Omnibus stables in the Rue d’Ulm were invaded
when a horse was introduced from Clichy where influenza raged.”
_Stables_ are fruitful sources of infection hence dealers’ horses and
horses travelling from place to place have long been objects of just
suspicion (Trasbot, etc.).
_Cars_ are often infected, and spread the disease widely. (Poucet,
Salle, Trasbot, etc.).
_Manure_ is especially dangerous. Trasbot gives a number of cases of the
infection of farms, by the manure taken from the Alfort Veterinary
College, and other infected stables in Paris. Friedberger conveyed the
disease experimentally in the manure.
The conveyance of the virus on the _clothes of attendants_ has been
alleged by Friedberger and Fröhner, and considering that it has been
noted to pass over intervals of about half a mile without the
intervention of any horse, it must have been wafted on the air, or
conveyed on the surface of man or non-equine beast.
Jensen and Clark allege that the contagium may be conveyed to mares by
_coition, for months_ after the stallion has shown all outward signs of
recovery. This would be entirely in keeping with the analogous fact in
swine plague.
_Inoculation._ Experimental inoculations have transmitted the disease
with difficulty and uncertainty. Those of Hertwig, Nocard, Arloing,
Labat, Friedberger, Trasbot, Pasteur and others came to naught. Even the
transfusion of the blood of the sick, proved as harmless as the
inoculation of the serous exudate. A probable explanation is found in
the extreme diffusibility of the germ of equine influenza, which spreads
over a city or county in a few days, attacking practically all equine
animals. Inoculation is necessarily made at the time of the prevalence
of influenza and at such a time all horses in a wide area are likely to
be suffering from the affection. Those that are unaffected and therefore
apparently available for experiment, are the immune animals. If they
were susceptible the probability is that they would speedily show the
disease through infection drawn from another source than the
inoculation. If the inoculated animal failed to contract the disease,
and yet very shortly afterward became infected by simple exposure, there
would be some basis for alleging that inoculation was always
inoperative. Dieckerhoff, on the other hand, transmitted the disease to
healthy horses by subcutaneous and intravenous inoculation of the blood
of the sick, and the same seems to be true of inoculations of the
cultures of the cocco-bacillus by Lignieres.
_Bacteriology._ Our knowledge of the bacteria of equine influenza is as
yet very imperfect and uncertain. Galtier and Violet found streptococci
and diplococci in the blood and tissues of cases showing intestinal
lesions, and held that they were derived from musty fodder. Injections
of infusions of such fodder into the trachea of the horse produced
broncho-pneumonia, double pleuro-pneumonia, and at times intestinal or
meningeal congestion. But there is no proof that the malady so caused,
passed with the certainty and rapidity of equine influenza from horse to
horse in the same stable.
The _cocco-bacillus_ found by Lignieres in the blood and exudate of the
patients has more plausible claims to being the specific germ. This is
an ovoid bacterium, somewhat smaller than that of chicken cholera, and
like it pigmented at the poles and clear in the central part, a
characteristic feature of the group of Pasteurella of Trevisan. This
group includes the nonmotile germs of swine plague, the septicæmic
pneumo-enteritis of sheep, wildeseuche, and septicæmia of rabbits and
chickens, as well as that of fowl cholera; all stain easily in gentian
violet and fuchsin, and all cause some form of hemorrhagic septicæmia.
The germ is ærobic and grows best in peptonized bouillon to which a
little serum has been added. It forms, in peptonized gelatin, round
colonies, at first transparent and later opaque or milky, and without
liquefaction. The cultures when inoculated subcutaneously proved fatal
to Guinea pig, rabbit, rat, mouse, dog, cat, sheep, pig, ox, ass, pigeon
and chicken.
Intravenous inoculation on the horse of 1 to 2cc. of the culture kills
in a few hours, the temperature having risen to 104° F., the mucosæ
acquire a dull brown tint, the eyes are swollen and weeping, enteritic
colics appear, the limbs may swell and there may be painful arthritis
and jaundice. At the necropsy the blood is black and incoagulable, the
muscles as if parboiled, the liver a deep violet, the intestinal mucosa
congested, a yellowish or reddish effusion in the pericardium and
numerous petechiæ on the serosæ.
Subcutaneous inoculation causes an enormous inflammatory œdema resulting
in a sanguinolent abscess, in case the subject survives. There are also
hyperthermia (106° F.), dulness, stupor, weakness, staggering, and
congested, swollen, weeping eyes.
Intratracheal injection is harmless to the horse.
Lignieres finds his cocco-bacillus in the expectoration at the outset
and in the nasal and guttural forms of the disease later, but not in the
blood nor lungs after death, as it is then replaced by streptococci, the
great reproduction of which is favored by its presence. In ordinary
cases of equine influenza it is often impossible to find the
cocco-bacillus in the lung or other organs after an illness of 8, 10 or
15 days. (Lignieres).
Lignieres appears to have omitted the obvious test of the infection of
other horses in the same stable, from the cases produced by his
experimental cultures, so that we must still call for more confirmatory
proof. Cadeac, indeed, assures us that cultures of cocco-bacilli taken
from cases of equine influenza, are often innocuous. Deadly as the germ
cultures of Lignieres prove, they appear to lack that element of extreme
infectiousness shown by equine influenza when the susceptible animals
come into proximity with the sick.
_Accessory Causes._ The recognition of the one essential cause in the
microbian invasion, need not exclude as accessory factors the many
unwholesome conditions which have long been recognized as contributing
to the severity of epizoötics. As the seed requires the rich field, the
rain and sunshine to bring it to an abundant harvest so the microbe of
equine influenza flourishes best where the conditions are most favorable
and the antagonisms least.
The _chill_ which comes from a sudden extreme fall of temperature, or
the standing in a cold draught when wet or perspiring, lays the system
open to this as to other microbian invasions.
The _electric tension_ preceding a thunderstorm, to which many of the
lower animals are excessively susceptible equally prepares the system to
succumb to the germs. It may here be noted that September 1872, the last
days of which witnessed the start of the great epizoötic, had no less
than eleven thunderstorms, while in September of the previous year there
were but two in the vicinity of Toronto. It is just possible that the
great and frequent electric tension, lowered the animal vitality,
allowing a violent invasion by the hitherto slumbering germ, and gave to
the latter that encreased potency which sent it forth on that year of
almost unparalleled epizoötic record.
The _high barometer_ and _low dew point_ similarly affect the animal
economy and encrease receptivity to disease. Rain fell at Toronto 16
days in September 1872 and but 8 days in September 1871.
_Impurities in the air_ whether originating in volcanic eruptions,
telluric emanations, close, filthy overcrowded buildings or compartments
or large collections of decomposing organic matter, impair the animal
vigor and lay the system open to a more violent attack. For this among
other reasons epizoötics of equine influenza are nearly always more
deadly in the closely packed city stables than in the pure country air.
_Overwork_ and _poor irregular feeding_ and _watering_ pave the way for
debility, prostration and severe invasion.
_Sudden vicissitudes of temperature_, which are so common in _spring_
and _autumn_, associated as they are with the _shedding and growth of
the coat_, materially encrease susceptibility and sometimes determine an
encreased severity in the attack.
_Youth_ has its influence, even if it means only that the system that
has never before been exposed to the poison, retains all its native
susceptibility, and has none of that acquired immunity which comes from
a previous exposure to the virus and successful resistance.
_Acquired immunity_ must of course be reckoned with. After a non-fatal
attack this is usually to be relied on for several years or even for the
rest of the lifetime, yet it varies with the individual animals, and,
under the baleful combination of a specially potent germ and strongly
conducive accessory causes, it may become worn out in a year. Yet the
older horses can always be trusted to show a large measure of this
immunity, so that in the absence of extraordinary epizoötics it is
mainly the young that suffer, and it is only when a country has had no
general invasion for a length of time, or when the germ has acquired an
unusual pathogenic potency, or when these two conditions conjoin, that
the invasion of the equine population becomes universal, as it virtually
was in the United States and Canada in 1872–3. Under other circumstances
the germ, temporarily shorn of its power, lingers in city and dealers
stables, biding its time until circumstances become more favorable for a
new general outbreak.
Immunity largely explains the comparative mildness of the last cases in
any particular locality. The more susceptible animals are attacked first
and most severely, while the partially immune ones, which for a time
resist, throw off the disease with greater readiness. The explanation
has been sought in a lessening potency of the germ, but though this may
hold true of some cases, it manifestly does not apply when slight
lingering cases only are left in one locality, and the disease is
advancing over the neighboring state with all its original force and
vigor.
_Incubation._ This appears to vary within certain limits. When during an
epizoötic a sick horse is brought into a new locality and stable, other
cases usually develope in from one to three days. Trasbot gives examples
of one day, Salle, Cadeac and others of two, others claim four, seven
and even, exceptionally, fifteen days. One reason for an apparently
prolonged incubation may be found in the seclusion of the germs in the
alimentary canal, so that they escape only when passed with the fæces.
The pathogenic potency of individual germs, and the varying
susceptibility of the animals exposed must also be taken into account.
_Symptoms._ Equine influenza is liable to show a special predilection
for a given set of organs in different epizoötics, so that we find
descriptions of the different forms as independent types or even
separate diseases: as the _catarrhal form_, _thoracic form_, _abdominal
form_, _bilious form_, _nervous form_, _pink eye_, _infectious
cellulitis_, and _rheumatic influenza_. These forms may, however, appear
in different subjects in the same epizoötic, and when they are not due
to complications, may be looked on as a concentration of the morbid
processes on one class of organs rather than another.
_Initial pathognomonic symptoms._ Certain prominent and striking
symptoms are so constantly present in the earlier part of the disease
that they may be held as virtually diagnostic. These are the _suddenness
of attack_, the _anorexia_, the _profound early prostration and
weakness_, the _high temperature_, _the swelling and watering of the
eyes_, and the specially _brownish red coloration of the conjunctiva and
other visible mucosæ_. The attack may come on with almost lightning
rapidity. The animal which yesterday, or it may be but an hour or two
ago, appeared to be in the most vigorous health and spirits, is found
with pendant head, resting perhaps on the manger, ears drooping, eyelids
swollen and half closed, epiphora, conjunctiva of a brownish red or
violet, lips loose and drooping, and one or two legs partially flexed,
while the body is balanced on the others. The patient is indisposed to
move, and when compelled to walk may sway and stagger from nervous and
muscular weakness. The arched back, cracking limbs, and their stiff,
rigid movement further indicate the suffering in muscles or joints or
both. Appetite is greatly impaired or lost, thirst marked, and
hyperthermia 102° to 105° or upward. Sneezing, cough or symptoms of some
other special localization may be present, but the above occurring in a
number of horses at once, without appreciable climatic cause, when one
or two new horses have been very recently acquired, or when influenza
has been prevailing in the vicinity or in a neighboring place, will
usually stamp the nature of the attack.
Cadeac considers the sudden attack, high fever, and profound nervous
prostration and stupor as the manifestations of the uncomplicated
disease, while the localizations in the lungs, bronchia, pleura, liver,
bowels, etc., are indications of complications by germs of other
diseases, which find the debilitated influenza system especially open to
attack. The _fever_ which always sets in early may be little above the
normal in mild cases, and may reach 107° or 108° F. in the more severe
ones. It may last thus for five or six days and then rather suddenly
descend to near the normal. In other cases it descends a little daily,
the lowest temperature for the day being seen in the morning. Shivering
is often nonexistent or passes unperceived.
The _pulse_ does not usually encrease in ratio with the temperature. It
may be at first only 40 or 50 per minute, though later, and especially
with extensive disease of important organs, it may reach 60, 70, 80 or
even 100. It usually lacks in firmness and force, even when the heart
beats forcibly, being soft, somewhat compressible, and often irregular
in successive beats, the weakest corresponding to the last part of the
inspiratory act, or when the lungs are full and the heart compressed.
The _heart_ impulse behind the left elbow is usually forcible and may
show variation in rhythm or even intermissions.
Mild _catarrhal symptoms of the nose and throat_ are usually present,
the discharge being at first serous and later muco-purulent. As a rule
this is complicated with more or less bronchitis, but this does not
indicate anything serious. Acceleration of the breathing, sneezing, and
cough are present. Cough may be at first nervous, husky and paroxysmal,
but later as the discharge is established it assumes a looser, mucous
character. It is liable to be roused by excitement, by drinking cold
water, by inhalation of dust, or by giving medicine. In connection with
these symptoms there are some indications that the digestive organs are
involved. The pharyngeal and submaxillary glands may be swollen and
tender. If the subject has been seized just after a full meal, there may
be slight tympany, and in any case, the fæces are passed in small balls,
a few at a time, hard and with a baked or glistening surface. These may
have an unusually strong or heavy odor, and laxatives are liable to act
with dangerous energy. The urine is scanty and high colored, sometimes
icteric.
In such mild attacks, which constitute the majority, improvement may be
noted as early as the fourth day, and a prompt recovery follows.
With extensive _thoracic lesions_, the symptoms are much more severe and
the danger greatly enhanced. These may occur in any patient, but there
appears to be a special predisposition in the young and still very
susceptible animals, in those crowded together in close, badly aired
buildings, in the overworked, poorly fed or in any way debilitated
subject, and in horses that have been especially excited and exposed, as
by railway travel.
In exceptional cases _congestion of the lungs_ may be so acute as to
lead to speedy death, and the objective symptoms do not differ greatly
from those of ordinary cases of this condition, if we except the very
high temperature in influenza, associated as it is with the fact of the
epizoötic prevalence of the disease.
In _pneumonic_ cases the lesions are usually double and have a tendency
to develop toward the lower borders of the lungs, just behind the elbow
or farther back, and less frequently in the centre of the organ. It may
be impossible to detect crepitation, but sounds of distant organs (heart
beats, bronchial blowing, intestinal rumbling) are heard with unwonted
clearness over the consolidated parts. A mucous râle can usually be
detected behind the shoulder blade, along the line of the larger
bronchia. Percussion sounds may be indefinite, as the area of
consolidated lung is usually small in ratio with the hyperthermia. The
area of flatness in ordinary fibrinous pneumonia is usually much greater
with a high fever, and if the lesions are on one side only, right or
left, it is still more suggestive. The crepitation too in pneumonia is
significant. When the pulmonary lesions are extensive by reason of
œdema, a marked infiltration may often be noted on the lower surface of
the trunk or in the limbs as well.
_Pleuritic_ symptoms may show in the same connection. The breathing
becomes more hurried and shorter, friction sound may be heard but it is
very transient and soon superseded by an absolute flatness on
percussion, rising to a definite horizontal line, representing the
boundary of the effusion in the lower third or half of the chest, and
usually rising to the same height on both sides. Tenderness of the
intercostal spaces may or may not be present. As the disease advances
creaking sounds may be heard from the stretching of the consolidated
false membranes. The combination of double pleuro-pneumonia constitutes
a very fatal type of the disease.
The symptoms of _pericarditis_ and of cardiac disorder usually accompany
those of pleurisy. The tumultuous heart beats, often associated with
soft, weak or even rapid pulse, and later, a deadening or muffling of
heart sounds, as in hydropericardium are characteristic when present.
With _endocarditis_ the early tumultuous heart beats, with small weak
pulse, irregular and sometimes intermittent, become complicated by a
blowing or hissing murmur with the first heart-sound. In such cases
clots of blood are liable to form in connection with the valves, and may
cause sudden and early death. When the heart is involved the tendency to
extensive infiltration of limbs and lower aspect of the trunk is much
enhanced. (See _diagnosis_ for table of phenomena in influenza,
fibrinous pneumonia and contagious pneumonia respectively).
_Symptoms_ of digestive disorder are usually in evidence. Even in the
thoracic forms the mouth is dry, hot, and has an offensive odor; the
tongue coated above, has often red margins and tip; it may even be
yellowish; the gums may be swollen and dark red or violet especially
around the incisors; mastication may be slow and unwilling; the pharynx
maybe swollen; the pharyngeal and submaxillary lymph glands may be tumid
and tender; and swallowing may be difficult.
Congestions of the stomach and intestines are indicated by inappetence,
sometimes flatulence, passage of flatus, constipation with small, round,
mucous-coated balls passed in small numbers, and by slight transient
colics, pawing, looking at the flanks, and retraction of the abdomen.
The retention of bile and destruction of blood elements are indicated in
a deeper yellow of the conjunctiva and visible mucosæ, and in a yellow,
brown or red color of the urine. There may be tenderness of the abdomen,
but this, like the colics, is moderate, the senses being blunted by the
attendant stupor which is usually even greater than in the thoracic
forms. Urination may become frequent with straining, and the urine may
become turbid, opaque, with flocculi of cystic epithelium and mucus, and
even albumen. In from three to five days diarrhœa supervenes, the fæces
becoming soft, pulpy, watery, glairy or bloody, and escaping through a
permanently dilated sphincter. The diarrhœa may alternate with periods
of torpor or complete inactivity, otherwise tenesmus of the rectum is
marked. The exposed rectal mucosa is congested, of a deep red or it may
be of a dark violet hue. Eversion is not unknown.
In the worst cases death may ensue by the third or fourth day, but in
others the diarrhœa is critical and heralds an improvement which goes on
to a speedy recovery. In still other cases the bowel troubles continue,
the fever does not give way and the privation of food and rapid
metamorphosis of tissue produce steady emaciation and fatal marasmus.
A striking feature of the gastro-intestinal disease is the extraordinary
susceptibility to laxatives. So much is this the case that I have known
of two drachms of aloes proving fatal by superpurgation in a large,
mature Percheron horse. It is never safe to use laxatives in equine
influenza until one has ascertained whether in the special form of the
epizoötic in question the gastro-intestinal organs are or are not
especially involved.
_Disorders of the eye_ are so common or constant as to have procured for
certain epizoötics the name of _pink eye_. They set in suddenly, and
equally in both eyes, with infiltration of the lids and particularly of
the mucosa which is of a more or less deep red, and may bulge between
the margins of the eyelids, (chemosis). The flow of tears is profuse,
seropurulent matter accumulates at the canthi and in the lachrymal sacs,
vision is impaired and there is intolerance of light. The cornea becomes
bluish, cloudy or milky white, with a red zone around its margin and,
above all, on the adjacent sclerotic. In some cases the aqueous humor
becomes turbid or flocculent, and the iris changes its clear, healthy
dark lustre for a dull brown or yellow tint. The tension of the globe
may be materially encreased. They are readily distinguished from
recurrent ophthalmia by the attendant weakness, stupor and hyperthermia,
and by their non-recurrence in case the patient survives.
The _nervous symptoms_ are especially manifest in the sudden seizure,
great prostration, extreme weakness, profound stupor or lassitude, the
staggering gait, in bad cases, insensibility to voice, slap or, it may
be, even to the whip, the rigidity of the loins, their insensibility to
pinching, the difficulty of turning in a short circle, or of backing.
The high fever, disproportionate to the appreciable local lesions, and
its sudden improvement at the critical period, the excessive weariness
and the disposition to lie down contrary to the habit of other
inflammatory chest diseases are further indications.
This may go on to coma, there may be more or less complete anorexia,
muscular trembling, paresis, especially of the hind limbs, or delirious
manifestations indicating meningitis.
_Rheumatoid attacks of the muscles and joints_ usually appear in the
advanced stages of the disease, but may appear earlier. They may occur
in any latitude but seem to be especially common in cold, damp,
inclement northern regions, and at seasons when climatic vicissitudes
are sudden and extreme. These may appear suddenly and disappear with
equal rapidity, or they may last for a time during and even after an
apparent recovery in other respects. When the joints are involved they
usually become engorged with exudates in the synovial membranes.
_Lameness_ in either _fore_ or _hind limb_ may assume an _intermittent
type_ developed by exercise and subsiding with rest, evidently
bespeaking local arterial embolism, and in such cases it is likely to
persist for months.
A tendency to _transudations_ and _dropsical effusions_ is common in
severe cases, showing especially in the filling of the legs, but in
certain epizoötics, these become strikingly prevalent and have secured
for such a special name (_epizoötic cellulitis_). Apart from the limbs
these affect particularly the inferior surface of the chest and abdomen.
The swellings are not necessarily hot nor painful nor petechiated as in
petechial fever, yet they may merge into that affection or they may
become phlegmonous and develop abscess.
_Complications_ of many kinds are to be looked for, pregnant mares may
_abort_; _laminitis_ may set in; the microbes of _strangles_,
_contagious pneumonia_, _cerebro-spinal meningitis_, _septicæmia_,
_pyæmia_, etc., may take occasion to attack the debilitated system, and
thus complex diseases and manifestations are developed.
_Morbid Anatomy._ The lesions may predominate in different organs in
different subjects and successive epizoötics. It is a protean disease
and may expend its main energy on any one of a number of different
organs or systems of organs.
In the slighter cases the lesions are often largely confined to the
anterior part of the respiratory organs. The _fauces_, _pharynx_,
_larynx_, _guttural pouches_ and _nasal mucosa_ are tumified, congested,
red and covered with mucous, and this condition may extend down to the
bronchia. In such cases the _blood_ is normal or may coagulate with
undue readiness and firmness. The pharyngeal and intermaxillary lymph
glands are red and congested in their outer zone.
In the more severe cases the _alterations in the blood_ are perhaps the
most constant of the morbid features. The blood is fluid and
incoagulable, or the clot is soft, diffluent and black, the red globules
are crenated or broken up, and show little tendency to adhere in
rouleaux. The escaped hæmatoidin accumulates in masses in the serum in
crystalline forms, giving it a high staining power when a line is drawn
with it on white paper. Fatty globules also float in the mass. The
leucocytes are relatively very much encreased and the red globules
diminished. Dieckerhoff found 30,000 and Trasbot 40,000 leucocytes in a
cubic millimetre.
The diffluence is not constant. Blood drawn in the earlier stages of the
disease, coagulates with extraordinary firmness, influenced, doubtless,
by the encrease of the leucocytes, the disintegration of the blood
globules, and the liberation of globulins. This serves also to partially
explain the early and sudden deaths from coagula in the heart and large
vessels, which are occasionally met with. Such clots in the heart are
often found adherent to the valvular or ventricular endocardium which at
such points shows cloudy swelling, thickening, cell proliferation and
even encreased vascularity and granular elevations.
In advanced cases, however, the prominent features are usually acidity,
blackness, and incoagulability of the blood, its resistance to oxygen,
altered and broken down red globules, free coloring matter, relative
encrease of white cells, and, if necropsy has been delayed, the
abundance of septic microbes (cocci and bacilli). Petechiæ are abundant
on the serosæ especially on the pericardium.
_Lesions of the alimentary mucosa_ are very constant. There may be
stomatitis, with tumid follicles and even ulcers (Kowalavsky). In the
_stomach_ the _right sac_ has its mucosa thickened, softened, red,
congested, petechiated and discolored. The summits of the folds may be
ulcerated (Labat). Similar lesions are presented in the _small
intestines_. The agminated glands may show many rounded elevations, with
or without open discharging follicles. The mucosa is covered with a
muco-purulent material. Otherwise, the small intestines, like the
stomach, are usually empty. The _large intestines_ present similar
lesions, the nodular elevations often representing the solitary glands,
and the masses of ingesta are likely to be dry and indurated, in the
earlier stages or semiliquid in old standing cases. The _peritoneum_ may
be congested, petechiated and at points infiltrated and usually contains
a reddish serum in variable quantity. The _mesenteric glands_ are more
or less enlarged and congested.
The _liver_ shows more or less congestion as in other infectious
diseases localized in the bowels. It usually has a parboiled appearance,
and yellowish gray areas of necrosis may be manifest, or again, fatty
degeneration may be present. Petechiæ, and even small blood clots may be
found on or beneath the capsule. The _pancreas_, and, still more, the
_spleen_ may be the seat of congestion or engorgement but this is far
from constant.
The capsule of the _kidney_ may be petechiated or elevated at points by
serous exudate or extravasation. The surface of the organ and of
sections show a mottling with darker and lighter areas, and petechiæ and
patches of congestion may be found on the bladder and urethra.
The _nervous centres_ exceptionally show meningeal congestions, and
exudations, and petechiæ as has been noted of other serosæ.
Lesions of the _eye_ may be confined to the mucosa, or they may extend
to the membrane of the aqueous humor, the iris, or even the deeper
structures.
Other lesions such as _laminitis_, _bursitis_, _arthritis_, like those
attendant on _abortion_ need no special description.
When _pulmonary lesions_ are extensive, the bronchial mucosa is not only
softened, opaque and covered with a serous, or muco-purulent discharge,
but deeply congested and petechiated. When the chest is opened there is
usually an effusion, pale straw, red or bloody and more abundant than in
contagious pneumonia. False membranes may exist and show a blackish tint
from extravasated blood. The lung fails to collapse and shows on the
surface and throughout its substance petechiæ and small black
infarctions. In some instances the whole lung is blood gorged, black,
almost jelly like, as in acute congestion. In others these are limited
infiltrations, concentrated especially in the anterior and lower parts,
and almost invariably affecting both right and left lungs. The
infiltration is circumscribed in area in comparison with the attendant
fever and constitutional disturbance, resembling in this respect, the
lesions of contagious pneumonia. It differs however in having a greater
tendency to liquid infiltration of the connective tissue, and but for
the lack of such tissues in the horse’s lung it would tend to
approximate to the lesions of lung plague in cattle. It shows a distinct
thickening of the interlobular septa, a tendency to extension to the
pleura, and to issue in pleural and subpleural infiltration, and to a
more copious effusion into the pleural cavity than in either fibrinous
or contagious pneumonia. The lung tissue may be granular and hepatized,
but far more frequently it is only splenized, the lung being the seat of
a bloody infiltration, yet retaining much of its elasticity and
coherence. Portions may be infarcted and black and large areas may have
a pale or parboiled appearance, and gangrene is by no means uncommon.
_Diagnosis._ This is based largely on the suddenness of the attack, its
epizoötic character, the numbers attacked in rapid succession, and over
a large area as contrasted with contagious pneumonia, the sudden and
extreme prostration and weakness, the swelling, watering and
discoloration of the eyes, the mildness of the average case, the
congestion of the upper air passages, and in the mild cases a
comparative immunity of the lungs, the irritability or congestion of the
gastro-intestinal mucosa, and the history of the case:—the arrival of
the infected horses within a few days from an infected place, or coming
through infected channels, or the attack of new arrivals in a previously
infected stable, or the known advance of the disease towards the place
where the patients are, will usually serve to mark the true nature of
the affection.
As a help to correct diagnosis we give below some of the prominent
conditions and phenomena of the three forms of lung disease known as
_fibrinous pneumonia_, _contagious pneumonia_, and the _pneumonia of
equine influenza_:
=Pneumonia=: =Pneumonia=: =Pneumonia=:
_Croupous Fibrinous._ _Contagious, of Equine _of Equine Influenza_.
Animals._
From climatic Slow succession of Rapid succession of
vicissitude, cases in the same cases in the same
exposure, etc. stable, irrespective stable or locality,
Attacks exposed of climate or irrespective of
animals only, and all exposure climate or exposure
at once
Prevails in inclement Any season: worse in Any season: worse in
seasons, spring, inclement season inclement season
autumn, (Winter)
Infection from close Infection spreads
proximity, contact, widely and rapidly
stall, manger, rack, through the air.
bucket, trough, etc.: Spread rapid and
Spread slow often general
Carried in manure, on Carried in manure, on
harness, wagons, harness, wagons,
clothes, etc. clothes, etc.
Incubation, 3–10 days Incubation, 1–2 days
Rigor may be late: Rigor early and well Rigor not always well
after exudation has marked, before marked
commenced exudation
Sets in slowly or with Sets in slowly, cough, Profound nervous
acute congestion; dulness, impaired prostration like
appetite and pulse appetite, pulse opium poisoning,
vary with rapid, prostration appearing early and
inflammation slight suddenly
Nasal discharge, watery Nasal discharge, yellow Nasal discharge,
or rusty, later watery, may become
muco-purulent yellow
Eye pink, dark red Eye yellow, rarely Eyelids bloodshot (pink
swollen or watery eye), violet, madder
hue, swollen, watery,
closed
Temperature rises with Temperature rises early Temperature rises early
inflammation and extremely, before and extremely, in
exudation, 104°–107° some hours, 104°–107°
Swelling of limbs rare Limbs swell rarely Limbs often swell
greatly
Rheumatoid arthritis Rheumatoid arthritis
may follow may set in; often in
advanced stage
Crepitation more Crepitation less Crepitation may escape
constant around the constant around the recognition
exudation exudation
Exudation Exudate affects lower Exudate less granular
(Hepatization) in or anterior border of than in pneumonia;
lung, lower, lung; often in small forms in or
posterior, anterior, isolated areas or gravitates to lower
or central, usually around bronchia; less part of lung.
undivided area blood engorgement Congestion passive
than in fibrinous
pneumonia
If pleurisy effusion Pleural effusion Pleural effusion
may be copious infrequent, or frequent and abundant
limited, though
pleurisy is common
Abscess not infrequent Abscess rare Abscess not infrequent
Pulmonary gangrene Pulmonary gangrene and Infarctions, sequestra,
infrequent sequestra frequent and cavities not
uncommon
Pericarditis infrequent Pericarditis frequent Pericarditis frequent
Blood, decrease of red Less altered than in Blood at first clots
globules; encrease of either of the other firmly, later
white, hæmatoblasts, forms. Shows becomes, thick,
fibrine formers and cocco-bacilli in the black, sizy,
soda salts earlier stages: hæmatosis tardy.
streptococci later Reaction acid.
Coagulation firm, buffy Coagulum loose, buffy
coat coat slight
Hepatic congestion, not Hepatic congestion Hepatic congestion
hepatitis excessive, hepatitis, excessive,
necrotic changes hæmorrhagic; fatty
degeneration
_Prognosis._ _Mortality._ As usually met with and under favorable
conditions, equine influenza is a mild disease. In 1872 when the
disease, sweeping the continent and hardly sparing an equine animal,
might be assumed to have reached its maximum, the actual deaths varied
from 2 per cent. in country districts to 7 per cent. in large cities.
The same holds for Europe where Friedberger and Fröhner gives 4 to 5 per
cent. Früs (Denmark) 1 per cent., Aureggio (Italy) 3 per cent.,
Siedamgrotzky 10 per cent. Much depends on conditions: In horses
infected in transit on a long railroad journey it may be 100 per cent.
and in fat dealer’s horses, out of condition for active work it usually
reaches a high figure. If the patients are kept at work the
complications and mortality run very high. The same applies to
debilitated animals kept in close, foul, ill-aired stables, or reduced
by exhausting or long standing diseases. The very young and the senile
suffer more than animals in middle life and vigorous condition. Finally
the parts invaded have a controlling effect. The milder cases affecting
the upper air passages only, nearly all recover, in those showing
abdominal lesions the indications are still favorable; while with double
pulmonary and pleural lesions the patient is too often in a hopeless
condition. Brain lesions are almost equally redoubtable.
The actual money losses, in an epizoötic of influenza, are more in the
way of the loss of work and the complete stagnation of trade in all
departments, than in the number of deaths. Yet even in this sense it may
prove more ruinous than would a disease having a less universal sway,
though far more fatal to the animals attacked.
_Treatment._ A disease like this, which tends to spontaneous and perfect
recovery, needs mainly dietetic and hygienic care in the vast majority
of cases. Rest is a prime consideration in a pure genial atmosphere. In
the summer season, in the absence of rainstorms, an open air life, at
pasture is the best. Shelter must be had in case of storms, and in the
cold season a clean, sweet, roomy well-aired loose box, with a sunny
exposure, is important. Clothing, bandages, blankets and even hoods may
be required if there is any tendency to chill. Food should be laxative,
cooling and of easy digestion. Bran mashes, scalded oats or barley,
ensilage, roots, potatoes, apples, fresh grass or scalded hay may be
suggested. Milk has been strongly advocated, from twelve to fifteen
quarts a day, and linseed tea as being especially adapted to the
irritable stomach and bowels. Food should be given often, in small
quantities so as not to destroy the appetite.
Costiveness is best met by injections of water, blood warm, or if there
is much hyperthermia, of cold water. This latter stimulates the
peristalsis more actively and at the same time lowers the temperature.
By unloading the large intestines it removes irritants, without danger
of encrease of congestion or diarrhœa.
If anything more is wanted for these mild cases, small doses of
stimulating diuretics or diaphoretics may be given. Sweet spirits of
nitre ½ oz. or liquor of acetate of ammonia 2 oz. may be given twice a
day, the latter in the drinking water or gruel. In the absence of these
saltpeter ½ oz, or potassium acetate ½ oz. may be given.
In the more _severe cases_ more active treatment is resorted to, but in
all cases one should avoid measures that tend to greatly depress the
vital powers and especially the circulation. Heroic treatment has been
all but universally condemned and yet Trasbot claims to have had
excellent results from a moderate venesection (2–5 qts.) in strong,
muscular, well conditioned animals. The blood became more fibrinous, the
general symptoms improved and complications were far less marked. During
twenty years, in a large number of cases, it had constantly the same
results, restoring appetite, opening the closed eye, imparting new life,
lowering temperature, and checking congestions. The results were best in
all cases when it was employed early, but they were almost equally good
when later congestions set in, or when the ordinary inflammatory
localizations were advancing, and he found the measure hurtful only
when, in the advanced stages, the animal was worn out, and destitute of
all power of recuperation.
_Antipyretics_ have been lauded and decried, and it is doubtless best to
use them with due discrimination and caution. Acetanilid, the agent in
most common use, is a powerful cardiac depressant, and in this disease
the heart is often already dangerously weak. Yet in cases with very high
temperature, seriously threatening life, acetanilid in doses of 2 drams,
repeated every second or third hour until the temperature falls, and
thereafter twice or thrice daily, for a day or two, may save the
patient. Similarly, where there are indications of violent headache
(drooping head, eyelids and ears, congested and watery conjunctiva,
stupor or irresponsiveness) a dose or two of acetanilid with the same
amount of sodium bromide will often give material relief. The general
suffering and disorder attendant on the cephalalgia, if allowed to
continue, prove a direct bar to improvement, and endanger complications
that might otherwise be escaped. On the other hand, there is constant
danger from too large doses, or a too long continued use of acetanilid
in influenza. Phenacetin may be substituted in 2 dram doses, the action
being somewhat more prompt and transient. As less dangerous than the
coal tar antipyretics, we may fall back on such agents as sodium
salicylate, ½ to 1 oz., or sulphate of quinia, 20 grs.
Elimination of toxins and waste products is to be secured and this is
more safely conducted by the kidneys or skin than by the irritable
alimentary canal. Plenty of pure cold water is one of the best and
simplest resorts. Aside from this, where there is much hyperthermia,
bicarbonate of potash or soda will serve the various purposes of an
antidote to the acid blood, an eliminant and an antithermic. Under the
same circumstances saltpeter may be resorted to in ½ oz. doses twice
daily. When, however, the heart is weak it is better to employ
ammoniacal or etherial diuretics:—spirits of nitrous ether, 1 oz. or
liquor of acetate of ammonia, 2 to 4 ozs. By combining these with
extract of belladonna and camphor a fairly standard prescription may be
prepared.
Inhalations of warm water vapor, rising from hot water or a hot mash in
a bucket, over one end of which a bottomless bag is drawn, while the
other end receives the nose of the horse, will greatly relieve the
irritation and the cough. It can be made even more soothing by
introducing a little alcohol, eucalyptol, menthol, camphor, poppy-heads,
or other anodyne. Or the water vapor may be set free in a close stall
from a boiling tea-kettle or a steam pipe, and an admixture of
sulphurous acid made by burning a few pinches of sulphur, more or less
according to the size and closeness of the stall. If the stall is tight
enough a steam bath may be given with much profit in the early stages.
Counter irritants applied to the throat, or, if need be, to the breast
and sides of the chest will often give material relief, acting as
derivatives and probably also by modifying the globulins in the exudate
and thus influencing the course of the disease. In case of sore throat
of a very high type it may be best to apply a compress or poultice, or
even a piece of sheepskin for a day or two, until, by antithermics,
cooling diuretics and soothing inhalations, the severity of the
inflammation has abated. The common mustard pulp made with tepid water,
rubbed in, and covered by paper, may be applied for an hour; or the
_soap liniment_ (soap 6 ozs., camphor 3 ozs., and proof spirit, liquor
ammonia and linseed oil aa 1 pint) may be rubbed on repeatedly; or a
blister of cantharides may be used.
The _ophthalmia_ may be treated by a moist atmosphere, a few drops twice
daily of a solution of atropine beneath the lids, a similar treatment
with pyoktanin, (1:1000), or a solution of mercuric chloride (1:2000).
In case of _gastro-intestinal inflammation_ elimination is to be sought
by ⅓d the usual laxative dose, supplemented if need be, by injections.
Half a pint of olive oil with 20 grs. calomel will usually be well
borne. Counter irritants may be applied to the abdomen, and the bowels
must be carefully watched and any inactivity or derangement corrected. A
slight diarrhœa is not to be too hastily checked as it may serve at once
to eliminate offensive matters and subdue mucous inflammation. Solutions
of flax seed, gum, or slippery elm in the drinking water may serve a
good end.
In case of _cardiac weakness_ with intermittent or irregular pulse,
hurried breathing, and an undue contrast between the violence of the
heart action and the weakness of the pulse, circulatory stimulants are
called for. Digitalis 10 grains twice daily, strophanthus tincture 1½
dr., strophanthin subcutem ¼ grain, caffeine 5 grains, veratrine ⅒th
grain, or strychnia 2 grains.
_Nervous symptoms_ will exceptionally demand the application of cold
water or even ice or snow to the head, with counterirritants to the
sides of the neck or chest, and the internal use of bromides, iodides,
chloral or other nerve sedative.
Other complications must be treated according to their indications.
As the skin becomes cooler and more moist, and the pulse slower and
fuller, a tonic and stimulating treatment may be desirable. Gentian 4
drs., saltpeter 4 drs., sal-ammoniac 2 drs. may be given night and
morning, or in case of great debility ammonia carbonate may replace the
sal-ammoniac. Or the gentian may be replaced by nux vomica, and the
ammoniacal preparations by alcoholic ones.
When prostration becomes extreme and stimulants and bitters appear
inadequate, transfusion of blood from a healthy horse may save the
patient’s life, or a normal salt solution sterilized may be introduced
into the vein.
The first method is accomplished through a caouchouc tube with a short
tube of silver inserted in each end; the jugular groove of each horse is
washed and disinfected, and the vein opened; the tube disinfected with a
salicylic acid solution, and cleared out with boiled water is inserted
upward into the vein of the sound horse, and when the blood begins to
flow the other end is inserted downward into the vein of the sick one.
In this way the blood is allowed to flow from the one to the other, the
finger being kept on the pulse of the patient to detect any faltering,
which like heaving up of the head or rolling of the eyes, may be taken
to indicate undue arterial tension, or disturbed brain circulation, and
should be the signal for an arrest of the flow. To effect this, pinch
the tube in the centre, and wait a minute or so; if the symptoms subside
the current may be reopened and a little more carefully admitted, but if
not the tube may be withdrawn and the wounds pinned up.
The normal salt solution, .6 per cent., is sterilized by boiling, and
placed in a sterilized vessel where it is allowed to cool to the body
temperature; then a caouchouc tube furnished with a silver tube at one
end and sterilized as for transfusion of blood, is filled with the
solution and the vessel containing the latter having been placed at a
level higher than the patient, the tube is used as a syphon. When the
liquid flows in full stream the silver tube is inserted downward into
the jugular of the patient and the liquid is allowed to flow in, subject
to the same precautions as regards sudden blood tension as in the case
of the transfusion of blood.
_Prevention._ No country appears to have attempted the absolute
exclusion of the disease or the extinction of the germ by a compulsory
quarantine and disinfection. The nearest approach to this is in Prussia
where in the event of an outbreak of equine influenza, the official
veterinarians and police authorities must send in reports to be
published in the official papers and communicated to the directors of
government breeding studs and to the army authorities. We have here the
germ of an effective system of extinction, for if those in charge of
government horses in an infected country can protect them against
infection, much more could such protection be secured by putting an end
to the infection which is now allowed to remain generalized. Moreover in
our great outbreak of 1872–3, when germ-potency and all but universal
susceptibility were so remarkable, effective quarantine showed the most
signal successes, in the resulting immunity of Vancouver’s Island,
Prince Edward Island, the whole of the West Indies except Cuba, Central
and South America, and isolated districts in Mexico.
Sanitary police in this disease has been abandoned mainly because the
virus is so diffusive on the air that quarantine must be more than
usually comprehensive to prevent extension of infection, and because the
disease is fatal only in a small percentage of cases, so that the loss
is apparently minimized. But a panzoötic like that of 1872–3,
prostrating 1,000,000 horses, asses and mules in the United States for
one to two weeks, and paralyzing the agriculture and commerce of the
continent for that length of time, may well make one hesitate to
supinely accept for all time an evil, which, experience has shown, can
be circumscribed and stamped out. When horse owners, legislatures and
veterinarians can be educated up to the needs of the case our yearly
local losses from equine influenza, and the occasional all pervading
epizoötics of this disease can probably be abolished by the extinction
of the germ on the Continent. To achieve this result an immediate large
outlay would be well spent. In a new generation, or a new century
perhaps, this desirable object may be achieved.
Meanwhile the individual owner can do something to secure a partial
protection. On farms and in barracks the animals may be secluded from
all other equine animals during the local prevalence of the disease.
Men, dogs, and wild animals can be similarly excluded. Litter, fodder,
bags, clothing, manure, vehicles, etc., from infected stables and places
must be carefully guarded against. Newly purchased animals, carried in
any public conveyance, or kept or fed in any public yard or stable must
be quarantined at a considerable distance from others, and treated by
disinfectant sponging and fumigation before they are allowed to mingle
with other equine animals. Stables where the disease has occurred must
be thoroughly disinfected, together with all manure made during the
epizoötic and for some time thereafter.
EPIZOOTIC CELLULITIS: PINK EYE.
Williams follows a popular fashion in describing under the above names
an affection which may be only a form of equine influenza, but which may
be named by itself until its true place can be defined by proof of its
actual pathogenic microörganism.
Beside the general constitutional disturbance, this condition is
distinguished by marked hyperthermia (103° to 104°), swollen, congested,
watering eyelids, cough, strong pulse becoming gradually feeble, firmly
coagulating blood, irritable bowels, painful passage of fæces, and,
above all, a frequent movement of the feet indicative of discomfort and
followed by swelling, often excessive, of the limb or limbs, by a
cutaneous and subcutaneous exudate. These various phenomena may all be
but manifestations of the rather protean disease, equine influenza, and
the cellulitis but variations of the rheumatoid and arthritic forms
which are so common in the regular type of that disease in cold or wet
climates, or seasons. Williams claims that a prominent danger is the
formation of clots in the heart and large vessels and advocates the free
use of the salts of ammonia and potash with stimulants. The treatment
does not essentially differ from that of equine influenza except in the
call for special applications to the inflamed eyes and infiltrated
limbs.
PETECHIAL FEVER. ACUTE HÆMORRHAGIC—ANASARCOUS—TOXÆMIA.
Synonyms. Definition. Causes, obscure, bacteria variable, pus microbes
no active contagion, toxic products, any toxin causing
vaso-dilatation, examples, toxins from fermenting ingesta, debility;
impaired innervation, nutrition and function; gravitation; primary and
secondary forms: predisposing diseases. Lesions: petechiæ and slight
blood extravasations in skin, subcutis, mucosa, submucosa, serosæ, and
solid tissues, largest in soft tissues; round cutaneous swellings one
to two inches across, patches, cracks, oozing, fissures, sloughs,
section shows yellow serous and blood infiltrations, capillaries
greatly dilated, infiltrated thickened mucosæ, blocked nasal passages,
ulcers, serous and bloody discharges, pharynx, larynx, lungs, stomach,
intestines, kidneys, blood firm or diffluent. Symptoms: Hyperthermia,
nasal petechiæ, extravasation, pink or yellow oozing, swellings on
nose, lips, face, limbs, oozing, cracks, sloughs, turning up of toe
from detachment of the flexors, metastasis from skin to lungs, or
abdomen, dyspnœa, colics, serous or bloody diarrhœa. Course. Duration:
acute two days, average one to three weeks, tardy one to two months,
Diagnosis: from glanders, anthrax, urticaria, malignant œdema, horse
pox. Mortality. Prognosis: 50 per cent.: hopeless and grave
indications. Sudden retrocession. Treatment: excellent sanitary
conditions, cleanliness, air, light, green food or mashes, pure water,
laxative food, or salts, diuretics, alkaline diuretics, vaso-motor
contractors, antiseptics, quinine, strychnine, phenic acid, lysol,
ichthyol, sulphites, etc.; locally aluminium acetate, cold water,
scarification, nasal injections and tubes, tracheal iodine injections,
argentum colloidale intravenously, antistreptococcic serum subcutem,
Menveux’s solution.
_Synonyms._ Purpura Hæmorrhagica; Morbus Maculosus; Anasarca (Fr.);
Typhus: Anthrax; Dropsy of Connective Tissue; Mal de Tete de Contagion;
Coryza Gangrenosa; Malleus Gangrenosa; Charbon Blanc; Diastashemia;
Leucophlegmasia.
_Definition._ An acute (or subacute), toxæmic, generally secondary
disease, manifested by capillary dilatation and petechiæ on the mucosæ,
skin, serosæ and elsewhere, and attended by extensive effusions of lymph
and blood into the skin and connective tissue, to form hot, tender,
nodular, diffused, or general swellings.
_Causes._ The causes of petechial fever are not clearly made out.
Bacteria are found in the early exudate, but these are not constant in
kind and it is not unreasonable to suspect that these may be results
rather than causes of the lesions. On the other hand there may be an as
yet undiscovered organism present, the products of which are capable of
producing the disorder. Or the latter may be due to a combination of the
toxins of two or more. Among the bacteria found may be named: The pus
microbes, cocci, streptococci, staphylococci, and bacilli, have been
found and adduced as causes, also diplococci, the bacillus hæmorrhagicus
of Kolb, the streptococcus of strangles, the microörganism of contagious
pneumonia and that of influenza, with a variety of others too great and
too inconstant to be accepted as proof of cause. The fact that rarely
more than one animal suffers in the same stable at the same time might
be held to oppose the idea of contagion and of a definite organized
germ.
Hence the theory of its causation by the presence in the system of the
toxic products of bacteria rather than the bacteria themselves.
(Dieckerhoff.) Cadeac supposes that any toxin which causes capillary
dilatation may determine the disease, and calls attention to the fact
that the injection of mallein (a vaso-dilator) aggravates the phenomena
of petechial fever and determines enormous local exudations and
engorgements. He notes further the potent vaso-dilator action of the
products of strangles, contagious pneumonia, and influenza which are
among the most frequent antecedents of petechial fever. Dieckerhoff also
looks on the phenomena as the result of poisoning by the absorbed toxins
of the microbes of suppuration, which modify the nutritive changes in
the walls of the capillaries and determine exudations and hæmorrhages.
Zschokke thinks that there is infection of the intima of the
capillaries, with the formation of coagula. Clots are not found,
however, apart from hæmorrhages.
The toxin theory receives indirect support from the absence of the same
specific lesions in simple mechanical congestion of the capillaries and
veins. Ranvier had no such results from tying the veins of a rabbit’s
ear. Roger tied the auricular veins of the rabbit, and then cut the
sensory nerves without effect: he then destroyed the cervical
sympathetic ganglion, when there supervened marked exudation, lasting
for three days. The complete blocking of veins by pressure or aseptic
ligature, does not produce a spreading œdema, whereas in ordinary
suppurative phlebitis, with abundance of toxins in the tissues this is a
constant result.
The toxin theory does not fully account for those cases that occur
suddenly, without any manifest pre-existing disease, and as the result
apparently of cold and chill. On the other hand, it is only a very small
proportion of horses exposed to the same degree of cold and chill that
contract petechial fever, and it might well be surmised that in these
few an unknown focus of suppuration or other lesion existed prior to the
chill or that toxins having the requisite devitalizing and vaso-dilating
properties had been absorbed from fermentations in the bowels or
elsewhere. The mere exposure is harmless to the very great majority of
subjects.
In any case it must be accepted that the debility and impaired local
innervation, nutrition and function, that attend on the exposure to cold
and toxins must be looked on as potent contributing causes. The
predilection of the swellings for dependent parts (limbs, venter, face)
shows the influence of gravitation and congestion. Whether there is
present any special microbe which has yet eluded discovery, but which is
the main pathogenic factor, must be left to the future to decide.
In cases that appear to be due to cold or chill alone, the disease is
held to be _primary_; in those following on another affection,
_secondary_.
Among the diseases on which petechial fever supervenes as a secondary
affection contagious inflammatory affections of the lungs and air
passages hold a bad preëminence. Strangles, influenza and contagious
pneumonia, about in the order named, are especially causative factors or
occasions of petechial fever. Among the other affections on which it
supervenes may be named pharyngitis, abscess of the nasal sinuses,
hepatic, renal and other internal abscesses, acute coryza, laryngitis,
or bronchitis, enteritis, abortion, aggravated grease, suppurating
wounds of the skin, infective abrasions by harness, suppurating sores
after firing, infective arthritis with open joint, amputation of the
tail, and castration.
_Lesions._ In certain cases these may be largely confined to petechiæ
and slight blood extravasations, which are distributed very generally
throughout the tissues, but show especially in the skin, subcutis,
mucosa and submucosa of the nose, eyes, pharynx, guttural pouches,
larynx, trachea, bronchia, mouth, stomach, intestine, bladder, vagina
and womb; also in and on the lungs, pleura, pericardium, heart, liver,
spleen, kidneys, peritoneum, pancreas, ovaries, bones, lymph glands,
brain and nerves. The largest extravasations are liable to be in the
softest tissues, and in the lungs they may reach the size of the closed
fist, though usually they vary from a mere spot up to this. The spleen
is sometimes engorged even to rupture. Beside the extravasations, and
associated with them in position, and probably largely as an effect of
them, there is more or less serous effusion infiltrating the tissues,
congestions, suppurations, degenerations, and necrotic changes.
The _skin_, if white, and the dark skins on section, are seen to be
marked by petechiæ. The cutaneous swellings may appear on any part,
commencing with nodular thickenings varying in size from a pea to a
walnut, and merging together into extensive elevated areas terminating
abruptly at their margins in the smooth skin. The larger and more
persistent engorgements settle on the lower aspect of the body and other
dependent parts like the limbs and face. Cracks, oozing, deep fissure,
and extensive sloughs are not uncommon. When the skin is incised it
shows serous infiltration and thickening, with spots and patches of
blood extravasation. The subcutaneous connective tissue is similarly
infiltrated and discolored, and often in the limbs, face, and under the
breast, sternum and abdomen so as to form a tremulous gelatinoid cushion
of several inches in thickness. The capillaries may be distended to more
than 20 times their normal calibre. The exudate may extend deeply
between the muscles, and sloughs may lay these freely open and invade
their substance. The muscular tissue is mottled with petechiæ, and apart
from these it is pale, yellow, or grayish, having to some extent
undergone granular or fatty degeneration. Detachment of the perforans
and perforatus from their insertions is occasionally met with.
The _nasal mucosa_ may show only petechiæ and circumscribed blood
staining, but in fatal cases it is more likely to present extensive
blood extravasations involving it may be the whole mucosa, and narrowing
the lumen almost to complete occlusion. Sloughing is not rare, and the
resulting ulcers may extend into the subjacent tissues, so as to
penetrate the septum nasi or the thin plate of the turbinated bone.
The _buccal mucosa_ and _submucosa_ are often involved in common with
the skin of the lips, cheeks, and intermaxillary space, the tissues
being involved in one common infiltration of blood and serum. In some
cases circumscribed necrosis and ulcerations are formed.
In the _pharynx_ and _larynx_ infiltration of the mucosa and adjacent
parts of a deep blood red, with or without ulceration, causes serious
narrowing of the passage, that on the vocal cords threatening
suffocation. Suppuration of the pharyngeal glands and guttural pouches
is not uncommon. Alimentary matters are frequently found in the larynx,
and bronchia.
Beside the petechiæ and hæmorrhages in the _lungs_, œdematous
infiltration in dependent parts, hepatization, abscess, and limited
areas of necrosis are met with. The pleural sacs often contain a
sanguineous effusion.
The _stomach_ and _intestines_ are usually more or less mottled with
petechiæ involving mucosa, serosa or muscular coat; they are raised in
rounded or irregular elevations by œdemas; or they are the seats of more
or less extensive and even perforating ulcers. The contents of the
bowels may be deeply discolored by the escaping blood.
The _kidneys_ may be pale except where blood stained and œdematous
infiltration of the surrounding tissue may be marked. Serous effusion
into the peritoneum is not rare.
The _eyelids_ are often implicated, infiltrated thickened, and rigid,
and the conjunctiva, bulbar and palpebral, the seat of extensive
petechiæ.
Barreau mentions extravasations on the divisions of the lumbosacral
plexus causing sudden paraplegia.
Petechiæ and hæmorrhages mark endocardium, pericardium and cardiac
muscle, otherwise the muscle is pale. The blood is sometimes in firm
clot, at others diffluent or nearly incoagulable.
_Symptoms._ If hyperthermia is not already present as a feature of the
pre-existing malady it usually shows itself early, at first slight, it
may be (101° F.), and afterward rising in some cases to 104° to 106° F.,
or even higher. The general symptoms are usually those of the
pre-existing disease (strangles, contagious pneumonia, influenza, nasal
catarrh, pharyngitis, bronchitis, etc.), pursuing, it may be, a
persistent course, or attended by special toxæmic symptoms of
prostration and other signs of depression of vital functions. In some
cases the hyperthermia is either absent at this stage or overlooked. On
the prostration supervene the petechiæ on the visible mucosæ, and often
also the swellings of the skin and subcutis. One of these may be seen
before the other and it is difficult to decide whether the petechiæ
always appear first as has been claimed. Cadeac claims that when œdema
is first seen it has been preceded by petechiæ in that tissue (skin).
The _petechiæ_ are usually first noticed on the nasal mucosa as fine red
points, pin’s heads, or up to half an inch in diameter, or a number of
these have coalesced to form extensive patches, and by and by to cover
the entire wall. At first the mucosa is spotted with purple, without any
marked elevation of the surface, but as the lesions extend it becomes
swollen and raised at the points of extravasation and immediately around
them and oozes a serous, sometimes a pinkish or yellow fluid. Even in
the smallest petechiæ the color is persistent and does not disappear on
pressure like the blush of the adjacent mucosa.
Usually _cutaneous swellings_ coincide with the petechiæ, or appear
within two days thereafter. The first manifestation is in the form of
rounded abruptly elevated nodules, about 1½ inch to 3 inches in
diameter, strongly resembling the eruption of urticaria. These show a
certain predilection for the more dependent parts of the body,—limbs,
abdomen, sheath, mammæ, sternal or pectoral region, nose, lips, face,
etc.,—but they may develop on any part or on the whole surface. Neither
tenderness nor heat is usually excessive. The swellings tend to run
together so as to form extended elevations enveloping the entire limb up
to a given point, forming a great pad under the chest and abdomen, or
distending the whole face or head so that it seems more like that of a
hippopotamus than of a horse. In such cases the lips and nostrils become
so thick and rigid that prehension is impossible, and breathing if it
can be accomplished at all is accompanied with a marked snuffling. The
swollen eyelids are closed, and the general turgid surface of the face
is hard and resistant and no longer pits on pressure.
Under the _chest_ and _abdomen_ the swellings show as a continuous pad
or cushion, on one side mainly or extending across continuously on both
sides, and from the breast to between the thighs. It usually pits on
pressure, and may shed the hair and become rough and scabby or ooze a
serous fluid from the surface.
On the limbs the swelling usually shows first on the fetlock or pastern
and gradually extends upward until it reaches the body.
As the disease advances chaps, cracks and fissures tend to form on the
swellings, showing about the head, on the lips or on the nose and
maxilla where the noseband of the halter crosses; on the lower part of
the body where the circingle crosses, or where the part is pressed upon
in lying down, and in the limbs in the flexure of the joints—behind the
pastern, or knee or in front of the hock. In many cases the skin and
connective tissue sloughs, and drops off exposing the muscles, the
tendons or the ligaments of the joints. In other cases the tendons are
involved in the degenerative process or necrosis and become detached
from their lower insertions so that the toe may be turned up or the
fetlock pad may come to the ground. The matrix of the hoof wall
(coronary band) may separate from the horn, leaving a gaping opening
which exudes liquid freely, and if the animal survives, the entire hoof
may be shed.
In other cases, and often quite early in the disease, the swellings may
suddenly subside and disappear, with it may be, a recovery, or, in other
cases, with an exudation into the lungs or chest, the digestive organs
or abdomen. In case the lungs are attacked, there is hurried oppressed
breathing merging into dyspnœa or asphyxia. In case the bowels suffer
there are colicy pains more or less acute, with much constitutional
disturbance, marked prostration and serous or bloody diarrhœa. These
mostly prove speedily fatal. Less redoubtable are those cases in which
the swellings alternately subside or moderate, and reappear or increase,
without implication of the internal organs. The absence of internal
lesions and the moderation and intermissions, of the external ones, give
good hope of the preservation of the vitality of the tissues and of
recovery.
_Course and Duration._ These vary much with the severity of the case. In
subacute and tardy cases with few petechiæ and restricted swelling in
the limbs, the symptoms become remittent and recovery finally takes
place after one or two months. In other cases the morbid phenomena which
developed rapidly may subside as quickly and recovery occurs in a few
days. In the more typical case the visible lesions may encrease or
remain stationary for one, two or three weeks and then terminate in
death or recovery. In the most violent types death may occur within
forty-eight hours. The average duration of the affection is found to be
about 16 days.
_Differential Diagnosis._ In typical cases of petechial fever, diagnosis
is easy. The supervention on a protracted or debilitating disease of the
respiratory passages of an access of hyperthermia, and marked
prostration, with the appearance on the nasal or other mucosa of
petechiæ and swellings of a dark red color throughout, and of cutaneous
swellings in the form of nodular elevations and more extended salient
patches, having a tendency to ooze blood or serum, to crack and fissure
is virtually pathognomonic.
_Acute glanders_ may resemble it but lacks the extended sloughs of
petechial fever, and the nasal ulcers that form in glanders are on a
yellowish base and periphery, whereas the purpura ulcer is on an
uniformly dark red base, and without the elevated margin seen in
glanders. In cases of doubt the mallein test is not available as the
purpuric patient is already fevered, or liable to be so at any moment,
and any wound in such a subject will give rise to extensive swelling.
In glanders the nodular submaxillary enlargement is almost pathognomonic
and still more so if the facial lymphatic vessels are thickened (corded)
and both symptoms fail in purpura. In cutaneous glanders with swollen
joints or limbs the attendant pain is much more severe, and the farcy
buds, forming on the thickened and indurated lymph vessels, bursting and
discharging an albuminoid fluid like oil have no counterpart in
petechial fever. In cases of doubt the search for the glander bacillus,
and above all the inoculation of a male Guinea pig in the flank and the
discovery of the bacillus mallei in the resulting exudate and diseased
testicle will decide.
From _anthrax_ and _emphysematous anthrax_ petechial fever is
distinguished by the absence of the large bacilli of these respective
diseases from the exudate. It is not communicable, like anthrax, to the
sheep, Guinea pig and rabbit, and does not crackle on manipulation, like
emphysematous anthrax. The swellings are much more generally diffused
than in anthrax and the hyperthermia much less.
_Urticaria_ furnishes a skin eruption which may be indistinguishable
from the earlier skin lesions of petechial fever, but these lesions are
not associated with the petechiæ in the nasal and other mucosæ, and the
swellings do not advance to great sanguineous engorgements, cracks,
fissures, necrosis, and deep and extensive sores as in purpura.
Urticaria is, moreover, usually traceable to some digestive disturbance
and fault in feeding.
_Malignant œdema_ is usually confined to the seat of the inoculation
wound and an extension around that, the exudate is very watery and may
be mixed with fetid gas bubbles, so as to crepitate slightly, and it
contains an abundance of its specific, round ended bacillus, often in
chain form. The carcass putrefies with great rapidity.
_Horse pox_ affecting the pastern and limb with attendant swelling is
distinguished by the absence of petechiæ on the mucosæ, and by the
formation on the affected part of little pea-like papules, which early
exude an abundant liquid, the concretion of which on the hairs forms a
remarkable yellowish encrustation, embedded in the angry red sores
beneath.
_Mortality._ _Prognosis._ The mortality has generally averaged about 50
per cent. Much, however, depends on the violence of the attack, and the
reduced and worn out condition of the patient. The most hopeful cases
are those in which the temperature remains near the normal, the strength
and appetite are well sustained, the swellings are comparatively slight,
and there is no indication of any internal complication. The unpromising
symptoms are: persistent high temperature; complete anorexia; great
dulness and prostration; excessive swellings not only cutaneous but in
the nose and throat as well; a marked oozing from the swellings with a
tendency to form cracks, fissures and sloughs; the serious obstruction
of breathing and prevention of hæmatosis by blocking of the nose,
pharynx or larynx by sanguineous and serous exudate; the appearance of
oppressed breathing and other indications of exudate with the lungs and
chest, or of colics, diarrhœa, and other suggestions of effusion on the
bowels or in the abdomen. Extreme fetor of the expired air and of the
fæces is a bad symptom, though not always a fatal one. Sudden
retrocession of the cutaneous swellings, may be the precursor of
internal exudations and death, yet in the absence of marked acceleration
of the pulse, and of the objective symptoms of disease of the chest or
abdomen, it is rather to be taken as a herald of recovery.
_Treatment._ Whatever may be the precise cause of petechial fever it is
largely connected with and maintained by an unhealthy condition of the
blood, and especially with the presence of toxins and waste products in
that liquid. The first consideration is to secure for the patient the
best possible sanitary conditions. A roomy loose box, dry, clean, well
lighted and well aired, nourishing, easily digested food—green food,
carrots, turnips, or mashes—and pure water are desiderata. A sunny
exposure is desirable especially in winter, and everything like chill
should be guarded against. Blanketing may be called for in cold weather,
but the circingle like the halter should be avoided as being calculated
to cause indentation, cracking or sloughing of the swellings.
A moderate action of the bowels should be secured by the nature of the
food (linseed meal or tea), or by small doses of saline laxatives
(sodium sulphate) or calomel. Suppression of the urine too, must be
counteracted by diuretics (saltpeter, oil of turpentine) when necessary.
Further internal medication has been aimed to correct the dilatation of
the capillaries, and to prove antidotal to or to eliminate the poisons
present in the blood.
As _vaso-motor_ stimulants have been employed ergot, belladonna, tannic,
sulphuric and hydrochloric acids, oil of turpentine, iron sulphate,
potassium bichromate and chlorate, quinia sulphate, and strychnia
sulphate and arsenate. The value of any one of these is dependent on its
early employment, the slight character of the lesions and the remissions
that so often occur even in severe attacks. None are of much account in
a violent attack at its worst.
In the slighter cases _ergotin_, 5 grains daily in two doses, has been
apparently useful. An objection is that its continued action on the
nerve centres and digestive organs is liable to prove depressing and
injurious. Of the acids, _tannic_ is liable to engender constipation,
locking up the injurious products to which, however, it acts to some
extent as an antiseptic. _Sulphuric_ and _hydrochloric_ acids have a
tonic effect, and the latter is a stomachic under ordinary conditions.
The same may be said of the _iron salts_ and to some extent of _oil of
turpentine_, which have both proved useful in favorable cases. Cadeac
condemns ol. terebinth as calculated to abolish kidney secretions. The
_potash salts_, _bichromate_ and _chlorate_, and _quinia sulphate_ are
decided antiseptics and though the admissible dose would not ensure the
destruction of bacteria, yet, acting in the system, with leucocytes and
leucomaines, they may serve by keeping them in check. The _chlorate of
potash_ is given to the extent of an ounce the first day, and of half an
ounce on succeeding days. The _quinine_ salt is given in half ounce
doses once or twice daily. In combination with bitters they seem to be
of material value. _Nux vomica_ (1 dram) or _strychnia sulphate_ or
_arsenate_ (2 grains) given twice daily has seemed to be among the most
promising agents of this class. As a potent vaso-motor stimulant, a
bitter tonic and stomachic, strychnia has seemed at times to rouse the
vitality and enable the system to throw off the load of poison that
depresses it. The wonderful power of _adrenalin chloride_ as a
vaso-motor stimulant more than warrants its use both locally and
generally. In using any one of these agents, we should not neglect
concurrent attention to the bowels and kidneys, to antisepsis internally
and externally, to hygienic and tonic measures generally.
_Antiseptic agents_ have been given by the alimentary canal, the skin,
the subcutis, and the air passages.
By the _stomach_ the following have proved more or less useful in
checking gastro-intestinal fermentations, and perhaps in hindering
absorption of toxins from the specific lesions on this track: _phenic
acid_, _creolin_, _lysol_, _ichthyol_, _boric acid_, _salicylic acid_,
_sodium salicylate_ and _hyposulphite_, and _calomel_.
To the _superficial swellings_, _fissures_ and _sores_ the same agents
may be freely applied, alone, or combined with astringents, such as
_alum_, _lead acetate_, _aluminum acetate_. In the hot season they may
be applied cold, whereas in the cold weather hot applications are often
preferable. Aruch claims excellent results from covering the engorged
head with a woolen cloth and irrigating it with cold water.
The question of drainage of the worst cutaneous swellings by
_scarification_, has been variously dealt with, Dieckerhoff advocating
deep incisions, while Friedberger and others forbid them as encreasing
the tendency to necrotic infection and sloughing. In the slighter cases
it can well be omitted, but in extensive swellings the disintegrating
and debilitating action on the tissues is so great as to well warrant
its prevention by incisions and drainage. It is well to first give the
surface a soapy wash, then apply a mercuric chloride or carbolic acid
lotion and lance it in the prominent and tense portions. As a further
precaution against septic infection it may then be covered by cotton
soaked in one of the above lotions and covered with a bandage. For
swellings beneath the abdomen or chest this may be held in place by
loose circingles. Scarifying becomes imperative in case of paraphymosis
arresting the flow of urine. Deep fissures and sores following sloughing
may be treated with mercuric chloride solution, (1:1000), creolin or
phenic acid (2:100), iodoform, dermatin, naphthalin or salol.
Disinfection of the _nasal passages_ has been attempted by pervading the
air with carbolic acid, creolin, cresyl, lysol, or naphthalin, by
hanging saturated cloths in the stall, or spreading them on the floor.
Perhaps a better method is to flush out the nose, by injecting each
chamber in turn with a piece of rubber tubing, one end of which is
introduced into the nose, and the other raised four feet and furnished
with a funnel. The injection may be 1 dram creolin to 2 quarts water, or
carbolic acid or alum may be substituted or alternated.
The swelling of the nostrils may be so great that it becomes requisite
to hold them open mechanically. The suture of the two altogether, across
above the nose has been practiced, or a tube of light wood or aluminum
can be inserted in each nostril.
_Injection of the trachea and bronchia_ with a solution of iodine 1
part, potassium iodide 5 parts, and water 100 or 200 parts, was
advocated by Dieckerhoff and met with a fair measure of success in mild
cases. In some cases, however, granular tracheitis and bronchitis
followed, and in others necrotic tracheitis and pulmonary gangrene, so
that the method has not been widely accepted. If resorted to, the weaker
solution is to be preferred, and may be injected through a tracheal
ring, or the membrane between two rings twice a day in doses of 3 to 5
centigrammes (45 to 75 drops).
_Injection into the veins of Argentum Colloidale_, 1 per cent solution
in doses of 1⅔ oz. (50 grammes) at intervals of 2 hours has been very
strongly advocated by Dieckerhoff who in four successive cases had
complete recoveries in from three to six days. After disinfection of the
skin a small trochar and cannula, or a hypodermic needle is introduced
into the jugular and the injection made. Local treatment for the
swellings was also applied.
Injection subcutem of the _antistreptococcic serum_ of Marmorec, has
been lauded as promptly overcoming the capillary dilatation, and
enabling the leucocytes to neutralize the toxins.
Finally Menveux recommends an artificial compound as possessing all the
good qualities of the antistreptococcic serum. This is composed of
sodium chloride 5 grammes, sodium phosphate 1 gramme, sodium sulphate 20
centigrammes, sodium carbonate 1 gramme, caffein chlorhydrate 10
grammes, boiled filtered water 100 grammes. Inject daily in three doses
135 grammes.
PETECHIAL FEVER IN CATTLE.
Synonyms. Causes: microbes, maturity, hard work, chill, poor hygiene,
drying of damp lands in summer and autumn, impermeable soils, corrupt
water, bacillus, diplococcus; resemblance to hæmorrhagic septicæmia.
Lesions: petechiæ and hæmorrhages on mucosæ, serosæ and skin;
gelatinoid exudates gravitating to the lowest parts of face, chest,
belly and legs; chaps, oozing, sloughs, depilation, exudate in tongue,
bloody diarrhœa, duration 14 to 40 days, mortality light; indurations.
Diagnosis: from anthrax, black quarter, malignant œdema and acute
hæmorrhagic septicæmia. Prevention: avoid infecting soils in summer
and autumn; drainage, cultivation; chills. Treatment: venesection:
laxatives, diuretics: intratracheal injections of iodine: colloidal
silver. Locally: antiseptic astringents: remove eschars: facilitate
breathing by surgical or mechanical means: good hygiene.
_Synonyms._ Purpura Hæmorrhagica. Anasarca. Inflammatory Œdema. Yellow
Water. Morbus Maculosus.
This malady presents phenomena very similar to those found in the horse,
and shows itself in mild and severe types. It has been noted by writers
on diseases of cattle from Vegetius down, though under quite a variety
of names.
_Causes._ These are uncertain, though much seems to point to microbian
invasion or intoxication by microbian poisons. In France, it has been
seen mainly in mature and robust working oxen after a hard day’s work,
when the animal has had time to cool off. Also in cows used in the yoke
and milked at the same time. Poor food, starvation and low condition
have also been cited as causes. In other cases, high feeding and
plethora have been incriminated. It shows itself most commonly in summer
and autumn, so that cold or chill must be looked on as a cause secondary
to another—probably microbian or toxic. Again, it is by far the most
common in the adult animal. What is more suggestive is its relative
frequency in localities characterized by swamps, springy fields, hollow
basins, damp hill-foots, bottom lands, and damp, impermeable or
undrained soils. Again, on heavy clays where the water is preserved
through summer in open ponds and often in a very corrupt condition. This
at once accounts for its common appearance in summer and autumn when the
offensive products of fermentation are most abundant, and corroborates
the doctrine of a toxic ferment. But its origin has not been definitely
traced to such products as yet. This, notwithstanding that Kolb
attributes it to _bacillus hæmorrhagicus_, and Robert, Fabert, and
Dinter found the exudates swarming with _diplococci_. This may
assimilate it to _septicæmia_ hæmorrhagica.
_Lesions._ In cattle killed during the early stages, circumscribed
hæmorrhages and petechiæ are found in the nose, trachea, bronchia,
gastric and intestinal mucosæ, cerebral membranes, pleuræ, peritoneum,
bladder, and skin. In many cases these are accompanied by congestion and
thickening of the walls of the lymphatics, and effusion in and under the
skin in different parts of the body, but especially along its lower
aspect—(belly, sternum, dewlap, limbs, lower jaw, tongue)—of a
gelatinoid exudate, which raises the skin abruptly in the form of a
thick cushion. At first this is soft and tremulous, but later it may
have coagulated giving a great degree of resistance to the structure.
Extensive cracks, fissures, and sloughs, and unhealthy sores form on
these swellings. Franck especially notes the enlarged tongue gorged with
blood and yellowish exudate as in gloss-anthrax. The blood extravasation
may be further evidenced in the black or blood-streaked fæces, the
reddish urine, and a rosy tint of the milk.
_Symptoms._ The animal is dull, sluggish, moves stiffly and with
difficulty, and shows hyperthermia, (102° to 106° F.), inappetence,
impaired or suspended rumination, heat of the roots of the ears and
horns, and of the dry muzzle; the spine, and usually certain points
beneath the sternum or abdomen at which swellings are about to appear,
are tender to the touch. On the affected parts of the skin the
temperature is raised, and there may be detected pea-like elevations
which become surrounded and enveloped in extensive swellings that pit on
pressure. The swellings show a preference for the thinner and looser
parts of the skin, and gravitate rapidly toward dependent parts. Thus,
the eyelids, roots of the ears, intermaxillary space, throat, muzzle,
dewlap, ventral aspect of the body, axilla, mammæ, scrotum, groin,
thigh, knee and hock are favorite spots, the liquid rapidly gravitating
downward through the loose connective tissue to the lowest points. The
face becomes infiltrated to unsightly dimensions, interrupting
prehension and threatening suffocation, the dewlap swells up to a great
size, the forearms or thighs become rounded and tense, and a thick pad
forms along the ventral aspect of the body. The white skin on such
swellings becomes red, they may ooze a yellowish liquid or blood, the
surface becomes depilated, scaly and rough, chaps and cracks appear,
going on, it may be, to deep fissures, more particularly at the flexures
of the joints, on the throat or muzzle, or on other points that are
subjected to pressure. Necrosis of great patches of skin is not
uncommon, and these sloughing off leave large wounds with unhealthy,
indolent surface and little disposed to rapid healing.
The petechiæ show early on the muzzle, the nasal and buccal mucosæ, and
on other mucous membranes. Exudations also appear and a serous, often
bloody, discharge escapes from the nose and concretes in colored
encrustations around the nostrils. The nose may be obstructed causing
the animal to breathe through the open mouth, protruding the tongue
which is often also the seat of extensive swelling, discoloration and
induration.
As the disease advances there is encreased dullness and prostration,
marked emaciation, and anæmia, sunken eyes, encrusted eyelids, extensive
areas of depilation including even the long hairs of the tail, and quite
often an abundant bloody diarrhœa.
The affection may last for 24 to 40 days and under rational treatment
the majority survive. There remains, however, in a certain number of
cases, a permanent enlargement and fibrous induration from the
organization of the exudate.
_Diagnosis._ A fully developed case is easily recognized. The fever and
constitutional disorder, complicated by petechiæ on the mucosæ and skin;
the extensive swellings suddenly formed, oozing serum or blood, and
tending to fissures and necrosis; and the discharge of blood from the
nose, bowels, kidneys and udder, in the absence of the bacilli of
anthrax, emphysematous anthrax, malignant œdema, and wildeseuche; the
slower progress; the low mortality; the occurrence on a damp, springy,
or impermeable soil, or one known to produce this disease; and
especially if in late summer or autumn, become virtually pathognomonic.
_Prevention._ Seclude cattle in late summer and autumn especially, from
soils known to be productive of this affection and above all from damp
wet clays, underlaid by hardpan, from swamps, from drying up ponds and
basins, from wet river bottoms and deltas and from springy fields
generally. Fields of this kind may be reserved for cultivated crops or
for raising hay. The fundamental remedy is thorough drainage, and a
subsequent abandonment of the land for a year or two to other crops to
allow of a dissipation of the poison. Sudden chills after being heated
or fatigued, and exposure in the pasture in cold nights are to be
avoided.
_Treatment._ The French writers up to the present extol bleeding for the
early stages. Its benefit must apparently depend on the diminution of
the blood tension allowing the distended capillaries to resume their
normal contractility, and in the lessening of the tendency to exosmosis,
and the encrease of endosmosis so that much of the poison in the blood
is removed and what remains is largely diluted and rendered
comparatively harmless. However well this may operate in the strong and
plethoric, it cannot be considered as applicable to the weak or anæmic,
nor to advanced cases in which the vital powers are already seriously
reduced by the abundant exudations and extravasations, and by the
narcotic and devitalizing action of the circulating toxins.
With us the demand is usually met by laxatives and diuretics, under the
idea that these are less debilitating and that if the morbid process can
be arrested recovery is more prompt and perfect. A purge of sulphate of
soda is followed by full doses of nitrate or acetate of potash, in
combination with iodide of potassium, or chlorate of potash; or
bicarbonate of soda associated with hyposulphite of soda. These or other
diuretics should be pushed so as to produce free diuresis. Stimulating
antiseptic diuretics like ol. terebinth, may be added. Iodine solutions
injected into the trachea have been recommended as for the horse (Huber,
Heuberger, Rohr,) and the serum or silver preparations or adrenalin may
be tried.
_Locally_ astringents and antiseptics have given good results. Solutions
of alum or lead acetate with carbolic acid and iodine; frictions with
soap liniment, with a mixture of aqua ammonia, oil of turpentine and
oil, or with mixtures of oils of origanum, cajeput and peppermint, and
iodine, or simple painting with tinct. of iodine may be cited. Fissures
and open sores may be dressed with mercuric chloride solutions (1:1000),
Lugol’s solution, phenic acid lotion, solution of creolin, lysol, or
chloronaphtholeum, camphorated spirit, or other antiseptic agent. The
nose should be injected, cleared of eschars, and if necessary propped
open.
An abundant, wholesome, easily digested diet, pure air, a dry stall and
protection against cold are essential.
CHICKEN CHOLERA. FOWL CHOLERA. CHICKEN TYPHOID. CHICKEN PASTEURELLOSIS.
Definition. Historic notes. Bacteriology: Bacterium choleræ
gallinaceæ, nonmotile, with polar stain, bleached by iodine,
non-liquefying, causes septicæmic lesions. Lignieres’ bacillus,
culture features non-gasogenic, acidifies dextrose; vitality in
disinfectants; survives drying. Accessory causes: new birds in flock,
or eggs for hatching, mingling of flocks, manure, watershed, streams,
ponds, dust, wild birds, buzzards, rabbits, insects, infected soil.
Susceptible animals: hens, doves, peafowl, pheasants, parrots, ducks,
small birds, guinea pigs, rabbits, white and gray mice. Effect on
sheep, horse, man, cow, frog. Incubation 18 to 48 hours. Symptoms: in
fulminant cases rarely seen, in acute, anorexia, depression, debility,
apathy, ruffled feathers, sunken head, neck, wings, tail, tremors,
nasal and buccal discharge, hyperthermia, sighing, violet comb and
wattles, thirst, pultaceous fæces, later glairy, green and fetid.
Temperature becomes subnormal, inability to rise, stupor, convulsions,
death in 1 to 3 days. Mild cases last 7 days. Cases caused by one
microbe have slough only. Lesions: congested, petechiated, hæmorrhagic
intestinal mucosa; contents of bowels watery, frothy, bloody;
epithelial degeneration and desquamation; abrasions, croupous
exudates, enlarged congested lymph glands, fermenting contents of
crop. Petechiæ general, spleen and liver swollen, congested, friable;
kidneys congested; lungs hyperæmic or blood gorged. Blood diffluent
with microbe. Anæmia. Emaciation. Arthritis. Diagnosis: by rapid
spread, infection origin, early excessive mortality, hæmorrhagic
lesions, microbe in blood and liquid ingesta. Prognosis: Mortality 90
to 95 per cent. at outset. Prevention: Quarantine new birds, inside
screens in summer; burn or acidify manure; exclude buzzards, vermin,
wild birds, and visitors; separate sick, kill, burn, disinfect; divide
infected flock in small lots; prevent wandering in fowls, destroy
insects. Phenic acid subcutem. Immunization: inoculate in breast with
one microbe (Salmon): or with weakened virus (Pasteur). Limitations.
Treatment: gastric and intestinal disinfection—copperas, mineral
acids, carbolic or salicylic acids, aromatics, quinine, naphthol, tar,
phenic acid subcutem.
_Definition._ A febrile hemorrhagic septicæmia of chickens and other
fowls (pigeons, ducks, geese, parrots, etc.) communicable to certain
rodents and other animals, and characterized by a short incubation,
rapid progress, great prostration, violent diarrhœa usually greenish,
and a high mortality (90 to 95 per cent.).
_History, Geographical distribution._ It is quoted as prevalent in
Lombardy in 1789, in East India in 1817, in France in 1825, and
generally in Europe and America in the last half century.
The _losses_ from the ravages of this disease are far greater than the
average value of the individual animal would lead one to suppose, but
with domestic fowls numbering 300,000,000 and a yearly egg crop
bordering on a billion dozens it may well be called enormous.
_Bacteriology._ Chicken cholera is caused by a very small ovoid
bacterium (B. Choleræ gallinaceæ) about 0.3 to 1.8μ long, as found in
the blood and tissues of the fowl. It has the general characters of the
groups which cause hemorrhagic septicæmia, thus: 1. It fixes, above all
at the poles, the ordinary anilin colors; 2. It is decolorized by the
methods of Gram and Wiegert (iodine solutions); 3. It grows on gelatine
without liquefying it; 4. It produces acute septicemic lesions; 5. It
tends to polymorphism when grown under different conditions. In the
peritoneum of the guinea pig it forms cocco-bacilli tending in acute and
violent cases to diplococci. Fed to rabbits it appears in the fæces as a
minute bacillus. Even the mode of staining causes a difference in
appearance. Fixed in alcohol-ether, and then stained in Ziehl’s phenated
preparation, coloring is polar, and the central area clear. If in place
of Ziehl’s fluid, hot fuchsin solution is used warm for ½ a minute,
bacillus or cocco-bacillus is shown (Lignieres). It is nonmotile, though
some observers have been misled by Brownian movements. There are no
flagella. In old bouillon cultures short chain forms are met with. No
spores are formed.
From fresh cultures, in flask or in animals, the bacterium grows readily
in alkaline culture media. In _bouillon_ a turbidity ensues, and after
some days pellicles form on the surface and walls, and the liquid slowly
clears. The addition of a little blood serum, sugar or glycerine
encreases and hastens the growth, while acid retards or prevents. This
is common also to other septicemic germs. In _gelatine_ growth is tardy,
but in two or three days there are whitish glistening colonies, becoming
opaque later, and appearing granular if slightly magnified. In punctures
minute colonies form along the line of culture and one at the surface,
at first translucent; later opaque. On _agar_ the colonies grow faster
with similar appearance. On _gelose_ at 37° C. the colonies are blueish
and iridescent, at first, and later opaque. If the germ has been
repeatedly passed through the Guinea pig, they are more translucent. On
_potato_ with alkaline surface, there is a delicate grayish yellow
growth after 48 hours; if acid, growth ceases. In _milk_ there is no
coagulation nor acidification for four weeks; then it becomes slowly
clear and opalescent. With _sugars_ it is not gas producing. With
dextrose it forms an acid solution; with saccharose or lactose an
alkaline one. Cultures in peptone gave a strong _indol_ reaction (V. A.
Moore). Lignieres found no indol in cultures in pancreatic bouillon.
The bacterium perishes when heated to 58° C. for fifteen minutes. It
dies in carbolic acid solution (1:100) in five minutes; in sulphuric
acid solution (0.25:100) in ten minutes; in lime water in ten minutes;
and in sulphur fumes in three hours. Easily destroyed by disinfectants,
it remains potent for months in flasks or buildings that are not
subjected to disinfection. It is not killed by drying (T. Smith and V.
A. Moore) nor by zero temperature maintained for seventeen hours.
The cultures, especially those made in agar have a very characteristic
odor.
_Accessory Causes._ Birds sent to poultry shows will often contract the
disease and introduce it into the home flock on their return. It may
also be imported in newly purchased birds, or on eggs obtained for
hatching. It is even alleged that it has been propagated by feeding
healthy hens on the eggs of diseased ones. When chickens run at large it
passes easily from flock to flock in the immediate vicinity. The
infected manure is, however, the most common channel of infection.
Carried on the feet or bill this contaminates the food and drinking
water, and washed into streams and ponds, it finally in any case reaches
the alimentary canal of the susceptible bird. Or drying up and raised as
dust it is inhaled into the lungs. Or finally from any such source it
infects any open sore. As granivorous birds, wild and tame, suffer from
fowl cholera, it is often introduced by the wild, especially coming from
infected poultry yards. Predatory birds, like hawks and buzzards, but
the latter especially, are common bearers of infection. Rabbits, which
contract the affection so readily, transmit it equally with birds, but
man or beast, soiled by the manure will convey it. Insects are among the
most prolific bearers, hence, as noted by Salmon, the infection may fail
to overstep a close fence in winter, but is subject to no such
limitation during the fly season. In this respect chicken cholera agrees
with Asiatic cholera, typhoid fever and other affections in which the
virus abounds in the alvine discharges. The sale and transportation of
the guano from the infected poultry yard is a direct cause of new
outbreaks. Feeding on the carcasses or offal of the infected birds is a
further cause. It must not be forgotten that the microbe is largely
saprophytic, living indefinitely in the organic matter in soils, and
determining new outbreaks when brought in contact with susceptible
animals. Thus a period of immunity may be followed by infection when new
birds are brought in or when young and susceptible ones grow up.
_Susceptible Animals._ Fowl cholera is preëminently a disease of
chickens, but the microbe is successfully transferred to pigeons,
peafowl, pheasants, parrots, ducks, canaries, sparrows and other small
birds, also to Guinea pigs, rabbits, white and gray mice. Guinea pigs
have abscesses in the seats of inoculation (Pasteur); the same is
alleged of sheep and horses (Kitt), and man (Marchiafava, Celli).
Injection into a cow’s teat caused chronic catarrhal mammitis in which
the microbe persisted for a long while (Kitt). Like other members of the
group of microbes causing septicæmia hæmorrhagica, the pathogeny and
even the morphology are liable to material modification as grown in
different environment (genera). Some of the forms of cholera occurring
among domesticated birds and held to be distinct diseases may find in
this an explanation. Rabieaux claims that under favorable conditions it
has been transmitted to the frog.
_Incubation._ This varies from 18 to 48 hours, the usual being 24 hours.
_Symptoms._ In some _fulminant cases_ the animal is found dead a few
hours after apparently blooming health; it may even have died on the
nest or fallen dead from the roost. Cadeac speaks of transient symptoms
even in such cases—extreme dulness, prostration, somnolence, seclusion
in a cool, dark place, ruffling of feathers, sinking of the head between
the wings, drooping, trailing wings and tail, violet comb, gaping,
discharge of glairy mucus from the bill, convulsions and death. These
symptoms last from two to five hours.
In _acute_ but less fulminant forms there is loss of appetite,
depression, debility, apathy, erection of the feathers, sinking of the
head, swaying when made to walk, drooping wings and tail, sitting on the
breast, convulsive tremblings, discharge of filmy or frothy mucus by the
nose or mouth, vomiting, hyperthermia (108° to 111° F. ), sighing,
breathing, inflation of the crop, violet colored comb, wattles and
mucosæ, great thirst and diarrhœa, at first pultaceous and light yellow,
later glairy, green and fetid. The feathers round the anus become soaked
and matted with the discharge. Temperature becomes subnormal, the
patient falls and is unable to rise, and finally dies in a stupor or
convulsions, the illness having lasted 1 to 3 days.
_Milder cases_ occurring chiefly towards the end of an outbreak when the
less susceptible animals only are left, or when the microbe has become
less virulent, show a larger ratio of recoveries. These show a lack of
spirit and vigor, impaired appetite, diarrhœa, emaciation, dulness,
prostration, moping, ruffling of the plumes, dark discoloration of the
comb, and often swelling of one or more important joints (femoro-tibial,
etc.). These may burst and discharge a reddish pus, or simply form dark
or grayish swellings. These cases may drag along for a week or more and
finally die in marasmus. The minute bacillus is not obtainable from
these (Lignieres).
Cases inoculated in the pectoral muscles with only one or two microbes
usually have only a circumscribed slough, with loss of condition, and
after the elimination of the slough and the healing of the sore the bird
proves immune.
_Lesions._ The alimentary canal is the main seat of morbid changes. The
intestinal walls, and especially the mucosa, have points and patches of
blood extravasation, extensive areas of congestion with ramified
redness, exudation and thickening. The intestinal contents are watery,
frothy, browned or blackened by effused blood, and swarming with
ferments including the specific bacterium. The mucous surface is
brownish or blackish, and epithelial degeneration and desquamation with
abrasions are not uncommon especially on the summits of the duodenal
folds and villi. Croupous exudates and swelling or ulceration of the
follicles are met with. The lymph glands at the base of the cæcum are
often enlarged and congested. The crop is full of watery, pulpy, frothy
or slimy contents, and its mucosa and that of the pharynx may be deeply
congested.
Elsewhere the lesions suggest rather the action of destructive toxins
and the profound changes in the blood. Pericardium and endocardium are
usually studded with dark petechiæ, and congestion and even slight
exudation may be present. The spleen is enlarged, soft, and gorged with
blood. The liver is swollen, congested, extremely friable, and mottled,
grayish white from degenerations. The kidneys are dark red, and friable.
The lungs may show slight hyperæmia only, or a blood engorgement and
consolidation, and are then easily reduced to a dark red pulp.
Friedberger and Fröhner say that respiratory changes are most frequent
in land birds; and intestinal and cardiac in water fowl.
The blood is diffluent coagulating loosely if at all, of a brownish red
color, reddening slowly and imperfectly in contact with air, and like
the tissues contains an abundance of the characteristic bacterium
staining deeply at the poles and clear in the center.
In birds that survive a few days there are marked anæmia and emaciation,
and the muscular system is of a grayish red color, with fatty
degeneration. In acute and fulminant cases on the other hand the muscles
may be full and of the normal red color.
In arthritic cases the congestion and thickening of the soft tissues,
and the excess of synovia, are supplemented by destruction of the
articular cartilage and by areas of bone abrasion. In the more tardy
cases collections of caseous matter are found.
_Diagnosis._ This is based on the demonstrably highly contagious
character of the disease, its rapid spread in a flock, and from the
first to nearby adjoining flocks in summer, the short period of
incubation, the constancy and nature of the diarrhœa, the speedy and
great mortality, and the hemorrhagic lesions of comb, bowels, heart,
lungs, liver, kidneys, spleen, and serous membranes. The demonstration
of the bacterium in the blood and affected tissues is conclusive. Kitt
points out that inoculation of a pigeon kills the bird in 12 to 48
hours, with dry yellow exudate in patches of from ½ to ¾ inch in
diameter on the surface of the muscles, and yellow discoloration and
nodular induration beneath.
_Prognosis._ The mortality reaches 90 to 95 per cent. The negative
chemiotaxis exerted on the leucocytes by the microbe, precludes
defensive phagocytosis, and the progress of the deadly microbe is
comparatively unhindered. Toward the end of a severe outbreak, and in
certain mild epizoötics the recoveries are much greater.
_Prevention._ All birds bought or otherwise acquired and all birds
returning from shows should be quarantined for one week before being
allowed to mingle with the flock. In summer this should be conducted
inside fly screens. The manure should be burned, carefully secluded, or
treated with dilute sulphuric acid. Buzzards and vermin as possible
bearers of the infection should be excluded from poultry yards. So with
human beings, dogs, etc., coming from infected places. In an infected
flock the sick should be at once separated, killed and burned or treated
with sulphuric acid. All manure should be treated in the same way.
Buildings, yards and runs should be thoroughly cleaned and liberally
sprinkled with a dilute sulphuric acid (2:100). If the birds can be
divided up in small groups (say of 5) the appearance of the disease will
only endanger that group. In small flocks or with very valuable birds it
may even be well to take the body temperature morning and night and
separate at once any bird showing a rise. Any diseased or suspected
flock should be kept where its manure will not be washed into wells,
running streams or ponds to which other birds have access. In a locality
where the disease exists fowls should not be allowed to run at large. In
winter this is very effective; in summer owing to the danger from insect
bearers, it must be supplemented by the most scrupulous cleanliness of
poultry houses and yards, and by a liberal sprinkling with dilute
sulphuric acid, or other disinfectant, to be made especially abundant
and frequent on the manure. Nocard cuts short the disease by injections,
subcutem of a 5 per cent. solution of carbolic acid.
_Immunization._ With valuable birds it may be desirable to secure
immunization by non-fatal inoculations. Salmon secured this by first
estimating the number of microbes in an mm. of the blood, then diluting
until five drops would contain but one, or at most two of these
organisms, and injecting this amount into the pectoral muscles. A
sequestrum forms in the muscle and is gradually sloughed out, and the
cavity heals, with resulting immunity.
Pasteur produced a weakened virus by exposing the artificial bouillon
cultures to air for from three to ten months, the strength decreasing
with the length of exposure. The weaker form produces slight illness
only, from which recovery is prompt. A second and stronger virus is used
ten or twelve days later and produces a real immunity.
The drawbacks to these methods are: 1st; that fowls are of too little
value, to warrant inoculation in healthy flocks; 2d; that in infected
flocks, where it is employed, the more susceptible birds are usually
already contaminated, and a large proportion die in spite of it; and 3d;
that it becomes a means of planting the infection in new localities
(Kitt).
_Treatment._ The disease is so deadly that little can be hoped from
medicinal treatment. It has been directed mainly to gastric and
intestinal disinfection. Copperas and sulphuric or hydrochloric acid in
the drinking water ½ to 1 per cent. of each is at once prophylactic and
curative. Friedberger and Fröhner add fennel or peppermint, and give a
tablespoonful every hour to an affected chicken. Other agents
recommended are: carbolic acid (5:100) by the mouth or subcutem
(Nocard), salicylate of soda, quinia (Cadeac), tannic acid (2:100),
salol, naphthol, tar water, etc.
DISTEMPER IN DOGS AND CATS.
Definition. Synonyms. Animals susceptible: dog, fox, jackal, hyena,
wolf. Historic notes. Causes: contagion, inoculation, immunity,
contact with sick, clothing, bedding, kennel: infection fixed—little
diffusible, dogs at large, chill, domestication, high breeding,
special breeds, shows, public conveyances, vegetable diet,
debilitating conditions, catarrhs, change of climate, recurrent
attacks, youth, native susceptibility, teething. Microbiology:
micrococci, bacilli, mixed cultures, Shantyr’s observations,
Lignieres’. Virulent products—all secretions and exudates. Vitality:
virus survives drying, freezing, dilution in water. Destroyed by
disinfectants. Forms of distemper: catarrhal, ophthalmic, cutaneous,
gastro-hepatic, bronchitic, pulmonary, nervous. Duration 20 to 30
days. Mortality 20 to 70 per cent. Prognosis: unpromising conditions.
Incubation 4 to 7 days. Symptoms: hyperthermia (103° to 104°),
dulness, debility, anorexia, staring coat, tremors, seeking warmth,
early fatigue, dry burning nose and footpads, irregular temperature,
simultaneous congestion of all visible mucosæ; Respiratory phenomena;
sneezing, congestion of nose, discharge, blocking, snuffling, rubbing,
cough, retching, vomiting; percussion flatness in lungs, in islets or
along the lower part; auscultation râles, wheezing, crepitus,
creaking, etc.; epiphora, swollen eyelids, weeping, photophobia,
muco-purulent discharge, sticking of lids together, opacities,
vesicles, ulcers; red, hot, buccal mucosa, costiveness, fetid
diarrhœa, tenesmus, weakness, emaciation; skin eruption, on delicate
areas, papules, vesicles with colored contents, pustules, sticky,
greasy exudate; irritability, restlessness, taciturnity, depraved
appetite, spasms, delirium, paresis, epilepsy, chorea. Lesions:
inflammation, degeneration, ulceration on air-passages, alimentary
tract, lymph glands, kidneys, liver, cerebral and spinal meninges,
leucocytic infiltration: offensive odor. Lignieres’ views of microbes.
Prevention: quarantine new dogs for 14 days, wash, disinfect all
collars, etc., avoid shows and meetings, exclude street dogs, protect
against mice, rats, birds, shut up all dogs during an epizoötic;
separate a pack into small lots; seclude the sick and all belonging to
them. Immunization: by lung exudate, by weakened cultures. Treatment:
hygienic, dietetic, warm baths, antipyretics, antiferments, calomel,
phenic acid, eliminants, expectorants, collyria, emetic, demulcents,
bismuth, etc., pepsin, quinine, nerve sedatives, tonics.
_Definition._ A contagious, febrile affection attacking dogs (and by
inoculation cats), and tending to local inflammatory and degenerative
lesions in the mucosæ, lungs, bowels, liver, skin, kidneys, and nervous
system,—a first attack usually immunizing against a second.
_Synonyms._ Contagious catarrhal fever; Dog ill; Bronchial Catarrh;
Intestinal Catarrh; _Fr._ Maladie des Chiens, Maladie du jeune age,
Typhoïde, Typhus des chenils, Variole du chien; _Ger._ Staupe; _It._
Cimurro.
_Animals susceptible._ Dogs, especially puppies and young dogs, and
other members of the canine race, fox, jackal, hyena, wolf. Cats suffer
from inoculation (Laosson), also apes (Cadeac). Old cats and dogs are
often immune, also all animals that have passed through one attack of
the disease.
_History._ The older English veterinarians quote the epizoötics in dogs
described by Virgil, Aristotle and even Homer as probably distemper.
Laosson attributes to it a canine epizoötic which prevailed in Bohemia
in 1028. It appears to have been unknown in Europe in the earlier third
of the 18th century though prevailing in Peru. According to Ulloa, it
was introduced from Peru into Spain in 1735, whence, it spread into
France (1740), Germany (1748), Ionian Isles, Greece (1759), England
(1760), Italy (1764) and Russia (1770), Sweden and Norway (1815),
Siberia (1821). Since that time it has prevailed in Europe and many
dependencies of European nations.
_Causes._ Its advent in Europe as a new disease in the second third of
the 18th century, its steady spread, its continued prevalence, and
extension, concur with the infection of kennels and districts by the
introduction of a sick dog, in demonstrating its purely contagious
nature, and this implies a living microbe transferred from animal to
animal. If any doubt remained it must be dispelled by the inoculations
which have been constantly successful when made on young puppies, or
dogs that have not previously suffered, and on cats. A first attack
confers immunity.
Among _accessory causes_ may be especially named _contact with the sick
dog_, its _clothing_ or _bedding_, and above all its _kennel_. A kennel
may retain infection indefinitely, especially if there is a constant
accession of puppies or susceptible dogs. On the contrary it is not
readily carried on the clothes of attendants, and the inmates of a
kennel often remain sound, though only separated by a yard from the
infected one, and though cared for by the same attendant. Yet so
universally diffused is the contagion that few dogs escape it until they
are a year old.
The habit of letting dogs run at large, to meet in roads and fields is a
most prolific cause, which might easily be done away with where
distemper is prevalent.
A _chill_ is a common condition, hence injudicious washing, swimming in
cold water, exposure of house dogs to cold storms, or outdoors at night,
sleeping in cold, damp cellars, on cold stones or metal plates, or in
passages in a current of cold air are frequent factors. Yet it often
spreads rapidly in the summer, the heat favoring the preservation and
diffusion of the germ.
_House dogs_ as a rule suffer more severely, as their systems are more
sensitive to the cold, and the resisting power to invading microbes is
lessened. Country dogs and those living in the open air are hardier and
more resistant and often have the disease in a mild form.
_High bred dogs_ suffer more severely probably largely from the greater
protection and care lavished on them and their consequent diminished
power of resistance. Newfoundlands, great Danes, pointers, pugs,
poodles, spaniels and greyhounds may be named as especially liable.
The exposure to infection at _shows_, and in traveling by _rail_,
_steamboat_ or _other infected conveyance_ must be considered as among
the prominent causes.
An exclusively _bread diet_ has been recognized as a predisposing cause,
by reason of its lowering the stamina of the carnivorous animal.
Any condition which induces _debility_ whether severe or continued
disease, parasitisms, impure air, under feeding, improper food,
rachitis, or scurvy, etc., must be admitted to operate in the same way.
Any _catarrhal disease_ of the nose or bronchia is especially conducive
to the affection by weakening the mucosa and making an easy entrance
channel for the germs.
_Change of climate_ is a strongly predisposing condition, which not only
hastens an attack, but even, at times, arouses anew the susceptibility
in dogs that have passed through a first attack. Dogs that suffered in
England have had a second attack in India, and some have even had a
third attack when brought back to Europe. Four attacks within a year, in
the same dog, and without change of climate, are recorded by Friedberger
and Fröhner.
_Youth_ is much more susceptible than age, even apart from the immunity
which comes to the mature dog from a first attack. Yet some puppies are
insusceptible from birth.
_Microbiology._ No one pathogenic organism has been proved to be the
constant infecting agent, yet two classes of investigators have
contended in favor of micrococci and bacilli respectively.
_Micrococci_, 1 to 3μ in diameter, singly or in chains of 6 or 8 have
been found in the blood, lungs, liver, kidneys and spleen (Semmer,
Friedberger, Krajewski, Rabe, Mathis, Marcone, Meloni, Kitt).
_Bacilli_ were found associated with micrococci by Semmer, Legrain and
Jacquot, Laosson, Millais, Schantyr, and Galli-Valerio. As observed by
the latter they were 1.25, to 2.5μ long, by 0.31μ broad and took the
Gram stain. Cultivated on gelatine the colonies were waxy, lustrous
points, which indented the gelatine without liquefying it.
Cultures of the mixed bacteria (cocci and bacilli) and their inoculation
on young dogs produced the symptoms of distemper with subsequent
immunity (Laosson, Millais). Legrain and Jacquot claimed immunity, as
resulting from inoculations with the cocci in pure cultures.
Galli-Valerio, using the mixed cultures produced all the symptoms
(pulmonary and cerebro-spinal) of distemper.
Schantyr, ignoring the cocci, describes three bacilli which cause three
different diseases (distemper, abdominal typhus, and typhoid), but the
distinctions are not clear nor generally accepted.
Lignieres and Even, in Argentina, and dealing with the more susceptible
high bred dogs (fox terriers, great Danes and carlins), found constantly
in the blood of the dog, in the early stages of the disease, a long,
delicate bacillus, nonmotile and easily stained in aniline, but not by
Gram’s method. Inoculated on the Guinea pig it shortens, approximating
rapidly in successive passages to a cocco-bacillus, and assumes the
general characters of Lignieres’s _pasteurella_. Different bacteria may
be found in the lungs, bronchial and nasal mucus, tears and vesicles.
Lignieres’s _pasteurella_ is inoculable on the Guinea pig, mouse,
rabbit, and dog, producing the symptoms of local or general infection.
Two centigrammes, subcutem, in the _Guinea pig_, produced a local œdema,
disappearing in four or five days and securing immunity. Five cc.
subcutem proved fatal in 48 hours; intraperitoneal in 24 hours. In the
_rabbit_ 1cc., subcutem, caused local œdema for 2 days and hyperthermia
(104°) for 3 days; 1cc. intravenously, caused fever for 3 weeks,
diffluent blood and hæmorrhagic lesions in lungs, liver, kidneys,
bowels, spleen, and serosæ. In the mouse, 4 to 8 drops, subcutem, caused
œdema, and recovery or death in 2 to 4 days. In such cases the microbe
was found in pure cultures in the blood or inoculated tissues.
Inoculations of the pure cultures on dogs produced in different cases,
gastro-enteritis, pneumonia, pleuro-pericarditis, and arthritis, in
various combinations. If the animal survives it is immune.
Grown on _peptonized bouillon_, _neutral_ or _slightly alkaline_, the
bacillus forms, in 24 hours, small granular colonies which fall to the
bottom, leaving the liquid clear. The addition of serum renders this
more abundant without causing opacity.
On _pancreatic_ bouillon the growth is very free without indol.
On _gelatine plates_ there are fine punctiform colonies, transparent,
but becoming white and opaque in 8 or 10 days. Similar colonies form in
stab and streak cultures. The gelatine is not liquefied. Cultures in
_milk_ cause neither coagulation nor acidity. There is little or no
growth in hay tea, on potato, nor in vacuum. The cultures have the
peculiar odor of the pasteurella.
_Virulent Products._ Infection is present sooner or later in all the
morbid animal products. The nasal mucus, bronchial exudate, saliva,
tears, contents of the cutaneous vesicle, milk, contents of the bowels,
and the blood have been successfully inoculated on susceptible subjects.
Inoculations with blood failed with Bryce, but proved successful with
Konnhauser, Krajewski, Even, Lignieres and Physalix, so that the first
named cases may be explained by a prior immunity, or by a too advanced
stage of the case which furnished the matter. The virulence is not lost
nor even diminished by drying at ordinary temperatures, freezing (10°
F.), nor by moderate dilution in water. Prolonged exposure at ordinary
temperature, however, reduces the virulence, which is greatly impaired
in 15 to 25 days (Laosson), or, if dried, in three months and upward
(Krajewski). Virulence is easily destroyed by disinfectants,—thorough
washing (Menard) hypochlorous acid (Trasbot), chloride of lime, mercuric
chloride, etc.
_Forms of Distemper._ This disease is extremely protean in its
manifestations. Many cases, in country districts especially, are
manifested by a slight fever, with a _catarrhal condition of the mucosæ_
of the nose, eyes, and throat. In other cases there may be simply a
slight _conjunctivitis or keratitis_, and in still others a _cutaneous
eruption_, papular, vesicular or pastular. In some instances there is
slight _gastric_ or _hepatic disorder_ with inappetence nausea, and
vomiting or some irregularity of the bowels. In such cases recovery may
take place in eight or ten days.
In the more severe forms, especially seen in house and city dogs, and in
high bred and confined dogs generally, the fever is high and persistent
and the disorders often predominate in particular organs, hence we see a
_catarrhal form_, a _conjunctival_, a _bronchitic_, a _pulmonary_, a
_gastro-intestinal and hepatic_, a _cutaneous_ and a _nervous_. The
severe cases may last for twenty or thirty days or even in their sequelæ
for several months. Exposure to cold contributes greatly to a pulmonary
attack even in inoculated cases (Lignieres).
The _mortality_ varies greatly. In country dogs it may be below 20 per
cent., whereas in city dogs and those kept confined in close quarters
and in large numbers it may rise to 50, 60 or even 70 per cent.
_Prognosis_ is especially unfavorable in severe cases; in those
profoundly affecting the brain, lungs or liver; in high bred or pampered
dogs; in the very young; in the debilitated, anæmic or rhachitic; in
those that have been recently imported from another climate and are as
yet unacclimated. Puppies from debilitated dams, or those raised in a
large litter with insufficient nourishment, or older dogs confined to a
purely vegetable diet show less power of recuperation. Profound
prostration and offensive odor, from excess of toxins are always to be
dreaded.
_Incubation_ in inoculated cases varies from four to seven days
(Krajewski). When contracted by simple exposure it may seem to have been
extended to fourteen or even eighteen days.
_Symptoms._ The _earliest symptom_ is hyperthermia (103° to 104° F.)
This is accompanied and followed by prostration, dulness, impaired
appetite, erection of the hairs along the spine, shivering, trembling,
seeking a warm place, fatigue on slight exertion, hot dry nose, burning
pads of the feet, sometimes taciturnity. Later the temperature may
descend even to the normal or there may be alternations of rise and
fall. One of the most characteristic symptoms of distemper is the
implication of more than one set of organs, so that morbid
manifestations referable to the nose, eyes, throat, stomach, skin and
nervous system occurring in the same subject are to be especially noted.
In enumerating the prominent symptoms caused by disease of one set of
organs therefore, it is not to be implied that the absence of others
referring to a different class of organs is to be understood. On the
contrary a complication of several is especially significant of this
disease, though the predominance in one class of organ will signify a
special form of the disease.
_Respiratory Symptoms._ One of the earliest symptoms is usually sneezing
with redness of the nasal mucosa, followed by a muco-purulent blocking
of the nose, and rubbing of it with the paws. With the implication of
the throat there is usually local tenderness and a hard, painful cough,
which may be accompanied by retching or vomiting. The breathing becomes
snuffling, especially in pugs and bull dogs, and rapid and even
oppressed in case of implication of the smaller bronchia and lungs. The
nostrils may become glued together, the discharge red or dark in color,
vesicles and sores may appear on the mucosa, and the cough gets
paroxysmal, small, weak and husky or gurgling.
Percussion of the lungs may reveal small areas of flatness from exudate
or collapse, and in case of pleurisy and hydrothorax there is a lack of
resonance up to a given horizontal line, varying in position according
to the position of the animal and always keeping to that part of the
thorax which may at the time be lowest. Auscultation will reveal various
sounds according to existing lesions. There may be a loud blowing murmur
over the large bronchia, or at points to which this sound is conveyed
through consolidated lung. Or a coarse or fine mucous râle may be
present indicating the second stage of bronchitis, or a line of
crepitation, around a non-resonant area indicating pneumonia, or there
may be friction sounds or, later, creaking murmurs from false membranes.
Wheezing and sibilant sounds are not uncommon, also sounds of the heart,
bronchia or bowels, heard in unwonted situations to which they are
conveyed through consolidated lung tissue. Dyspnœa may become extreme,
with puffing out of the cheeks, labial soufle, and violent inspiratory
action. Fœtor of the breath is common. Emaciation, marasmus, sunken,
pale or dark red eyes, putrid diarrhœa and nervous disorders usually
precede death.
_Eye Symptoms._ Conjunctival congestion is one of the earliest and most
constant symptoms. Weeping, swollen eyelids and red turgid mucosa.
Photophobia may bespeak keratitis. Soon the watery tears become
muco-purulent, matting together the lashes and even the lids, during the
night especially, so that they must be sponged to get them apart in the
morning. The exudate may accumulate under the lower lid, or may become
flocculent, and usually flows down the cheeks causing matting and even
shedding of the hair. Vesicles exceptionally appear on the conjunctiva;
more frequently it becomes cloudy and opaque, and at points near the
centre, degeneration of the epithelium leads to the formation of ulcers
no larger than pinheads, but extending into the cornea and sometimes
perforating it so as to allow protrusion of the membrane of Descemet or
the escape of the aqueous humor. The formation and extension of the
ulcers are favored by the general debility, the rubbing of the eye with
the paws, and the infection of abrasions, by pus microbes. This
infection may extend to the lining member of the anterior chamber and
even of the posterior with panophthalmia, but, in the absence of
perforation, internal ophthalmia is rare. When the ulcers heal, white
cicatricial spots, or black points caused by the adhesion of the uveal
pigment remain.
_Digestive and Hepatic Symptoms._ Anorexia and vomiting may usher in the
disease. Buccal congestion, dryness, clamminess and fœtor are marked
symptoms and there may be some yellowness of the mouth and eye. The
patient is at first costive, but diarrhœa often sets in early, with
tenesmus, much fœtor, mucus, froth and even blood, also abdominal pain
and tenderness. The abdomen is habitually tense and contracted. The
alvine flux may rapidly exhaust the animal, or it may continue for a
month in dysenteric form with intense fœtor, weakness, emaciation and
exhaustion. Ulceration of the mouth, gums and rectum, invagination,
prolapsus ani, jaundice, septic pneumonia, paralysis, chorea,
convulsions, or cutaneous eruptions are occasional complications. The
abdominal type of distemper is especially fatal. Even in its early
stages debility, prostration and even drowsiness are marked features.
_Cutaneous Symptoms._ Skin eruptions are observed in the great majority
of cases, at some stage of the disease, and may remain as a sequel for a
time after apparent recovery. Friedberger and Fröhner note cases in
which the high fever and skin eruption are the only prominent symptoms,
and recovery may be looked for with some confidence. The lesions are
most patent on white skinned dogs with short hair, and on the more
delicate parts of the skin (abdomen, scrotum, perineum, inside of the
thighs and elbows) but they may extend over the whole body and even
extend on the mucosæ. They vary much in different cases and stages.
There may be punctiform reddish spots, changing to hard elevated
papules, and, in the case of a certain number, to vesicles and even
pustules. Some vesicles may be small and pointed, but more commonly they
are rounded and flat, and as large as a lentil or small pea. When first
formed, the contained liquid exudate may be clear and transparent, but
often it is reddish or even violet. The individual vesicles tend to
speedily burst, and dry up, but others appear, and thus the eruption
will continue for weeks, the skin meanwhile exuding a sticky, greasy,
offensively smelling exudate which mats the hairs together. Itching is
usually slight, yet in given cases excoriations and sores are produced
with considerable moist discharge. It tends to spontaneous recovery when
the general health improves and appears to be little affected by local
treatment.
_Nervous symptoms._ These are shown more or less from the beginning. The
great dulness, depression, apathy and weakness, which usually usher in
the disease, are indications of this. Drowsiness may be early shown.
Even the early nausea and vomiting may be largely central in its origin.
In some cases, however, the brain symptoms are more active and violent.
The dog is restless and irritable, getting up and moving from place to
place, starting from sleep, yelping, snapping, with twitching of the
muscles of the face or limbs, rolling of the eyes, and excessive heat of
the head. Krajewski even describes rabiform paroxysms, depraved
appetite, spasms, furious delirium, fawning, or threatening, and finally
paraplegia and maxillary paralysis Occurring in a country where rabies
is familiar it would have been more satisfactory if inoculations had
been made from such cases with results negativing rabies. Epileptic
attacks may appear at any stage of the disease. Chorea, tonic spasms,
paresis and paralysis are on the contrary habitually late manifestations
and often seem to be sequelæ determined by toxin poisoning of the nerve
centers, or degenerations of their structure. Choreic movements may be
confined to the head, or a limb, or they may affect the whole body.
Tonic spasms often affect the neck, turning the head rigidly to one
side. Among other nervous disorders may be named, amaurosis with dilated
pupil and atrophy of the optic nerve, deafness, anosmia, and dementia.
_Lesions._ These vary as do the symptoms. The nasal pharyngeal, and
laryngeal mucosæ show congestion, swelling, infiltration, ecchymosis
with vesicles, pustules and ulcerations. They are covered by a foul
muco-purulent exudate. The same condition may often be traced to the
final ramifications of the bronchial system. In pulmonary cases, the
lungs show inflammation, inflammatory exudation and consolidation,
collapse, splenization, œdema, and even suppuration in points or large
areas. The bronchial lymph glands and often the pharyngeal are enlarged,
congested and may be suppurating. The pleura over the congested lung may
be the seat of exudation and false membrane, and a bloody serum may
occupy the pleural cavity. The heart may show parenchymatous
degeneration.
In the digestive organs there may be buccal congestion, with
degeneration and the desquamation of the epithelium and formation of
more or less extended ulceration. The stomach shows similar congestions
and degenerations, the ulcer appearing particularly on the summit of the
folds. Together with the intestines this often presents numerous
petechiæ and ulcerations, and is covered by a foul but often tenacious
mucus. The agminated and solitary glands are usually swollen and
infiltrated, and the mesenteric glands are swollen, congested and
infiltrated.
The kidneys are often congested, and show points of blood extravasation
and tissue degeneration.
The meninges of the brain and cord are often inflamed with
infiltrations, false membranes, and especially exudation into the
subarachnoid and ventricles. Centres of congestion and softening have
been noted in the brain and cord with embolism of capillaries and
softening and degeneration of their endothelium. Nocard and others have
noted a leucocytic infiltration of the perivascular lymph spaces. In old
standing cases sclerosis is an occasional feature.
In nearly all cases there is marked emaciation and a very heavy
offensive odor comes from the skin, the tissues, the contents of the
bowels and the exudates on the respiratory passages.
Lignieres alleges that in the early stages, the specific bacillus is
found in the blood and viscera, but that later it is only exceptionally
found and that other bacteria (streptococcus, etc.,) usually take its
place. In the nasal discharge it may be found at times, but in the more
tardily appearing cutaneous vesicles its absence is the rule, and in the
brain matter and meningeal and ventricular fluids, in cases of paralysis
or chorea, it is not to be detected by culture. Hence the case cannot
always be diagnosed by a successful search for, or culture of the germ,
and hence also the frequently unsuccessful inoculations with the blood,
tears, liquid of vesicles, and even the lung tissues or nasal
discharges.
_Prevention._ Distemper, like any other contagious malady may be
excluded from a city or district by the simple expedient of shutting out
animals that bear the infection. From a kennel or pack of hounds, new
arrivals should be quarantined for a fortnight, until danger is past,
and should only be admitted after a good soapy wash. All clothing,
collars, brushes and other material that came with them should be
thoroughly disinfected. Dog shows and other meetings are to be avoided
as far as possible, and any animal that has returned from one should be
quarantined and all his belongings purified. Dogs that run at large
should be carefully excluded from kennels where valuable dogs are kept,
and from all possible contact with them. Even mice, rats, and birds have
to be considered if the disease exists in the near vicinity. When the
disease exists in a district a sound sanitation would demand the
shutting up of all dogs on their owner’s premises, unless carefully led
on chain and prevented from coming in contact with other dogs.
When the disease has broken out in a pack of hounds, or a populous
kennel, the dogs should be separated into small lots of 3 or 4; the
temperatures of all should be taken twice a day; any lot in which one
shows a high temperature should be instantly removed to a safe distance
and placed in quarantine; and the enclosure where they have been and all
their belongings should be thoroughly disinfected. The enclosures where
the sick are kept must be carefully quarantined so that no infection may
escape on food, water, brushes, utensils, clothing, attendants, cats,
vermin, or even birds.
The dogs that are still healthy should have spacious, well-aired
dwellings, open air exercise (as much as possible in the fine season),
good but not too stimulating food (in part at least fresh animal food),
pure water, and protection against undue fatigue, cold, icy baths,
especially when exhausted, rain or snow storms and cold stone or
metallic beds. In the cold season artificial heat in the kennel is
desirable.
_Immunization_ may be sought in various ways based on the use of the
toxins and antitoxins on the one hand, and of a weakened type of virus
on the other. Bryce (1882) and others inoculated with the blood and
pulmonary exudate, and produced in three-months-puppies, local swellings
mainly, with subsequent immunity. The mortality from the inoculation did
not exceed 10 to 15 per cent. These losses imply that in certain cases
the material inoculated conveyed the microbe of the disease, and the
survivors acquired all that immunity which comes from a first attack. In
the cases that show local lesions only, it may be presumed that few
microbes or none were inserted, while the results came mainly from the
toxins or antitoxins. This would be entirely in keeping with Lignieres’
observation that the blood and pulmonary lesions often failed to furnish
the pathogenic microbe, as tested even by attempts at artificial
cultures. The protection secured from the antitoxins alone is
shortlived, terminating with the elimination of these elements, while
that coming from the action of the toxins on the leucocytes, and the
stimulation by these to the production of defensive products, is much
more lasting and in ratio with the quantity of the stimulus introduced
and the profundity and duration of its influence on the leucocytes. This
may partly explain the occasional early exhaustion of the immunity and
the reinfection of the animal within a year after inoculation.
Physalix working in Chauveau’s laboratory has found the best results
from the use of weakened artificial cultures. He cultivated the microbe
of Lignieres in peptonised bouillon having 6 per cent. of glycerine, and
allowed successive cultures to rest (without reseeding a new culture
fluid), after they have attained to their full growth. The strength of
the culture is in inverse ratio to the period that elapsed between
successive cultures, leading up to this one, and the first inoculation
is made with the weakest product that will produce a very limited local
swelling which is fully developed in 48 hours, and disappears in a few
days. Three or four inoculations are made successively with cultures of
gradually encreasing potency, after which immunity persists for years.
It is to be understood, that an overdose will overcome the immunity at
any time; also that the passage of a culture of lessened potency through
a dog or Guinea pig will raise it to its original virulence. Physalix
operated only on young dogs, that had not shed their milk teeth, and
injected 2 to 3 c.c. of the culture as a dose with only 2.5% mortality.
Others had less success.
_Treatment._ To secure good results in the treatment of distemper every
attention must be paid to good hygiene. An open air life in summer, and
a roomy, clean, well-aired, warmed building in winter are most
important. Chills, foul air, and filth generally are to be carefully
guarded against. Food should be moderate in amount, easily digested and
nutritious. Milk is especially good (sweet, skim or buttermilk); then
biscuit and milk, or in patients accustomed to animal food, lean meat,
minced, scraped or pulped. Warm baths are often advantageous, but they
must be given with great caution to avoid chill.
Medicinal treatment is largely symptomatic. An excessively high
temperature (104° and upward) may be met by warm baths, or
antipyretics—quinine, acetanilid, salicylate of soda, antipyrine,
phenacetin, or even damp compresses to the sides. As a rule, however, it
is not well to continue such agents as acetanilid, antipyrine or
phenacetin longer than is absolutely needful to reduce excessive
temperature.
Attempts have been made to check microbian proliferation by
antiferments, such as quinine, calomel, creolin, phenol, and phenacetin.
The tonic action of quinine specially recommends it but like all bitters
it is obnoxious to a dog with a delicate stomach. Calomel is especially
recommended by Fröhner as a gastric and intestinal antiseptic and its
indirect action on the liver renders it valuable in many cases. Creolin
and carbolic acid exhaled from saturated cloths tend to disinfect the
air passages and give tone to the mucosa. My colleague Dr. P. A. Fish
gave carbolic acid, 2 per cent., and afterward 4 per cent. in normal
salt solution, and in doses of ½ to 1 drachm, subcutem once and twice a
day. In the initial stages, it seemed often to be of great value,
quieting the nervous excitement, improving the general symptoms, and in
some instances apparently cutting short the affection. Trasbot
recommended strong infusion of coffee, and Zippelius sodium chloride,
while others gave ergotin, or better hydrogen peroxide in spray or as a
draught.
_Eliminative treatment._ As in all depressing contagious diseases, we
must favor elimination of the toxins, and in this case without risking
any material encrease of debility. Calomel (7 grs.), sodium salicylate
or benzoate (4 grs.), sodium bicarbonate (7 grs.), potassium iodide (4
grs.), chlorate (7 grs.), or nitrate (7 grs.) may be cited. Digitalis (1
gr.), strophanthus, or caffeine are especially recommended by their
power of encreasing the tone of the heart when that has become weak or
exhausted.
For the _respiratory_ symptoms we may employ the antiseptic inhalations
already named, or, in place of these, iodine or sulphurous acid. The
nervous cough may be met by syrup of poppies, or anise, by morphia, or
codeia. (Recipe: morphinæ hydrochloras 0.1 grams: aquæ amygdal. amar. 10
grams, aquæ distill. 150 grams. M. A teaspoonful three or more times a
day. _Fröhner_). As expectorants, ammonium chloride (5 grs), or acetate,
senega, or apomorphia (⅒ gr.), may be used. In vigorous subjects
ipecacuan (½ to ¾ gr.), or antimonial wine (1 drop). Hydrogen peroxide
in doses of a teaspoonful is often useful. Among counterirritants and
derivatives the warm bath and cold compresses are especially valuable,
or tincture of iodine, or camphorated spirit, or equal parts of aqua
ammonia and olive oil serve a double purpose as furnishing at the same
time an expectorant inhalant.
Special pulmonary complications must be dealt with on general principles
as advised for the special diseases, bearing in mind always the profound
prostration and the need to avoid depressing agents.
For _conjunctival symptoms_ bathing with tepid water to soothe
irritation and remove adhesions and crusts, may be followed by a drop of
aqueous solution of pyoktanin (1:1000) under each lid, twice a day, or
cocaine (3:100), or silver nitrate (½:100); may be used. Fröhner advises
creolin (½:100); Cadeac, cresyl (½:100); Müller, mercuric chloride
(1:2000) or boric acid (1:40). Other Collyria may be substituted (see
diseases of the eye). In violent inflammations atropia will find a place
and in ulcerations boric acid, silver, pyoktanin, calomel, or hydrogen
peroxide. When irritation and rubbing are persistent a cocaine solution
may be dropped into the eye every few hours. When the ocular troubles
persist during general convalescence tonics with good nourishment and
hygiene are demanded.
With _digestive symptoms_ the attendant vomiting will usually have
cleared the stomach of irritant contents. In the exceptional cases it
may be unloaded by apomorphia (¹⁄₁₀₀ gr. subcutem), or ipecacuan wine a
teaspoonful by the mouth. More commonly a check must be placed on
persistent vomiting by bismuth nitrate (3 grs.), laudanum (5 to 10
drops), creosote (5 drops), or chloroform (5 to 10 drops), and small
pieces of ice. A derivative to the epigastrium is sometimes useful. The
food should be of the simplest and most easily digested kind, milk,
meat-soup skimmed of fat, meat juice, scraped or pulped raw meat.
Demulcents like gum water, slippery elm bark, or decoction of marsh
mallow may be resorted to, and in case of extreme irritability
nourishment may be given by rectal injection. As vomiting may be kept up
by irritants in the intestines a tablespoonful of tincture of rhubarb
may be required to be repeated twice a day until relief is secured.
Calomel and chalk (1:12) in grain doses will sometimes serve a good
purpose. Also dilute hydrochloric acid in water (1:60) in doses of a
teaspoonful with pepsin, gentian, quinine or nux vomica will often
contribute much to restore tone and function. Septic intestinal
fermentations may be met with beta-naphthol, naphthalin, (7 grs.),
chloral hydrate (10 grs.) lactic acid (buttermilk), or salol (5 grs.).
The attendant fœtid diarrhœa may demand in addition opium or silver
nitrate (½ to 1 gr.). The gastric secretion is usually suspended so that
it largely passes into the intestines unchanged. Of course it should not
be used along with muriatic acid.
The _skin eruption_ is usually considered of little consequence, or, by
some, beneficial (Cadeac). If treatment is desired it may consist in
dusting powders, demulcent soothing dressings and perhaps stimulating
liniments as found under _skin diseases_. It usually disappears with the
elimination of the toxins and the restoration of vigorous health.
For the _nervous symptoms_ treatment must correspond to the morbid
phenomena. Extreme prostration may demand diffusible stimulants. Spasms
and other indications of congestion may be met by cold to the head, and
inhalations of ether, followed by potassium or sodium bromide (8 grs.),
sulphonal (20 grs.), trional (15 grs.) chloral hydrate in mucilage, or
hypnal (15 grs.). Paralysis must be met by tonics, stomachics, easily
digestible, rich food, and good hygiene. Pepsin, muriatic acid, nux
vomica (½ gr.), arsenite of soda solution (5 drops), arsenite of
strychnia (¹⁄₂₀ gr); orexin(3 grs.), strong coffee infusion, wine, and
electricity may be tried, in addition to stimulant liniments. Chorea
must be treated on the same corroborant plan. Cold douches after which
the patient is carefully rubbed dry are sometimes successful, (see
Chorea).
During _convalescence_ and in all cases of debility and anæmia a similar
corroborant treatment is demanded. Pulped raw meat, rich soups,
stomachics, tonics including the preparation of iron, and in extreme
cases transfusion of blood or a normal salt solution may be resorted to.
In _cats_ a parallel course of treatment may be pursued, allowance being
made for the smaller size of the animal and the great susceptibility of
the feline patient to phenol.
INFECTIOUS BRONCHIAL CATARRH. BENCH SHOW DISTEMPER.
Under this name Glass describes an affection, milder than the usual
distemper, but showing similar lesions and demanding an equivalent
treatment. It is not self-limiting the same patient having suffered
twice in the same year (an occurrence which is occasionally seen in
distemper.) The incubation is 3 to 5 days. Diarrhœa is invariably
present from the first, and the fæces slimy and at the end of a week
slightly bloody. The affection is characterized by the predominance of
the digestive disorder, the absence of skin eruption, the free shedding
of the hair in long coated animals, the ulceration of the gums, tongue
and lips, and the low mortality.
Bacteriological research must be invoked to determine whether this is
only a form of distemper or if it is one of a group of diseases which
have hitherto been known by that name.
EMPHYSEMATOUS ANTHRAX.
Definition. Historic notes. Geographical distribution. Animals
susceptible: Young cattle after weaning, sheep, goats; horses, asses
and white rats, have local swelling; dog, cat, pig, bird and man
immune. Immune animals succumb if injected with lactic acid, or
proteus vulgaris, or violently exerted (sarco-lactic acid). Causes.
Bacillus anthracis emphysematosa, 3 to 10μ by 5μ, stains violet with
iodine, anærobic, sporulates in living body, hence seen as rod, club,
and round, spore. Lives in exudate, not in blood nor on surface. Table
comparing with anthrax bacillus. Vitality: resists drying, cold, 98°
F., weakened by 139°, sterilized by 212° F. for 20 minutes, by strong
antiseptics. Lives in dense clay, hard pan, and waterlogged soils
holding little oxygen. Accessory causes: lactic and other organic
acids, overwork, potash salts, alcohol, salt, proteus vulgaris,
micrococcus prodigiosa, low condition, debility, plethora, chills,
change to warmth, youth, melting snows, freshets, drying of wet lands.
Symptoms: incubation a few hours, disease 12 to 70 hours.
Hyperthermia, swelling in loose connective tissue, shoulder, quarter,
arm, thigh, neck, trunk, palate, base of tongue, pharynx, tender
point, rapidly enlarges, spreads, crepitates, percussion resonance,
finally cold, insensible, and withered. On incision black, bloody
pulp, or frothy. Peripheral gelatinoid exudate. Subsidiary lymph
glands enlarged. Cases with deep seated exudate. Diagnosis: from
malignant œdema and anthrax. Lesions: early decomposition, bloating,
in swelling blood extravasation with gas bubbles and lymph exudate,
muscle beneath dirty brown or black, breaking down when pressed, shows
waxy or fatty degeneration, and many leucocytes and cell forms. Lymph
glands and plexuses blood gorged. Extravasation may be in internal
organs. Liver congested. Spleen rarely enlarged. Treatment: Chloride
of iron internally, ammonia iodide and ol. terebinth externally.
Scarify and use hydrogen peroxide or potassium permanganate.
Antitoxins. Prevention: drain and till soil, apply quicklime to muck,
exclude new animals just from infected districts, disinfect buildings,
close infected wells and streams, seclude the sick, burn, cook or
dissolve carcasses, or fence graves. Bleeding purgation, diuresis,
uniform good feeding, setoning. Immunization by heated and sterilized
culture; by toxins passed through a porcelain filter; by minimum dose
intravenously; by injection into trachea; by inoculation on tip of
tail; by inoculation with Pasteur weakened virus; by heat sterilized
virus.
_Synonyms._ Symptomatic Anthrax; Black Quarter; Quarter Ill; Black Leg;
Rauschbrand; Charbon Symptomatique.
_Definition._ An acute infectious bacteridian disease manifested by
hyperthermia, lameness, and a localized, hot, painful swelling on the
shoulder, quarter, leg, neck, trunk or elsewhere, tending to emphysema,
and gangrene and when incised showing black extravasated blood, clotted
or frothy.
This affection was long confounded with anthrax proper, but was
differentiated by the observation of Wallraff (1856), Boulit-Josse,
Vernant, Pfisterer, Feser, and others and finally Bollinger in 1875
found the motile bacillus. Arloing, Cornevin and Thomas (1879–84)
thoroughly substantiated this position, and devised a method of
immunizing by inoculation. Feser had however seen the motile sinuous
rods in the exudate as early as 1860, and even produced the disease by
the inoculation with mud from infected Alpine pastures.
_Geographical distribution._ Emphysematous anthrax prevails in limited
areas, and particular buildings in Europe, Asia, Africa, Australia and
America, and in all climates from the tropics up to the sub-Arctic. It
is however most prevalent in spring, summer and autumn. It is not
uncommon at the breaking up of the winter snows. It is especially
prevalent on damp, undrained land or on such as has dried up in the
heats of summer, and has become less prevalent in many localities in
connection with drainage and careful cultivation.
_Animals susceptible._ The disease is especially common in young cattle,
from three months to four years of age. Calves fed on milk are rarely
attacked, being in a sense carnivorous and sometimes immunized by toxins
from the dam. Cattle over four years usually escape, having already
become immune if kept in an infected locality. If brought from a
noninfected place they are, at any age, as susceptible as the young.
Sheep and goats contract the disease only exceptionally, but like the
Guinea pig are easily infected by inoculation. Horses, asses and white
rats have only a circumscribed swelling in the seat of inoculation, and
foals and buffalo calves sometimes contract it casually. Carnivora and
omnivora, (dog, cat, pig, bird, man), and the rabbit are virtually
immune.
Immune animals may, however, be made to succumb under special treatment.
In a rabbit inoculated at the same time with the microbe of black
quarter and proteus vulgaris, or micrococcus prodigiosus, or if injected
with a little lactic acid, the disease develops promptly and fatally.
Over-exertion, producing sarco-lactic acid will also lay the system open
to attack. The reduction of the vitality and resistance of the muscle of
the rabbit by a contusion, bruise or lacerated wound, or by injecting it
with acetic acid, potash salts, alcohol, or common salt, will render the
inoculation pathogenic. Again, the introduction of the black quarter
microbe into the aqueous humor of the rabbit, where there are so few
defensive leucocytes, entails an active proliferation and a fatal
result.
_Causes._ The essential cause of emphysematous anthrax is a rod-shaped
germ, variously known as =bacillus anthracis emphysematosa=, =bacillus
Chauvæi=, =Rauschbrand bacillus=. This is a rod-shaped microbe, with
rounded ends, found singly or connected in pairs, or very short
filaments. The bacilli are 3 to 10µ long, by .5µ broad, or when
sporulating, 1.1 to 1.3µ. They form spores even in the body of the
affected animal, often assuming a club shape by reason of the spore
formation near one end. If the spore develops in the center they appear
fusiform. They take aniline colors readily, and iodine slightly,
assuming in the last case a violet tint. The staining is unaffected by
heating in melted balsam. The bacillus grows readily in ordinary culture
media, (peptonized gelatine, bouillon, milk, etc.), but, being anærobic,
only under the surface in stick cultures, or under a neutral gas or
vacuum. It grows most rapidly at a temperature of 36° to 37° C. but also
as low as 15° C. The bouillon at 37° C. becomes milky and opaque in 24
hours, and later it clears up, the microbes being precipitated as a free
white powder. In gelatine cultures liquefaction takes place in three
days, and in twenty days the whole mass may be dissolved and the
microbes precipitated to the bottom. Spores may form in the living body
and as these are set free by the granular degeneration of the bacilli,
the virulent exudate and cultures usually show the microbe in three
different forms: 1st; the straight, motile bacillus of one thickness
throughout its whole length; 2d; club-shaped or fusiform bacilli, the
thickening of the end or median part being due to the endogenous
formation of a refrangent spore or spores; and 3d; the free refrangent
spores which have been set free by the degeneration and destruction of
the sporulating bacilli. The microbe is not found on the surface of the
living animal, nor in the blood, for in both the supply of oxygen is too
abundant; it forms its colony under the skin, in the tissues, and above
all, in the mass of extravasated blood or gelatinoid exudate which its
irritation has produced and where air is lacking.
The most marked differential features of the microbes of anthrax and
emphysematous anthrax are contrasted in the following table:—
=Bacillus Anthracis.= =Bacillus of Emphysematous
Anthrax.=
5 to 20μ × 1.25μ. 3 to 10μ × 0.5 to 0.6μ.
Ends square or cupshaped. Ends rounded.
Occurs singly in the living body. Often in pairs or threes in body.
Long filaments in cultures. No long filaments.
Nonmotile. Motile (sluggishly).
Ærobic. Anærobic.
No spores formed in living body. Sporulates in living body.
Sporulates in air; in surface Sporulates in vacuo; deep in soil.
soil.
Bacilli only. Bacilli; sporulating bacilli; free
spores.
Multiplies freely in blood stream. Dies in blood stream unless
charged with toxins.
Rabbit very susceptible; man less Rabbit, pigeon and man immune.
so.
Produces no gas. Gas producing.
Inoculation swelling very Inoculation swelling very
restricted. extensive.
Bacillus destroyed by Not destroyed by putrefaction.
putrefaction.
_Resistance of bacillus of black quarter to physical and chemical
agents._ The microbe is possessed of great vitality. Thoroughly dried at
a temperature of 95° F. it retains its virulence. The spores may be
preserved indefinitely in dry soil, buildings, fodder, litter, harness,
etc. Cold is equally harmless to it. It has been exposed to a
temperature of 98° F. below zero without losing its virulence. Its
virulence is lessened by exposure for an hour to 139° F., and it is
sterilized at a temperature of 212° F. for twenty minutes. The dried
spores are virulent after six hours of the boiling temperature but are
sterilized at 230° F. if maintained for the same length of time.
Diffused in water the virus is sterilized in thirty-five minutes at the
boiling temperature. Some waters at ordinary temperatures destroy the
virulence in twenty-four hours; others not for many months. It is
destroyed by the more potent disinfectants, mercuric chloride (1:1000),
silver nitrate (1:100), acid salicylic (1 to 2:100), acid carbolic (2 to
4:100), copper sulphate (20:100), boric acid (20:100), muriatic acid
(1:2). Quicklime, copperas, zinc chloride, sulphuric acid and an
alcoholic solution of phenol have proved unsatisfactory.
In clay soils, hard pans, waterlogged soils, and in some that are over
manured so that the atmospheric air is excluded, it may be preserved
indefinitely. Feser, Gotti and others have produced the disease by
inoculating with the washings of infected marshy soils, and this is
doubtless a common source of casual cases of the malady.
_Accessory causes_ are important. The predisposing influence of lactic
acid, of other organic acids, and of overwork have been already named.
Potass salts, alcohol, common salt and the products of proteus vulgaris,
or micrococcus prodigiosus increase the susceptibility. Low condition,
debility, or suddenly induced plethora have a similar influence. Sudden
changes of weather, chills, and particularly the access of hot weather
in spring, when the animal is changing its coat lays, the system open to
attack. Youth, after the period of suckling, and under three years old,
seems to increase the predisposition, though this is largely the result
of the absence of a previous exposure. Then impermeable, clay, wet,
marshy soils, or those charged with organic matter are conditions of the
presence of the microbe. It often appears in spring in connection with
the melting of the winter’s snows, the occurrence of freshets, and the
washing out of soil infection which would otherwise remain buried. Also
in advanced summer and autumn when swamps, ponds, basins, deltas, river
bottoms, etc., are drying out and furnishing pasture. Pease records its
great prevalence in the rainy season in the swamp districts of the
Punjab and North Western provinces of India, and the same is largely
true of our Gulf coast states.
_Symptoms._ Emphysematous anthrax develops suddenly, the incubation in
experimental cases, lasting only for a few hours, and the whole course
of the disease does not usually exceed ½ to 3 days. The local swelling
may be the first observed symptom or there may be first febrile
disturbance followed by the local swelling. _The swellings_ show where
the connective tissue is loose and abundant as on the shoulder, quarter,
arm, thigh, neck, face, or trunk, and practically never where the
areolar tissue is very spare and dense as on the end of the tail, or
ear, or on the limb below knee or hock. They sometimes form on the
palate, base of the tongue, or pharynx. The muscular system is
especially liable to suffer, the looseness of the texture and the
presence of lactic acid making a particularly favorable field for the
propagation of the microbe. The comparative absence of muscle in the
region below the metacarpus, the tail and ear is an important cause of
this immunity.
The _swelling_ is at first very small and tender, but it encreases
rapidly, and in a few hours may extend to one, two, or three feet in
diameter. At first smooth, rounded, pitting on pressure and destitute of
crepitation on handling, it becomes softer and less sensitive and when
pressed or kneaded it gives a crepitant sensation and sound, or it even
appears to gurgle. When percussed the resonance is drumlike. Finally,
the skin may become cold, insensible, and withered like a piece of
parchment. When incised the tissues are found to be gorged with blood,
and of a black or dark red color; they break down under pressure into a
bloody pulp, and from the wound flows a bloody fluid which may be red in
the early stages, black in the advanced, and frothy in the latest. Where
the connective tissue is very loose and abundant, the bloody
extravasation is surrounded by an extensive straw colored œdematous
infiltration. The swelling is sometimes single, but more frequently
several appear and become confluent. The lymph glands in the vicinity
become greatly enlarged.
_Fever_ is a constant condition as the swelling advances and sometimes
it precedes the local engorgement. There is erection of the hair, with
it may be, distinct shivering, recurring again and again. Then general
stiffness, dulness, prostration, loss of appetite and rumination,
accelerated breathing sometimes attended by a grunt or moan, and rapid
pulse. The temperature usually reaches 104° F., and may rise to 109° F.
The breathing becomes more and more labored and plaintive, colicy
symptoms may set in, the prostration advances to complete adynamia, the
patient can no longer stand, the temperature drops to 100° F., or 98°
F., and death supervenes in from eight hours to two days from the first
sign of illness.
In some cases the swelling may be invisible because it is situated
deeply or it may perhaps be entirely absent, and the constitutional
symptoms are the only ones observed.
_Diagnosis._ From _malignant œdema_, which it resembles in producing gas
and crepitating tumors, emphysematous anthrax is distinguished by the
greater length of the microbe, by its formation of spores at the pole
and not in the centre of the bacillus, by the more sluggish motions of
the germ, by the restriction of the germ to given infected districts
instead of being generally diffused as in malignant œdema, by its not
attacking man, rabbit, nor pigeon, which are subject to malignant œdema,
by its deadly action on mature cattle which are usually immune from
malignant œdema, and by the abundant blood extravasation on the
swelling.
From _anthrax_ it is distinguished by the motility of the bacillus, by
its polar sporulation and club shape, by its rounded ends, by its
absence from the blood in the earlier stages, by the presence of gas and
crepitation in the swellings, and by the deadly action of the infection
on Guinea pigs, but not on rabbit, man, nor pigeon. Anthrax is easily
inoculable on a cutaneous sore or intravenously whereas emphysematous
anthrax is not.
_Lesions._ The carcass is liable to be bloated with gas and a reddish,
frothy liquid often escapes from mouth nose and anus. Gas is
particularly abundant in the substance of the tumor, and the skin
covering it may be dry and crackling. An incision made into the swelling
exposes a mass of blood extravasation and lymph exudate, the blood
predominating in the centre so that it may appear clotted and black, and
mixed with gas bubbles, while the yellowish lymph forms the periphery of
the tumor, yet streaked more or less with blood, or even pink
throughout. The abundance of gas is usually in inverse ratio to the
amount of œdema. The muscles beneath or surrounded by an exudate are of
a dirty brown or black, and are disintegrated so as to break down
readily under pressure of the finger into a blackish pulp. They are
infiltrated with gas, crepitate under pressure and assume a golden
yellow color on exposure to the air. The gas is comparatively inodorous
immediately after death, being mainly carbon dioxide and carbide of
hydrogen. Later it may show distinct and even offensive odor, from the
formation of hydrogen sulphide, or lactic acid. The muscular fibres are
easily teased apart, and show under the microscope masses of blood
globules, leucocytes, lymph cells, free nuclei and granules, with, in
some points, fatty or waxy degeneration of the fibres, or granular
masses that are stained black by osmic acid. The bacillus is present in
large numbers, and this with its absence immediately after death from
the blood becomes characteristic. The lymph glands near the swelling are
usually enlarged and gorged with blood. The lymph plexuses and vessels
contain bubbles of gas.
The swellings may be subcutaneous, or submucous in the tongue or
pharynx, but they occur also in the pleuræ, lungs, heart, pericardium,
mediastinum, the peritoneum, the sublumbar connective tissue, and even
the walls of the stomach or intestine. It is not uncommon to find a pink
effusion into one of the serous membranes. The liver is usually
hyperæmic, as may be also the kidneys, but the spleen is rarely
enlarged. In this and in the integrity of the blood globules this
affection differs from anthrax.
_Treatment._ This disease is so often speedily fatal, cutting off its
victim in eight hours, often during the night, that no opportunity is
allowed for treatment. Even in those that survive for two days, the
affection must always be looked on as exceedingly grave, and as little
amenable to treatment. Yet much depends upon the patient and the
country. Dr. Phares in Mississippi found that it yielded readily in many
cases to ½ oz. doses of tincture of chloride of iron every four hours,
and a local application composed of equal parts of tincture of iodine,
aqua ammonia and oil of turpentine. Galtier tells us that recoveries are
frequent in Algeria, while they are rare in France. Tisserant gives the
French recoveries as 2 per cent. It is probable that in districts and
countries where the malady is all but ubiquitous, the surviving animals
are racially immune, or they have been largely exposed and in some
degree virtually immunized at an early age.
Wallraff mentions a success from applying a tight ligature around an
infected limb, above the seat of the tumor and freely scarifying the
latter so as to freely admit the air. For swellings elsewhere,
scarifications and the free application and injection of peroxide of
hydrogen or potassium permanganate (2 to 3:100) would be rational
treatment. The same agent might be given by the mouth in doses of 2 or 3
ozs. at frequent intervals. Antiseptics and tonics have been freely
employed, including phenol, salicylic acid, sodium salicylate, potassium
iodide, quinia, alcohol, phosphorated oil, ammonia acetate, and as an
eliminant soda sulphate, but with no very good result. Locally,
scarification, antiseptics and caustics, have been employed.
Another line of treatment which deserves to be further exploited is the
use of antitoxins on infected animals. An immunized animal may be again
and again inoculated at intervals of a week or two until it has been
stimulated to produce antitoxin in large amount. Then after three weeks
interval its blood serum or blood, may be sterilized by heat, the
resulting coagulum washed in distilled or boiled water, and filtered,
and the filtrate injected subcutem on the infected animal.
_Prevention._ This is most effectively secured by sanitation of the soil
and buildings. Thorough drainage to secure perfect and constant æration
leads to destruction of the anærobic germ, or the suspension of its
pathogenic quality. Thorough culture contributes largely to this
sanitary æration, while baking of the surface counteracts it. When
thorough drainage is impossible it may be desirable to subject the land
to gardening or to the production of crops that are to be used for human
consumption and not for domestic animals. Kitt’s suggestion, to soil
cattle on hay, produced on such lands, and to exclude from the infected
lands all animals that by wounds or sores near the feet, or by raw gums
from shedding of teeth, furnish infection atria for the poison, is
insufficient, as stalled cattle occasionally suffer.
When an open porous soil maintains the infection by reason of the
presence of an excess of decomposing organic matter, that may be largely
remedied by a free application of quick lime. This hastens the
decomposition of the organic matter and after a year or two, when that
has been largely disposed of, the good effects may be expected.
An important measure is to exclude from fairs, markets, and above all
from clay or other dense wet soils into which they might convey the
germs, all animals brought from infected soils.
Disinfection of the buildings where diseased and infected animals have
been is an essential measure. Wells and streams receiving the drainage
of infected lands must be carefully avoided.
Diseased animals must be carefully isolated, and all their droppings,
and products of every kind disinfected.
The carcasses are best cremated or rendered under superheated steam
under pressure. Solution in sulphuric acid may be employed. If none of
these are available they may be deeply buried in dry porous soil well
apart from any risk of drainage into wells or water supplies. The area
occupied by the graves should be fenced in so that no cattle nor sheep
can gain access to it, and any vegetation grown on the graves should be
burned. The danger of the germs being raised to the surface by soil
water or earth worms must be recognized and any consequent evil guarded
against. The carcass should not be cut open but buried in the hide, or
if the latter is preserved it should be treated with a chloride of lime
solution. If a carcass is opened for scientific purposes, great care
must be taken to avoid the distribution of the bacillus in soil
appropriate to its preservation. The meat should not be preserved for
human consumption unless it has been cooked under pressure at a
temperature of 240° F. The object is not to destroy any poison which
would be fatal to man, but rather to prevent the spread of the spores on
new soil and the extension of the area of infection.
The reduction or prevention of sudden plethora was formerly availed of
to lessen the number of victims and it is well to still bear in mind
that this has an appreciable though limited effect. As a means of
reducing plethora a free bleeding was resorted to when the period of
yearly prevalence approached, and no less when the disease had already
appeared in a herd. I can mention an instance in which infection was
carried on the fleam from the first animal bled (the sick one) and
caused the fatal infected swelling around the phlebotomy wound in the
next seven animals operated on. Another objection to phlebotomy is the
tendency to a rapid reproduction of blood, which the depletion brings
about, and the supervention of a greater danger than before, in the
course of a month or more. Purgatives and diuretics are somewhat less
objectionable in this sense. Careful feeding to keep the animal
constantly in good condition does something to obviate sudden plethora
and its attendant dangers, and thus an allowance of grain or linseed
cake through winter and early spring, or when the pastures are bare,
will bring the animals through in fine condition, and ward off the
danger that comes from a sudden access of rich aliment.
Another measure was the insertion of a seton in the dewlap. The theory
was to counteract plethora but the benefit probably came rather from the
formation of an actively granulating wound, which came in contact with
the ground and received the bacillus, but in which the abundance of air,
and of active leucocytes checked the propagation of the germ and the
occurrence of a fatal infection. A certain grade of immunity was the
natural result in many cases.
_Immunization._ As the first attack of emphysematous anthrax secures for
the subject of it immunity against a second, we are furnished with a
reasonable basis for the practice of artificial immunization. This has
been attained by a variety of methods, the essential feature of each
being the subjecting of the system of the animal to be treated, to the
action of the toxins of the specific bacillus.
1st. A culture of the bacillus made in the thermostat at 42 C. (107.6°
F.) so as to prevent the formation of spores is then sterilized by
heating to 100° C. for one hour and then injected subcutem in a dose of
2 drams, to be repeated on the second day. This, like all the other
methods named should be done by some one accustomed to bacteriological
manipulation and the sterilization completed by superheating the neck of
the vessel containing the mixture. Any germs escaping on the hands,
instruments or other objects used will prove fatal in spite of all the
appearance of precautions.
2d. Roux sterilized his cultures by filtering them through a porcelain
(Pasteur) filter and using only the filtrate for injection. This
requires even greater precaution in manipulation as what is left in the
filter is most virulent, and must be thoroughly sterilized to obviate
dangers from its dissemination.
3d. Intravenous injection of a small quantity of virus, containing but a
few bacilli produces no local swelling, but only a slight temporary
hyperthermia and permanent immunity. The greatest care is necessary in
the manipulation, to prevent any contact of the bacillus with the
subcutaneous tissues or the walls of the vein. The virulent exudate
swarming with bacilli is taken and a drop or two added to a normal salt
solution, which is diluted and shaken in a stoppered bottle, until each
drop contains but one, or at most two bacilli. Then the hands having
been thoroughly washed with soap and warm water and rinsed in a 5 per
cent. solution of carbolic acid, and the instruments having been boiled,
the vein is raised as for bleeding, and penetrated by a short cannula
and trochar, which after boiling has been dipped in the carbolic acid
solution, the trochar is withdrawn, and the nozzle of the syringe
containing the virulent solution is inserted through the cannula, so
that its point is free in the centre of the blood stream, into which a
few drops of the virulent solution are discharged. The nozzle is left in
place for a few seconds to ensure the washing of any infecting matter
from its point, when it is withdrawn, followed immediately after by the
cannula. Great care should be taken to avoid any scratching of the inner
coat of the vein with the cannula, trochar or nozzle.
4th. Another method of immunizing is by the injection of the virulent
liquid into the trachea and bronchia. This appears to bring it so
directly in contact with the blood, that the microbes are destroyed as
rapidly as if it were introduced into the blood stream direct. The
injection is made between two tracheal rings, the manipulation being
essentially the same as in the cases of the vein, the tissues being
first perforated by a sterilized cannula and trochar, and the sterilized
nozzle subsequently inserted through the cannula.
5th. Inoculation into the tip of the tail can be successfully employed,
the coldness of the region and the scantiness of the connective tissue
preventing any dangerous increase of the bacilli in the cooler season.
In the heat of summer, however, this is to be avoided as dangerous. The
tail is first washed with soap and water followed by a 3 per cent.
solution of phenol. It is then punctured with a fine trochar or needle,
(sterilized), within two inches of the tip and in a downward direction
and the instrument is moved slightly from side to side so as to form a
small sac, and is then withdrawn. The sterilized nozzle of the
hypodermic syringe is now inserted in the opening and a few drops of the
virus injected into the sac. When the nozzle has been withdrawn the
thumb may be placed on the external orifice and the end of the tail
manipulated to diffuse the virus in the connective tissue. This is
usually followed by an insignificant swelling, and a slight rise of
temperature. Should the swelling exceed the size of a duck’s egg or if
others appear higher up on the tail, they may be freely scarified and
covered with a carbolic acid bandage. Or the tail may be amputated above
the highest swelling and the stump treated with antiseptics.
6th. The virus prepared by the Pasteur institutes, that of Arloing,
Cornevin and Thomas, is the most extensively employed. Forty grammes of
the diseased muscle are dried rapidly at 32° C (90° F.) and triturated
in 80 grammes of water. This is divided in 12 equal parts and put on
plates in two thermostats, six at 100° C. (212° F.) and six at 85° C.
(185° F.) where they are kept for six hours, when it forms a dry,
brownish powder. One tenth of a gramme (1½ gr.) of this powder is
dissolved in five grammes of distilled or boiled water and will furnish
ten doses. The animal to be protected is first injected in the tip of
the tail or elsewhere with the virus prepared at 100° C., and ten days
later with that prepared at 85° C.
By the use of this method in hundreds of thousands of animals on
infected lands the mortality has been reduced to less than one tenth of
its former amount. It is attended by the one danger which is not always
duly appreciated, that unless its use is restricted to herds on ground
that is already infected, it endangers the infection of new districts.
The spores are not absolutely sterilized at 85° C. Arloing and Cornevin
and later, Nocard and Roux have shown that the addition of lactic acid
to the liquid which has been weakened for inoculation, restores it to
its former virulence, making it a most deadly agent. Galtier says that
the virus weakened by heating to 100° C. for seven hours until it will
no longer kill a mature Guinea pig, will still kill a new born Guinea
pig and acquire all its original virulence in the act. Also that the
injection of large enough doses will not only kill the full grown Guinea
pig, but at the same time restore the microbes to their former
virulence. While recognizing the great economy of the judicious use of
such weakened virus, we cannot but condemn the reckless sale by the
Pasteur institutes of their products, to be used on animals on all kinds
of lands, the uninfected as well as the infected. A great and valuable
prophylactic measure should not be used in such a way as to increase the
area of prevalence of the disease which is to be prevented, and also the
yearly demands for more of the preventive agent. This may appeal to the
business instinct, but this should ever be held subordinate to sanitary
considerations. The danger might be avoided by making the state the sole
distributor of such prophylactic agents, but in any case their use
should be forbidden, and as far as possible prevented, upon dense and
wet soils that are not yet contaminated by the bacillus.
7th. Kitt secured immunization by inoculating once only, with dried
virus which had been subjected for six hours to steam at 100° C.
8th. In different outbreaks, I have taken the blood from the sick
animal, or one that has just died, and heated it for over one hour in a
water bath, at 100° C., then broken up the coagulated mass in well
boiled water, filtered the liquid and used the filtrate for inoculation
in doses of 2 drams, repeated the second day. Great care is taken in
keeping the whole mass at 100° C. for the requisite length of time; then
in heating the upper part of the vessel, which was above the contents
and the water so as to char anything adhering to it; to see that hands,
instruments, and all articles used have been thoroughly sterilized; and
to dip the hypodermic nozzle in carbolic acid before each injection.
It is not claimed that this method is perfect, since severe, advanced
cases may have bacilli and even spores in the blood, and the latter
would not be sterilized but only weakened. It has, however, several
manifest advantages that may be held to more than counterbalance this
danger.
_a._ It almost infallibly secures the toxins of the disease prevailing
in the particular herd, thus escaping the danger of using the weakened
virus of emphysematous anthrax on some other disease (anthrax,
Wildeseuche, Barbone, etc.), which has been mistaken for it, and which
may not be prevented by this purchased product.
_b._ During life the blood of emphysematous anthrax is usually free from
the microbe, and even where that is present it is liable to be in very
small numbers, so that we secure either the pure toxins, or if a few
germs are present they are so scanty, that weakened as they are by heat,
they are without danger to the animal operated on. I have never had
occasion to note evil results.
_c._ There is no danger of the spread of the bacillus to new territory,
as we secure the material from a herd in the already infected territory,
and use it only on the animals on the same land.
The certainty of results with this method, and the comparative absence
of danger of injury to the animal operated on, and of all risk of the
extension of the area of infection appeal to me so strongly, that I
would not willingly resort to the purchased products, except where it
proves impossible to secure the virus on the spot.
ANTHRAX.
Definition. Synonyms. History and geographical distribution. Etiology:
Bacillus anthracis. Susceptible animals: small rodents, sheep, horse,
camel, ox, goat, deer, stag, man, swine, dog, white rat and bird when
chilled, frog when heated; young most susceptible, races long exposed
to infection are least. Soils, wet, dense, impermeable, basins,
swamps, rich river bottoms, deltas, rich meadows, below tanneries,
alkaline soils, wells with surface drainage; season: wet, hot and dry,
late summer and autumn; flies; infected buildings, harness, vehicles,
fodder, litter, butchers’ knives and wagons, surgical instruments;
insolation; privation of water: plethora, starvation: overwork,
exhaustion. Bacillus anthracis: rod, nonmotile, 5 to 20μ by 1 to 1.5μ,
square ends, isolated in blood, often filamentous in cultures,
sporogenous, ærobic, stains easily in aniline and iodine, killed at
131° F. (spores at 203° to 282° F.), action under chemical
disinfectants, or septic ferments: air favors sporulation and
survival; in shallow graves, water. Infection atria: ingestion,
inhalation, inoculation, insects, placenta. Forms: fulminant,
internal, febrile, local,—external,—gloss-anthrax, pharyngeal,
hæmorrhoidal, subcutaneous. Lesions: blood normal in fulminant, dark,
diffluent, crenated or disintegrated globules in prolonged cases,
tissues brown or yellow, heart pale; liver enlarged, softened, pale,
hæmorrhagic: spleen enlarged, blood-gorged, ruptured; lymph glands
hyperæmic; serosæ congested, petechiated, hemorrhagic; lesions embolic
and like the blood swarm with bacilli. Toxins, ptomaines. Incubation 1
to 6 days. Symptoms: _internal cases_: hyperthermia, constitutional
disorder, mucosæ dusky, brownish, yellowish, bleeds, bloody urine,
rectal mucosa congested, blackish, colics, pharyngeal anthrax, blood
diffluent, black, broken down red globules, bacilli, abortions, death
in 12 to 48 hours: fulminant cases in cattle and sheep. Local
(external) anthrax, cutaneous, swellings: gloss-anthrax; pharyngeal,
hæmorrhoidal; sheep and goats; horse; swine; dogs; cats; birds.
Differential diagnosis: deductions from symptoms, condition of blood,
animals attacked, environment or conditions of life, presence of the
bacillus. Examination for bacillus. Post mortem lesions; gelatinoid,
bloody exudate, petechiæ, blood-gorged spleen, lymph glands, and
liver, diffluent blood, bacilli in capillaries. Inoculation
intravenously. Cultures. Prognosis. Mortality often 70 per cent.
_Definition._ Anthrax is an acute infectious bacteridian disease
occurring casually in the herbivora and omnivora and, under favorable
conditions, communicable to carnivora, birds and batrachians. Its
special features are the presence of the _bacillus anthracis_ in the
diseased parts, the destruction of red globules, the arrest of
hæmatosis, the occurrence of capillary embolism, extravasations and
exudations, and of necrotic processes in the affected parts, and a
sanguineous engorgement of the spleen.
_Synonyms._ Malignant pustule; Splenic apoplexy; Splenic Fever; Charbon;
Miltzbrand; Woolsorter’s Disease; Malignant Carbuncle; Contagious
Carbuncle.
_History and Geographical Distribution._ As anthrax prevails in damp,
undrained lands where agriculture is backward, it is not wonderful that
it can be traced to near the dawn of human history when the whole race
lived under primitive conditions. Moses records its ravages on the
bottom lands of the Nile (Ex. ix. 9), Homer, on the plains of Troy
(Iliad, Bk. 1st), Ovid, Plutarch, Dionysius, Livy, Lucretia, Columella,
Virgil, Pliny and the Arabian physicians all show a familiarity with a
disease of this nature. Later, Heusinger collects evidence of its
prevalence in certain areas in all parts of the world from the equator
to the Arctic circle. The mortality was often very high, thus Kirchner
records the death of 60,000 people in a single epidemic in 1617, in the
vicinity of Naples, Placide-Justin, that of 15,000 in St. Domingo in six
weeks in 1770, and on the Russian and Siberian Steppes it is not
uncommon for hundreds of thousands of domestic animals and thousands of
human beings to suffer in a single year.
The geographical distribution of the disease is largely influenced by
soil and climate. On dense, impermeable clays and hardpan subsoils, on
river bottom lands, dried lake basins and deltas, rich in organic
matter, and with the air driven out by water or gaseous fermentation
products, the germ is preserved and propagated if once introduced. Thus
it is common around the mouth of the Nile, and along the occasionally
inundated banks of the Vistula and Danube, the Spree, Oder, Elbe, Rhine,
Eure, Loire, Seine and Marne, and in England in the Fen district. On the
rich, undrained, black soils of Siberia it is extremely prevalent and
fatal. In the rich Genesee Valley, N. Y., the writer has seen 200 cattle
in one herd and three human attendants attacked in the course of a
fortnight, and in different meadows receiving the drainage of tanneries,
the affection prevails every summer and autumn. It is much more
prevalent in the rich lands of the Southern States and a widespread and
deadly epizoötic prevailed in Louisiana in 1896. Where the soil is
favorable, the germ may be preserved indefinitely, even in mountainous
districts, and near Los Angeles, Cal., where the disease was introduced
in imported sheep some years ago it has become permanently domiciled, on
the dry ranges which have moist lands (Cienegas). When an outbreak
occurs, the herds or flocks are usually moved to higher soil, and the
carcasses being left unburned and unburied the infection is spreading
year by year (McGowan, Morrison).
_Etiology._ Nothing is more certain than that the disease is due to the
introduction into the blood or tissues of the bacillus anthracis or its
spores. These microbes are always found in the anthrax lesions and in
the blood of the victim in the advanced stages. When grown in bouillon
cultures to the hundredth generation they retain their virulence
unabridged and determine the same lesions in the animals inoculated.
When the infecting culture has been passed through a Pasteur filter the
virulence is lost with the removal of the bacilli. The fresh anthrax
blood containing bacilli but no spores when subjected to compressed
oxygen (50 atmospheres) becomes noninfecting. The same liquid when
boiled proves non-virulent.
Certain conditions, however, contribute to the propagation and reception
of the bacillus and these may be considered as accessory causes.
_Animals susceptible._ The receptivity of the animal exposed is of first
importance. Young animals are the most susceptible. The small rodents,
the mouse, Guinea pig and rabbit are susceptible in the order named,
followed by the sheep and horse and these again by the camel and ox.
Among the wild herbivora the goat, deer and stag have a high
susceptibility. Man is less susceptible yet contracts the disease
readily by inoculation, inhalation or ingestion. Swine and dogs are
comparatively little susceptible, yet they often contract the disease by
eating the carcasses or discharges of anthrax animals. White rats and
birds are held to be insusceptible, yet the latter contract the disease
readily when the vitality of the system has been reduced by immersing
the body in water, or giving antipyrine. A similar result is observed in
the otherwise immune frog if the body is heated above the normal cold
blooded temperature. The receptivity may vary, however, in the same
genus and species. The Algerian sheep is virtually immune from anthrax,
perhaps because its ancestors have been so constantly exposed that only
the insusceptible strains survived. Swine, birds and carnivora may have
similarly acquired a fair measure of immunity by the survival of the
fittest. Apart from this, however, a flesh diet is to a certain extent
protective, thus Feser’s rats if fed vegetable food proved susceptible
to inoculated anthrax, while if fed on animal food they were
comparatively immune.
The animal that has survived an attack of anthrax is thereafter strongly
immune. This serves to partly explain the apparent immunity of animals
bred in an anthrax district, the young animal becoming habituated to
infinitesimal doses of the toxins, conveyed in the secretions of the
uterine glands or mammæ.
_Soil_ is a factor so far as it preserves and propagates the bacillus.
As already stated, soils that are naturally wet by reason of their
impermeable character, their position on or near the water level, their
conformation in basins which dry out in late summer or autumn, are
especially favorable to preservation of the bacillus. Again soils that
are specially rich by reason of an excess of decomposing vegetable and
animal remains, or because of excessive manuring, tend to preserve and
multiply the microbe. Rich, flat meadows below tanneries or abattoirs,
and irrigated from these or occasionally overflowed are especially
dangerous to stock placed upon them. Soils with an alkaline reaction
from the lime, potash or ammonia present are very favorable to anthrax.
Wells receiving surface drainage are common factors in carrying
infection.
_Season_ is a contributing factor in various ways. Damp seasons
sometimes bring the germ to the surface of the soil by the gradual
elevation of the water level, or by causing inundations and the
deposition of the bacillus on areas of pasture or forage that were
previously free, or finally by bringing the earth worms to the surface
and leading to the deposition in their casts of the bacillus brought
from the infected graves or retentive subsoils. Dry seasons are,
however, the anthrax seasons _par excellence_, as they dry up swamps,
fens, ponds, lakes, basins, deltas and bottom lands, and render them
available for pasture. The germladen mud of these drying lands is also
raised in dust and deposited on the vegetation to be taken in by the
animals. Again on the drying basins and bottom lands the tempting green
vegetation is often pulled up by the roots with adherent, infecting mud.
For the above reasons, even in an anthrax region the malady is most
prevalent in the late summer and fall, and in certain valleys like those
of Corsica the stock is considered safe until the dry autumn weather
demands their removal to the mountains.
Another reason for the summer epizoötics is found in the transference of
the germ by flies. House _flies_, horse-flies, blowflies, mosquitoes,
etc., carry the bacillus on their feet, mandibles or piercing apparatus,
and even in their stomachs (Bollinger) and transfer it from one
individual to another. It is worthy of note that the great majority of
cases of local anthrax in man occur on the habitually uncovered parts of
the body (face, neck, hands and arms) and start from a centre like the
bite of an insect.
_Stables_, _stable utensils_, _harness_, _shafts_, _poles_, _fodder_ and
_litter_ are familiar bearers of the virus. Butchers’ knives and wagons
and surgical instruments are further media of contagion.
Certain conditions of the animal system expose it to attack. The fever
and constitutional disturbance which are caused by _the extreme heats of
summer and autumn_ are strongly predisposing, especially if alternated
with frigid nights as seen on the Siberian Steppes. _Privation of water_
raises animal temperature and thus the _drying up of the customary
drinking places_ becomes an important factor. _Plethora_ and
_starvation_ are alike predisposing, probably by lessening the resisting
power of the system. _Overwork_ and _exhaustion_ predispose, as Roger
showed by making the immune white rat turn a wheel until worn out and
then successfully inoculating it. The addition of lactic acid to the
virulent liquid (1:500) greatly encreases its potency (Arloing, Cornevin
and Thomas) and the further addition of fermentescible sugar and rest
enhances this still more (Kitt). The production of lactic acid by
muscular overexertion is thus a potent accessory cause in fatigue.
_Bacillus anthracis._ This was first demonstrated in anthrax blood and
exudates by Pollender and Brauel in 1849 and 1850 but as they failed to
find it in all cases they concluded that it was not the essential cause.
Davaine who found the bacilli in 1850 suspected that they were
pathogenic and by 1863 he had shown that blood which contained no
bacilli was non-virulent, while that in which these organisms were
present was constantly infecting. Klebs and Tiegel in 1871 filtered
anthrax blood through an earthenware vase and found that the clear
filtrate (bacillus-free) was noninfecting.
The _bacillus anthracis_ as found in the blood is a nonmotile rod-shaped
organism, 5 to 20μ long by 1 to 1.5μ broad with ends apparently square,
but really slightly cup shaped as seen in the stained specimens when two
have remained connected end to end. Under favorable conditions a clear
hyaline envelope may be seen around the bacillus. Though usually
isolated in the living blood, yet in bouillon cultures the bacilli grow
out into long flexible filaments, made up of separate segments which are
easily distinguished in the stained specimen. In all cultures out of the
living animal body, in the presence of air and at a suitable temperature
spores form endogenously in the bacilli and are set free by the granular
degeneration of the latter. In peptonized bouillon this may occur in
four days at 14° C., or in eight hours at 37° to 40° C., but not above
42° C. (Schreiber. Centr. S. Bact. 1896). Sporulation never occurs in
the living animal body.
The bacillus is ærobic, yet it will grow at the bottom of a stick
culture in solid media. It fails to grow in an atmosphere of CO_{2}, H,
or N. It stains readily in aniline colors, and also by Gram’s method. It
grows freely on a variety of culture media (blood serum, aqueous humor,
urine, vegetable infusions, milk, meat bouillon, peptonized gelatine,
potatoes, etc.) at a temperature of 20° to 38° C. Growth ceases below
12° C., and above 45° C. Growth is most active in neutral or slightly
alkaline media, and is arrested by that which is decidedly acid.
_Action of physical and chemical agents on the bacillus anthracis._ The
bacilli survive a temperature of −45° C. (−49° F.), but they perish in
10 minutes at a temperature of 100° C. (212° F). A temperature of 55° C.
(131° F.), proves fatal if sufficiently prolonged. The spores are much
more resistant. They have survived −130° C. (−202° F.) and though they
may die in 10 minutes in liquid media kept at 95° C. (203° F.), yet when
old and dry it may require several hours at 140° C. (282° F.) to
sterilize them.
Even the bacilli are comparatively resistant to ordinary disinfectants,
and, as spores form in the body very rapidly after death, and in
virulent products, it is always best to assume their presence. In a
moist medium Cl. 44.7% destroyed the spores in 3 hours: HCl (1:1100) in
2 hours: HgCl (1:1000) in a few minutes: HgI_{2} (1:20000) in 2 hours:
Malachite green (1:40,000) in 2 hours: Methyl violet (1:5000) in 2
hours: Aseptol (1:10) in 10 minutes: Carbolic acid (4:100) with HCl
(2:100) in 1 hour.
_Action of septic ferments on the bacillus anthracis._ Rapid
putrefaction in the anthrax carcass which has not been opened tends to
speedy granular degeneration and death of the bacillus anthracis, so
that the blood and tissues may be no longer infecting after six days in
summer. In such cases the irrespirable gaseous products of decomposition
drive out the oxygen without which the bacillus cannot live. If,
however, spores have already formed or if air is freely admitted the
infection survives in spite of decomposition. The search for the bacilli
may thus be fruitless as soon as decomposition is well advanced and the
material can only be virulent through any spores that may have formed.
Eventration serves to retard sepsis and admit air to form spores, and
salting operates in a similar manner.
The infected hides, the nasal, buccal, kidney and bowel discharges, and
spilt blood and exudates mingling freely with the air tend to form
spores and to preserve and propagate the contagion. On the contrary
prompt and deep burial, without opening the carcass and before spores
can have formed will usually ensure its destruction. The main danger in
such cases comes from infecting matter (adherent to the surface of the
body) which sporulates easily. This serves to explain the great danger
of working in anthrax hides, leather, horn, wool, hairs and bristles. It
also explains sporulation and preservation of infection when the
virulent excretions, blood, etc., mix with the surface layers of soil.
This may happen at a greater depth (3 or 4 feet) in a very porous soil
and where the temperature is sufficiently elevated (above 14° C.) It may
even occur in water. The dried spores are mostly carried in dust, hay,
fodder, and running streams.
Since 1892 anthrax has prevailed along the banks of the Delaware river
for a distance of 40 miles in N. J. and Del., destroying from 70 to 80
per cent of the farm stock. The great morocco industry on this river
draws infected hides from India, China, Russia, Africa and South
America, and the spores are carried and distributed by the tides.
_Infection-Atria._ Infection may occur by a variety of channels as: 1st,
by _ingestion_, giving rise most commonly to anthrax of the mouth,
throat or intestines; 2d, by _inhalation_, giving rise to pulmonary
anthrax (wool-sorter’s disease): 3d, by _inoculation_ through contact of
abrasions, wounds, etc., with infecting bodies, including surgical
instruments: 4th, by flies and other insects: and 5th, by transmission
to the fœtus in utero. This last form is very rare in the larger
animals, but has been repeatedly seen in Guinea pigs, rabbits, goats and
even in one case (Pangalli) in man.
_Forms of Anthrax in Domestic Animals._ In the lower animals anthrax
manifests itself differently according to the seat of invasion and the
amount of the virus. The worst forms, seen especially in cattle and
sheep, are so sudden that they have been called _apoplectic_ or
_fulminant_. Without premonitory symptoms there is sudden loss of
appetite, trembling, haggard expression of face, uneasy shifting of the
feet, irregular movements backward or to one side, dyspnœa, cyanosis,
plaintive cries, convulsions, ejection of blood by the nose or with
urine or fæces, and death in a time varying from a few minutes to four
hours. The second type is the _anthrax fever_, known also as _splenic
fever_, _splenic apoplexy_, or _internal anthrax_. In this form there
may be prodromata, especially in sheep, excitability, restlessness, and
above all, a rise of temperature of often 3° or 4°. There may be
distillation of drops of blood from the nose, eyes or ears, the mucosæ
become congested, and in sheep this may show on the finer parts of the
skin, as inside the forearm or thigh. Tremors, erection of the hairs,
dulness, prostration, lagging behind the flock or herd, insensibility of
the loins to pinching, inappetence, ardent thirst, grinding of the
teeth, colics, tympany, mucus coated, bloody or liquid fæces, bloody
urine, tumultuous heart beats, dyspnœa, dark, congested mucosæ,
amounting to cyanosis, and spasmodic contractions of the muscles of the
back, neck or eyes. If blood is drawn it may appear abnormally dark in
color and very slow to brighten under the action of the air, it may have
a thick, tarry appearance, and form a very loose clot. Death, (usually
in coma or convulsions) will supervene, in sheep under 24 hours, in
cattle in 2 to 5 days, and in horses in 1 to 6 days. The third type is
the _local_ or _external anthrax_, assuming in cattle the special forms
of _gloss-anthrax_, _pharyngeal anthrax_, _hœmorrhoidal anthrax_,
_cutaneous_ and _subcutaneous anthrax_. In horses most of the same forms
appear, in the tongue, throat, neck, shoulders, withers, flank or thigh.
These swellings have a firm or doughy feeling, are comparatively and
sometimes wholly insensible and show a marked tendency to necrotic
changes. When incised they show extensive blood extravasation, or a
pale, straw-colored exudate mixed with sanguineous lines or patches, and
manifest no tendency to suppuration, nor to emphysematous crepitation.
These features distinguish them from phlegmon and emphysematous anthrax.
When suppuration ensues it is tardy and indolent and is, on the whole, a
favorable indication. In all cases the bacillus may be found on
microscopic examination of the exudate.
_Lesions._ Putrefaction of the carcass is usually rapid. In the very
rapidly fatal cases the changes in the blood and tissues are often
little marked, and after the removal of the enlarged, engorged spleen
and infiltrated internal organs, the carcass might often be placed on
the market without much suspicion. In more prolonged cases the blood is
profoundly changed, being very dark, not subject to rapid æration, and
incapable of coagulating firmly or at all. The red globules are crenated
or otherwise distorted, adhere to each other in irregular masses, and
have parted with much of their hæmoglobin which diffused in the serum
stains the intima of the blood vessels and other white tissues. The
leucocytes are relatively very much encreased. The bacteria are easily
found in the intervals between the globules. The heart is often soft,
discolored, as it were parboiled, with the endocardium deeply stained
and the contained blood dark and diffluent or liquid. The liver is
usually enlarged, softened, friable, and as if parboiled, with many
hæmorrhagic patches. The spleen is materially, often enormously
enlarged, irregular in outline from extreme engorgement with blood, and
in exceptional cases even ruptured. An encrease to two or three times
the normal is common. The bacilli are present in great numbers in the
spleen, alike in the pulp, in the blood vessels and in the trabeculæ.
The lymph glands are almost always hyperæmic, hypertrophied, and
softened, especially in the vicinity of the localizations of the tissue
lesions. They may be merely petechiated, or they may seem like a mass of
black blood, and under pressure may break down readily into a
sanguineous pulpy mass. Like the spleen they are favorite centres for
the accumulation of the bacilli. The marked alterations in these glands
will often indicate the channel by which the infection entered the body.
The serosæ are usually hyperæmic, with many hæmorrhagic points and even
extensive exudations, and they often enclose a sanguineous liquid. The
hyperæmia and points or patches of extravasation are to be found in any
part of the body in which the bacilli have been colonized, thus they are
common in the tongue, the throat, the lungs, the stomach or bowels, the
mesentery, the omentum, the skin, the connective tissue, or the muscular
system. There may be bloody or gelatinoid exudation, but there are
always the capillary embolisms by irregular masses of blood globules,
and bacilli. These embolisms, the arrest of hæmatosis and the
destructive action of the toxins on the red globules go far to account
for the extreme fatality of the disease.
_Morbid poisons._ Hoffa found in anthrax cultures a ptomain which killed
with anthrax symptoms. Hankin obtained a deadly albumose which in small
doses procured immunity. Brieger and Fraënkel separated a toxalbumin,
and Martin too, a protalbumose and a deuteralbumose together with a
ptomain. Marmier separated a toxin which did not give the reactions of
the albuminoids, albumoses, peptones nor alkaloids. This was not
poisonous in small doses, to animals possessing immunity—natural or
artificial. It was weakened but not destroyed by 110° C., and was
rendered harmless by treatment with alkaline hypochlorites. Immunity
could be induced by its use in small non-fatal doses. This is present in
the bacilli and being soluble in water can be secured from these by
diffusion in watery fluids and especially so if aided by heat.
_Incubation._ The implanted bacillus begins at once to multiply in the
tissues, but the encrease is at first slow and the resulting morbid
phenomena slight, so that there appears to be a period of incubation. In
experimental inoculations in which this can be certainly noted it
extends from one to two and even three days in the rabbit and Guinea
pig, from two to four days in sheep, and from three to six days in
horses and cattle. It may be shortened by giving an overdose and
especially if this is introduced intravenously, the chemical poisons
apparently acting at once. In young animals, too, the period is
shortened, unless they have been rendered refractory by a milk diet or
otherwise.
_Symptoms._ These vary according to the species affected, and the seat
of the disease, general or local, _internal_ or _external_. In the
latter case the febrile and constitutional disturbance is delayed. In
the _internal_ cases the fever is early and of a high type. Even before
the animal appears to be seriously ill, while still keeping with the
herd and showing life and vigor, there may be high temperature, 104° to
106° F., pulse and breathing accelerated, heart beats tumultuous,
tremors or shivering or perhaps only staring coat, anorexia, and
grinding of the teeth. Later there may be drooping head and ears,
dulness, a disposition to lie, apathy, stupor and somnolence. Nervous
excitement and delirium have been noticed. The patient becomes weak,
especially behind, comatose, and the temperature declines to, it may be,
97° or even 94° F., prior to death. The visible mucosæ becomes dusky,
brownish or yellowish, and streaks of blood may appear in the nose or
elsewhere. The urine may be red, the fæces covered with mucus, or blood
streaked, and the rectal mucosa of a violet tinge, or blackish and blood
gorged. In this the vulvar mucosa often participates. Local swellings
may appear in the tongue or pharynx, even if not on the surface, or
colics indicate implication of the digestive organs. The examination of
the blood early reveals the presence of the bacillus, and as the disease
advances, its black, incoagulable, tarry, or coffee-grounds appearance
becomes characteristic. Pregnant animals are liable to abort. Death
occurs in 12 to 48 hours. Most cases are fatal at the beginning of an
outbreak, while later the great majority often recover.
_Fulminant cases_ (Anthrax acutissimus) occur mostly in cattle or sheep,
in high condition, the victim being found dead in pasture or stall,
without previous observation of illness, or, if seen during life there
is the sudden attack, leaving food, muscular tremors, anxious expression
of countenance, hyperthermia, dyspnœa, dark red mucosæ, it may be
streaks of blood on them, plaintive cries, rolling of the eyes, spasms
or coma, and death in a few minutes to one or two hours. In _sheep_
there may be separation from the flock, pawing, stretching, shaking of
head, turning in circle, dyspnœa, falling, convulsive struggling,
passing of blood by nose, kidneys or bowels and death.
_Local Anthrax in Cattle. Symptoms._ In _cutaneous anthrax_ the
circumscribed swellings appear suddenly, and may grow to considerable
dimensions on different parts of the skin, head, neck, breast,
shoulders, abdomen, axilla, sheath, udder, or flanks. There may be one
or many, and they lack the acute early tenderness, and later crepitation
of black quarter. On white skins they are dark red, or violet, and when
incised, show a gelatinoid, bloody, non-suppurating mass, abounding in
bacilli.
_Gloss-anthrax_ implicates the whole, or it may be the roots only, of
the tongue and the fauces. There is profuse salivation, perhaps bloody,
intermaxillary and pharyngeal swelling, anorexia, and the tongue is
found protruding, swollen, violaceous, vesiculated or with rounded
nodules, or sloughs and ulcers, with lardaceous or blood stained
bottoms. Hyperthermia and constitutional symptoms are present.
_Pharyngeal anthrax_ is manifested by swelling of the throat, profuse
salivation more or less marked with blood, complete dysphagia, attending
on the marked febrile and constitutional symptoms already described.
_Hæmorrhoidal anthrax_, a common complication of the constitutional
disease, is manifested by infiltration, blood extravasation, violet
discoloration and often enormous swelling of the rectal mucosa, seen
mainly during straining, but sometimes also as a constant protrusion.
=Local Anthrax in Sheep and Goats.= External anthrax swellings may form
on the face, throat or udder with the general characters of those of the
ox, but this form is much more rare than in cattle and horses. The usual
form is the internal one, with engorgement of spleen, liver, and perhaps
some other internal organ, and it is relatively very fatal.
=Local Anthrax in the Horse.= _Symptoms._ In anthrax districts, tumors
form in the seats of inoculations on sores, insect bites, or sometimes
without apparent local cause, as a result perhaps of a general
infection. The infiltration takes place suddenly into or beneath the
cutis, mostly on the head, tongue, throat, neck, breast, shoulder,
inguinal region, mammæ, croup, or thigh, encreases rapidly, but without
crepitation, or suppuration, the incision showing the general characters
described in the ox, and early attended by the constitutional disorder.
The general fever is often later in developing, less intense, and, on
the whole, less fatal than the purely internal forms.
=Anthrax in Swine.= _Symptoms._ Swine are, on the whole, less
susceptible than cattle, and on the strength of his laboratory
experiments Pasteur denied their susceptibility. The mistake gained
a wide acceptance, yet experienced practitioners knew that they were
occasionally infected by eating the carcasses or droppings of
anthrax cattle. I had seen a number of swine die in common with
cattle in an outbreak at Swineshead, Lincolnshire, in 1863, and a
like occurrence took place in East Lothian, and similar cases are
reported by McFadyean, Trombitas and Von Ratz, while Crookshank and
Perroncito have respectively inoculated the pig with success. In my
experience at East Lothian a shepherd skinned an anthrax bullock and
then castrated several litters of pigs, all of which died of
anthrax. Much doubtless depends on the condition of the animal as
regards food (flesh or vegetable), the presence of lactic or other
organic acid, the coincidence of infection with anthrax bacillus and
one of those conditions, which habitually enhances its virulence.
There may be named venesection (Rodet) or its counterpart anæmia,
the presence in the blood of inert powders—precipitates (Bardach),
fatigue—sarco-lactic acid (Charrin and Roger), starvation—dyspepsia
(Canalis and Morpurgo), privation of water (Pernice and Alessi), the
products of previous or coincident illness (Galtier).
The pig, infected by ingestion, suffers especially from pharyngeal and
intestinal anthrax. There is marked swelling of the throat with
stiffness, dysphagia, champing of the jaws, salivation, frothing about
the lips tinged with blood, dark, violet discoloration or ulceration of
the fauces and tonsils, retching, vomiting, hoarseness of grunt,
extension of the swelling to the face, with petechial spots and patches,
diarrhœa with frothy or bloody fæces, great muscular weakness, a
disposition to lie, it may be actual paraplegia, with the usual
accompaniments of hyperthermia, constitutional disorder, cyanosed, or
dusky brown, reddish or yellowish mucosæ, and the black, incoagulable
blood, with destruction of the red globules.
=Anthrax in Dogs.= _Symptoms._ In the outbreak at Swineshead,
Lincolnshire, in which the pigs suffered, one shepherd dog contracted
the disease from eating the carcasses. It took the pharyngeal and
intestinal form, with dysphagia, vomiting, bloody diarrhœa and high
fever. Straus found that young puppies were very susceptible and old
dogs refractory probably because of flesh diet and exposure. The
excision of the spleen encreased the susceptibility to 76 per cent.
instead of 20 per cent. (Bardach). Cornevin saw 5 dogs die the same
night out of 7 that ate from an anthrax carcass. Much depends on the
previous exposure and existing condition of the dog.
_Cats_ have been observed to suffer under similar conditions. At Geneseo
in 1877 I found that a cat and three young horses died from licking the
blood from a stoneboat on which an anthrax hide had been carried.
=Anthrax in Birds.= _Symptoms._ Birds (chickens) are naturally less
susceptible than swine, yet they succumb readily to inoculation, when
the body has been cooled by partial immersion in cold water. Caplewsky
found that, apart from artificial chilling, young pigeons of certain
breeds were easily infected, and Œmler successfully inoculated small
birds, sparrows, finches, canaries, yellow hammers, red breasts. The
larger birds are more resistant but succumb readily if dosed with
chloral hydrate, or antipyrin (Wagner). Birds of prey seem to be immune.
In chickens the disease is very acute, of rapid progress and fatal. A
few hours after inoculation they are seized with dulness, debility,
sunken head, drooping wings and tail, ruffled feathers, and dark red or
black discoloration of comb and wattles. Dark colored anthrax swellings
may appear on these last, on the eyes, tongue, palate or feet, and the
obstruction of breathing may cause general cyanosis. Weakness is
extreme, the bird staggers or is unable to rise, has violent tremors or
convulsions, with bloody diarrhœa and perishes after a few hours or a
day’s illness. The presence of anthrax in the locality, or in other
species, will be to some extent a safeguard against confounding chicken
cholera, entero-hepatitis or malignant œdema with this affection. The
crucial diagnosis is based, as in other animals on the discovery of the
characteristic bacillus.
_Differential Diagnosis._ The suddenness of the attack, hyperthermia,
dusky, cyanotic, petechiated mucosæ, the escape of blood from mucous
surfaces, the dark, tarry blood, brightening imperfectly on exposure to
the air, its comparatively loose coagulum, the crenation and destruction
of red globules, the staining of the serum with hæmatoidin, the
leucocytosis, the engorged, enlarged liver and spleen, and the
gelatinoid or bloody swellings, not gasogenic as in blackquarter or
malignant œdema, together present a picture which is strongly suggestive
of anthrax. If the malady affects domestic animals generally, is
especially virulent in cattle, sheep and horses, and attacks even man;
if the district is subject to anthrax, or of a rich damp soil which
would be favorable to the preservation of bacillus anthracis; if it is
in the line of watershed from stock markets, abattoirs, tanneries,
rendering works, glue factories, packing houses, sausage factories, or
phosphate works; if forage or new stock has been introduced from an
anthrax district; and if the outbreak has taken place with a high water
level, or during a dry hot season the case for anthrax will be
strengthened.
The final tests are, however, by the microscope and inoculation. To
discover the bacillus a power of 400 to 500 diameters is desirable. From
the living animal take a drop of blood, exudate, or hæmorrhagic
extravasation, make a thin film on a cover glass by drawing across it
the straight edge of another one, dry the film, then pass it three times
through the alcohol flame film downward, stain in anilin dies, or clear
with acetic acid and examine. The bacillus is large (5 to 20µ by 1 to
1.5µ), nonmotile, of uniform thickness throughout, and sharply cut off
at the ends. The bacillus of blackquarter is shorter, often club-shaped
because of a spore in one end, has rounded ends, is flagellate, motile
and gasogenic. That of malignant œdema is much thinner, has rounded
ends, sluggish movements and is gasogenic. The bacillus subtilis (hay
bacillus), is short, thick, with rounded ends each bearing a flagellum
and is motile. The proteus vulgaris (common septic saprophyte) is small,
short, with rounded ends, and very active movements. If the subject is
dead we may examine the blood, or the scraping from the cut surface of
the spleen, liver, kidney, congested lymph gland or other part bearing
the lesion.
If we find in the carcass exudates gelatinoid or bloody (especially the
latter), petechiæ, dark, uncoagulated blood, brightening little on
exposure, blood gorged spleen, congested or hæmorrhagic condition of one
or more internal organs, muscle or connective tissue, (particularly of
the lymph glands), if the muscles of the loins, quarters, thighs,
diaphragm or elsewhere, are soft, as if parboiled or salmon-colored,
clammy, friable, or if reddish, yellowish, brownish, with petechiæ, and
capillary embolism the case will require critical examination. If the
first examination fails to show the bacilli, repeat it from different
lesions until thoroughly satisfied of their absence, or until another
cause for the condition has been discovered. The blocking of the
capillaries with bacilli in the various lesions is a most important
point, never to be overlooked.
In case of uncertainty, inoculation of a Guinea pig, mouse or rabbit
should be made. The blood or scraping from the seat of a lesion is made
into an emulsion if necessary, and injected subcutem. A single bacillus
will destroy a mouse or Guinea pig in from one to four days, and the
blood shows the characteristic bacilli.
One must, however, exclude the possibility of septic bacteria, excluding
or obscuring the bacillus anthracis, by taking the inoculating material
from the blood of the living animal, or from the same or the tissues as
shortly after death as possible. Fifteen hours may be altogether too
late for inoculation. To exclude the anærobic bacteria of black quarter,
malignant œdema and septic affections, make an emulsion of the suspected
material in sterilized water, filter through a boiled cloth and inject a
strong dose into the auricular vein of a rabbit. The anærobic bacteria
perish in the blood and if anthrax bacilla are present they are found in
pure cultures.
In inoculating suspected water or infusion of forage the intravenous
method should be adopted.
Another resort is to make two artificial cultures, one in free air, and
the other in an atmosphere of nitrogen or carbon dioxide. The bacillus
anthracis develops in the first, the anærobes in the second.
_Prognosis. Mortality._ Fulminant cases are uniformly fatal. _Acute
intestinal_ cases are usually fatal in 70 to 90 per cent. of the
subjects at the beginning of an outbreak. Toward the decline most cases
may recover. In a herd of 200 head, at Avon, N. Y. in 1875, 40 fat
bullocks died in two weeks, and 50 more showed a marked hyperthermia,
yet under a change of pasture, and antiseptics, all but two of the
latter recovered. As serving to identify the disease, three attendants
suffered from malignant vesicle, but recovered.
SUPPRESSION AND PREVENTION OF ANTHRAX IN HERDS.
Less simple or easy than in plagues. Germ survives in soil and water.
Extinction not always possible. Killing: conditions demanding it: when
unwarranted. Kill without shedding blood, or opening carcass. Body
burned: if buried, 5 feet deep, in porous soil, distant from wells,
ponds, and rivers. Fence graves, burn grass. Disinfection of hides,
litter, fodder, manure, excretions, stalls, etc.: of bodies that must
be moved, of buildings, yards, utensils, etc. Isolation of unaffected
on porous soil; surveillance. Sales interdicted. Milk, butter, cheese.
Immunization: by toxins which stimulate leucocytes to form defensive
products: antitoxins. Eosinophile cells, action of spleen, and liver.
Mellituria. Protection by a minimum dose: by weakened virus—modes of
lessening potency, Pasteur’s “vaccine”, its drawbacks and dangers, its
technique; by soluble toxins in sterile solution, author’s experience,
apparent failures, advantages. Drainage—Æration of land. Prevention of
importation and diffusion. Therapeutic treatment.
Prevention of anthrax in animals is equally important for the sanitation
of herds and human beings. It involves the purging from the anthrax
bacillus of the infected lands and the drinking supplies, and in this
respect the disease is much less amenable to thorough and speedy
extinction than is a simple plague in which the germ does not live and
multiply outside the animal body. In some localities the extinction of
the germ may be confidently counted on and secured; in others, it may be
impossible and other measures of protection must be resorted to.
_Killing of the Sick and Disposal of the Carcass._ This is not always so
imperative as in the obligatory parasitic infections, since the
destruction of the sick, still leaves the germ present in the soil and
water. If, however, the infection has just been introduced, on hitherto
uninfected soil, by the arrival of new animals, and, if the new location
is in any way favorable to permanent colonization by anthrax bacillus,
and, if the diseased and suspected animals cannot be kept secluded so as
to absolutely exclude these dangers, or again, if the diseased herd or
its remnant is to be moved on to another locality, slaughter is the
obvious sanitary measure.
The animal should be killed on the premises to avoid the danger of
scattering the infectious discharges in transit; it must not be bled,
nor cut open, as the admission of air determines the formation of the
resistant spore; and the carcass must be burned, boiled, or rendered in
superheated steam under pressure, or finally dissolved in strong mineral
acids. If buried, it must be in open, porous soil, well apart from any
well, pond, river, or bank where the liquids may leach out, and the body
must be wholly covered to a depth of at least five feet. The graves must
be well fenced in from all stock, for a number of years, and no forage
grown on them can be safely fed to animals, as the bacillus can be
brought to the surface by earth worms. I have known cattle to become
infected through licking the fluid which escaped above a stratum of
clay, on the deep bank of a river, at some little distance from where an
anthrax carcass was buried in the surface sandy loam. A covering of coal
tar, chloride of lime or of sand charged with sulphuric acid is an
admirable precaution.
As a measure of economy the skins may be removed, if at once, on the
spot, plunged for 12 hours in a 5 per cent. solution of carbolic acid,
or cresyl, or creolin, or in a two per cent. solution of sulphuric acid,
and, if the knives and other implements used are placed in boiling water
for half an hour. The same will apply to fleeces.
_Disinfection._ All litter, fodder, manure, urine, and other excretions,
or products; all stalls, feeding troughs, sheepfolds, covers, halters,
harness, wagons, poles, shafts, and other objects used about the
animals, or soiled by them or their products, should be disinfected by
burning, flaming or scalding (boiling), when applicable, by one of the
above-named disinfectants, by mercuric chloride (5:1000), by formalin,
or other potent antiseptic. Extensive dung heaps, too wet to burn, may
be sprinkled freely with strong mineral acids, or mercuric chloride in
solution, piled into compact mass, covered with chloride of lime, and
finally with a thick layer of earth, and fenced in from all stock.
If carcasses must be moved to the grave, rendering works, or elsewhere,
they should be sponged with carbolic acid solution, formalin, or
mercuric chloride, and each of the natural openings firmly plugged with
tow or cotton soaked in the same material, so that no infecting material
may drop on the way. They should on no account be dragged on the ground,
but carried on a wagon or stone boat, which should be afterward
carefully disinfected. Men or animals, entering an infected place,
should be disinfected on leaving; especially hands and feet.
All roads, yards, and pastures where the sick have been, and, above all,
where manure, urine, or saliva has fallen, should be subjected to
thorough disinfection, or the surface layer removed and deeply buried.
Where available, a concrete or asphalt floor should be placed in the
buildings.
_Isolation. Movement from Infected Ground._ It has long been known that
the movement of an infected herd from the contaminated pasture to
another, will often, at once, check the development of new cases. In
Sardinia and Auvergne the flocks and herds were yearly moved on the
approach of autumn, from the rich valley, and bottom lands, to the drier
hill pastures, to avoid or lessen the decimation that otherwise
inevitably overtook them. This is in keeping with the enzoötic nature of
the malady which arises more from the microbe preserved in the soil than
from the sick animal direct. Two precautions are necessary in making
such a change of locality: 1st, Animals already infected should not be
moved on such new pasture; and 2d, the pasture to which the stock is
moved should be entirely free from the impermeability (clays, hard
pans), and saturation with water (swamps, basins, low bottoms), which
would ensure the permanent preservation of any microbe planted there.
Elevated, sandy, argilaceous or loamy soils are to be selected. To these
the animals of the infected herd which by their appearance and
thermometry may be pronounced sound, should be removed, and kept under
careful supervision, especially as regards thermometric tests. Any
showing symptoms of anthrax should be at once taken back to the infected
herd. If they have stood in stalls, for milking or otherwise, these
should be disinfected, and they should be carried in wagons, or driven
by unfrequented roads. Their droppings should be carefully disinfected.
If, in the absence of anthrax symptoms, animals must be kept in the
infected lot, or returned to it, they should be immunized.
_Interdiction of Sales._ No animal in the infected herd which shows a
rise of temperature, should be sold even for slaughter. No animal should
be sold for stock purposes until the disease has completely subsided.
Any animal in the infected herd, which shows no hyperthermia nor other
sign of anthrax, may be sold for immediate slaughter, subject to a
critical expert examination of the cadaver for anthrax. Milk, the
product of an infected herd, and butter and cheese made from such milk,
should not be used as food. If those members of the herd, that show no
hyperthermia or other symptom of anthrax, can be held apart as a
separate herd, in a disinfected place and under careful thermometric
observation, their dairy products may be used.
_Immunization._ A number of different methods have been practiced of
rendering animals refractory to the bacillus anthracis, but all are
apparently based on the production in the system of defensive products,
as the result of a nonlethal poisoning with anthrax toxins. It is true
of anthrax as of many other infections that a first attack protects
against a second. In all animals there is a certain measure of defensive
power against the bacillus anthracis, amounting in some cases to virtual
immunity and in others having a very little effect. The object in
immunizing is to stimulate to the increase of these defensive products
in quantity or power until an ordinary dose of the bacillus will fail to
colonize the tissues or the blood. In considering this subject a clear
distinction must be made between the simple bactericidal and the
antidotal or antitoxic products found in the serum of immune animals and
the toxins which are produced by the bacilli. The soluble antitoxic and
bactericidal agents found in the serum of the immune, may be employed
for therapeutic purposes to preserve life in an animal which has
received a lethal dose of the bacillus anthracis, but as these are
rapidly eliminated from the system, their protective power is very short
lived, and if some bacilli survive the period of their presence and
potency, or if they are introduced into the system later, the animal may
fall a victim to anthrax as if no such protective agent had been used.
Behring showed that the blood serum of the white rat proves fatal to the
bacillus anthracis, but Metchinkoff pointed out later that it must be
brought in contact with the bacillus in order to prove effective,
whereas if the serum and bacillus were injected at different parts of
the body no protection was obtained. The antidotal or bactericidal
action of the serum of an immunized animal acts at once, whereas a
permanent immunity cannot be established before about fifteen days. The
serum of the immune animal contains the following elements antagonistic
to anthrax: _Antitoxin_ or _leucomain_ which may be poisonous to the
bacilli, or chemical antidotes to their products: _globulicidal
principles_ which distort or disintegrate the blood globules and release
their contents including the bactericidal nuclein, and probably others.
All such agents when injected into the system are present only for a
limited time and while they may be made subservient to a temporary
immunity, they can give no permanent protection and must be considered
mainly as therapeutic agents.
A permanent immunity must depend on a stimulation or education of the
system to the production of these protective agents _de novo_ or in
increased quantity. This must be done by exposure of the tissues to the
toxins of the bacillus anthracis, and is accomplished slowly. Precisely
what tissues are stimulated to the production of the defensive agents is
not fully known, though certain indications may be drawn from observant
facts. The eosinophile cells of the blood are presumably important
factors as the natural sources of the leucomaines. The spleen as the
seat of important blood changes and as preëminently the seat of election
of internal anthrax is probably involved. The dogs from which Bardach
had removed the spleen were found to be three times as susceptible to
anthrax as were the dogs that had not been operated on. Leo’s rats, in
which he had produced mellituria by the administration of phloridzin
were found to be much more susceptible to anthrax. The liver is also a
favorite seat of election of internal anthrax. The products of the
healthy liver, are probably in some measure protective.
No matter where the defensive products are formed, the practical problem
is to secure their production without imperilling life.
_By Minimum Dose._ Chauveau and Colin secured this in the larger animals
by intravenous injection of a minimum dose,—one or two bacilli. This is
more lasting in effect if a second and stronger dose is injected some
days later.
_By Weakened Virus._ This has been secured by heating the defibrinated
blood to 55° C. for ten minutes (Toussaint); Pasteur, Chamberland and
Roux accomplished the same end by making anthrax cultures at 42° to 43°
C. in presence of air; Chauveau by subjecting the virulent culture for
eight days to oxygen under a pressure of 8 atmospheres at a temperature
of 38° C.; Chamberland, Roux and others have cultivated the bacillus in
weak antiseptic bouillons as phenic acid (1:600 or 1200), bichromate of
potash (1:2000 or 5000), sulphuric acid (2:100).
Other methods have been followed, as growing the bacillus in the blood
or serum of immune animals (dog, chicken, pigeon, white rat, frog).
Of these different methods that of Pasteur has been most extensively
adopted. The temperature of culture (42° C.) prevents the formation of
spores and the duration of exposure to air gradually lessens the
virulence until in 12 or 13 days it is not fatal to the Guinea pig and
after 31 days it fails to kill the young mouse. Thus preparations of
varying grades of virulence, and adapted to the varying susceptibility
of different animals, are secured. The protective inoculation is made by
preference in spring, when there is less chance of complication by a
coincident accidental infection, it is to be avoided if possible in
animals at hard work, in advanced gestation, in full milk, in extreme
youth, or in ill health. To secure the best results it should be
repeated with a stronger preparation 12 to 15 days after the first
injection. The acquired immunity lasts a year and over, and it is
probably perpetuated by new and non-fatal doses taken in casually, on
the anthrax pastures. Hundreds of thousands of live stock in all parts
of the world have been treated in this way with the result of reducing a
mortality of two, five or ten per cent. to insignificant proportions. It
can only be safely adopted on anthrax lands, as elsewhere it may lead to
the stocking of new areas with a malignant germ which in young and
susceptible animals reacquires its original virulence.
It can never be safely ignored that we are dealing with the living seed
of a most deadly infection. Though robbed of a large part of its
virulence by artificial culture at 107:5° F., yet many accidental
conditions, contribute to a relapse to its original potency, and when it
has once killed a victim, the reacquired virulence is usually
persistent. If the virus employed for protective purposes in cattle and
sheep, is inoculated on Guinea pigs of 1 to 30 days old, from these on
those of several months, and from these last on sheep, the virulence is
constantly and persistently enhanced. The same is true of the microbe
which is inoculated on a succession of pullets of steadily encreasing
ages (Roux and Chamberland), or on a succession of pigeons
(Metchnikoff). The germs reinforced in potency in any such way are
liable to be the starting points for dangerous infections in animals and
permanent contamination of soils and waters. Fortunately an occurrence
of this kind is rare, yet with a wide application of the Pasteurian
inoculation the opportunities also are great, and with the free sale and
distribution of the mitigated virus (anthrax “vaccine”), the evil may
grow indefinitely. The method departs from the ideal one, aimed at a
final extinction of the disease, and accepts in place a mere temporary
protection of the herd or flock, and though in this affection
eradication cannot always be secured, every effort should be made to
gain it and above all to prevent an encrease of the area of infection.
_Technique._ The weakened virus (1st “vaccin”) is sold in tubes holding
enough for 100, 200, or 300 sheep. Of this ⅛ cc. is injected subcutem on
the inner side of the thigh of the mature sheep, and 12 or 15 days later
a similar dose of the stronger preparation (“2d vaccin”). For the ox or
horse double the amount (¼th cc.) is used, being injected behind the
shoulder, and on the side of the neck in the respective animals. The
dose is graduated in the different subjects according to the size and
age, yet a considerable latitude is permissible. The syringe must be
disinfected before and after inoculations by a 5 per cent. solution of
carbolic acid, or by boiling, and the nozzle should be dipped in strong
carbolic acid immediately before and after each insertion. This will
greatly obviate infection of the liquid used, and of the wound by any
virulent germs lodged on the surface of the skin. The liquid to be
injected should be used as soon as possible after preparation, and if
kept should be in a dark cold place, and if the tube is once opened the
whole of its contents should be used the same day,—never kept over. The
second, stronger preparation should never be used until the system has
been prepared for it by the use of the first.
_By the Soluble Toxins in Sterile Solution._ In 1884, in an outbreak of
anthrax in Skaneateles, N. Y., I drew blood from an anthrax cow,
subjected it to 212° F. for 30 minutes, dissolved out the soluble toxins
in boiled water, and injected the product subcutem, in the dose of 2 to
4cc. according to size, into every apparently healthy member of the
herd, excepting one, which was left as a check. The check animal died of
anthrax while all of the others escaped.
Since that time I have personally used it in every herd where
opportunity offered, and with equally good results. In an outbreak near
Elmira, Dr. Moore adopted it in a large dairy herd, and the disease was
suddenly arrested.
In several experimental cases (one cow and 2 Guinea pigs) at the N. Y.
S. V. College, the outcome was not so satisfactory and in a herd in
Oneida Co., N. Y., it is said to have failed to check the disease.
Notwithstanding these untoward results in other hands, I am still
confident that we have in this a measure of no small value, and worthy
of application in suitable cases. A certain percentage of failures in
immunization are to be looked for. Even cowpox vaccination is not always
protective against itself; I knew one man who was successfully
vaccinated every three years in a comparatively long series. Many
habitually self-limiting diseases relapse in particular individuals.
Even in the case of anthrax excess of glucose in the system, and the
lack of some unknown influence of the spleen are respectively
destructive of immunity. Even after the Pasteurian inoculation a certain
number of inoculated animals are lost, it may be between the first and
second injection, or it may be “two or three months” after the latter
(Galtier). We must also bear in mind that in an infected herd or flock,
there are always a certain number already infected at the time of the
protective inoculation, and as the protective conditions are slowly
established, through the action of the leucocytes, it is unreasonable to
expect that serious illness and death can be obviated in such animals.
In inoculation with the Pasteur lymph, the bacillus is held not to enter
the blood, a position supported by the researches of Bitter, Perroncito,
Wissokovicz, Lubarsch, Metchnikoff, Chamberland and Roux, so that the
resulting immunization must come from the toxins. Add to this that
Chauveau (1885), conferred immunity on a sheep by injecting
intravenously, anthrax blood, defibrinated and sterilized by heat:
Arloing obtained immunity in the sheep by injecting, subcutem, the clear
supernatant liquid from old bouillon cultures of anthrax, from which all
bacilli had been precipitated. Roux and Chamberland obtained the same
result by using the pulp of an anthrax spleen treated with essential oil
of mustard, so as to destroy the life of the bacillus, and then
evaporated in vacuo to remove the essence. Smaller doses proved
effective, than when the splenic pulp had been filtered or sterilized by
heating to 58° C.
The advantages of using sterilized toxins are numerous:—
1st. As the material can be derived from a case of the outbreak in hand,
there is no risk of using the anthrax protective inoculation for black
quarter, hæmorrhagic septicæmia or other disease which is so often
confounded with it.
2d. There is no danger of the sudden enhancing of the potency of a
weakened microbe on account of some condition of the animal inoculated,
as no living microbe is employed.
3d. There is no possibility of planting the anthrax bacillus, on new
soil, as is so liable to take place in using the weakened microbe.
4th. There is no necessity for the care and cost of holding the
inoculated animals apart by themselves, under official veterinary
control for 15 days, of withholding their products from market, or of
disinfecting the place where they have been kept. On the contrary the
animals inoculated can be treated in every way as if no such injection
had been made.
_Thorough Drainage and Æration of Land._ The most thorough and permanent
method of eradicating anthrax is by thorough æration of the soil. In
dry, sandy, or gravelly soils, having a good natural or artificial
drainage, and not underlaid by an impermeable damp stratum, the bacillus
is never permanently found, and, if introduced, is slowly robbed of its
virulence by the action of the oxygen. When a soil can be well and
permanently ærated by thorough underdrainage, a few years suffice to rob
it of its infecting property and render it salubrious. In many
localities, however, this is actually or economically impossible, so
that the owner is thrown back on the alternatives, of abandoning the
soil for stock, or of immunizing all the animals placed on it.
_Prevention of Importation of Anthrax._ To prevent the introduction of
anthrax into a country or district, the usual control must be exerted on
trade in cattle and their products, as in the case of other infectious
diseases. The exclusion of livestock from an anthrax-infected country or
district, or the admission after 6 to 10 days of quarantine and the
disinfection of the surface of the animal. Dried hides, horns, hoofs,
hair, wool and bristles are even more dangerous, as they are liable to
hold the microbe in the spore form which will survive indefinitely and
plant the disease widely. The recent great extension of the disease
along the Delaware River, in connection with the morocco factories,
which draw their hides from the most virulently anthrax regions (India,
China, Russia, Africa, S. America) is a strong case in point, and nearly
every tannery planted on a favorable soil is an example on a smaller
scale. Disinfection of all such products on arrival is essential. But
this should be thorough, and no question of trouble nor expense should
stand in the way. If the trade cannot stand the expense, it has no right
to exist where it is, at the expense of threatened ruin, local and
ultimately general, of agriculture, on which all other industries are
based. Similar control is demanded of live stock products from infected
regions in America.
The control of home markets, stockyards, and abattoirs is no less
important. Fortunately the disease is shortlived and deadly, and is much
more easily discovered and arrested than in the case of plagues with
prolonged incubation and frequently occult form (glanders,
tuberculosis). An inspection of the various markets, and the detention
of herds that have shown anthrax infection would do much to limit
extension. This would entail the disinfection of the infected places,
cars, boats, harness, clothing, and other things, and of the skins of
the healthy animals of the infected herd.
_The Therapeutic Treatment_ of anthrax in animals must in the main
follow in the same lines given below for the human being; locally,
antiseptics (mercuric chloride or iodide, Luzol’s solution, hydrochloric
acid, phenic acid, iodized phenol, creoline, cresyl, oil of turpentine,
formalin, salicylic acid, scarification, excision of the primary sore or
swelling with antisepsis, antiseptic injections into the swelling.)
Internally, there have been employed, dilute phenic acid, creolin,
terebene, calomel, quinine, hydrochloric acid, bichromate of potash,
tincture of iron chloride, etc. (see below).
ANTHRAX IN MAN.
Causes: infection from animals and their products, from soil, by
flies, by dust. An industrial disease, of workers among animals and
animal products. Wounds as infection atria, ingestion anthrax,
inhalation. Lesions: malignant vesicle, anthrax œdema, intestinal
anthrax: pulmonary anthrax. Symptoms: malignant vesicle, œdematous
anthrax, intestinal, pulmonary. Prevention. Treatment: caustics:
antiseptics, excision of nodule and subsidiary glands, mercurial
ointment, iodine, sodium bicarbonate. For intestinal anthrax: emetic,
oleaginous purgatives, potassium iodide, sodium salicylate, iron
muriate, heart stimulants. For pulmonary anthrax: inhale chlorine,
iodine, bromine, phenic acid, eucalyptol, oil of cinnamon, sterilized
cultures of prodigiosus, pneumococcus of Friedländer, bacillus
pyocyaneus, staphylococcus aureus, or streptococcus: blood serum of
immune animals: blood serum (sterilized) of anthrax cattle.
_Causes._ Anthrax in man is usually the result of contamination by
infected animals or their products. It is quite possible that man, like
animals, may be infected directly from the soil or water, or from the
same source through the medium of flies or windblown dust, yet undoubted
cases of this kind are rare or unrecognized. The animal origin of the
disease, as regards man, makes this largely an industrial affection,
attacking shepherds, cattlemen, horsemen, farmers, drovers, butchers,
veterinarians, tanners, and workers in hides, wool, hair, bristles,
furs, hoofs, bones, rags, felt, glue, and even leather. The sound skin
is sufficient protection, but the slightest abrasion may form an
infection atrium. Workers in tanneries and those who live near them are
notoriously subject to anthrax. The hides must of course be drawn from
an anthrax region. Russian, Armenian, South American, Australian and
African hides have an especially bad reputation. The _British Medical
Journal_, May 21st, 1898, records cases occurring in postal clerks who
had to handle foreign parcels bound with strips of hide. Proust records
cases from handling Chinese goat skins (Bull. de l’Acad. de Med. 1894).
Infection may also occur through leather made from infected hides as
proved experimentally on Guinea pigs.
Hair has long been recognized as a frequent medium of infection and
outbreaks among brushmakers have been recently recorded by Gerode,
Sarmont and Chauveau. (Compt. Rend. de l’Acad. des Sc. 1893). Trousseau
reports twenty cases in Paris, all contracted from South American horse
hair. Wool from infected countries is often dangerous and has given rise
to special names for the disease (wool-sorter’s, rag-picker’s) which may
be developed in the lungs from inhalation of the dust. In the same way
those who handle bones about fertilizer, glue and rendering works, are
particularly exposed. The agency of insects in man is undoubted. In
sixty cases recorded by Dr. Bell, fifty-four were on the face, two on
the hands, one on the wrist and one on the forearm. This is mainly due
to blood-sucking flies, yet Heim incriminates the coleoptera as well
(Compt. Rend. de Soc. de Biol. 1894). Wounds of all kinds contribute to
inoculation, hence, the presence of burdocks, thorns, thistles and the
like in the matted wool or hair is often a direct cause of infection.
The infection may be transferred on surgical instruments, and in these
days of hypodermic medication the greatest care is necessary to prevent
infection through the needle.
As in animals man suffers from ingestion and inhalation of the bacillus;
and sometimes widespread mortality comes in this way. Meat just killed
may be thoroughly disinfected by the secretions of a healthy stomach,
yet the bacillus may pass through in an envelope of fat, in an
undigested mass or during an attack of dyspepsia, and infect the
intestines. The spores are proof against the gastric juice, and as they
are produced in a few hours after death the meat of an anthrax animal
must always be considered as exceedingly dangerous.
Man is much less susceptible than some other animals and the disease
wherever inoculated tends to remain for a time localized, in the skin,
the lungs or the bowels. The forms of the disease are _malignant
carbuncle_ (pustule), _malignant œdema_, _intestinal anthrax_, and
_pulmonary anthrax_.
_Lesions._ The morbid histology is in the main the same as described in
animals. In the protracted cases there is the same dark nonærated blood,
forming a loose coagulum, the crenated or distorted blood globules
aggregated in irregular masses, the escape and solution of the
hæmoglobin so as to stain the white tissues, the enlargement of the
spleen which is gorged with dark blood, and the hyperæmia of the liver
and lymph glands. There is in the affected tissues and usually in the
blood the characteristic large bacillus anthracis.
In the _malignant vesicle_ there is first a minute, firm central, dark
nodule like an insect bite with a lighter colored areola, and showing
not only hyperæmia, but blocking of the capillaries, and minute areas of
extravasation. Somewhat later the dark centre is surmounted by a small
vesicle, beneath which the tissues are becoming necrotic, and the area
of congestion and extravasation has extended and thus the local disease
advances by a constant invasion of new tissue which in its turn becomes
the seat of coagulation necrosis. On microscopic section the central
necrotic part shows the cells of the rete Malpighi separated by a finely
granular coagulum, and the papillæ are greatly swollen by serous and
hæmorrhagic exudate. The cell nuclei are necrotic and no longer take a
stain. The capillaries are gorged with red globules and bacilli. In the
surrounding tissues there is much congestion and exudation, with
numerous points of extravasation, but the abundant multinuclear cells
retain their staining power.
In _Anthrax Œdema_, which appears in parts like the eyelids, neck and
forearm where there is an abundance of loose connective tissue and a
scanty blood supply, there is no firm central nodule, but a diffuse soft
infiltration, with points or patches of a yellow or reddish color. The
capillaries are congested, with minute emboli and extravasations and
there is an excessive and rapidly spreading exudation. It shows a great
tendency to early general infection and may end in vesication and local
gangrene or in favorable cases in resolution.
In _Intestinal anthrax_ (intestinal mycosis) the lesions are usually
concentrated on the small intestines, while the stomach and large
intestines in the main escape. The walls of the bowel are of a dark red,
and greatly thickened by exudation and extravasation which also mixes
with the ingesta giving it a dark bloody tinge. At intervals on the
mucosa are nodular hæmorrhagic swellings, from the size of a linseed to
a pea, with commencing necrotic changes or the formation of sores. The
mesenteric glands are swollen, infiltrated and hæmorrhagic, and like the
other lesions abound in bacilli. Hyperæmia and engorgement of the liver
and above all of the spleen are the rule.
In _pulmonary anthrax_ (wool-sorter’s disease) a sanguineous liquid is
found in the lower trachea and bronchia, and not infrequently in the
pleuræ and pericardium. The bronchial glands are swollen, hyperæmic and
often hæmorrhagic, and exudations and extravasations may be found in the
mediastinum and lungs. Lesions of the intestines and spleen are common,
and in all alike the bacilli are found.
In certain cases the anthrax lesions may be found in the brain, or any
part of the body but in all they show the same general characters and
the same specific microbe.
SYMPTOMS: DIAGNOSIS.
_Malignant Vesicle_ (_pustule_). Symptoms may vary somewhat but are in
the main as follows: An itching papule appears in the seat of
inoculation, which might be mistaken for an insect bite but for the dark
red color of the centre. Occurring on an uncovered portion of the skin,
in an anthrax district, or near a factory where anthrax products are
likely to be used, this should at once create suspicion. Soon the dark
centre is covered by a small vesicle with clear contents which later
become bloody. Within 24 or 48 hours the vesicle dries up, becoming
firm, resistant and brownish red or blackish gray, and apparently
gangrenous. The swelling has meanwhile extended to ½ or ¾ inch in
diameter and a row of fresh vesicles may appear which in their turn give
place to a necrotic slough. In this way extension may take place, the
sore retaining a more or less rounded form, and necrosis extending from
the centre in every direction. The necrotic mass, however, remains
firmly adherent to the adjacent tissues until separated by the work of
suppuration which ensues in favorable cases. The disease is attended
with more or less fever, chill, hyperthermia, nausea, diarrhœa, with
aching of head, back, and limbs and unfavorable cases may merge into
acute and fatal general anthrax. The mortality is about 20 per cent.,
though in special epidemics it has reached 80 per cent. (With the
pustule on the face 25 per cent.; on the lower limb 5 per cent.,
Norris). The prognosis is favorable with a free concentration of
leucocytes, a moist condition of the wound and above all a liberal
invasion of pus cocci. It is unfavorable when the wound is dry, when the
drying slough remains firmly adherent and when the adjacent lymph glands
become implicated. In non-fatal cases it may be difficult to find the
bacillus.
_Anthrax Œdema._ This is less easily diagnosed than malignant vesicle,
and appears where the connective tissue is loose, abundant and little
vascular, from direct local inoculation, or as a concomitant of internal
anthrax. It is a flat, rapidly extending swelling, with the skin
comparatively unaltered, though at points yellowish or reddish
discoloration indicates congestion and extravasation. Not being limited
by firm tissues nor aggregations of accumulating leucocytes it tends to
a speedy general infection with all the febrile manifestations of that
condition. Thus chills, nausea, hyperthermia, dusky reddish or brownish
mucosæ, cephalalgia, rachialgia and profound prostration assist in
diagnosis. The bacilli in the blood and exudate would serve to confirm
the conclusion.
_Intestinal Anthrax._ Here again the ingestion of anthrax products, and
the simultaneous attack of a number of people who have taken such
materials will often assist in diagnosis. There may have been for some
days indications of local bowel lesions, such as chilliness, elevation
of temperature, nausea, headache, and giddiness. Suddenly these become
more violent, there is vomiting and sanguineous diarrhœa, extreme
anxiety and debility, cyanosis, dyspnœa, and it may be the appearance of
petechiæ on the skin and mucosæ or even of local swellings. In some
cases there are convulsions or other symptoms of nervous disorder and in
others extreme prostration and collapse. The bacillus is not always to
be found in the circulating blood, but may be detected in sanguineous
excretions, or by cultures.
_Pulmonary Anthrax._ (Woolsorter’s disease). Here again the occupation
of the patient assists in diagnosis. For two to five days prodromata
similar to those of intestinal anthrax may be noted. The difficulty in
breathing, dyspnœa, cough, cyanosis and sense of constriction of the
chest are especially diagnostic. Suddenly all these symptoms are
aggravated, respirations become 30 to 40 per minute, the pulse 120 to
150, the temperature 104° to 106°, and there is a frothy bloody
expectoration in which the bacilli may be detached. There may be
indications of intestinal, cerebral or nephritic lesions, and bloody
discharges. Death usually occurs in 12 to 48 hours from collapse, or
coma, from asphyxia or in convulsions. The few recoveries are tardy and
tremors and spasms persist for a length of time. In the most favorable
cases the disease does not proceed beyond the initial stage.
PROPHYLAXIS AND TREATMENT.
Prevention is the most important consideration and this will include all
that has been stated above with regard to the restriction of the disease
in flocks and herds, the drainage and improvement of anthrax lands, the
seclusion, destruction, deep burial or cremation of carcasses without
autopsy or incision, the disinfection of stalls, secretions and all
contaminated products, and the suppression of all traffic in anthrax
products—meat, milk, blood, guts, bones, horns, hoofs, hair, wool,
bristles, etc., or the thorough disinfection of the same. Above all, is
the adoption of personal precautions. No one should handle anthrax
animals, nor suspected products who has any sore or abrasion on hands or
face, or such sore may be temporarily covered with a film of albuminate
of silver, or the hands may be washed with a solution of mercuric
chloride (1:500), or chloride of lime (1:200). If persons must work in
wool or textile products which are open to suspicion a respirator is an
obvious precaution, and this may be disinfected by live steam at
intervals.
_Treatment of malignant pustule_ is mainly surgical. At the outset the
thorough destruction of the dark central point or nodule with a red hot
needle or powerful caustic will be sufficient. Even when the pustule is
fully formed, its free excision with as much of the surrounding
infiltrated tissue as can be safely accomplished and the free
application of caustics will usually succeed. Potassa fusa, or zinc
chloride (1:3), or mercuric chloride or iodide in powder with or without
calomel, or pyoktanin, or formaline, or iodized phenol may be named as
especially applicable. Injections of carbolic acid (5 or 10:100) into
the indurated centre and infiltrated periphery have proved very
successful. In the case of Kaloff, when the excision of the nodule
followed by the local use of carbolic acid solution, failed to prevent
implication of the inguinal and pectoral glands, violent fever,
prostration, and diarrhœa; the excision of the affected glands and the
free use of phenic acid solution (5:100) in the adjacent tissues led to
speedy improvement. Some surgeons make a crucial incision of the pustule
and apply caustics freely. Muskett has been successful in excising the
nodule, filling the wound with ipecacuan powder and giving the same
agent internally. Many mild cases, or those that occur in refractory
systems will however recover spontaneously or under a less drastic
treatment. In the anthrax districts of Russia mercurial ointment is
rubbed on the sore, and the application of tincture of iodine or iodized
phenol to the raw sore or incised nodule and surrounding infiltration is
often successful.
Camescasse has claimed great success by incising the swelling, applying
tincture of iodine freely, and then wrapping in cloths kept wet with a
solution of 5 drachms of bicarbonate of soda in a quart of tepid water.
When systemic reaction has set in it is desirable to have resort to
general medication as for internal anthrax.
_Treatment of Anthrax Œdema_ must follow the same rule. Free incisions
into the œdematous tissues with the application of antiseptics, solution
of mercuric chloride or biniodide (1:1000), or the injection of the
whole infiltrated area and around it with the same agents, with phenic
acid (5 or 10:100), or with pyoktanin (1:1000) will prove useful, and as
in the malignant pustule the surface should be kept disinfected by a
compress wet in solution of the mercuric chloride or biniodide, carbolic
acid, iodized phenol, formalin or pyoktanin. If the pain of these
applications is very acute cocaine will be demanded or even ether. If
ether is applied to the surface its evaporation will cool the parts and
retard the proliferation of the bacillus. Under other conditions cold
water, pounded ice or snow may be applied.
_Treatment of Intestinal Anthrax._ When anthrax flesh has been eaten, or
when there are symptoms of incipient intestinal anthrax, the first
resort is an emetic of ipecacuan, followed by an active oleaginous
purgative to clear the _prima viæ_ of bacilli and their toxins. To these
may be added potassium iodide, pyoktanin, sodium salicylate, quinine or
tincture of muriate of iron, by way of keeping in check the
multiplication of bacilli. To counteract depression and heart failure
digitalis, strophanthus or strychnia with alcoholic stimulants may be
resorted to.
In _Pulmonary Anthrax_ the same principles are applicable. The patient
may be made to cautiously inhale gaseous chlorine, iodine or bromine or
a solution of iodide of potassium in an atomized condition. The vapor of
carbolic acid, eucalyptol, or oil of cinnamon may be tried.
The irritable stomach may be soothed by oxide of bismuth, with milk,
beef tea and other bland nutritive or stimulating draughts.
The grave character of internal anthrax, however, is such that resort
may be had to one of the various antitoxins, antidotal cultures, serums,
and immunizing agents that have proved useful in different hands.
Unfortunately such agents do not seem to act in the same manner on all
genera, and what has been effective in one of the lower animals may fail
in the human being. Thus Roger found that sterilized cultures of
bacillus prodigiosus retarded or obviated anthrax in rabbits, but
hastened its progress in the Guinea pig.
The sterilized cultures of the pneumococcus of Friedländer (Buchner) of
the bacillus pyocyaneus, or of the staphylococcus pyogems aureus,
(Pawlowsky) when injected subcutem have proved antidotal to anthrax.
Emmerich has successfully used erysipelas serum subcutem in the
treatment of anthrax. (Münch. Med. Woch. 1894). The sterilized cultures
of the streptococcus erysipelatos therefore offer themselves as
promising curative agents. The same is true of the sterilized cultures
of the bacillus pyocyaneus (Woodhead and Cartwright-Wood).
The blood serum of animals that are naturally immune (frog, white rat,
pigeon, dog,) is bactericidal and to a certain extent antidotal to the
bacillus anthracis, but that of an animal which is naturally susceptible
but which has been artificially immunized has proved much more potent.
In the experience of the writer this potency attaches no less to the
blood of an animal in the advanced stages of the disease. In adult
cattle he has found the symptoms of anthrax subside under two successive
daily doses (4cc.) subcutem of the sterilized blood serum of one of the
herd which had just died. Relapses were observed several days after the
serum treatment was abandoned. In experiments on rabbits two check
animals with anthrax inoculations died at the end of 3½ and 4 days. Of
six inoculated with anthrax and injected from one to three times with
sterilized (anthrax) blood serum one recovered, and the others died, one
at the end of the 7th, two of the 6th and two of the 5th day. In this
connection it may be stated that successful treatment by leucocytes is
claimed, (Pawlowsky) and that one of the effects of serum treatment is
the destruction in part of the globules and the release of nuclei, and
in this we may have an explanation in part at least of the therapeutic
action of the serum from the infecting and immunized animal.
Protective serums may be utilized by hypodermic injections daily or
every second day for a week, giving time for the disposal of the bacilli
present in the system. In the intestinal anthrax they may be given by
the mouth and injected into the peritoneal cavity. In pulmonary anthrax
they may be introduced into the trachea, bronchi and pleural cavity.
GLANDERS.
Synonyms. Definition: Acute, infectious, microbian disease, often
localized in lymph glands and plexuses of nose and air passages,
etc.; with hyperplasia, degeneration, necrosis, liquefaction.
Affects solipeds, and, by inoculation, man and all domestic animals
save cattle, chickens and (usually) swine. Geographical distribution
and historic notes: known in Ancient Greece; now where solipeds live
and fresh subjects are exposed; Central Europe; great horse trade
and movement; war, Franco-German, Napoleonic, Afghanistan, American
Civil War, Boer War. Unknown in Australia. Susceptibility: solipeds,
Guinea-pig, rabbit, goat, cat, dog, pigeon, sheep, and swine in low
condition. Cattle, chickens, white and house mice, linnets,
chaffinches, and frog immune. Microbe lives in frog in water at 86°
F. Cause: Bacillus mallei. Accessory causes: trade in solipeds,
mingling of sound and sick, crowding, common feeding and drinking
troughs or buckets and racks, debility, low condition, starvation,
overwork, damp, dark, draughty stables, carriage in transports or
cars. Insular quarantined lands—Australia, Tasmania, and New Zealand
exempt. Bacteriology: Bacillus Mallei; 2 to 5μ by 0.5 to 1.4μ,
nonmotile, ærobic grows in ordinary culture media, stains tardily
but is easily bleached. Spores uncertain, easily killed by
disinfectants, preserved in stables, does not grow in infusion of
hay, straw or horse manure, lives 15 to 20 days in water; infection
by coitus, and through placenta, by ingestion, by blood transfusion,
through dust; microbe in all lesions and discharges, (unless
sometimes in milk, sperm, etc.). Infection-atria: skin wound,
mucosa, hair follicles, lungs. Forms: Acute, chronic, nasal,
pulmonary, cutaneous (farcy), orchitic, arthritic, abdominal,
occult. Symptoms: nasal; incubation, 3 to 5 days, languor,
weariness, stiffness, horripilation, tremors, inappetence, thirst,
hyperthermia, epiphora, snuffling, nasal discharge, serous, viscid,
agglutinating, purulent, swollen alæ, violet mucosa, elevated spots
and patches with central ulceration, may become confluent, and
involve submucous tissues; submaxillary lymph glands swollen,
nodular, not tender, non-suppurating, swollen (corded) facial
lymphatics, from nose, eye or lymph glands; swellings, cutaneous and
lymphatic in skin of limb or body, ulcers (farcy buds), deposits in
throat or lungs; chronic cases; slow, indolent, persistent, nasal
discharge—unilateral (or bilateral), viscid or not, nodules on
mucosa with whitish centres or points; red areolæ, later ulceration,
puckered white cicatricial lesions, submaxillary swelling, nodular,
large or small, insensible; cutaneous cases; arthritis with
lymphangitis, skin engorgement, corded lymphatics with ulcerating
nodules, sanious discharge, intermuscular abscesses. Occult cases:
lesions in internal organ;—cough, leucorrhœa, enlarged testicle, low
condition, weakness, lack of endurance. Diagnosis: inoculation of
male Guinea-pig in flank or peritoneum,—ulcer and orchitis, cat,
dog, old soliped; mallein test,—swelling, involving lymphatics,
fever, 1.5° to 2.5 F. and upward above normal, at 10th to 18th hour,
lasting two days. Lesions: cell proliferation in nests in fibrous
stroma, pea upward, central degeneration, fatty debris, ulcer or
abscess, hyperplasia of lymph vessels, on nasal mucosa like
sand-grains, peas, patches, centre grayish or yellowish, blood
extravasation, necrotic degeneration, ulcer with ragged edges;
fibroid degeneration—cicatricial lesion; lesions in guttural pouch
or tube, larynx, trachea, bronchia; lungs—peribronchial, lobular or
interlobular inflammation, cell proliferation in foci,
degeneration—nodules—and caseation; skin,—cell proliferation,
degeneration, rupture, fibroid hyperplasia of lymphatics, exudates
in connective tissue; dependent lymph glands congested,
hypertrophied, cell proliferation, caseation; lesions in pharynx,
spleen, kidney, heart, brain, testicle, scrotum, mammæ, vagina,
uterus, joints, bones; bone fragility. Glanders in swine, sheep,
goat, rodent, dog, cat.
_Synonyms._ Malleus, Equinia, Farcy.
_Definition._ An acute infectious disease caused by the bacillus mallei,
which tends to localize itself in the lymphatic glands and plexuses,
especially of the nose and upper air passages but also in other parts of
the body, where it produces a progressive hyperplasia, with a strong
tendency to degeneration, necrosis, and liquefaction. It occurs casually
in horses, asses, mules and other solipeds, and is communicable to man
and all domestic animals except the bovine races, chickens, and, under
ordinary circumstances, swine.
_Geographical Distribution._ Glanders (Malis) appears to have prevailed
in asses in Greece as noted by Aristotle. Its contagious prevalence in
horses is recorded by Absyrtus in the time of Constantine, and again by
Vegetius Renatus in 381 A.D. At the present time its existence is almost
coextensive with the equine family, but its prevalence is in a direct
ratio with the facilities for the infection of fresh subjects. In the
central countries of Europe where the equine population is greatest and
where there is the most extensive trade and movement among horses it
secures the greatest relative number of victims. War with its constant
opportunities for infection, in crowded cavalry and artillery stables
and the successive changing of place, tends greatly to enhance its
ravages. Thus in the German army it rose from 966 to 2058 per 100,000
per annum in the year of the Franco-German war; in Spain it was
practically unknown until the Napoleonic war in the Peninsula, but after
this it proved a veritable scourge; in Hindostan it was hardly known
until the Sepoy rebellion yet its ravages greatly hampered the army
movement in Afghanistan in 1879; and in the United States it became very
prevalent in the armies during the Civil War of 1861–4, and was widely
scattered over the whole country on the sale of the army horses and
mules. Since that time, as before, it has been most prevalent in the car
stables of the great cities, though it has also gained a wide extension
in many great horsebreeding establishments in the Rocky Mountain region,
where however it proves much less destructive than in the East.
It is unknown in Australia, whence it is excluded by a rigid system of
quarantine.
_Susceptibility of Different Animals._ Horses, asses and mules are the
most susceptible, and it is only exceptionally that the disease is
contracted casually outside the class of solipeds. The Guinea pig and
rabbit are susceptible to glanders in the order named and the former is
especially available for experimental diagnostic inoculations. The goat,
cat and dog sometimes contract the disease from living in stables with
glandered horses, but infection is much more certain when they are
inoculated. The pigeon is also susceptible. In the dog the disease is
rarely fatal, but the ulcerations tend to heal in 14 days and recovery
ensues. In sheep and goats too, many cases recover though in other cases
an internal infection takes place followed by death. Swine are
comparatively insusceptible, but they may be successfully inoculated
when in ill health and low condition. (Spinola, Cadeac and Malet).
Cattle and chickens have uniformly proved refractory even on
inoculation. White and house mice and rats, have proved immune, also
linnets and chaffinches and the frog at ordinary temperature. If however
the frog is placed in water at 30° C., he may be successfully inoculated
and, though it does not prove fatal, the bacillus may be found in the
blood and tissues after a lapse of 50 days.
_Etiology._ As already stated this disease is due to the presence of a
microörganism, the _bacillus mallei_. Many secondary causes, however,
contribute to its propagation. The activity of movement and commingling
of horses has been already noticed. Crowding in close yards where the
animals bite each other, snort out the virulent discharges on each other
and eat and drink from the same troughs, leads to a rapid extension.
Even on the western ranges where the disease tends to be mild, Billings
observed a deadly extension when yarded during winter storms. Debility
from chronic ill health, starvation, overwork and damp, dark, draughty
stables, is so conducive to the disease that it was at one time
considered as the sole cause. Close confinement in impure air is at once
a cause of increased susceptibility and a means of concentration and
transmission of the poison. Hence confinement, between decks, of
military and other horses, carried by sea, is a source of wide
extensions. On the other hand insular places from which strange horses
are excluded or into which they are admitted under careful inspection
and quarantine have succeeded in preserving immunity. Australia,
Tasmania and New Zealand are examples.
_Bacillus Mallei._ Christot and Kiener claimed to have found a bacillus
in the lesions of glanders in 1868. In 1881 bacilli were found by
Bouchard in a glander abscess in man, and these were cultivated _in
vitro_ and inoculated in a number of animals, by Capitan and Charrin in
1882. Independently in the same year (1882) Löffler and Schütz
discovered the bacillus, cultivated it _in vitro_, and successfully
inoculated it on animals. The microbe is rod-shaped, 2 to 5μ long, by
0.5 to 1.4μ thick, the same length as the bacillus tuberculosis but
thicker. It is nonmotile, ærobic (facultative anærobic) and grows
readily in a variety of culture media at a temperature of 37° C. On
neutral bouillon of the flesh of horse, ox, calf or chicken with or
without peptone, it grows readily, producing cloudiness in one or two
days. In peptonized gelatine it forms a whitish flocculent mass. On
glycerine agar with milk it forms in 48 hours a milk white layer,
changing to yellowish brown. On potato it forms long slender filaments,
in yellow, viscous, glistening colonies, changing to fawn and darker. It
grows best at 35° to 39° C. and growth ceases below 25° C., and above
42° C. It stains tardily in aniline colors, and not at all by Gram’s or
Weigert’s, but will readily take Kuhne’s stain prepared as follows: take
of phenic acid in solution (5:100) 50cc., absolute alcohol 10cc., and 1
to 2 grammes methylin blue. The stain is very easily bleached by acid,
differing in this from the bacillus tuberculosis. For decolorizing
Löffler recommends 10cc. distilled water, 2 drops of strong sulphuric
acid, and 1 drop of a 5 per cent. solution of oxalic acid. Sections
should be left in this not longer than 5 seconds. The bacillus often
appears granular, and unequally stained in its different parts. It may
be difficult of discovery in old standing lesions of horses, but comes
out clearly in recent lesions of experimental cases in Guinea pigs and
donkeys.
Baumgarten claims sporulation but this is uncertain.
The bacillus has only limited power of resistance to destructive
physical and chemical agents. It is killed in 10 minutes at 55° C., in 2
minutes at 100° C., or by mercuric chloride solution (1:5000), or by
phenol (5:100), or by permanganate of potass (1:100). In warm dry air
and sunshine it is sterilized, in thick layers in 2 months (Peuch), in
moderate layers in 4 to 15 days (Galtier), and in very thin layers in 3
days (Cadeac and Malet). In moist, cool air and in the shade it is much
more resistant. In stables it may remain virulent for three or four
months, and thus the disease has often reappeared among the newly
introduced horses after a stable has been abandoned for a length of
time. The microbe does not grow in infusions of hay, straw or horse
manure, and it is doubtful if it can maintain an active saprophytic
existence. Its vitality and virulence, however, persists in putrefying
materials for 14 to 24 days, and in water from 15 to 20 days. Hence it
is largely propagated through drinking troughs and occasionally through
ponds, lakes and sluggish streams. Again the virus is likely to be
preserved in and transmitted by rotten or even sound woodwork, as of
mangers, racks, buckets, shafts and poles, and by harness, halters,
blankets, combs, brushes and rubbers. Sometimes direct transmission
takes place in snorting or coughing, or by the animals biting or licking
each other. As the virus is spattered on surrounding objects, the walls,
stable utensils, soiled fodder and feed, and even the attendant’s
clothes may be the medium of transmission. Contagion during copulation
is not unknown, nor infection of the fœtus _in utero_ from a diseased
mother. Carnivora (dog, cat, lion) fed on the diseased carcasses have
become infected. Experimentally infection has been conveyed by
administering, by the mouth, balls containing the virus (Renault,
Coleman, etc.), and again by transfusing the blood from a bad case of
glanders into the veins of a sound horse (Viborg, Coleman, Renault,
Hering, Chauveau, Nocard). Transmission through the air on dust is
counteracted by the speedy destruction of virulence on dust, and horses
often stand side by side in adjacent stalls for months without
communicating the infection. Such escapes may, however, in some of these
cases, be attributed to the immunity secured by a previous exposure and
slight attack. That the germs may be exceptionally conveyed through the
air appears to have been proved by Viborg and Gerlach, who collected the
floating dust in a stable containing infected animals and successfully
inoculated with it.
The microbes are especially found in the visible lesions of glanders, in
the mucous, cutaneous and subcutaneous swellings and abscesses, in the
swollen lymph glands, in the nodules and ulcers of the mucous membranes
and skin, in the morbid discharges, from the nose, eyes, pharynx,
guttural pouches, larynx, trachea and bronchia, and in the discharge of
farcy buds and abscesses. They are not necessarily distributed through
all the tissues, and in chronic cases, with strictly local lesions, the
infection appears to be often confined to these or nearly so, and the
contamination of other animals is slow and uncertain. When, however, the
disease is acute and advanced, or generalized, every part must be looked
upon as probably infecting. Thus virulence has been shown in the blood,
the exhalations of the serous membranes, saliva, the aqueous humor
(Cadeac and Malet), the tears, (Viborg), the muscles, and the bones.
Galtier says the milk, sperm, bile and intestinal mucous are
non-virulent, also the vaccine lymph raised on glandered animals, but
much must depend on the grade and stage of the disease and no one would
care to run unnecessary risks with these liquids.
_Infection Atria._ Inoculation on a skin wound or abrasion, is a most
effective mode of transmission, but the virus undoubtedly enters in
certain cases with the air, food or water, or by accidental lodgment of
a speck of the virus on the mucosa of the nose or eye or other natural
opening. Through the healthy mucosa the bacillus may enter by
penetrating the soft epithelium, or entering the mucous follicles, but
it will find the way smoothed for it, if there has been friction,
abrasion, desquamation or congestion. The skin in its healthy state is
usually resistant, but Babes has conveyed infection by rubbing on the
virus mixed with vaseline, and without displacing the epithelium. The
channel of entrance was the hair follicles. Injected into the blood,
intravenously, or into a serous cavity, the bacillus infects with great
certainty and promptitude.
There is ample evidence that primary lesions appear not only in the skin
and nasal mucosa, but also in the bronchia, intestines, and other parts.
Much time and ink have been wasted in attempts to prove that pulmonary
lesions are always secondary, and doubtless many are so, but the cases
in which the lesions are confined to the bronchia or parenchyma, and the
many parallel cases of direct infection of the lungs by other diseases
(tuberculosis, lung plague, contagious pneumonia, influenza, etc.,)
furnish conclusive enough evidence that the germ may be inhaled and
colonize this part first. Cases of inhalation bronchitis, are equally
corroborative, and not only may the grosser solids be aspired, but
infection droplets can easily gravitate down when from congestion or
inflammation the action of the tracheal and bronchial cilia, is
suspended.
FORMS AND LESIONS OF GLANDERS IN SOLIPEDS.
Glanders appears in two primary forms—_acute_ and _chronic_, and each of
these is further divided according as the lesions are exclusively or
mainly seated in one part of the body or another. The generic term
_glanders_ is habitually used to designate that form in which the
lesions are situated in the nose, the nasal sinuses, and the
submaxillary lymphatic glands—_nasal glanders_. When the principle
lesions are situated in the lungs and lymph glands of the chest, the
case is one of _pulmonary glanders_. When the skin and subcutaneous
lymphatics are most prominently affected it is known as _farcy_ or
_cutaneous glanders_. When the skin and nose are simultaneously affected
the name _farcy glanders_ is sometimes applied. But as the bacillus may
enter by very varied channels the primary lesions may appear in still
other organs. Thus in stallions the first symptom is often a glanderous
orchitis. In other horses it may be a glanderous arthritis, and in still
others infected by ingestion it may be an abdominal infection.
_Symptoms of Nasal Glanders in Solipeds._ _Acute._ After an incubation
of three to five days the subject shows prostration, weariness,
stiffness, erection of the hair, and even tremor or shivering,
inappetence, thirst, hyperthermia, rapid pulse, weeping eyes, the
discharge becoming purulent, snuffling breathing, and a discharge from
the nose, at first serous, with a remarkable viscidity which tends to
glue together the long hairs or even the margins of the nostrils. This
discharge may be reddish, greenish, or brownish and may become
distinctly purulent and opaque. The _alæ nasi_ are swollen, hot and
painful, and the mucosa red, congested, thickened, with a blackish or
violet tint especially along the median part of the _septum nasi_. On
these, violet patches appear on the second or third day, pronounced
elevations of very varying size indicating the centres of active
hyperplasia. They are usually yellowish or grayish, surrounded by a deep
violet areola, and may become confluent forming patches. The centre of
each undergoes rapid degeneration, forming a rounded ulcer with salient
edges, a yellowish base, more or less pointed or streaked with red, and
a viscid seropurulent or bloody discharge which may concrete in crusts
or scale. The whole septum may become one continuous ulcer with
excavations of various depths surrounded by hyperplastic elevations, and
involving not only the mucosa, but even the cartilage and leading to
perforations.
From an early stage of the attack the submaxillary lymphatic glands and
the investing connective tissue become swollen, forming a mass of firm
bean- or pea-like nodules, with no excessive heat nor tenderness, and
with little disposition to suppurate and discharge. If this has lasted
for some time the glands often become more firmly attached to adjacent
parts (maxilla, tongue) by the contraction of the exudate.
The swelling of the alæ nasi also often extends to the skin of the face,
and firm, rounded cords formed by the swollen lymphatics stretch upward
toward the eye, or the submaxillary glands. Upon the turgid lymphatics
may appear more or less rounded nodules from the size of peas to hazel
nuts, which, unlike the submaxillary glands, tend to soften, burst and
discharge a viscid, glairy, sanious liquid.
At the same time the morbid process is liable to show itself in the
cutaneous lymphatics of one limb, usually a hind one, in the form of
firm cords, with degenerating or ulcerous nodules (farcy buds) and pasty
patches. Or the throat or lungs may become involved, with local
swellings, violent cough, dyspnœa and fever. The swellings of the
cutaneous lymphatics usually follow the course of the veins, in the hind
limbs the branches of the saphena, and extend from below upward, and the
first nodules may be on the fetlock or hock.
_Symptoms of Chronic Nasal Glanders in Solipeds._ The chronic form of
the disease follows an indolent course, and local symptoms are often so
slight or equivocal that the true nature of the malady is unsuspected.
If the patient is well fed and cared for and not overworked, the malady
may run a course of three, five or seven years, and the victim may pass
through many hands leaving infection in every stable it occupies.
Diagnostic symptoms, more or less clear, may be obtained from the
discharge; the lesions of the mucosa and the submaxillary glands.
The _nasal discharge_ may be bilateral, but if confined to one nostril
is strongly suggestive of glanders. It may be profuse or scanty,
continuous or intermittent, of a yellowish, purulent tint, or greenish,
or grayish and with a special tendency to viscidity. In some indolent
cases the nostrils may be clean but if there is any matting of the long
hairs, or adhesion of the alæ nasi, the case is specially suspicious. If
it is sanious, flocculent, or bloody it is all the more characteristic,
and suggests the supervention of an acute attack.
The _lesions of the pituitary membrane_ are varied. Hyperæmia of a
purple or violet color is common, especially along the septum, and the
mucosa is liable to be somewhat tumid or œdematous. Nodules the size of
a pin’s head, a pea or larger appear inside the inner ala, or on the
septum or turbinated bones, and at first red from extravasation and, as
it were vesicular, become grayish, whitish or yellow with points of red
and surrounded by a deeply congested areola. Larger nodules forming in
the submucosa approach the surface and stand out the size of the tip of
the finger and with the same general character as the smaller. Sooner or
later these degenerate and form ulcers which bear a resemblance to those
of acute glanders but are less angry, and when small and solitary may be
taken for simple erosions. In other cases they become thickened and
indurated with sharply defined projecting margins, and a yellowish base
with points or lines of red. The presence of red, black, green, or brown
crusts may also be noted.
Another lesion frequently observed in indolent cases is a cicatricial
white spot or patch in which the hyperplasia has become partially
developed into tissue and shows no tendency to ulcerate. The mucosa may
even be drawn or puckered around the cicatrix, making the illusion all
the more complete.
The _submaxillary swelling_ is even less sensitive than in acute
glanders and produces the same sensation as of an aggregation of small,
hard, pea-like, masses with no tendency to ulcerate.
_Symptoms of Cutaneous Glanders (Farcy) in Solipeds._ Acute cutaneous
glanders has been already referred to under nasal glanders. The chronic
type is often less characteristic, yet may be detected by careful
observation of the symptoms. The main symptom may be the swelling of a
joint with more or less engorgement of the limb from attendant
lymphangitis. There can usually be detected around the margins of such
swellings firm, tender cords representing the larger lymphatic vessels
and often branching in their course. In the absence of the engorgement,
or when it is slight, these _cords_ may be the main evidence of the
disorder, and in the hind limb usually follow the course of the flexor
tendons on the inner side of the digit, metacarpus and thigh. At
intervals along the line of the _cords_ appear nodular masses (farcy
buds) varying in size from a pea to a hen’s egg, and showing a great
disposition to soften and discharge a glairy, sanious or more or less
bloody liquid. The inner sides of the fetlock and tarsus are favorite
seats of these nodules but they may form at any point. On the trunk also
the corded lymphatics and nodules follow the lines of the veins and
lymphatics, and here there may be the complication of large
intermuscular abscesses often in connection with the groups of lymphatic
glands.
_Latent or occult glanders_ is often met with, the indolent, specific
lesions being confined to some internal organs, like the larynx, lungs
or womb, or to the testicles, the nasal diagnostic symptoms being
absent. A chronic cough, with a slight purulent discharge from the nose,
a chronic leucorrhœa, a swollen testicle, or simply a persistent low
condition or weakness without apparent cause, may be the only
indications, and special means of diagnosis are demanded.
_Special Means of Diagnosis._ In occult cases, the disease may be
identified by inoculation, or by the mallein test.
_Inoculation_ is best performed on a very susceptible animal. If the
suspected discharge from the nose, vagina, open sore or preferably from
a freshly incised nodule is inoculated subcutem in the flank of a male
Guinea pig, or better in the peritoneum, there develops a local ulcerous
sore and on the second or third day a violent orchitis in which pure
cultures of the bacillus can be obtained. The caseous and purulent
centres are found not only in the testicle but along the line of the
spermatic cord, affecting the tunica vaginalis and connective tissue.
Death usually follows in four to fifteen days. The cat and dog can also
be utilized, inoculation being made on the forehead. Old wornout, but
otherwise healthy asses, and even horses make very available subjects,
inoculation in the nose speedily developing acute glanders. In the
absence of a good subject the suspected animal is sometimes availed of,
scarifications being made in the nose and the morbid product rubbed in
freely. The rapid development of ulcerous wounds is characteristic. If,
however, the case is chronic, and if a fair measure of immunity has been
acquired this test may prove misleading.
_Test by Mallein._ Mallein is the sterilized and concentrated toxic
product obtained from a pure culture of bacillus mallei in a peptonized
glycerine bouillon. When injected hypodermically in a small
physiological dose this has no effect on a sound horse, but in one
affected with glanders it develops in several hours an extended swelling
in the seat of inoculation, hot, tense and painful, which continues to
enlarge for 24 to 36 hours and does not subside for 4 or 5 days. From
the margin of the swelling, swollen lymphatics may often be traced
running toward the adjacent lymphatic glands. There is also decided
dulness, prostration, inappetence, staring coat and tremors. The body
temperature rises 1.5° to 2.5° and upward from the eighth hour after
inoculation attaining its maximum from the tenth to the eighteenth hour
and subsiding slowly to the forty-eighth to the sixtieth.
Mallein must be used under precautions like tuberculin. It must be
obtained freshly prepared from a reputable maker. If preserved for
months its force may be largely lost. The animal to be tested should be
in his customary environment, and not just arrived from a railroad
journey nor other cause of excitement. He must not be fevered as any
rise of temperature is then equivocal, and a fall of temperature, which
sometimes occurs in the febrile system under mallein, is no sure
evidence of glanders. Reaction sometimes fails in advanced cases of
glanders, but in such a case other symptoms are usually diagnostic so
that mallein is superfluous and should not be misleading. The greatest
care should be taken to prevent infection from the syringe, nozzle,
skin, hands, etc., as other infections may give rise to local swelling
and hyperthermia (see tuberculin test). If a first test leaves the
matter in doubt, the animal should be secluded and tested again in a
month (some prefer 3 months).
_Pathological Anatomy._ The colonization of the bacillus mallei in a
tissue usually determines a concentration and multiplication of
leucocytes, so as to form rounded nests of small lymphoid cells in a
scanty fibrous network. These may be miliary or by aggregation they form
masses the size of a pea or larger, which bear a close resemblance to
the neoplasms of tuberculosis. As in tubercle the central cells of the
group, degenerate, forming a granular fatty debris, and constituting an
ulcer or abscess. In certain cases with a proliferation of fibrous
tissue a cicatricial material is developed. Another characteristic
lesion is the occurrence of hyperplasia in the walls of the lymph
vessels so as to constitute firm tender cords, and the infiltration of
the adjacent lymphatic plexus.
In the _nasal mucosa_ the bacilli form prolific colonies at different
points of the membrane and submucosa with the active production of
lymphoid cells, followed by granular fatty degeneration and ulceration.
Hence may be found different lesions representing the different stages.
First there may be miliary deposits with clear contents and standing out
like grains of sand. Then there are the larger pea-like nodules with
congested vessels and minute hæmorrhages, but made up largely of the
nests of lymphoid cells. These may bear on the surface a distinct blood
extravasation, or the epithelium may be raised from the corium layer by
a liquid exudation. The more advanced nodules show the centre light
colored, grayish or yellowish with a distinct granular degeneration of
the cells. Later still the degeneration involves the superficial layers
and epithelium and an open ulcer is formed with a strong tendency to
extend in depth and width. The formation and degeneration of numerous
foci of cell proliferation gives the ulcer a very uneven outline. The
continuous growth of fresh centres of proliferation may cause marked
elevations between the ulcers, constituting extended patches, or the
entire nasal mucosa may be thickened as the result of the morbid
deposit. The cicatrices resulting from the apparent healing of deep or
extensive ulcers or from a fibroid, transformation of the neoplasm
consist of condensed connective tissue with small scattered nests of
lymphoid cells and bacilli. In chronic cases the bacilli are very
scanty.
The mucosa of the _Eustachian pouches and tubes, the larynx, trachea and
bronchia_ often present lesions similar to those of the pituitary
membrane.
The _lungs_ are usually marked in chronic cases by circumscribed lobular
pneumonia, interlobular and peribronchial inflammations and miliary or
larger areas of degeneration resembling tubercles. These may begin as a
minute congestion and ecchymosis, which later shows in the centre a
translucent or gray mass of lymphoid cells, with a surrounding area of
congestion. Later still this central mass becomes yellowish and caseated
from granular and fatty degeneration and this gradually extends so as to
involve the whole area of the nodule. The peripheral portion may
condense into a fibroid envelope, but usually this is less smooth and
evenly rounded than in the case of an inspissated abscess or
bladder-worm. The bacilli are found in the affected tissue but not
always abundantly.
In _cutaneous glanders_ the lesions may begin in the papillary layer by
active congestion and infiltration and proliferation of lymphoid cells
which cause an eruption of rounded papules like small peas that
degenerate and soften and form superficial ulcers. When the derma is
mainly involved the inflamed area becomes the seat of larger hard
nodules which are at first deeply congested, with capillary thrombi,
minute extravasations and rapid cell proliferation; later on section
they show numerous caseated centres with a dense fibroid framework and
surrounded by an area of active congestion and capillary hæmorrhage;
later still the caseation and softening has caused rupture of the
investing epithelium and the discharge from the ulcerous cavity of a
yellowish, glairy, grumous liquid (open farcy buds). Sometimes the
nodule undergoes fibroid induration and fails to ulcerate, becoming the
counterpart of the cicatrices in the nose. When the infective
inflammation extends to the subcutaneous connective tissue, diffuse
engorgements and extensive swellings occur from the general infiltration
of the abundant lymph plexuses. Lymphoid cells accumulate in the
perivascular sheaths and lymph plexuses, the walls of the lymphatic
trunks running out of these swellings become swollen and indurated and
at intervals, mostly on the seat of the valves there is the
proliferation of small round cells to form farcy buds. In chronic cases
the fibroid thickening involves the skin, subcutaneous connective tissue
and walls of the lymph vessels binding the whole into one dense
resistant mass, more or less studded with corded lymphatics, firm
nodules, and ulcerous sores.
The _lymphatic glands_ in the line of circulation from the infected
centres are constantly involved. Hypertrophy, congestion, serous
infiltration, and rapid cell proliferation are present and a section
will usually show caseated or caseopurulent centres confined by the
outer dense fibrous envelope. Exceptionally, these necrosed contents
will escape through an ulcerous opening, forming a deep cavity which is
slow and difficult to heal. In the vicinity of these glands and in the
loose intermuscular connective tissue abscesses of the size of an egg or
an orange or larger are sometimes met with.
Nodules and ulcers are found on the pharyngeal and intestinal mucosa,
similar to those of the larynx.
The spleen, and less frequently the liver, may be the seat of caseating
nodules exactly comparable to those of the lungs. Glanders of the kidney
is rare.
Nodules have been seen on the ventricular endocardium and one case of
nodules of the choroid plexus (Boschetti).
In stallions, glanderous, caseating foci in the _testicle_ and dropsy of
the scrotum are common, while mares may have similar formations in the
mammary glands or ulcers of the vaginal or uterine mucosa.
Infiltrations of the joints and other synovial cavities are not uncommon
and glanderous infiltration of the bones with caries is also found. In
chronic cases, fragility of the bone is marked, and the blood contains
an excess of leucocytes. These may be traced to disease of the bone
marrow, as well as of the spleen and lymphatic system.
GLANDERS IN SWINE.
The healthy, vigorous pig is practically immune. Experimental
inoculations have uniformly failed to produce the disease. Exception
must be made when inoculation is made into the aqueous humor, in which
there is comparatively little resistance by leucocytes. Sacharoff
succeeded in giving the disease in a fatal form to a young pig in this
way. To weak and debilitated pigs, on the other hand, the disease may be
conveyed as shown by Spinola, and Cadeac and Malet. The symptoms were
engorgement of the tissues in the seat of inoculation with the formation
of glanderous nodules, which undergo molecular degeneration and
ulceration; swelling of the lymph vessels extending from the infected
point, and of the adjacent lymph glands; the formation of glander
nodules in the lungs, liver and spleen, and of nodules and ulcers on the
nasal mucosa.
GLANDERS IN SHEEP AND GOAT.
Casual glanders is uncommon in the small ruminants, yet it has been seen
in goats that fed on the soiled provender left by glandered horses
(Ercolani, Trasbot, Mesnard). Sheep have suffered after inoculation
(Renault, Bonley, Gerlach, Bollinger, Croker, Peuch, Galtier) showing
nodules and ulcerous swellings in the seat of inoculation, with
extension in some cases to the nasal mucosa and lungs, and a fatal
result. In other cases the lesions remain localized and the disease
progresses to recovery.
GLANDERS OF RODENTS: RABBIT, GUINEA-PIG, MOUSE, RAT.
The _Guinea-pig_ is especially susceptible, and like the rabbit and
mouse may contract the disease by eating the soiled fodder of glandered
horses. It is usually selected for inoculation for diagnostic purposes,
because in the male, the insertion of the virus in the peritoneum
determines a rapid swelling of the testicle and cord, with a glistening,
violet engorgement and tension of the scrotum, suppurative adenitis and
death in three to six days. In other situations the inoculated part
swells rapidly and ulcerates, the adjacent lymph glands become swollen
and tender, similar lesions form in other parts and notably in the nose
which discharges profusely a whitish, sticky fluid, the breathing is
hurried, and emaciation is marked. Death occurs in a few days and
ulcers, and abscesses are found in the lungs and other internal organs,
as well as in the nose. In less susceptible subjects or under smaller
doses of the virus the local swelling and ulceration in the seat of
inoculation are slight, but there persist engorgements of the adjacent
lymph glands, swelling (cording) of the lymph vessels adjacent, and
nodules and abscesses, (cutaneous, subcutaneous, intermuscular,
intravisceral), arthritis, emaciation, dyspnœa and death in two to four
months. In some cases with a very small dose of the poison, there is no
local swelling, and no generalization nor subsequent manifestation of
the disease.
In the _rabbit_ the lesions are less certain and often less marked.
There is sometimes no swelling in the seat of inoculation, in the
neighboring lymph glands, nor elsewhere, and the rodent might have been
supposed to have escaped, only that successful inoculation of the ass
may be made from the tissues inoculated (Galtier). In such a case a
certain immunity of the rabbit must be inferred. In less resistant
rabbits, or with a larger dose, an ulcerous swelling forms in the seat
of inoculation, the adjacent lymph glands become engorged or even
purulent, corded lymphatics intervene, and nodules and caseous
degenerations appear in the lungs, nose, spleen, liver, and other
organs.
The _hedgehog_, _ground squirrel_, the _field mouse_, _house mouse_,
_mole_ have been successfully inoculated.
The _frog_ immersed in water at 30° C., forms a good culture ground for
the bacillus which may be found in its blood, in pure cultures, from the
second to the fifty-fifth day. These cause no local lesion, nor obvious,
constitutional disorder. It seems possible that, in summer, the
infection may be propagated by frogs in the drinking water.
GLANDERS IN CARNIVORA.
All carnivora are liable to contract glanders by eating the flesh of
glandered horses, asses and mules, and this has been noted especially in
menageries. _Lions_, _tigers_, _bears_ and _wolves_, have shown the
ulcerous lesions in the nose, and the nodules in the lungs, spleen,
liver, kidneys and elsewhere. The carcass of the diseased horse is,
however, often devoured without evil result, and even when the carnivora
become affected the disease is not always fatal.
In the _dog_, experimental glanders has been closely studied by many
observers. Casual glanders has been contracted by living with the
glandered horse; by licking his nasal or other discharges, and by eating
his flesh. The disease has also been conveyed from dog to dog by licking
each other. In many cases even inoculated glanders produces only a local
ulcerous inflammatory lesion with or without hard swelling of the
adjacent lymphatics, and engorgement of the lymph glands. After a rather
tardy granulation and cicatrisation, the symptoms subside and the animal
is restored to health. Yet such benignity does not depend on any
lessened virulence of the bacillus, for an inoculation of the discharges
on the ass produces acute and fatal glanders.
GLANDERS IN MAN.
Recognized by Lorin 1812. Causes: infection from soliped, man less
susceptible; infection from man, clothing, stable bucket, inhalation,
etc.; industrial disease; native immunity. _Symptoms_: incubation;
mistaken for carbuncle, small pox, measles, erysipelas, anthrax;
anamnesis; anthrax focus has darker center, no caseation, no corded
lymphatics; nodules and ulcers in nose, swollen submaxillary glands
and lymph vessels, general illness, diarrhœa, vomiting, dyspnœa,
mental derangement, stupor, coma, internal deposits, bloody sputa,
fœtid breath, hepatic pain, icterus, muscles, bones, bowels, typhoid,
pyæmic, osteo-myelitic, or acute tuberculous symptoms. Death in 3 days
to 4 weeks. Chronic cases, cutaneous, muscular, osseous, skin nodules
in group or chain, glandular swellings. Diagnosis from pyæmia by lack
of chills, and the sanious pus; from syphilis by futility of potassium
iodide, and history; inoculate ox or white mouse; find bacillus.
Lesions: as in horse, more early coagulation necrosis, ulceration,
abscess; pus more viscid than in pyæmia, walls of abscess more
irregular, lymphoid cell proliferation more abundant and extended
(glands, spleen, liver, lung, nose, etc.), history; distinguished from
variola, rötheln, and erysipelas by the many miliary or pea-like
neoplasms with cellular caseating centres; lymphoid deposits in bone
marrow, with friability.
Until the early part of the present century glanders in man was not
traced to its origin in the soliped. Lorin in 1812 recorded a case in
which the human hand had been accidentally inoculated from handling a
horse suffering from farcy. Soon other cases were put on record by
Waldinger and Weith, Muscroft, Schilling, Rust, Sedow, and a host of
followers. Later Rayer, Tardieu, Virchow, Leisering, Gerlach and Koránye
have thrown much light on the subject.
_Etiology._ Man is manifestly less susceptible than the soliped,
considering the great number of exposures relatively to the victims. Yet
the infection of man is altogether too common to be lightly passed over.
The infection is almost always derived directly or indirectly from the
horse, yet a number of cases have been derived from the human being
through handling the dishes, towels or handkerchiefs of a patient,
dressing his wounds, or performing a necropsy. Other cases like that of
Dr. Hoffmann of Vienna, came from handling artificial cultures of the
bacillus mallei.
Glanders is preëminently an industrial disease, attacking persons of the
following occupations: hostlers 42, farmers and horse owners 19, horse
butchers 13, coachmen and drivers 11, veterinarians and veterinary
students 10, soldiers 5, surgeons 4, gardeners 3, horse dealers 2,
policeman, shepherd, blacksmith, employe at a veterinary school, and
washerwoman, 1 each.
The modes of transmission are essentially the same as in the animal. In
the great majority of cases there has been the direct contact of the
infecting discharges with a wound of the human victim. Handling the
diseased horse with injured hands, giving him a bolus and scratching the
hand on the teeth, examining the nose, sleeping under a blanket which
has been used on a glandered horse, removing the dressings of such an
animal or performing a post mortem examination on him are familiar
examples. The particles scattered by the diseased animal in snorting,
will infect the mucous membrane of the eye or nose, and all the more
readily if these are already sore or abraded. Infection of man by
ingestion has been discredited mainly because the carcasses of glandered
horses have often been eaten with impunity; but this may be largely
accounted for by cooking, the bacillus being destroyed by a temperature
of 131° F. Carnivora such as dogs, cats, lions, polar bears and prairie
dogs have been infected by feeding. Men also have been infected through
drinking from the same bucket after a glandered horse. After making full
allowance for the inimical action of the gastric juice, we must admit
that this has often failed, and there is the added danger of abrasions
of the lips, mouth and throat and of the entrance of the microbe into
the tonsillar follicles and gland ducts. Still other cases are recorded
of men sleeping in stables, but not handling horses, who contracted
glanders, presumably, through the dust borne bacillus inhaled. The
bacillus, is however, so readily destroyed by thorough desiccation that
this mode of transmission is exceptional. Some men are immune to
glanders, and suffer only when predisposed through a course of ill
health, and yet a large proportion of the cases on record have been in
strong hearty men.
_Symptoms of Glanders in Man._ In man as in the horse, glanders occurs
in the _acute_ and _chronic forms_. In the _acute_ supervening on an
external inoculation, _incubation_ is from one to four days. When it
enters through other channels it may seem to extend to a week or more.
When a skin abrasion has been inoculated it will show in a few days a
soft inflammatory swelling or a firm nodule with a puffy reddish areola,
and it may be mistaken for a carbuncle. In not a few cases the small
nodule has been mistaken for small pox. In my experience a horsemen on a
ranch on which over a hundred horses showed glanders, died of an
ulcerous skin affection which was variously supposed to be a malignant
small pox and measles, though neither malady was known to exist in the
district. Other cases are confounded with gangrenous erysipelas. The
absence of these other affections from the locality, and the fact that
the patient was employed about glandered horses, should go far to
correct such mistakes. The early supervention of ulceration is further
diagnostic, and discovery of the bacillus mallei in the products will be
conclusive. From anthrax it is easily distinguished by the absence of
the dark centre of the sore in the early stages, and of the large sized
bacillus anthracis. The caseation or liquefaction of the necrotic centre
further distinguishes it from the characteristic anthrax slough, and the
thickening and induration of the lymphatic walls are not present in
anthrax. Sometimes the inoculated case proves mild and recovers in two
or three weeks with healing of the ulcer, but in other cases there is an
extension to adjacent tissue and a general infection with the
supervention of nasal glanders.
There is a spread of the erysipelatoid inflammation and swelling, and
the formation in such newly invaded tissue of nodules and ulcers in
successive crops. In acute cases too, the nasal mucosa becomes involved
with the formation of the nodules and ulcers that are so pathognomonic
in the horse. The discharge is then somewhat sticky and often tinged
with blood. In acute cases according to Senn, the nose may be completely
destroyed and deep facial ulcers may be formed in a week. The
submaxillary glands are enlarged and painful and the facial lymphatic
vessels leading from these to the nose may be red, thickened and tender.
Suppuration and ulceration of the glands may ensue. Headache,
prostration, nausea, inappetence and vomiting with diarrhœa usually
supervene. Then follow dyspnœa, wakefulness, troubled dreams, anxiety,
nocturnal delirium, stupor and coma. The pulse may rise to 120 and the
temperature to 104° F.
There may be various complications as deposits in the lungs with pain in
the chest, weak cough, aphonia, bloody expectoration and offensive
breath; or the morbid process may take place in the liver or spleen with
pain in the hypochondrium and much prostration and even icterus; or the
muscles, bones, joints or testicle may suffer and the symptoms may
suggest typhoid fever, pyæmia, osteomyelitis, or acute general miliary
tuberculosis. The bacillus can usually be detected in the blood.
Acute glanders may prove fatal in three days or it may be prolonged for
two, three or even four weeks.
_Chronic glanders_ in man usually confines itself to the cutaneous
muscular and osseous systems. It may take on an indolent type with the
formation of skin nodules in groups or chains which remain hard and show
no tendency to soften nor ulcerate. The adjacent lymphatic glands may
become enlarged and indurated and the affection strongly resembles
tuberculosis of the skin. Later when the nodules have softened and
formed irregular and obstinate ulcers with swollen lymphatic glands, the
disease is easily mistaken for syphilis. From pyæmia and septicæmia it
is usually to be distinguished by the comparative absence of chills, and
by the more sanious character of the pus. From syphilis it may be
distinguished by the futility of a course of potassium iodide, and the
general history of the case and probable exposure of the patient, and
for tuberculosis the same principles will apply. In case of uncertainty,
inoculation may be resorted to on the horse in suspected syphilis and on
the pig when there is suspicion of tuberculosis. Or conversely the ox
may be employed for the latter disease as he is altogether insusceptible
to glanders. As a last resort the discovery of the bacillus may be made
or the mallein test may be adopted with the concurrence of the patient.
_Pathological Anatomy and Diagnosis._ This is fundamentally the same as
in the horse. The bacillus and its toxic products act on the infected
tissues to produce clusters of lymphoid cells in a fibrous stroma after
the manner of tuberculosis. Like that disease it also tends to affect
primarily the lymph channels and glands, showing a particular tendency
to the respiratory mucosa and has a great disposition to early
coagulation, necrosis, ulceration, suppuration and abscess. The giant
cell of tuberculosis is not a prominent feature in glanders, and the
disposition to suppuration is greater especially in the human being so
that the disease often resembles pyæmia. As in solipeds, however, the
glander abscess has somewhat more sanious or glairy contents and the
investing wall is not smooth and regular, but uneven and ulcerous from
the successive softening and discharge of the clusters of degenerating
lymphoid cells in the adjacent tissue. The pallor of the adjacent
tissues from exudation and from the presence of numerous nests of
lymphoid cells, the thickening of the efferent lymphatics, and the
presence of numerous lymphoid neoplasms in the adjacent glands, and
tissues, and often in the internal organs such as the liver and spleen
and in the nasal mucosa or lungs together with the history of the
patient’s exposure to glanders serve to diagnose from pyæmia. From
smallpox and rötheln the skin lesions are distinguished by the presence
of a central coagulation necrosis bathed in a glairy seropurulent fluid,
and by the infiltration and thickening of the efferent lymphatic trunks.
It differs from erysipelas in the same way by the presence in the
affected tissues of the small hard lymphoid masses of embryonal tissue,
and in a more advanced stage by the granular fatty debris resulting from
their fatty degeneration. The presence in the affected tissue of these
miliary or pea-like neoplasms in all stages of development from the
primary congestion, through the embryonal tissue to the coagulation
necrosis and caseation or softening is characteristic of the lesions of
glanders. The sanious, sticky or glairy pus is especially noticed in the
newly opened abscess, as after exposure to the air it is speedily
infected with pus microbes, and the discharge becomes less serous and
more creamy. Another characteristic of glanders in man is the frequent
implication of the bone marrow, and the formation of the lymphoid
deposits in the cancellated tissue until the bone may be reduced to a
mere friable shell. Even when the disease is localized in the nasal
mucosa it extends rapidly, not only to the skin and muscles, but also to
the cartilage and bones of the face, so that deep, wide, perforating and
destructive ulcers are common. The enlarged ends of the long bones of
the limbs are favorite seats of the lesion, and the synovial membrane of
the joints and the articular cartilage often bear centres of lymphoid
proliferation. Though usually small the intermuscular neoplasms may form
abscesses as large as a hen’s egg. The affected muscle appears pale,
degenerated and granular with foci of lymphoid cell growth. The swelling
of the lymph glands is usually less than in the soliped though the same
in character. The pulmonary neoplasms are histologically almost
indistinguishable from tubercle, though the comparative absence of the
giant cell, the different staining qualities of the bacillus, and the
coincident lesions in the upper air passages, with the cord like
infiltration of the walls of the lymphatics may assist in diagnosis.
Diagnostic inoculation may be made on the basis of the susceptibility of
the ox and white mouse to tuberculosis, and their insusceptibility to
glanders; also the partial insusceptibility of the soliped to
tuberculosis and his marked susceptibility to glanders.
The characteristic nodules and abscesses may be found in different
internal organs such as the stomach, intestine, liver, spleen, kidneys,
testicles and brain, especially in acute cases, whereas the lesions of
the skin and nose are more common in chronic cases.
PROPHYLAXIS AND TREATMENT OF GLANDERS.
Extinction. Exclusion, in Australia, New Zealand, English army.
Occision of infected, and disinfection of stables, harness, vehicles,
utensils, manure and other infected things, mallein diagnosis;
attendants should avoid handling suspicious horses, except with sound
hands, and disinfect latter. Sheep living in horse stables, tested
before slaughter, or inspected after. Malleinization on Plains and in
high, dry air, in secluded herds: less hopeful elsewhere. Mallein test
for all solipeds from glanders districts, and imported horses.
Treatment illegal in many states, so that justice would require
extinction with indemnities. Successful on high tablelands and
mountains. Demands careful segregation and disinfection. Acute cases
always hopeless: chronic skin cases more promising. Antiseptic
injection of unbroken nodules (carbolic acid, potassium permanganate),
also of open sores (mercuric chloride, iodized phenol, cupric
sulphate, saturated, zinc chloride), excise nodule. For delicate
mucous surfaces Lugol’s solution of iodine or iodized phenol diluted.
Tonics: arseniate of strychnia, copper biniodide, baryta nitrate, iron
sulphate, sulphites, bisulphites, hyposulphites, phenic acid, open air
life at pasture, or thorough ventilation, sunshine, moderate exercise,
generous, partly grain diet. Mild cases in separate herd, in secluded,
wide pasture with rich diet, including grain, and shelter in clean,
comfortable shed at will, under tonics and antiseptics, tested by
mallein at intervals, to be restored individually to work after two or
more tests without reaction. Serum of immune animals subcutem.
Treatment in man: surgically as in the horse, excision, curetting,
antisepsis, abscesses opened and disinfected; iodoform insufflations,
antiseptic gases, sprays and solutions. Internally: tonics,
sulphocarbolates, iron muriate, iodides, phenic acid, quinia,
strychnia, arsenite, stimulants, serum treatment, pure air, out door
life, rich, digestible food.
Radical efforts at prevention must look to the extinction of the disease
in the soliped, and its complete exclusion from Australia and New
Zealand shows that such a result is not unattainable. In the English
army where every glandered horse is at once killed and all pertaining to
him disinfected, the disease is now virtually unknown except in the case
of newly purchased horses or regiments operating in the field. In the
French army which formerly lost 9 per cent. per annum from glanders, now
under similar precautions loses but .5 percent. A law providing for the
prompt destruction of every glandered soliped and the safe disinfection
of carcasses, stables, harness, vehicles, utensils, fodder, litter and
manure that have been exposed to contamination, if enforced, would soon
eradicate the disease. But this law should provide efficient machinery
for its enforcement, and, under suitable safe guards, an appropriate
indemnity for the owner. With the use of mallein in all infected studs,
as a diagnostic agent, the campaign can be made sharp, short and
effective, instead of waiting as in the past for the slow development of
occult cases.
The greatest and most fundamental error in veterinary sanitary
legislation is the lack of a guarded indemnity for the animals killed. I
strongly urged this fact on the committee of the N. Y. legislature in
1898 but to no purpose. A bill was passed forbidding all indemnity for
glandered horses, and an impetus thus given to the spread of the disease
is daily bearing fruit in our great cities especially, disastrous to the
health of the horses, and a constant menace to that of humanity as well.
The law makes it the duty of veterinarians to report all cases of
glanders, but in great horse establishments such a report would stop the
use of the whole stable, at a loss of thousands of dollars per diem, and
put a sudden end to the employment of the reporting practitioner by the
firm or corporation in question. The owner of one or two horses can
afford to report, the loss of these and their work does not mean
absolute ruin, but the owner of hundreds can not safely report. For
owner and practitioner alike the alternatives are presented of obedience
to the law with personal ruin on the one hand, and the surreptitious
dealing with cases of glanders and the preservation of their livelihoods
on the other. Whatever may be said as to the constitutionality of the
law which destroys private property without compensation under the right
of eminent domain, this is certain, that, as applied to animal plagues,
this course is unjust, oppressive, and not only useless, but positively
injurious, in that it drives the owners of animals to such courses as
favor the spread of the plague in place of restricting it. To-day in New
York City glanders is extensively prevalent, but large horse owners dare
not adopt the legal measures for its extinction, with the certainty of
great loss or ruin staring them in the face as the result. It should be
further considered that any law is at once bad and vicious in its
tendency which places before the citizen the alternatives of
disobedience with profit, and obedience with loss or ruin. Such a law is
the worst possible economy because in preserving the infection, it not
only perpetuates the disease and its attendant losses for all time, but
perpetuates forever the official expenses of keeping it in check, when a
prompt extinction of the infection would once for all time abolish all
loss and all outlay for surveillance.
Until provision can be made for the enforcement of our laws against
glanders, all who handle horses should be warned of the danger of
working about strange solipeds, or those that show suspicious symptoms,
while they have any sores on the hands, and in case they must run any
risk of contact with infection, to promptly wash hands and face in a
solution of hydrargyrum chloride (1:2000), or carbolic acid (2:100).
Animals of susceptible races (sheep, etc.) which have lived with
glandered horses should be made to pass the mallein test before they can
be put upon the market for human food.
In the high, dry altitudes of the Plains and Rocky Mountains, where most
cases of glanders are mild and the majority recover, resort may be had
to malleinization provided the patients are kept safely secluded from
all other horses. In some horses with a native tendency to immunity, the
oft repeated inoculation with 0.5cc. of mallein will render the animal
refractory to the infection. Animals that have recovered from casual
attacks show the same immunity. Among those who have experimented with
mallein may be named: Straus, Schneidemuhl, Semmer, Bonome, and Vivaldi,
Mowry and Michel, Schweinitz and Kilborne. Sacharoff apparently secured
immunity in the horse by inoculation with virus modified by passing
through the cat. Straus found that dogs which had received mallein
intravenously could be made immune against intravenous inoculations,
but, as Galtier had already pointed out, were still susceptible to
cutaneous inoculations. Finger, experimenting on the rabbit, found that
immunity only resulted after a long series of inoculations. The
frequency of successful auto-inoculations in chronic cases of glanders
in the horse would tend to discredit the alleged value of single
injections of mallein, so that a long series is necessary if we would
aim at good results.
Altogether attempts at immunizing the equine population generally, are
not hopeful where it is dense, where they must be kept stabled, where
the climate is moist and where glanders is deadly, or tends to persist
in the chronic form for years in the same animal.
Considering the prevalence of the disease in a mild form on many of the
western breeding ranches it is well to test all horses arriving from the
west. The same applies to solipeds imported from abroad.
TREATMENT OF ANIMALS.
In the majority of the states the treatment of a glandered horse is
prohibited by statute. Yet without providing definite machinery for the
administration of the law, and without indemnities for horses disposed
of, such laws are largely inoperative. On the other hand treatment is
quite successful on the pastures of our dry table lands and mountains.
It can, however, be sanctioned only when careful segregation and
disinfection are provided for. Acute cases of glanders are hopeless in
any region, but chronic cases and especially such as have the lesions
confined to the skin are much more hopeful.
The unbroken nodules may be injected with carbolic acid solution
(1:200), or permanganate of potash (1:60). The open sores on the skin
may be treated with the same solutions, with mercuric chloride (1:2000
to 1:5000), with iodized phenol, with cupric sulphate (saturated
solution), or with chloride of zinc. A primary nodule may be excised and
the sore treated with antiseptics. When the lesions are very extensive
the less poisonous agents should be made use of, or tincture of iodine
may be substituted. The nose lesions may be treated by the weaker
solutions of iodine or of iodized phenol.
Benefit also comes from a course of tonics the most successful of which
have been arseniate of strychnia, binodide of copper, sulphate of
copper, nitrate of baryta and sulphate of iron. The sulphites,
bisulphites and hyposulphites and phenic acid are desirable adjuncts. An
open air life at pasture is the ideal condition. Otherwise thorough
ventilation, sunshine, moderate exercise and nourishing easily
digestible food including grain are very important.
When conditions are favorable and an absolutely secluded pasture can be
secured, with shelter from storms, and where civic or state authorities
do not take effective measures to stamp out glanders, nor compensate
owners for animals killed, mild, chronic and cutaneous cases and occult
ones that have reacted to mallein without showing any other symptom, may
be subjected to treatment. They should have an open air life, a generous
diet, including grain, perfect cleanliness and pure air in the
shelter-shed, an antiseptic and tonic medication (sulphites, tonics) may
be given, and every three months a new mallein test may be applied. If
the individual horse passes two successive tests without reaction, and
shows no other indication of glanders, if his general health appears
perfect and his condition good, he may be returned to work as a sound
animal. With effective measures of extinction in force on the other
hand, and indemnity for the slaughtered animal, any such measure would
be entirely unwarrantable.
Treatment by injecting the serum of immune animal subcutem has given
encouraging results. Helman, Semmer and Itzkovitch, Pilavios, Bonome and
Vivaldi, Johne, Schindelka, Prieur and others record recoveries in
recent cases and there need be no doubt of its value in subjects that
are naturally somewhat refractory to the germ. Babes introduced the
blood serum of the ox, which is naturally immune, and Prieur speaks with
confidence of the treatment of cutaneous glanders in man and certain
cases of pulmonary glanders in the horse.
TREATMENT IN MAN.
The surgical treatment of glanders in man does not differ materially
from that given for animals. It is more frequently possible to deal with
the local lesion in its early stages and then a thorough cauterization
of the infected sore, and a little later the complete excision of the
primary nodule, or the limited regional infiltration, the curetting of
the adjacent parts and the maintenance of thorough disinfection by
irrigation, sponging and compress will often be followed by success.
Where such radical measures are inadmissible the infected parts should
be excised and curetted as far as safe and the adjacent parts subjected
to carbolic injections (1:200). Abscesses should be evacuated, fistulæ
slit open, and thorough disinfection applied. For the affected
air-passages, iodoform insufflations and antiseptic gases, sprays, and
solutions should be freely used.
Internally, antiseptics such as sulphocarbolates and tincture of muriate
of iron, iodides, and carbolic acid have been largely employed. Whitla
recommends 5 grains of quinia in 15 grains of tincture of muriate of
iron every four hours. Tonics (arsenate of strychnia), and stimulants,
ammoniacal or alcoholic, may be called for. Special symptoms such as
pain, rigors, nausea, vomiting, diarrhœa and profuse perspirations must
be met by suitable remedies. Finally blood serum from healthy cattle or
from immunized animals may be employed subcutem. Pure air and
nourishing, easily digestible food are very essential. Every effort
should be made to check the disease at its outset, as generalized acute
glanders is speedily fatal, and recoveries in chronic cases usually
leave a broken down constitution.
LYMPHANGITIS SACCHAROMYCOTICA (FARCINOIDES: EPIZOÖTICA:ULCEROSA.) FARCY
IN CATTLE.
Geographical distribution and nature: Japan, Northern Europe, France,
Guadaloupe; caseating nodules in skin, subcutem, in mucosæ and
internal organs. In _horse_ skin nodules, and glandular abscesses,
with thick ovoid refrangent bacterium; saccharomyces (Hitt); swellings
first local, then multiple, and general, extending along lymph vessels
to glands (Hitt); along air-passages to lungs, from prepuce or scrotum
to peritoneum (Hitt), or from conjunctiva to other parts in the orbit
(Caparini and Ferner). In _cattle_, multiple, subcutaneous,
nodules—hazlenut to walnut, isolated, hard, painless. Suppurate
slowly. Same saccharomyces (Tokishige, Nocard). May invade lungs with
fatal result in a year. Mallein test gives no reaction. Treatment:
actively antiseptic; open, curette, pack with antiseptic gauze,
sublimate bandages; internally, tonics, antiseptics.
Horses and cattle in certain countries (Japan, Sweden, Finland, France,
Guadaloupe) are subject to a chronic lymphangitis resembling cutaneous
glanders, but associated with the development of bacilli or fungi in the
nodular, caseating swellings in the skin, subcutem, in mucosæ and in
internal organs.
Nocard describes the affection in the horse as characterized by skin
nodules (buttons, boils), which burst and discharge a thick, grumous, or
thin, oily, yellowish or bloody pus. The surrounding lymph plexus swells
up into corded lines, with at intervals nodules or abscesses. The
infection extends to and implicates the lymph glands and general pyemia
may follow. The thick ovoid refrangent, pathogenic, bacterium stains in
Gram’s solution.
In Northern Europe and Asia, Southern Europe and Guadaloupe an analogous
affection is described by Rivolta, Claudio-Fermi, Aruch, Tokishige and
Nocard and Leclainche. Hitt attributes this to saccharomyces. The
infection attacks horses and cattle, entering by sores and abrasions of
the skin of the limbs, or under the harness (back, breast, rump, head).
Confined at first to the point of infection it becomes multiple, being
conveyed from place to place, through the soil, floor, stall, harness,
blankets, brushes, combs, straw, etc., and may extend on the mucosæ. The
wounds fester, forming pus and crusts over a more or less considerable
swelling. In a variable time, (one to twenty weeks) the surrounding
lymphatics become swollen and tender (corded), and nodular swellings
appear on their course which fluctuate, burst and discharge a whitish or
yellowish pus, sometimes oily or slimy. The disease extends along the
lymphatics, invading the lymph glands and even the internal organs.
Tokishige describes cases in which it extended along the respiratory
mucosa, causing constriction of the nasal passages and larger bronchi,
with dyspnœa, and finally, invading the lung. In other cases it spread
from the prepuce, or scrotum, upward along the tunica vaginalis,
spermatic cord and testicle. Caparini and Ferner describe it in the
orbit, affecting the lids, nictitans, conjunctiva and adjacent parts,
with nodules and abscesses. Mazzanti describes the case of a filly which
died with pea-like nodules on the colon, and ulceration, with dirty,
black, purulent centres, and indurated borders. Tokishige describes the
affected cattle as showing a vast number of subcutaneous, hard, painless
nodules, varying in size from a hazel nut to a walnut and covered by
light colored skin. The nodules were isolated and not connected by
swollen, beaded lymph vessels. They encrease and suppurate much more
slowly than in the horse. In three cows microscopically examined he
found apparently the same branching fungus (saccharomyces), as in the
horse cases. The mortality is about 10 per cent.
In the _farcy of the ox_ of Guadaloupe there form subcutaneous nodular
abscesses, with cordiform swelling of the lymph plexus and trunks, often
proving fatal in a year through extension to the lungs. The abscess
breaks, discharging a whitish, creamy or caseous, or grumous contents,
containing a bacillus (Nocard). The abscesses usually appear under the
sternum or belly and later extend to the thighs and legs. In all such
cases the mallein test is inoperative.
The _treatment_ of such cases should be actively antiseptic to destroy
the germ while still local. After opening and evacuating the abscesses,
excise or curette the diseased tissue, or destroy with the actual
cautery, pack the cavities with pledgets soaked in tincture of iodine,
iodized phenol creolin, lysol, mercuric chloride, zinc chloride, or
copper sulphate, or dusted with aristol, iodoform, or iodized starch.
The surrounding swelling, if any, may be painted with tincture of
iodine, or covered with cloths wet with a sublimate lotion or other
antiseptic. Internally, tonics and antiseptics may be given: arsenite of
strychnia, quinia, iron or copper sulphate, sulphites or hyposulphites
of soda or potash.
RABIES AND HYDROPHOBIA.
Synonyms. Definition: Acute, infectious, cerebral disease, of domestic
and wild carnivora, shown by intellectual, emotional, and aggressive
nervous disorder, and extreme nervous excitability. Animals
susceptible: canine and feline animals, biting animals and those
bitten, of all warm blooded kinds; receptivity greatest in carnivora.
Geographical distribution: where population is most dense, trade and
movement most active—north temperate zone. Australia, Tasmania, New
Zealand, Azores, St. Helena immune—protected by quarantine. Islands in
Elbe, places with enforced muzzling. Causes: contagion; inoculation;
rutting; skunk bites; absence of flowing robes (men, children).
Virulent matters: saliva, bronchial mucus, flesh, blood (not in
sheep?), milk, (in advanced stages), nerve tissue. Morbific agent
particulate; filtered liquid noninfecting: blastomyces, bacillus,
found but not uniformly: claims of brain symptoms from each.
Viability; saliva virulent for 11 days; brain 3 weeks at 32° to 63°
F., for months aseptic and in contact with carbon dioxide; water 20 to
38 days; body in grave 44 days; virulence lost by drying in thin layer
yet kennels remain long infecting; glycerine preserves; robbed of
virulence by iodine, citric acid, bromine, chlorine, sulphurous and
mineral acid and cupric sulphate. Bites of men effective to 50 per
cent., protection by clothes, wool, flow of blood, cleaning of teeth
by succession of bites. Infection by licking, sneezing, coughing,
inhaling, feeding. Incubation 15 to 60 days in dog, 20 to 45 days in
horse, 14 to 60 days in sheep, swine and cattle, 14 to 64 days in man.
Prolonged cases doubtful. Symptoms in dogs: change in disposition,
more amiable or morose, dull, apathetic, excitable, unwonted silence
or howling, restless, depraved appetite, swallowing small objects,
searching, tearing sticks or clothes, licking cold stone or genital
organs, hiding in dark corner, dull expression, irritation where
bitten, hoarse voice, rabid howl, eyes follow unreal objects, snaps at
them, listens for unreal sounds, irritability, fury when threatened
with stick or shown another dog, bites without growl, bears master’s
blow in silence, eyes red, fixed, pupils dilated, squinting, lonely
wandering, biting, swimming rivers; restless excitement alternates
with torpor and seclusion, slouching gait when worn out; in _paralytic
form_; weakness, paresis, palsy of lower jaw, hind limbs, body, dull,
prostrate, apathetic; in lethargic form; no fury nor paralysis, but
profound prostration and apathy, no coaxing, threat, punishment not
even another dog will rouse. Paralytic and apathetic forms wind up the
furious; cases with intermittent attacks. Diagnosis: by marked change
of disposition or habit, voice, appetite, any hypersæthesia,
strabismus, watching or snapping at unreal objects, taciturnity, fury
in presence of other dog or stranger, snapping, biting without giving
voice, fury when threatened with stick, open mouth without disposition
to paw it, lack of muscular coördination, paresis, paralysis.
Distinction from lactation anæmia, bone in palate or throat,
dislocation of maxilla, stomato-pharyngitis, cutaneous hypersæthesia,
pharyngeal anthrax, epilepsy, pentastoma, cysticercus, filaria
immitis, nematodes, and tæniæ, auricular acariasis. Symptoms in
_cats_: changed voice, depraved appetite, hiding, restlessness,
irritability, bites, scratches, man or dog. Symptoms in solipeds:
trembling, hyperæsthesia, easily startled, ears and eyes alert,
dilated flashing pupils, roused by dog or stranger, attacks with teeth
and heels, mischievous, pawing, kicking, rolling, rising, straining to
urinate or defecate, neighing, sniffling, snorting, everting upper
lip, grinding teeth, biting, stiffness or impaired control of limbs,
generative excitement, spasms, paralysis, hyperthermia, perspiration.
Symptoms in cattle: irritability, restlessness, alert head, ears,
eyes, squinting, dilated pupils, loud bellowing, lashing tail, or
docility, yet pursues a dog, using horns, heels, (exceptionally
teeth), stamps, paws, has genital excitement, anorexia, spasms,
weakness, paraplegia. Symptoms in sheep and goat: hyperæsthesia,
irritability, genital excitement, fury in presence of dog, stamps,
butts, paws, snorts, bleats, grinds teeth, becomes paretic, and
paraplegic. Symptoms in camels and deer: camels show furious and
paralytic forms, biting and snorting; deer have hyperæsthesia merging
into paralysis. Symptoms in swine: extreme irritability, restlessness,
start at slightest cause or none, tremors, squealing, jerking,
grinding teeth, clenching jaws, bite especially a dog, or not,
weakness, lethargy, paralysis. Symptoms in rabbits and Guinea pigs;
may be furious, more often paralytic. Symptoms in birds: restlessness,
ruffling of feathers, pecking or striking man or dog, or at phantom,
palsy. Symptoms in wild carnivora: lose fear of man, approach and
attack him, are furious and later paralytic. Skunks bite slyly.
Symptoms in man: irritable cicatrix, anxiety, sighing, tremor,
insomnia, bad dreams, fever, thirst, spasms of throat when seeing,
hearing or taking liquids, dyspnœa, retching, vomiting, spasms, roused
by noise, squinting, dilated pupils, mental delusions, reticence,
taciturnity, suspicion, mania, exhaustion, paresis, paralysis.
Lyssophobia, its detection and cure.
_Synonyms._ Canine madness; Rabidus Canis; Lyssa; Lytta; Cynolyssa.
_Definition._ Rabies is an acute, infectious disease, affecting the
cerebral and medullary nervous centres and characterized by
intellectual, emotional, aggressive and other nervous disorders and by
extreme reflex excitability.
_Animals susceptible._ While the disease is seen most frequently in the
canine races (dogs, wolves, foxes and jackals), and in the cat family
(cat, lion), it is liable to spread widely among animals that use the
teeth as weapons of offense, and such as they can readily attack. When
inoculated, all warm blooded animals contract the disease. Thus the
carnivora and omnivora (dog, wolf, fox, hyena, jackal, cat, lion, badger
and skunk and, to a less extent, the pig and horse) may become active
propagators of the infection, which may spread widely among their
herbivorous victims (cattle, sheep, goats, deer, rats, mice, chickens
and pigeons) through their bites. Man suffers mainly through the attacks
of dogs, cats and, in certain localities, wolves or skunks, but he is
also liable to become infected from handling rabid domestic herbivora.
Different genera differ in susceptibility, the receptivity being
apparently greatest in the carnivora.
_Geographical Distribution._ Rabies is confined to no country nor
climate but it attains its greatest prevalence in the north temperate
zone, where there is the densest population and where activity of travel
favors the propagation of infection. The facility for inoculation is the
one determining cause, thus the islands of Australia, Tasmania, New
Zealand, the Azores and St. Helena have never suffered and the first
three exclude the disease by rigid inspection and quarantine. During the
Hamburg epizoötic of 1852–53, the islands in the Elbe escaped though
both banks were ravaged. Again, where the muzzling of all dogs has been
rigidly enforced, as in many German cities and districts the disease has
been practically extirpated.
_Etiology._ Long before the days of pathological bacteriology rabies was
recognized by veterinarians as a disease due to infection alone. Its
absence from the various countries above named, and from South and West
Africa, its rapid propagation in other countries (La Plata, Malta, Hong
Kong) into which it had been introduced for the first time, and its
restriction and disappearance wherever muzzling had been strictly
carried out, had practically settled this question. The development of
the disease in animals which had been experimentally inoculated was no
less significant of this truth.
Other alleged causes are based on secondary factors that favor
inoculation. The alleged evil influence of the hot season (dog days) is
accounted for by the period of _rutting_ of the dog which occurs in
spring, and brings together troops of jealous dogs following individual
bitches and fighting for their favors. This gives a great impetus to the
propagation of the disease which accordingly becomes more prevalent
during succeeding months. The statistics of Bouley show, however, that
the season of its greatest prevalence in France is March, April and May,
that it subsides slowly up to midwinter and encreases again in spring.
Boudin’s statistics show the greatest number of cases in man toward
midsummer which is explained by the long period of inoculation after
bites sustained in the spring, but also because clothing is lighter in
summer and infection more likely to reach the skin, and because the heat
of the weather tends to cause hyperthermia and encrease susceptibility.
The large preponderance of male dogs among the victims of rabies (7:1)
has led to the theory that sex predisposes, but the explanation is
rather that the males bite each other in their jealousy while they
respect the female, the object of their sexual passion. In inoculated
cases, males, females, and castrated contract the affection
indifferently and with equal readiness.
The skunk is found to be infected in certain localities, and it has been
claimed that the affection is native to this animal, and that the form
differs from that which prevails in the dog, but the restriction of the
disease to sharply circumscribed areas in Michigan and Kansas, while
skunks elsewhere show no such malignant quality, demonstrates that this
is but an accidental infection of the family of the Mephitis in a given
locality.
Men and children suffer in far greater numbers than women, the
difference being mainly due to the protection furnished the female by
the flowing skirt, though also in part because of the more frequent
contact of men with dogs.
_Virulent Matters._ In 1813 Gruner and Count Salm demonstrated the
virulent properties of the saliva of the rabid dog. This has been many
times repeated, though as shown by Pasteur, Raynaud, and others,
inoculations with saliva often kill in one or two days by reason of the
presence of other infective germs, or suppuration ensues and destroys
the rabific virus so that oftentimes not more than one in four develops
rabies. Galtier succeeded in inoculating 3 rabbits, 1 dog and 1 sheep
with the juice expressed from the salivary glands, and Nocard,
Leclainche and Peuch have found this to be very virulent. Paul Bert
found the bronchial mucus virulent. Rabies has been frequently conveyed
by consuming the bodies of rabid animals, yet Peuch and Galtier have
failed to convey infection by the flesh. Eckel and Lafosse successfully
inoculated the blood of goat to sheep, of man to dog and of dog to dog.
Yet many of the older observers agree with Peuch and Galtier in
pronouncing the blood non-virulent. Pasteur, Roux, Bujwid, and Helman
failed to obtain virulent cultures from blood. Peuch and Nocard have
found the milk virulent, and Bardach found the same to be the case in a
woman for two days before her death of rabies. In some partially
refractory animals like the sheep, the blood seems to destroy the virus,
as intravenous inoculations have been made with impunity. The
probability is that the blood is habitually non-virulent in the early
stages and in mild cases, but becomes virulent in violent and advanced
cases. Pasteur first showed that the virus has a special election for
the brain and nervous matter and that the central nervous organs are
constantly infecting. Rossi inoculated with a piece of nerve trunk, and
Doubouc and Babes advanced the hypothesis that the virus advances along
the nerve to reach the brain.
It was formerly supposed that the saliva of omnivora and herbivora was
non-virulent but repeated experiment has proved it to be infecting. The
blunder was due to the fact that these animals did not often transmit
the disease by biting. Some writers even deny that rabies exists at all
as an infectious disease. One alleges that the danger of rabies is
“_less than the gallows_.” Experiment shows most conclusively that it is
much more certain when the conditions are fulfilled. One may live a long
lifetime without seeing a genuine case of rabies, but so he may without
seeing leprosy or plague, and he is no more entitled to doubt their
existence than he is the existence of Manila, or of the other side of
the moon.
_Morbific Agent._ The actual factor which produces rabies is not
certainty known so that we cannot speak of its bacteriology. That it is
due to a specific particulate germ is now indisputable. Paul Bert and
Nocard filtered the virulent fluid through plaster and found the clear
fluid that had passed through non-virulent. Rivolta, Babes, Bouchard and
Peuch severally passed a solution of the rabific brain matter through a
Chamberland filter and found the clear filtrate harmless. The virulent
agent is therefore not a body in solution but a solid (organism) which
is held back by the filter. Hallier, Klebs, Galtier, Gibier, Pasteur,
Fol, Babes and Dowdeswell have respectively attempted the cultivation
and inoculation of organisms found in rabific liquids but none has stood
the test of further experiment. Memmo found a blastomyces in the brains
of six rabid rabbits and one hydrophobic child. It stains with the
aniline dyes but not by Gram’s method; when thrown into the peritoneum
of Guinea pigs it produced clonic spasms and death in 24 hours, and in
the dog, after an incubation of 8 days caused emaciation, salivation, a
disposition to bite, paralysis of the hind limbs and death in 48 hours.
Bruschettini using agar or bouillon, containing lecithin or cerebrin and
defibrinated dog’s blood, inoculated with pieces of the brain of an
inoculated rabbit, obtained in 24 to 36 hours a group of small
transparent drop-like colonies at first microscopic, but becoming larger
with each new culture on fresh media. These colonies contained a very
small, short, thick bacillus, which stains readily in Ziehl’s
carbol-fuchsin, and then presents a central clear band giving the
appearance of a diploccus. In fluid media spherical forms are produced,
but in fresh cultures the diploccus aspect reappears. Injected
subdurally in rabbits it gave rise to what appeared to be paralytic
rabies and could be inoculated from animal to animal, with similar
results. It failed to grow in the usual culture media from which the
brain products are absent, thus fulfilling the conditions, of a microbe
the point of election of which was the nerve cells. Marx who has sought
for Bruschettini’s organism in 60 cases of rabies has only once found
anything resembling it and concludes that it was merely a contaminating
organism, which caused a paralysis (Centr. f. Bacter. 1896.)
_Viability of the poison._ Galtier found that the virulent saliva
remained potent for 11 days if preserved from drying. It persists for 3
weeks in the brain and medulla kept at 0° to 12° C., for a month in
sealed tubes, or for several months if protected against septic microbes
and in contact with carbon dioxide.
In water it is preserved for 20 to 38 days so that water soiled with
saliva may easily become a means of infection. In graves it has been
found virulent as long as 44 days after burial so that in medico-legal
cases results may be obtained by exhuming a suspected animal (Galtier).
Haubner found that drying the saliva in thin layers rendered it
non-virulent and Pasteur has shown that the rabbit’s medulla loses its
virulence in 14 or 15 days when dried in contact with air, and apart
from putrefaction. Such laboratory results must however be qualified by
the facts recorded by Blaine, Youatt and others in which hound after
hound died of rabies from living in a dry kennel in which a rabid animal
had preceded them. Until we know something of the living germ itself of
rabies, it is unwise to infer too positive results from experiments on
that microbe, in what may be but one stage of its existence.
The virus is very resistant to cold, having survived a temperature of
−60° C. (−76° F.) for several hours (Roux), −10° C. (−14° F.) for ten
months (Jobert). Virulence is destroyed however by a temperature of 48°
C. (118.4° F.) in five to twenty minutes (Galtier). Light destroys the
virulence in 14 hours at 30° to 35° C. (Celli), but encreased pressure
has little effect on it (16 atmospheres, Nocard and Roux).
Glycerine at room temperature preserves the medulla in its full potency
for four weeks, but destruction ensues if it is heated (Protopopoff). An
aqueous solution of iodine (6:100) destroys the virulence (Galtier), as
does also citric acid, bromine, chlorine, sulphurous acid, the mineral
acids and cupric sulphate.
_Ratio of successful inoculation to bites of rabid animals._ As rabies
is usually transmitted by the bite, it is well to note that not all the
bites of rabid animals are effective. Of 183 dogs confined with and
bitten by a rabid dog 91 contracted rabies; of 73 cattle bitten 45
became rabid; out of 121 sheep bitten 51 succumbed and of 890 persons
bitten, 428 took hydrophobia. Of 440 persons bitten by rabid wolves 291
contracted the disease. The escape of such a large proportion is
variously accounted for. Wolves naturally attack the face, throat or
hands where there is no protection by clothing, and inoculation is
therefore much more certain. Dogs, especially in cold weather usually
bite man through the clothes which wipe off the virus from the smooth
conical teeth before they reach the skin. Long haired animals are often
protected in the same way. In other cases the bite is sustained on a
very vascular part and the free flow of blood washes out the poison. In
still other cases the rabid animal making a number of snaps in rapid
succession comes to the last with the teeth wiped clean and harmless.
Again the prompt washing or cauterizing of the wound tends often to
protect against infection.
Under favorable circumstances however every bite infects, and the writer
has seen six animals, bitten in the same stable, all contract rabies,
while a man bitten through the coat sleeve by the same dog, and
cauterized an hour later entirely escaped. If the bites are multiple,
deep and irregular, the danger is greater.
The licking of wounds is an occasional mode of infection, the rabid dog
in the early stages of the disease sometimes showing an unusual
disposition to fawn upon his owner.
Again particles of saliva may be projected by sneezing or otherwise and
lodge on sores, or on the mucosa of the nose, eye or lip so as to cause
infection. Galtier has conveyed the disease experimentally to rabbits in
11 cases out of 75 by making them breathe the atomized infecting liquid,
or by dropping it into the nose. In the same way he infected Guinea pigs
and sheep.
Galtier and Bujwid have conveyed the disease, exceptionally, to rabbits
and rats by feeding infecting emulsions. Galtier has also produced
rabies in ⅒th to ⅓d of the cases operated on by instilling the virus
into the eye.
_Incubation._ The duration of incubation varies with the species,
individual, the seat and character of the bite, the amount of virus
instilled, the potency of the virus, the age, size and weight of the
subject, the excitement of _rutting_, climatic or weather vicissitudes,
fatigue, and nervous or febrile disorders.
In the _dog_ incubation ranges from 15 to 60 days, and perhaps 4 to 6
months. It is claimed to have lasted a year but this is somewhat
doubtful. In _cats_ it has varied from 15 to 60 days.
In _solipeds_ it ranges usually from 20 to 45 days. The extremes stated
are 15 days and 20 months.
In _cattle_ it ranges from 14 to 50 days (exceptionally 70 days), in
_sheep_ and _swine_ from 14 to 60 days. It has been claimed to have
lasted 4 months in swine and 5 months in sheep.
In _rabbits_ subdural inoculation has an incubation of 15 days,
shortening in 25 removes to 8 days, and finally to 6.
In _man_ incubation is alleged to be even more varied. The rule is from
14 to 64 days, but it is claimed to have been as short as three days and
as long as 1 to 12 years (Chabert). In the human being, however, there
is always the danger of the disease caused by simple dread (lyssophobia)
and until these protracted cases can be verified by successful
inoculation on the lower animals, they must be held as extremely
doubtful. The Montpellier cadet has been often quoted who left, a few
days after he had been bitten, spent ten years in Holland, then
returning to the school and learning for the first time that his fellow
cadet, who had been bitten by the same dog, had gone mad, he too became
rabid without loss of time. Such cases have often been cured by moral
suasion and have been seized upon to corroborate the heresy that there
is no such thing as genuine rabies in man.
Any incubation, in man or beast which has exceeded 40 days should be
considered as doubtful, until certified by the successful inoculation of
rabbits or other small animals. For casual inoculations the incubation
rarely varies much from the time embraced between 16 and 30 days. It is
abridged by a special receptivity; by an overdose of the poison; by the
inoculation of a virus of unusual potency; by the youth of the animal
inoculated; by great heat of the weather; by all forms of violent
excitement; by _rutting_; and by the inoculation of the virus on the
head and above all on the cerebral meninges. By this last method
incubation may be reduced to 6 days.
_Symptoms in Dogs._ In dogs as in other animals rabies is manifested in
two great types: the _furious_ and the _dumb_ or _paralytic_, which,
however, usually succeed each other in fully developed cases. Yet the
_furious_ phenomena may be entirely omitted, and again the victim may
die in the early _furious_ stage so that the paralytic does not appear.
The prominence of one form over the other is to some extent determined
by the germ derived from a previous case of the same kind or by the
family, temperament and habits, bull dogs and hounds being specially
subject to the furious type, and house and pet dogs having rather the
paralytic form.
The _premonitory symptoms_ are in the main the same for both types, and
as these may enable us to recognize the disease before the period of
extreme danger, it is especially important that they should be well
understood.
Some marked change in the disposition or habits of the animal is the
first obvious variation from health, and in a district or country where
rabies exists any such change should be the warrant for instant
seclusion of the dog before there is any disposition to bite. The
unwonted habit may be of almost any kind. The lively, amiable dog may
become suddenly dull, apathetic or taciturn; the quiet, unexcitable dog
may become unusually affectionate, fawning and demonstrative, licking
the owner’s hands and face and perhaps infecting him before any
suspicion is aroused. Sudden capricious changes from fawning to apathy
or sullenness, or the opposite, should be dreaded. The noisy dog may
become suddenly silent; while the silent dog may take to howling without
apparent cause. A great restlessness, watchfulness or nervousness, a
tendency to start at the slightest sound, and a disposition to move at
frequent intervals in search of an easier position or place to lie in,
are most dangerous symptoms. A morbid appetite, with a disposition to
pick up and swallow all sorts of nonalimentary objects (straw, thread,
cord, paper, pins, nails, coal, marbles, pebbles, cloth, earth, dung or
urine), in a mature dog is most suggestive. Searching around, scraping,
tearing sticks, clothes and other objects to pieces, licking of smooth
cold stone or metal, of his penis, or of the generative organs of a
bitch, are often early phenomena. The dog may hide in a dark corner,
going to sleep and grumbling or growling when disturbed. He may make
night hideous with his howls, _baying at the moon_. He may stand with a
dull, melancholy, hopeless expression of countenance, as if beseeching
his master for relief from his nameless suffering. But as yet there is
no disposition to bite. The dog still responds to the call of the
master, but with dulness and apathy, in marked contrast with his usual
prompt, alert and loving response. There may be congestion, itching and
irritation in the seat of the bite, and it may be licked, scratched or
gnawed until raw, tender or bleeding. An early change in the voice may
be noticeable. There is at first a certain hoarseness, which gradually
develops into the pathognomonic rabid howl which is quite recognizable
at a distance. The dog turns his nose upward, and with open mouth, emits
a howl which, at first hoarse and low, rises into a shriller and higher
note before completion and which may be repeated several times without
closing the mouth. It is not an ordinary howl but rather a cry of
distress, and, to the educated ear a grave note of warning. Sometimes
the dog is dumb from the start.
Close observation will often detect evidence of mental delusions and
hallucinations even at this early stage. The apparently sleeping dog
suddenly starts up with an air of suspicion and excitement. His eyes may
turn after phantom flies or other objects at which he will presently
snap. He moves hither and thither with a curious, inquisitive air,
searching in dark corners, or under curtains or articles of furniture
for some imaginary object. He may stand in attentive attitude listening
to fancied sounds, and then bound in that direction in spite of an
obstructing wall or utensil. If recalled to reality by his master’s
voice his healthy attitude and affection may be completely though
temporarily restored. He may compose himself to rest or sleep, and soon
again start a victim to further delusions.
The _furious stage_ is ushered in by a more pronounced manifestation of
the above symptoms. The rabid howl is more frequent and characteristic.
The insomnia and the restless movements, change of place, searching,
scratching or tearing are likely to be more prominent. The delusions and
the watching or snapping at phantoms are more marked. The causeless
sniffing and scraping may imply disorder of the sense of smell. The
exalted hyperæsthesia and reflex excitability is usually a most marked
feature, frequently modified by a sinister, inimical or malevolent
disposition. Some subjects show evidence of intense itching, most marked
perhaps in the seat of the wound; others are abnormally sensitive to
currents of cold air; they start at the slightest noise, a flash of
light, a touch, or the approach of a stranger. A paroxysm of fury may be
caused at once by shaking a stick at the patient, but, above all, by the
test of presenting a dog before his eyes. He at once rouses himself and,
with flashing eyes, dashes himself on his supposed enemy and bites
viciously, but without bark or growl. The sudden and mute attack is
pathognomonic. But there may be symptoms suggestive of some
hypoæsthesia. A blow from the dog’s master is usually borne in silence.
The animal shrinks from the blow but does not yelp nor howl. During a
paroxysm he will lacerate his gums or loosen his teeth by biting on a
stick or iron bar; he will even seize a red hot bar without shrinking.
He will often gnaw his limbs or body so as to expose and even lacerate
the muscles, driven by the pruritus, or the insatiable disposition to
bite. Yet he has still an instinct of self preservation, retiring from a
light, or blazing brand, and seeking to evade the tongs used to seize
him.
The eyes assume a remarkable expression. They are often fixed, and at
times the pupils are widely dilated allowing the reflection of light
from the brilliant tapetum lucidum, resembling flashes of fire, and
adding greatly to his ferocious appearance, and the sense of terror that
he inspires. The conjunctiva is congested, of a dark red and the general
expression of the eye is very striking. The soft, trusting, affectionate
eyes may still for a moment meet those of the loved master, but there is
in them a dull, hopeless, anxious and suffering expression, which
appeals for pity and should be viewed with dread. To others there is
likely to be less of the affectionate appeal and more of the sinister,
suspicious, resentful and malicious expression. To the stranger,
therefore, the eye may be a better guide than even to the owner.
Squinting of the eyes and closure of the lids for a few seconds are not
uncommon. As the disease advances the dilatation of the pupils is more
marked, indicating the paralysis of the optic nerve.
In this stage the disposition to wander is characteristic. The rabid dog
leaves his home and wanders off a long distance, say ten or twenty
miles, snapping in his travels at man or beast that may irritate him,
returns dirty and exhausted, and seeks anew his dark place of seclusion,
or he may snap at and bite even his master. To those who come in contact
with him at this time the dog is especially dangerous from his extreme
irritability though weak and exhausted.
If the wandering rabid dog meets a strange dog he attacks him and bites
without growling or barking. If the bitten dog does not yelp nor
retaliate, but simply flees, the rabid animal moves on, but if he bites
back, or howls, he worries him, rolling him over and biting again but
always in silence, in marked contrast with an enraged but healthy dog.
If he comes up with a herd of cattle or pigs or a flock of sheep or
fowls, the result is similar. If they remain perfectly still they may
possibly entirely escape, but if they scamper off with noise as usually
happens, he rushes at them and bites one after another, so that in a
confined yard or park all may suffer. A man meeting the dog increases
his danger by making an outcry, whereas if he remains perfectly quiet he
may possibly escape. Bouley says that a canine attendant is, in a sense,
a measure of protection to a man, as the rabid dog attacks first the
animal of his own species, giving the man a chance to escape.
In his wanderings the rabid dog will swim rivers, having _no dread of
water_, just as at home he will plunge his nose in water though unable
to swallow. When abroad in this way he exhausts himself by his paroxysms
and may perish in one of them, or he may meet his death from man or
animal. He may in his exhausted state seek a dark secluded place where
he may remain for a time and renew his travel later, or he may pass into
the paralytic condition and gradually sink.
When shut up, and his vagrant disposition curbed, the paroxysms are
liable to appear intermittently, a period of torpor and quiet
alternating with one of restless movement, searching, scraping, howling,
biting of any animals within reach and later of men, beginning with
strangers. A paroxysm can usually be roused by shaking a stick at him
and always by presenting another dog.
There is sometimes a difficulty in deglutition, the dog acting as if he
had a bone in his throat which he was trying to dislodge, and fatal
bites have been sustained during well meant attempts to remove the
hypothetical bone. This bears a resemblance to the pharyngeal spasms
which are such a marked feature in the hydrophobic man. But it is not
roused, as in man, by the sight or sound of water. On the contrary,
water is sought and often swallowed at first and even, exceptionally,
throughout the disease. He may even take his usual food for a time. The
bowels are usually torpid, and any fæces passed are black and fœtid.
Diarrhœa may set in later.
In the early stages the rabid dog walks or trots like any other dog. It
is only when exhausted by wandering, or violent paroxysms, or both, that
he droops his head and ears, hangs the tail between the legs, and
slouches along with arched back, and unsteady, swaying limbs. The
appearance of these last symptoms implies advancing debility and
paresis, and the near approach of paraplegia. The symptoms may, however,
be temporarily relieved by a period of seclusion and quiet.
In _dumb_ or _paralytic rabies_ the striking peculiarity is the omission
of the preliminary furious stage, and the disease merges at once into
paralysis after the premonitory symptoms. In these cases the early
nervous symptoms tend to prostration, weakness and dulness or even
stupor, there is no disposition to escape, but rather to seek seclusion
and quiet, there is rarely howling and then only at first, and soon
there is paralysis of the masseters and dropping of the lower jaw, and
there is neither ability nor desire to bite. From this the paralysis
extends to the hind limbs and then to the fore limbs and trunk. In other
cases one limb is the first to suffer, followed by the face, limbs and
body. The most prominent feature is the widely opened mouth, the
flaccid, hanging tongue and drivelling saliva. The buccal mucosa, at
first red and moist, becomes bluish, dry and powdery. The eyes are dull,
mournful, suffering or altogether without expression and the pupils are
usually widely dilated. The hind limbs are usually utterly helpless and
often the fore ones as well, the prostration is extreme and the patient
lies quiet and helpless until released by death in two or three days.
A third form, known as the _lethargic_, is a modification of the
paralytic. There may be neither delirium nor marked paralysis, there is
no drooping maxilla, pendant tongue nor stringy, hanging saliva, but
only a profound, nervous prostration and complete apathy. The patient
curls himself up in some dark, quiet corner and cannot be roused by
coaxing or punishment, by hunger or thirst. In this, as in the dumb
rabies, the common test of presenting another dog fails to rouse
excitement or paroxysm. If left undisturbed, these patients may live to
the tenth or fifteenth day.
Beside the typical forms there are all intermediate grades, inclining
more or less toward the furious, or the paralytic or lethargic. Galtier
mentions cases that showed aphasia, scarcely any disposition to bite,
swaying movements of the body and limbs, muscular incoördination, tucked
up, tender abdomen, rolling the body like a barrel, and marked dyspnœa.
Others show at first a slight disposition to bite which is quickly
checked by a very early paralysis of the masseters. In still others the
attempts to bite are still seen after dropping of the jaw, but though
still moved, it cannot be completely closed.
In exceptional cases rabid dogs have shown _intermissions_ of apparent
soundness extending over eight days (Youatt), two months (Pasteur), or
even six months (Perrin). Rare as these are they must apparently be
accepted, and must qualify to some extent the trust reposed in
immunization.
_Diagnosis._ The early diagnosis of rabies in the dog is of supreme
importance as enabling the owner to destroy or seclude the dangerous
animal before he has developed the disposition to bite and to propagate
the disease. If the dog himself is known to have been bitten, every
premonitory symptom should be carefully looked for and critically
studied. Any change in the general habit, unusual liveliness or dulness,
restlessness, or somnolence, unwonted affection or taciturnity, special
watchfulness with vision, or hearing, change in the character or tones
of the voice or the disposition to use it, propensity to swallow foreign
nonalimentary bodies, retching, vomiting or costiveness, propensity to
hide away in a dark corner or to leave home and disappear for a day or
more, disposition to gnaw and tear up wood or clothing, or hyperæsthesia
affecting any of the senses should be carefully noted. Note especially
any exaggeration of the generative instinct, any strabismus, or redness
of the eyes, any turning of the eyes or head after imaginary objects or
snapping at them, any disposition to anger or attack when another dog or
cat is presented and any disposition to growl at or to bite a stranger.
This tendency to anger and resentment though not always present is
usually a symptom of the very greatest value. If a dog is known to have
bitten or attempted to bite any person or animal he should be tied or
shut up in a safe place for four days at least, under veterinary
supervision, and set free only on condition that no symptoms have
developed at the end of this period. A hasty decision that a suspected
dog is not rabid must lay a veterinarian open to the most serious
charges, in case rabies occurs in man or beast from the bites.
Diagnosis is less difficult after the paroxysmal stage has set in. Then
there is the extreme irritability and hyperæsthesia, the appearance of
reflex spasms of the pharyngeal muscles and chest under the influence of
any peripheral excitement, the derangement of the senses, the dilated
pupil, the flashing eye, the squinting, the taciturnity and the
propensity to bite. Later still the lack of coördination of movement or
the paralysis, especially of the hind limbs and of the jaws.
The symptoms may be simulated by those of some other diseases. Thus the
bitch which has been exhausted by lactation may show delirium with
taciturnity and a disposition to snap. The dog, which is habitually
struck or threatened by passers by, may acquire a sinister look and a
disposition to bite on every occasion. The presence of a bone or other
foreign body fixed between the upper molars, and various injuries of the
jaws, teeth or throat may cause inability to swallow, change of the
voice and a morose disposition and expression. In such cases there may
be vomiting, rubbing the jaws with the paws as if to disengage something
and salivation, but there is neither delirium, fury, muscular weakness
nor paralysis. In paralytic rabies on the other hand, along with the
open mouth and drivelling saliva, there is no disposition to paw the
mouth nor face, the buccal mucosa is not simply red but of a deep
violet, and there is attendant weakness or paralysis of the hind parts.
Galtier has seen inability to swallow and dropping of the lower jaw from
violent stomato-pharyngitis, and from dislocation of the maxilla.
Great tenderness of the skin from inflammation due to blistering or
caustic agents or from rheumatism may cause such alert apprehension and
disposition to bite in self defense that it may simulate hyperæsthesia
of rabies.
From pharyngeal anthrax and violent angina, rabies is distinguished by
the extreme exaltation of the special senses, the marked hyperæsthesia
and reflex excitability, and, as in the other diseases mentioned, by the
perfectly lucid intermissions. Epilepsy is not to be roused by sudden
noise, movement nor attempts to swallow, it is not associated with
hyperæsthesia and in the _haut mal_ the spasms affect the muscular
system more generally. A disposition to bite, and spasms and other
nervous symptoms, resembling to some extent those of rabies, have been
seen in cases of pentastoma in the nasal sinuses, cysticercas in the
brain, filaria immitis in the blood, nematodes, and tænia in the bowels,
and auricular acariasis, but there is no such hallucination nor visual
delusion, no alteration of the voice, no cutaneous anæsthesia, no
exalted reflex excitability. Cadeac finds rabiform symptoms with
disorders of the special senses in animals dosed with various essential
oils, but the odor of these essences about the mouth and in the breath
would serve to distinguish.
_Symptoms in Cats._ The disease makes a rapid progress, and often ends
in death in three or four days. There is a marked change of voice, the
calls being hoarse and bass, having been compared to that of a cat in
heat. As in the dog, there is a disposition to pick up and swallow
objects that are in no sense food, perhaps even its own urine or fæces.
There is a great tendency to hide away under furniture or in secluded
corners so that the malady may be far advanced before anything is
suspected. If seen the patient shows restlessness and frequent movement,
with a marked excitability under noise or other disturbing influence.
Any disturbance may arouse a paroxysm, accompanied by occasional wide
dilatation of the pupils, with flashes from the bright carpet in the
vitreous chamber, and the patient may spring at human beings and bite or
scratch the hands, face or other uncovered portion of the body. It shows
the same disposition to bite small animals, and especially dogs. A
glairy often frothy saliva is found in the mouth and often around the
lips. As the disease advances and paresis sets in, the cat usually
crawls into some dark secluded corner and there dies.
_Symptoms in Solipeds._ These may vary much in different cases but the
leading characteristics, as seen in the dog, are prominent also in the
soliped. There is marked restlessness, trembling, and extraordinary
hyperæsthesia, as seen in starting at sounds, sudden flashes of light or
other causes of disturbance. The ears are held erect and watchful for
sounds; the eyes are red and mostly vigilant with at times pupillary
dilatation and flashing. The sight of a dog rouses him instantly to
attack it with teeth and heels. A stranger is liable to be similarly
treated though the horse is still docile and kind to his keeper. There
may be itching of the skin and above all of the seat of the bite. During
a paroxysm the movements are usually violent, dangerous and even
mischievous. There is constant restless movement, pawing, kicking the
ground, the stall or attendants, lying down, rolling, rising, straining
to urinate, or defecate, eversion of the rectum, shaking the head,
muffled neighing, sniffing, snorting, everting of the upper lip,
grinding of the teeth, or biting. In the absence of such paroxysms
deglutition may be difficult, and the appetite depraved, the patient
preferring earth or manure to the natural food. With spasms or paralysis
of the pharynx, the food may be returned through the nose. In some cases
a stiffness or impaired control of the limbs has suggested inflammation
of the feet. In the uncastrated male and female generative excitement is
the rule, the protrusion and erection of the penis, the swelling and
rigidity of the clitoris, with frequent straining to pass water, the
whinnying of the animal for its mate; attempts at copulation and even
ejection of semen may be observed. The seat of the bite may be red,
angry and itchy, so that the horse rubs, nibbles or gnaws it, often
breaking it open anew. There is usually ardent thirst, and no dread of
water, even when swallowing is difficult or impossible.
During a violent paroxysm the horse often bites the halter, blanket,
manger, rack or stall, seizes the adjoining horse with his teeth, or
gnaws, or tears strips of skin from his own shoulder, breast or limbs.
In the same way he uses his feet with the most evident purpose of
injuring man or beast that may approach him, or he breaks down his
stall.
Even at an early stage there may be spasmodic movements of the eyes,
face or body, and later there appear signs of paresis, often commencing
in a hind limb and extending to paraplegia and general paralysis.
Sometimes paralysis begins in the muscles adjoining the seat of the
bite. The temperature, at first normal, may rise to 104° F. in the
advanced stages, breathing and pulse are greatly accelerated, and the
skin may be bathed in perspiration. Spasms are not entirely superseded
by paralysis, and death often takes place during a convulsion, from the
fourth to the sixth day. In apoplexy death may ensue in one day.
Cases in which paralysis is not preceded by a furious stage are not
uncommon in horses.
_Symptoms in Cattle._ Cattle are frequent victims of rabies, which
assumes mostly the furious type, yet in certain outbreaks the paralytic
or lethargic form predominates. There is first a strange irritability
and restlessness, very unlike the habitual quiet disposition of the
animal. The head is raised, the ears alert, the eyes prominent, red,
fixed, with occasionally widely dilated pupils and brilliant flashes
from the tapetum lucidum. Sometimes they roll or squint. They may appear
wild and ferocious or dull and hopeless. Loud and terrified bellowing is
not uncommon, switching of the tail, drivelling of saliva, and
exceptionally there are attempts to bite. More commonly the natural
weapons of offense are employed, the animal kicks, stamps, paws and,
above all, tries to gore man or beast, but especially any dog which may
appear. They even make such attacks on purely imaginary beings and
without any real, tangible enemy present. The bull, cow or heifer
present the usual signs of genital orgasm. Appetite is lost or depraved
and rumination arrested. Pharyngeal spasms or paralysis is not uncommon,
and signs of colic with frequent defecation may be seen. Violent
paroxysms are easily roused by the sight of a small animal and
especially of a dog. In these attacks the animal may break his horns or
teeth or otherwise injure himself. Sometimes the infection wound becomes
irritable, itchy and red or even abraded and raw by licking.
The animal becomes rapidly exhausted and even emaciated by the violence
of the paroxysms, and paresis sets in with dragging movements of the
hind limbs, which advance to paraplegia and general paralysis. Rolling
of the eyes, squinting and pupillar dilatation may be present. Death
usually takes place from the fourth to the sixth day.
The purely _paralytic rabies_ is not uncommon in cattle. There may be
persistent yawning or other sign of nervous exhaustion or depression,
halting on one or more limbs, usually behind, which advances to complete
paralysis. In other cases the symptoms are those of mental dulness, and
profound lethargy with gradually advancing emaciation. In paretic and
paralytic cases the characteristic paroxysms on presentation of a dog
may be absent.
Ladague claims to have seen intermittent cases with an interval of 27
and even 36 days.
_Symptoms in Sheep and Goat._ In these there is the same regular
succession of symptoms through intense hyperæsthesia and excitability,
fury and genital excitement to the terminal paralysis, or the palsy may
set in early without premonitory violence. Among the marked features
have been noticed, a change of expression, the pupils dilate, eyes
flash, they lick or mount their fellows, they lick or rub the bitten
part, snort, stamp or scrape with the fore feet, setting themselves in
the attitude of attack, they may butt other sheep, fowls, and other
animals, above all dogs, or they may deliver the attack in the air only,
at some phantom enemy. They may bleat hoarsely or brokenly, grind the
teeth, or work the jaws with the formation of froth about the lips.
Galtier says they may even attempt to bite. Sooner or later weakness of
the limbs, muscular incoördination, swaying and staggering bespeak
enervation, the sheep lies constantly, and if raised stands with
unsteady semi-flexed limbs, has trembling or convulsions and dies
paralytic in from two to five days. Death has been delayed till the
twelfth day (goat) or thirteenth (sheep). In some cases paralysis has
been present from the start, the subject lying prostrate from the first.
_Rabies in the Camel and Deer._ In Algiers camels are often times bitten
by rabid dogs and contract the disease showing both furious and
paralytic symptoms. They are especially dangerous because of their
propensity to bite, and to scatter the virulent product by sneezing.
In England rabies has prevailed extensively in parks of deer, which shut
inside high walls have been bitten remorselessly by rabid dogs that had
gained admittance. The symptoms of hyperæsthesia and paralysis followed
the same general course as in other animals.
_Symptoms in Swine._ Rabid pigs are usually very restless, excitable and
sensitive to all causes of disturbance. They will hide under the litter
in the darkest corner but soon start without apparent cause, turn around
and lie down again, or they bound up with grunt or scream and rush off
as if pursued, push or leap against the wall, stand with ears pricked as
if listening, and start violently at any noise or a flash from a
lantern, trembling, squealing, or having muscular jerking. The eyes are
at times fixed, or may roll, squint or flash from pupillary dilatation.
The voice is hoarse, deglutition difficult, there is frequent clenching
of the jaws, or grinding of the teeth, and frothing around the mouth.
The victim may tear with his teeth the boards of his pen, or gnaw pieces
of wood, he may swallow wood, pebbles or earth, and plunge his face in
water or other liquid without fear or apparent dread or dislike. The
disposition to bite may be viciously shown, and he may strike
dangerously with his tusks, while in other cases it may be entirely
absent. Peuch quotes cases in which no paroxysm was aroused by the sight
of a dog, and others in which the pig would rise and grunt without
showing any desire to bite.
Sows will sometimes bite or devour their offspring during a paroxysm,
yet nurse and care for the survivors during the intervals.
Emaciation, weakness, exhaustion, lethargy and paralysis appear early,
the victim remains down, or, if raised, moves weakly and unsteadily and
no longer pays attention to noises nor blows. Death may ensue from the
first to the sixth day.
_Symptoms in Rabbits._ Experimental cases in rabbits are now very common
and usually assume the paralytic or lethargic type, there is weakness in
the hind parts, advancing in a few hours to paraplegia, the fore limbs
may be used for a time while the hind are flaccid and dragged behind, or
the animal lies on the sternum and belly with the head sunken and
resting on the feet, or he lies extended on his side, in a state of
insensibility. In the early stages he may still masticate, with froth
collecting on the lips, but there is difficulty in swallowing. If a foot
is pinched it is drawn up often with a cry. The bowels are torpid though
a few small, round, hard pellets are sometimes passed or a little urine.
Incubation is shorter than in the dog, and the virus retains this habit
when inoculated on other animals.
In the experimental cases in the Anti-rabic Institute in St. Petersburg,
Helman found that the rabbits inoculated with virus from dogs having
furious rabies, contracted furious rabies, while those inoculated from
the less furious type of street rabies had the disease in the dumb form.
_Symptoms in the Guinea-pig._ In this animal as in the rabbit the
disease has been mainly seen in the experimental form, and has assumed
the paralytic type. It trembles, moves stiffly or weakly, lies most of
its time and passes rapidly into paralysis. There is usually no tendency
to bite, yet Peuch in a case of intraocular inoculation from a rabid cat
observed the most violent excitement, loud hoarse screaming, bounding in
different directions, biting of the wires of the cage, and other
manifestations of violent rabies. In both forms there are liable to be
convulsive movements of the jaws, accumulation of frothy saliva, and a
free discharge of urine.
_Symptoms in Birds._ Chickens bitten by mad dogs have been seen to prove
restless, erecting the feathers and moving aggressively toward man or
dog or phantoms of their imagination and attacking with bill or spurs or
both. This, however, rapidly advances to paralysis and death. In cases
due to intracranial inoculation on the other hand, somnolence, lethargy,
or coma appeared early, and was quickly followed by paralysis. This
affects especially the legs and neck. Recoveries are common and the
animal is thereafter immune. Subsidence, with complete intermission of
symptoms, is more common than in rabbits, the disease reappearing later,
and perhaps finally ending in recovery.
_Symptoms in Wild Carnivora._ The rabid wolf, fox, jackal, hyena,
coyote, ferret, polecat and skunk lose their fear of man, and approach
and attack him either in field, village or city. The disease has its
furious and paralytic stages as in the dog, and the animals attack
according to their nature, wolves being dangerous from flying at the
face and throat, and skunks from stealing up and biting without warning.
_Symptoms in Man._ After the period of incubation prodromata may be
present, or there may be suddenly and without any premonition, violent
spasms of the pharynx and inability to swallow. The premonitory symptoms
when present consist in irritability of the cicatrix which becomes red
or blue, swollen, itchy or pricking, and an aura or shooting pain may
extend from this toward the heart. There is anxiety, sighing, tremor,
restlessness impelling to frequent change of place, insomnia,
disagreeable or painful dreams, weariness, and gloomy forebodings. The
face is pale and drawn, and the eyes wander or have a look of
apprehension. There is some fever and often marked thirst, and the
attempt to swallow rouses slight spasm or a sensation of tightness in
the throat. The fauces, pharynx and eyes are congested, reddened and it
may be swollen. Pulse and respiration are both quickened, the
inspiration being often prolonged and sighing, and the expiration
sobbing. At first the intellect is unimpaired; there is no illusion nor
hallucination.
In cases in which premonitory symptoms are lacking, violent spasms of
the throat and chest are commonly roused by an attempt to drink and this
is so painful that the patient cannot again be induced to try. After
this any suggestion of drinking, the offer of drink, the noise of
trickling water, the sight of water, the sight of a vessel in which the
water was contained, or even of a clear shining surface of glass or
metal is likely to bring on a paroxysm. This hydrophobia is peculiar to
man being rarely seen in rabid animals. During a paroxysm dyspnœa is
extreme, respiration is gasping or sighing, and in the attempt to
dislodge the tenacious mucus which is present in the throat, hoarse or
shrill inarticulate sounds are emitted which have been supposed to
resemble the bark of the dog. There is a sense of closure of the throat
and of rising of the stomach, and retching or even vomiting may ensue.
Hyperæsthesia, reflex irritability, and exaltation of the special
senses, now become extreme, so that a paroxysm may be brought on by the
slightest disturbance, a current of air, a bright light, the rustling of
a dress, the noise of a footfall, the noise even of talking, or a slight
touch. The “tendon reflex” and skin reflex are often much encreased.
During a paroxysm there are muscular trembling and clonic
spasms,—sometimes opisthotonos. The intervals of complete relaxation,
however, serve to distinguish from tetanus. The face is red and drawn,
the eyes congested and sometimes squinting, the pupils dilated and the
expression one of suffering, apprehension and horror. Mental disorder
appears sooner or later, the speech is disconnected, with indication of
delusions from which the patient may at first be recalled by the
attendant. There is, however, a constant disposition to be reticent,
morose and above all, suspicious, as shown by the absence of a direct
look, and the frequency of side glances as though in expectation of a
hidden danger. This may even rise to mania, the patient charges those
about him with having caused his sufferings, or with conspiracy to
injure him, and he may seek to defend himself with hands, feet, teeth or
any available object. The necessary restraint aggravates and prolongs
the attack. On its subsidence the patient collects his scattered senses,
regrets, apologizes, and warns against future occurrences of the same
kind which he realizes to be beyond his control. Sometimes the delusions
continue during the remission as well. Sexual excitement is common in
man as in animals.
The convulsive paroxysms may last ½ to 1 hour, and they tend to encrease
in duration and force. A violent paroxysm may cause sudden death from
asphyxia or apoplexy.
Sooner or later exhaustion and paresis appear. The convulsions become
gradually weaker, the reflex irritability and hyperæsthesia abate, and
the patient may become once more able to swallow, but an ascending
paralysis, beginning in the limbs spreads over the body and death occurs
in from one to eighteen hours. In the paralytic stage there may still be
slight jerking of the muscles, or tremors, but violent convulsion no
longer occurs, and there is extreme prostration, with hurried, rattling
breathing, small, weak, irregular pulse and finally, stupor and coma.
_Diagnosis in man._ The only additional point, to those already stated
for animals, is in regard to _lyssophobia_. This false form of
hydrophobia is usually fortified by the fact of a bite, but as a rule it
lacks the exaltation of common sensation and of the special senses which
characterizes genuine hydrophobia. Very often also there is a flaw in
the history, the dog that inflicted the bite is unknown and may still be
alive, in which case no medicine is so good as to bring the healthy dog
into the presence of the patient. The dog may have been killed by an
excited community without any identification of his symptoms as those of
rabies or any post mortem examination to throw light on his case. The
attack may have come on after a conversation on the subject of the bite,
or of rabies, and perhaps, as in the case of the Montpellier cadet, long
after and when the patient had for the first time heard that the dog
that bit him had been mad. It may be that rabies does not exist in the
district and that no other victim in man nor beast can be adduced. It
may be that the patient has a nervous organization or is subject to
hysteria, and therefore specially predisposed to any disease of the
imagination. Such cases cannot be accepted as rabies until a successful
inoculation has been made on one or more animals.
RABIES AND HYDROPHOBIA. LESIONS. TREATMENT AND PREVENTION.
Lesions: blood fluid or clot diffluent. Fauces, pharynx and larynx
congested, exceptionally ulcerated. In dog, mouth cyanotic, with
tenacious mucus, sublingual petechiæ and erosions, stomach contains
many foreign bodies, but no food, small intestines and cæcum empty,
and like stomach congested: petechiæ on skin and elsewhere, cutaneous
and cardiac veins gorged, hyperæmic liver, kidneys and bladder: brain
congested, capillaries dilated or blocked, hæmorrhagic, leucocytic
collections in lymph spaces, nerve cells swell up with hyaline bodies
near nuclei, and neuroglia has hyperplasia, especially near the
respiratory centre. Congestion of nerves. Leucocytosis. Therapeutic
treatment: Orrotherapy: of little avail. Nerve sedatives; darkness,
quiet, nutritive enemata, chloroform, chloral, etc. Prevention:
eradicate the virus; muzzle all dogs absolutely, under heavy penalty,
for one year; Gower’s view; examples of muzzling; collar with name and
owner, shoot all unmuzzled dogs, cage for 6 months bitten dogs and
cats, also all imported dogs, shut up in cage for 10 days all dogs
that have bitten; treatment of bites, tourniquet, cup, suck through
tube, wring wound, cauterize—hot skewer, cautery, mineral solid
caustic, mineral acids on pledget or through a tube; Pasteur method:
emulsion of spinal cord (of rabid rabbit) after aseptic æration in
vitro for 3 to 14 days, injected in graduated doses for 21 days, table
of doses, table of mortality; Orrotherapy: by blood serum of immune
animal: advantages, disadvantages—technique: Use of sterilized brain
matter from rabid animal: experiments; protection by snake venom.
_Pathological Anatomy._ The blood is fluid or the clot diffluent.
Congestion of the fauces, pharynx and larynx is patent during life but
may have disappeared after death. Yet I have seen extensive ulceration
of the vocal cords in a rabid cow. The congestion may extend to the
trachea bronchia and lungs. In _dogs_ the buccal mucosa is often
cyanotic, covered with a thick mucus, and may present sublingual
ecchymoses and erosions, and wounds of various kinds made by objects
bitten or swallowed. The stomach in the same animal is usually almost
pathognomonic, being filled with foreign bodies of all kinds—straw, hay,
hair, wood, coal, pebbles, pieces of metal, cord, leather, cloth, earth,
sand, etc.—the result of the depraved appetite. There is an absence of
normal food principles in stomach and small intestines and the cæcum and
colon are usually empty. The gastric mucosa is congested, and may be
wounded and its contents mixed with blood. Such a condition of the
stomach in a dog, that has been bitten, and which after a customary
incubation period has shown symptoms like those of rabies, is virtually
diagnostic.
The following lesions are common to man and animals: Marked emaciation,
cyanosis or petechiæ in skins that are naturally white, early sepsis,
cutaneous veins and heart gorged with dark inspissated blood, hyperæmic
liver and kidneys, and slightly congested, petechiated empty bladder.
The most important lesions, however are those of the central nervous
system. In seven cases out of nine, Gowers found these very distinct.
There were vascular disturbance, capillary dilatation, capillary clots,
minute hæmorrhages, and accumulations around the affected capillaries of
leucocytes occupying the lymph spaces. Benedikt and Babes attach much
importance to the formation of hyaline patches in the thickened walls of
the vessels and around them, compressing the vessels in some cases to
virtual obliteration. The nerve cells swell up, and show small hyaline
bodies in the vicinity of the nuclei, and these latter finally
disappear. Germano and Capobianco found in addition marked hyperplasia
of the neuroglia. Babes, who looks on these changes as pathognomonic,
takes a small portion of spinal cord, hardens it in alcohol for 24
hours, stains it with aniline red and examines for the characteristic
hyaline nodes.
These brain lesions have been found mainly in the medulla near the floor
of the fourth ventricle and the respiratory center, but they are also to
be found in other parts of the encephalon and spinal cord. The greater
constancy of the medullary lesions serves to explain the characteristic
symptoms.
Congestions of the peripheral nerves have also been found. Lüttkemüller
found in rabies a moderate increase of the white blood corpuscles and a
great number of microcytes.
_Therapeutic Treatment._ It was long thought that rabies was necessarily
fatal, as indeed nearly all developed cases are to the present day. For
this reason and much more on account of the risk of preservation and
propagation of the deadly germ, the attempts at curative treatment in
the lower animals have been looked on as utterly unwarranted or
absolutely criminal. Yet it is now known that very exceptionally a
recovery takes place, and in that case immunity for the future may be
counted on. Yet the frightful danger attendant on the preservation and
treatment of a rabid animal, may well forbid the keeping of any of the
lower animals affected by rabies unless it be in the safest seclusion
and for the production of immunizing or curative products.
_Orrotherapy_ with the blood serum of an immunized animal is of little
value, and attended by risk from the rabid animal, but will be noticed
below as a prophylactic.
In man when the disease is manifested, palliation has been obtained and
very exceptionally recovery, under darkness, quiet, nutritious enemata
and antispasmodics or soporifics. Among such antispasmodics and nerve
sedatives may be named chloroform, chloral, curare (3 alleged
recoveries), eserine (1 recovery), pilocarpin (1 recovery), morphia,
datura, atropia, and bromide of potassium. Others have recovered without
any medicinal treatment, so that the mildness of the attack must be duly
considered in every case.
_Prophylaxis._ The most effective way of preventing rabies is to
eradicate the virus from the country. All immunizing measures resorted
to after the infecting bite has been sustained, are of little value as
compared with this, they may save the bitten individual, but they do
nothing to prevent others from being bitten in the future, and
indirectly they contribute to the maintenance of the disease by drawing
attention from such radical measures as would rid the country forever of
the scourge. In his great work on Diseases of the Nervous System, Gowers
puts this not a whit too strongly when he says: “The enforced muzzling
of dogs for a period of one year would almost certainly stamp out the
disease. That such a measure is not adopted is a national disgrace,
which is accentuated by the fact that the Government derives part of its
revenue from a tax upon dogs. The opposition to the use of the muzzle is
one of the strangest developments of morbid sentiment. There are
apparently thousands of well-meaning people who would prefer that
hundreds of dogs should perish every year of a painful disease, that
many human lives should be annually lost, and scores of persons should
be subjected for months to acute mental agony—rather than that dogs
should be made to wear an apparatus which causes them a trifling
annoyance. This perverted sentiment ought to be met with universal
abhorrence as a disgrace to humanity.” Such a statute, backed by a
penalty in some degree commensurate to the homicidal criminality of the
person who would leave his dog free to inflict this horrible disease on
humanity would doubtless be effectual, but some nations have such laws
on their statute books, and yet allow them to become dead letters.
Others have enforced them to good purpose. Berlin in 1853 had many cases
of rabies and muzzling was enforced. In three years the disease was
completely eradicated and the city enjoyed nine years of immunity or so
long as the law was enforced. Similar successes were met with in
Holland, new cases occurring only on the borders or in imported dogs.
London in 1889 had 123 cases and muzzling was enjoined. In 1892 the
cases were reduced to 3, and the muzzling law was suspended, and a
steady yearly encrease resulted, until the 1st three months of 1896
furnished as many as 72 cases.
In the absence of this radical measure muzzling should be enforced for a
year in any locality where a case of rabies has occurred, and every dog
should wear a collar with the name and residence of his owner inscribed
on it. All stray dogs and all unmuzzled ones should be summarily shot.
Dogs and cats that have been bitten by rabid animals should be destroyed
or shut up in cages for six months under veterinary supervision.
Imported dogs should be similarly secluded. Dogs that have bitten
animals or men should be shut up for ten days under supervision, when,
if rabid, the animal will develop unequivocal symptoms.
_Treatment of bites._ Absorption from a wound in a limb may be prevented
by applying a tourniquet. Wounds on the body may be cupped, or sucked
through a tube. Or the wound may be wrung to encrease the flow of blood.
As soon as possible it should be thoroughly cauterized. A hot skewer, a
Paquelin cautery, a stick of silver nitrate or zinc chloride or caustic
potash or a crystal of cupric sulphate will meet this end. If liquid
caustics are to be employed they can be applied to all parts of the
wound by means of a pipette, a glass tube, or swab.
With thorough cauterization shortly after the bite there is practically
nothing to fear, and even if it has not been applied for hours after, it
is still valuable in destroying the poison left in the wound from which
a continuous infection of the brain, by the transmission of the unknown
germ and its toxins, would otherwise take place. It has besides in the
human being a good moral effect against lyssophobia by giving the bitten
person a certain sense of protection.
_The Pasteur Method._ This is based on the fact that the spinal cord of
the tetanic rabbit when removed aseptically, and kept _in vitro_ in a
dry atmosphere, loses in virulence day by day, until on the fourteenth
day it is harmless. To render the air more drying, caustic potash is
introduced into the flask. The culture of the poison in rabbits
intensifies its virulence, until the virus becomes the strongest known
and when inoculated subdurally, reduces the incubation to six or seven
days.
In Pasteur’s early experiments he began injecting the emulsion of the
cord desiccated for 14 days, following with that of the 13th day, and so
on to that of the 5th. It was soon found that this was comparatively
ineffective when inoculation had been made with a strong virus or in a
large dose, and the treatment for such cases was modified to what is now
known as the intensive method. The weaker forms of the virus are given
at shorter intervals on the first days of treatment, and the stronger
forms repeated again and again, and, in place of a 15 days, course of
treatment, this is extended to 21 days. The following table illustrates
the course:
│ _Number of │
_Day of │ Days that │
Treatment._ │ cord had │_Dose Injected._
│ been │
│desiccated._│
───────┬────────┼────────────┼────────────────
1st day│morning.│ 14 days. │ 3cc.
„ │ „ │ 13 days. │ „
───────┼────────┼────────────┼────────────────
„ │evening.│ 12 „ │ „
„ │ „ │ 11 „ │ „
───────┼────────┼────────────┼────────────────
2d „│morning.│ 10 „ │ 3cc.
„ │ „ │ 9 „ │ „
───────┼────────┼────────────┼────────────────
„ │evening.│ 8 „ │ „
„ │ „ │ 7 „ │ „
───────┼────────┼────────────┼────────────────
3d „│morning.│ 6 „ │ 2cc.
„ │evening.│ 6 „ │ „
───────┼────────┼────────────┼────────────────
4th „│ │ 5 „ │ 2cc.
5th „│ │ 5 „ │ 2cc.
6th „│ │ 4 „ │ 2cc.
7th „│ │ 3 „ │ 1cc.
8th „│ │ 4 „ │ 2cc.
9th „│ │ 3 „ │ 1½cc.
10th „│ │ 5 „ │ 2cc.
11th „│ │ 5 „ │ 2cc.
12th „│ │ 4 „ │ 2cc.
13th „│ │ 4 „ │ 2cc.
14th „│ │ 3 „ │ 2cc.
15th „│ │ 3 „ │ 2cc.
16th „│ │ 5 „ │ 2cc.
17th „│ │ 4 „ │ 2cc.
18th „│ │ 3 „ │ 2cc.
19th „│ │ 5 „ │ 2cc.
20th „│ │ 4 „ │ 2cc.
21st „│ │ 3 „ │ 2cc.
Under this treatment the system becomes educated in the production of
antitoxins, and perhaps also in phagocytosis so that when subjected to
the lethal doses of three, four, five and six days preservation, it
successfully resists them. The most conclusive argument in favor of its
efficacy is this undeniable fact that the individual escapes death under
injected doses which in any unprotected system would prove fatal.
The results as given by the report of the Pasteur Institute are
furnished in the following table, from which are excluded such cases
only as developed the disease during the course of treatment, which
therefore remained incomplete.
_Years._ _Persons Treated._ _Deaths._ _Mortality per cent._
1886 2671 25 0.94
1887 1770 14 0.79
1888 1622 9 0.55
1889 1830 7 0.38
1890 1540 5 0.32
1891 1559 4 0.25
1892 1790 4 0.22
1893 1648 6 0.36
1894 1387 7 0.50
1895 1520 5 0.33
1896 1308 4 0.30
1897 1521 6 0.39
The following table gives the number of individuals treated who had been
bitten by animals which had been proved rabid by successful inoculation
of other animals, and of those bitten by reputedly rabid animals, and
their respective mortality.
_Died._ _Mort. per ct._
Bitten by animals proved rabid by
inoculation 2,872 20 0.69
Bitten by animals pronounced rabid by
veterinarian 12,547 61 0.48
Bitten by animals suspected of rabies 4,747 15 0.31
————
Average mortality 0.46
The Pasteur treatment by its great success in persons who have already
been bitten has in a great measure robbed hydrophobia of its terrors,
only it must be resorted to as early as possible in the period of
incubation. It has also been advocated as a means of immunizing subjects
that have not been bitten but are more or less liable to be so, and on
this basis a large number of dogs have been passed through it. This is
not likely to be adopted in the case of the human being, the more so
that a few, although on the whole a very limited number of persons, have
developed rabies long after the taking of the Pasteur treatment. This
has been attributed to the retention of latent germs in the system, and
argues besides a remaining susceptibility to the poison.
In spite of its brilliant success and the great boon it has been to
humanity, the Pasteur treatment is not an ideal one. Its success does
not consist in an entire extinction of rabies, but merely in the
reducing of its evil results; its success is indeed based on a
preservation and propagation of the germ and a continuous danger of
infection of new subjects; finally, the proposition to end the disease
by passing the whole canine race through the treatment, is open to the
objections that this would require a fabulous outlay, and that even then
some rare cases are not found to be fully protected. To continue the
disease, when it may be exterminated, and to palliate its results by the
treatment of generation after generation of dogs, must be promptly
condemned by the political economist, to say nothing of the
consideration of probable human infection.
_Orrotherapy._ It is not surprising that essays were made in the line of
serum treatment. Babes and Lepp in 1889 had some encouraging results in
transferring the blood of an immune animal into a healthy one. But
Tizzoni, Schwarz and Centanni have especially worked out this method.
These have shown that the blood serum of immunized animals destroyed the
virulence of the rabic poison, whether mixed with it before injection,
or injected with it, or injected within twenty-four hours afterward. A
very small amount of the serum is required and though delayed until the
end of the first half of the incubation period, it is only necessary to
multiply the amount by six or eight times. In this it has a great
advantage over the antitoxin of diphtheria or tetanus, the former of
which has to be multiplied 20 to 100 times, and the latter 1000 to 2000
times in the later stages of incubation. Further, it is possible by
drying to secure the serum in a permanent form which will remain active
for a length of time if secluded from air and light.
This has the decided advantages over the Pasteur treatment, (1) that it
employs the antitoxin already formed instead of waiting for its
formation in the body of the subject injected with the attenuated virus,
and (2) that it does not introduce into the system a virulent germ
capable of propagating in a favorable medium, but only an agent which is
antidotal to that germ.
It has the disadvantage as compared with Pasteur’s method that its
action is purely therapeutic in the sense of acting as an antidote,
while it produces no permanent immunity. It does not like the toxins
educate the cells to produce an encrease of antitoxin, and it can only
protect so long as it remains in the system. Whenever it is eliminated
or destroyed, the susceptibility to rabies returns. Hence it is
important to continue its administration as long as the microbe remains
in the system. As in tetanus and diphtheria antitoxin treatment, it is
also important to destroy the microbe and its toxins in the infection
wound.
The animal which is to furnish the antitoxin is immunized as in the
Pasteur method by a succession of graduated doses of rabic virus. After
a treatment of 20 days the rabbit or sheep furnishes a serum which is
protective when injected in the proportion of 1 of serum to 25,000 of
body weight, even though its use be delayed until 24 hours after the
introduction of the virus. The sheep can be immunized in 12 days by
doses of 0.25 gramme of emulsion of the infected cord to every
kilogramme of body weight. To maintain the serum at its highest standard
the treatment must be repeated at intervals of 2 to 5 months, as the
animal may be able to bear it without loss of condition.
_Treatment with Sterilized Brain Matter from a Rabid Animal._ In 1886 I
sterilized with heat an emulsion of the spinal cord of a man who died of
hydrophobia and injected two rabbits with 3 one drachm doses each, and a
third with 4 one drachm doses on as many successive days. These rabbits
were afterwards inoculated with virulent spinal cord and remained well
for nine months, while three control rabbits injected with virulent
cord, but which had received no previous treatment died rabid.
Puscarin and Vesesco have shown that the virus is rapidly weakened by
heat up to 60° C. at which point the virulence is destroyed. It becomes
easy therefore to secure in this way a toxin uncomplicated by any living
microbe.
Theoretically the sterilization and use of infecting nervous substance,
should share with the Pasteur method the advantage of the selective
action of the medullary matter in uniting with the toxins and robbing
them to a greater or less extent of their toxicity. It has the
additional recommendation that it introduces no living germ, and thus
obviates any possible danger of the propagation of disease through the
animal operated on.
Fernandez claims an immunity from rabies for dogs that have survived the
bite of a viper. Many facts and experiments are adduced in support of
this.
TETANUS.
Synonyms. Definition: infectious disease, due to bacillus, and shown
by tonic spasms of groups of voluntary muscles. Animals susceptible:
warm-blooded animals—dogs and chickens least: ⅔ds solipeds, ⅐th
cattle. Pathology and Causes: Bacillus tetani: 4 to 5µ by 0.2 to 0.3µ,
often enlarged by spore at one end; anærobic, liquefying, tardily
motile, until spore forms, grows in ordinary, alkaline media under
hydrogen, death point 60° to 65° C. (140° to 149° F.), for spores 80°
C. (176° F.), for an hour, dried it lives for years, in putrid matter
2½ months, stains easily, saprophytic in garden mould, in ingesta of
man and horse, abundant in tropics; infection local, killed by oxygen
in blood, toxins tetanize: tetanin, spasmotoxin, toxalbumin, diastase;
spasms first local near wound, then abruptly general, intravenously
causes general spasms first, theory of fermentation in blood; changes
in nerve cells, neuroglia, ependyma, peripheral nerves: muscles soft,
pallid, red, ruptured fibres, ecchymosis; rigor mortis early, marked:
sarco-lactic acid. Accessory causes: traumas and their causes,
parturition, umbilical infection, alimentary. General symptoms:
incubation 3 to 15 days, minimum 6 hours; tonic contraction of muscle
groups of locomotor system beginning near infection wound,—trismus,
orthrotonos, opisthotonos, emprosthotonos, pleurosthotonos, ocular
muscles; costive, difficult urination, hyperæsthesia, irritability,
perspiration, hyperthermia, mastication, deglutition, sucking.
Symptoms in _horse_: neck raised concave above, nose elevated,
nostrils wide, eyes sunken, haw protruded, ears rigid, pricked, facial
muscles rigid, prominent, mouth drawn back, muscles of back hard, tail
elevated, trembles, limbs extended outward, stiff, stilty, jaws
clenched or open slightly, stands. Symptoms in _cattle_; _sheep_ and
_goat_; _swine_; _dogs_; _birds_: Course: violent cases with short
incubation are rapid and fatal; mild ones with prolonged incubation
hopeful; cattle slow, sheep, goats and dogs acute. Mortality: sheep
and pigs 100 per cent.; horses 75 to 85; cows 70 to 80; lambs very
fatal. Death from asphyxia, hyperpyrexia, or exhaustion. Lesions:
trauma, often healed; congested nerves, gray horns of myelon, increase
of cells and granules in nervous matter of cord, corpus striatum,
cerebellum; blood extravasations at torn muscle fibres, intestinal and
cystic congestion. Diagnosis: from _strychnia poisoning_ by slow
advance, and persistence of spasm; from _rabies_ by absence of bite,
the continuous masseteric spasms, by absence of resentment, mischief,
hallucinations or depraved appetite; from _rheumatism_ by the
persistent trismus, hyperæsthesia and excitability; from _meningitis_
by the trismus, perfect mentality, absence of clonic spasm; from
_tetany_ by shorter and less perfect remissions, failure to develop
under nerve pressure, or improve under thyroid extract; from
_laminitis_ by the absence of high early hyperthermia, heat and
tenderness of the feet, and advance of hind legs under the body.
Treatment: best in slight cases, after long incubation, with slow
progress; antispasmodics; rest, darkness, absolute quiet, no litter,
nor visitors, slings, sloppy food, gruels, milk, green food, at level
of manger; clothing to favor perspiration; excision or antisepsis of
wound, carbolic acid, bleeding, opium, prussic acid, potassium
cyanide, bromides, physostigma, eserine, chloroform, sulphonal,
trional, tartar emetic, tobacco, apomorphia, lobelia, phenacetin,
acetanilid, cocaine, chloral, phenic acid, iodine terchloride, iodide
of potassium, orrotherapy, antitoxin; best as a preventive, value
decreases with development of disease; cerebral injections; brain
emulsion; use up toxins in blood; no use if nerve centres are already
in combination with toxins, only to ward off fresh toxin. Toxins
produce leucocytosis. Prevention: disinfection of all dirty wounds,
injections of phenic acid, or iodine; remove foreign bodies, use
muriatic and carbolic acids; antisepsis of navel; disinfection of
stables, feet, careful shoeing; immunization.
_Synonyms._ Lockjaw. Trismus.
_Definition._ An infectious disease of animals and man, characterized by
tonic spasms of the voluntary muscles in a given region or more
generally, with exacerbations, and dependent on the bacillus tetani.
_Animals susceptible._ Immunity cannot be claimed for any class of warm
blooded animal. Experimentally the dog and chicken prove among the most
refractory, in keeping with the comparative insusceptibility of the last
named animal to strychnia, but neither can be held to be in any sense
immune. Inoculated frogs become tetanic if the temperature is maintained
above the normal standard. In 208 cases in domestic animals recorded by
Cadiot and Hoffmann, 140 were in horses, 10 in mules, 5 in asses,
(solipeds, 155), 28 in cattle, 9 in sheep, 5 in goats, 5 in pigs, and 6
in dogs. Such statistics are liable to prove misleading when we have no
means of comparing them with the members of the different genera from
which the cases were drawn and the relative exposure of each genus to
traumatic lesions (infection atria). Solipeds lead with practically ⅔ds
of the entire number of cases, but these were presumably the most
numerous of the domestic animals, and preëminently the work animals and
therefore the most liable to traumatism. Cattle follow with ⅐th of all
cases but here again the large numbers to be drawn upon, and the
proportion of work oxen and wounds, are to be considered. The omnivora
and carnivora are comparatively little susceptible and among these the
chicken may be included. The omnivorous rat is quite susceptible.
Tetanus occurs in 1 per 1000 sick horses in the Prussian army
(Friedberger and Fröhner), and in 1 per 3000 sick in that of Wurtenburg
(Hering). It is so prevalent in San Domingo that a gelding costs twice
as much as a stallion (Wagenfeld). Heat and filth favor its
preservation.
In man tetanus is most frequent as the result of wounds (in feet and
hands) which are most likely to come in contact with the soil, and it
has visibly decreased in connection with the general adoption of
antiseptic surgery.
_Pathology and Etiology._ Sir James Simpson suggested in 1854 that
puerperal and surgical tetanus was due to the absorption of a poison
produced in the wound (Woodhead). Spinola charged it on infection in
wounds in horses. Carle and Rattone in 1884 successfully inoculated 11
out of 12 rabbits with the products from the wound of a man suffering
from tetanus. A year later Nicolaier produced tetanus in animals by
inoculating them subcutem with garden mould or street dust, and found in
the suppurating wounds in connection with various other microbes a
minute bacillus longer but thinner than that of mouse septicæmia to
which he attributed the tetanizing action. In 1886 Rosenbach inoculated
two Guinea pigs with the pus of a tetanic man, and found in the sores of
the tetanic pigs the bacillus of Nicolaier in company with another
larger spore-forming bacillus. In 1889 Kitasato succeeded in making pure
cultures of the bacillus tetani, and successfully inoculated the disease
on mice, rabbits, and Guinea pigs producing typical tetanic symptoms and
death. This was promptly corroborated by Tizzoni and Cattani and later
by a great variety of observers.
_Bacillus Tetani._ This organism is a minute rod 4 to 5μ in length by
0.2 to 0.3μ in thickness, with slightly rounded ends. In many mature
forms the one end is enlarged by the formation of a spherical,
refrangent spore which gives the bacillus the appearance of a pin or a
“drum-stick.”
The bacillus is anærobic, liquefying, tardily motile, and sporogenous.
When spores form the bacillus loses its motility. It grows at room
temperatures, in ordinary culture media which have a feebly alkaline
reaction, and in an atmosphere of hydrogen, but more actively at a
temperature of 36° to 38° C. Below 14° C. growth ceases and the bacillus
is killed at 60° to 65° C. The spores, however, can resist a temperature
of 80° C., in water for an hour, and 100° C. for four minutes. It was
this unusual resistance of the spore to heat that enabled Kitasato to
kill off the contaminating organisms and obtain pure cultures from the
surviving spores. The spores will survive desiccation for years,
retaining their virulence, and may live 2½ months in putrefying
material. The addition to the culture medium of 1½ to 2 per cent. of
glucose makes the growth much more rapid and abundant, and causes
opacity in the medium. The upper portion clears up in 6 or 7 days by the
precipitation of the bacilli as a grayish mass. In a glucose culture
medium growth is not prevented by the presence of oxygen at the surface.
The colonies formed in gelatine plate cultures show an opaque centre
with fine divergent rays, and a similar radiating growth is shown in
deep stick cultures. At the end of the second week the gelatine begins
to liquefy and form a little gas, and finally the whole mass becomes
soft and sticky. The bacillus does not liquefy blood serum. Cultures
have a disagreeable aromatic odor.
The bacilli stain readily in aniline colors and by Gram’s method. The
spores may be stained by Ziehl’s method. To 10 parts of a 10 per cent.
alcoholic solution of basic fuchsin, add 100 parts of a watery solution
of carbolic acid. Float the cover glass upon this, heating gently for
three to five minutes until steam begins to rise, wash well in water,
and decolorize in nitric or sulphuric acid, 25 per cent. solution, then
in 60 per cent. alcohol to remove color from albuminous background. Wash
in water and mount. By placing the specimen for two minutes in a watery
solution of methylene blue a contrast is obtained, the bacillus blue and
the spore red.
Outside the animal body the bacillus has a saprophytic life in rich
garden mould, street dust, stables, yards and drains, and the cracks of
floors. Nicolaier failed to obtain it in soil from forests and from the
deeper layers of garden earth. Marchesi found it to a depth of two
metres but no more. Again it is much more abundant in tropical countries
than in temperate and cold ones, and appears to be to a great extent
limited to particular localities. It has been found in the intestinal
contents of man and horse (Babes, Sormani), and in horse manure, and
this mingling with the surface soil and generating an abundance of
ammonia determines the anærobic conditions which favor the growth of the
microbe. This serves to explain the remarkable prevalence of the disease
among those living or working about stables, gardeners, agricultural
laborers, soldiers on campaign, and children and others walking with
bare feet. The contact with rich infected soil greatly favors
inoculation in any accidental wound.
An important feature in the pathology of tetanus is that the bacillus is
confined to the seat of the inoculation wound. The many attempts to
transmit the infection by blood, nervous matter, and by one or other of
the tissues have uniformly failed, though the pus of the infected wound
has proved virulent. Similarly, the attempts of Kitasato and others to
obtain cultures from the animal liquids or tissues apart from the wound
have been futile.
By inoculating the toxins remaining in the pus of the infection wound,
however, or in virulent cultures from which the bacilli have been
removed by filtration or in which they have been destroyed by heat, all
the symptoms of tetanus can be produced (Kitasato, Kund Faber, etc.) In
such cases too, the symptoms appear at once, as soon as the toxin is
absorbed, and not after a definite period of incubation as in
inoculation of the unaltered virus. Kitasato, Vaillard and Vincent
reached this conclusion by another channel. They inoculated mice at the
root of the tail with virulent tetanus cultures, and at definite
intervals after, namely, half an hour, one hour, and one and a half
hour, they made a circular incision round the wound and thoroughly
cauterized the whole, thus destroying all the inoculated bacilli. They
found that tetanus was prevented in those animals only which were
operated on at the first half hour. Again, Kitasato injected mice with
0.2 to 0.3cc. of the blood from the heart of a fresh tetanus cadaver,
and thereby produced typical tetanic symptoms and death in 1 to 3 days.
Various poisons have been separated from cultures of bacillus tetani.
Brieger isolated three substances—tetanin, tetano-toxin and
spasmotoxin—which in large doses caused tetanic symptoms and even death.
Brieger and Fränkel later isolated a toxalbumin which proved of
incomparably greater potency. Again, Brieger, Kitasato and Wehl
separated what appeared to be an enzyme or diastase which proved 500
times more potent than atropia. This was in the form of yellow,
transparent flakes, soluble in water, but which was not destroyed by
drying, nor in the dry state by absolute alcohol, chloroform nor
anhydrous ether, but which, like the virulent cultures of tetanus, was
easily destroyed by acids, alkalies, hydrogen sulphide, or heat. Like
the natural virulent product this may be kept unchanged for months on
ice, apart from the light, or with the addition of 0.5 per cent. of
carbolic acid, or its own bulk of glycerine. It kills the Guinea-pig in
a dose of 0.000025 gramme, and the mouse in a dose of 0.00000025 gramme.
While the propagation of the bacillus in the animal body appears to be
local, and the general tetanic symptoms are caused by the absorption of
the poison, it remains to be seen on what organ this directly operates,
and what accessory conditions favor its efficiency.
In _cases due to inoculation_ the spasms are at first local in the
vicinity of the inoculation wound and later become general. Kund Faber
shows that there is no gradual transition from the local manifestations
to the general, but the latter appear abruptly and in force as a new and
independent phenomenon. When we consider further that in inoculation
with pure cultures (uncontamininated by pus or saprophytic microbes) the
wound often heals promptly, without any sign of remaining local
irritation, we may conclude that simple nervous irritation in the sore
cannot be invoked as a cause of the early local spasm. It is more likely
due to the local diffusion of the poison into the peripheral nerves
while the little that has been absorbed is as yet too much diluted in
lymph and blood to seriously derange the nerve centres.
When general spasms set in it must be assumed that the poison has
reached the nerve centres in toxic quantities, either through the
circulation or as is alleged by Babes and others through the nerve
trunks. When the poison is injected intravenously the general spasms are
the first to appear. Again the section of the nerves of a limb before
inoculation prevents spasms in its peripheral muscles when all the body
beside has become tetanic (Tizzoni and Vaillard). The removal of the
brain from a tetanized frog had no effect, while the removal of a
portion of the spinal cord abolished the spasms in the muscles
corresponding to that part. Moreover Gumbrecht cut the whole of the
sensory nerves of a limb but the spasms occurred in its muscles
notwithstanding. It must be admitted, therefore, that the general
tetanic spasms are induced by disorder caused by the poison in the
spinal nervous centres.
Gumprecht and Goldscheider claim that the poison reaches the spinal
centres by way of the nerve trunks basing the conclusion on the
observation that the spasms sometimes remain for a time more marked on
that side of the body on which the wound or inoculation was made.
Absorption through the circulation also is conceded.
Courmont and Doyon claim that the product of the bacillus tetani only
operates as a ferment, which produces in the blood the real tetanizing
agent, basing the conclusion on an apparent delay in its action, in man,
as compared with strychnia, and on the prompt action of the injected
blood of a tetanic animal in which this poison is presumably preformed.
It should be noted, however, that the disease in man is only seen after
accidental inoculation of the bacillus, and that time must be allowed
for the increase of the microbe.
Vaillard and Vincent have shown that the promptitude and certainty of
the result depend on the age of the culture employed. A culture of 5
days in bouillon at 20° to 22° C. will not harm a Guinea pig in a
hypodermic dose of 0.25cc. to 0.5cc. A culture of 20 days old is deadly.
The action on the nerve cell of the spinal cord has been investigated by
Goldscheider and Flatau, who found degeneration of the chromatin
granules within a short time after inoculation. (Centr. für Allg. Path.
Anat. 1897). W. K. Hunter found that the ganglion cell stained more
diffusely than normal cells. There were also some capillary dilatation
and punctiform hæmorrhages in certain cases (Brit. Med. Jour. 1897).
Péchoutre examined the lumbar enlargement of tetanic rabbits, by Nissl’s
method and found the following lesions in the motor cells of the
anterior horns: 1st. A partial or total disappearance of the distinct
outer marginal line; enlargement of the cell and pericellular space;
diffuse coloration of the achromatic substance; a disappearance of the
regular concentric disposition of the granules of Nissl which were in
part reduced to a fine powder; 2d. Encrease of nucleus and nucleolus.
Others have observed encrease of the cerebro-spinal fluid, thickening of
the ependyma, nuclear proliferation in the neuroglia, and softening of
the cord, but in many cases no appreciable lesions in the nerve centres
have been found, and none can be affirmed as constant. Neuritis in the
region of the wound is sometimes found especially if the lesion is a
contused or painful one.
The muscles often show lesions the result of the violent contractions.
There may be points of ecchymosis and partial rupture of individual
fibres, they may be of a deep red, or again pale, soft and as if
parboiled. There may be hyperæmia or œdema of the lungs, congestion of
the larynx, ecchymosis on the pericardium and other serous and mucous
membranes, and congestion of the liver, spleen and kidneys. Rigor mortis
sets in rapidly and is usually very persistent. The muscles contain an
excess of lactic acid.
_Accessory Causes._ Whatever contributes to traumas must be classed in
this list. Solipeds, work oxen, and dogs are especially exposed in this
sense. In all animals castration wounds; in horses and lambs amputation
of the tail; in solipeds pricks, bruises and fistulæ of the feet; all
kinds of surgical wounds; in females the parturient condition; and in
the new born the umbilical sore form infection atria. The tendency to
infection in wounds of the feet in animals, and of the hands and feet in
man, is easily explained by contact with the virulent earth or dust.
Children running barefoot, or injuring their bare knees and soldiers
sleeping on the ground are similarly exposed. The contamination of the
clothes is the main condition. It has been held that infection never
takes place from the gastro-intestinal canal, but the facts that the
bacillus is frequently present in the prima viæ and that the mucosa is
often perforated by blood-sucking parasites, suggest that some cases
(idiopathic) are probably due to intestinal infection. The gland ducts
also and the follicles of Peyers’ patches and of the solitary glands
offer available fields for the colonization of the bacillus and for
infection atria.
_General Symptoms in Animals._ In experimental cases, in which there has
been a large intravenous injection of the blood of a victim of tetanus
the symptoms may set in speedily and violently. In casual cases,
however, there is usually an _incubation_ period varying on an average
from three to fifteen days in the _horse_ while it may be as short as
two days in _cow_ and _sheep_. Hoffmann quotes one incubation in the
horse as but six hours after a wound in the neck, and another as
twenty-five days, following a castration. The last is rather unreliable
as infection may have taken place long after the operation. He quotes
cases in the pig and goat, after castration as eight to fourteen days,
and one in the dog almost immediately after a bite on the loins.
Following the incubation the marked phenomena are tonic contractions of
groups of muscles beginning usually with those near to the seat of the
infected wound and extending with varying rapidity to the locomotor
muscles generally (limbs, croup, back, loins, neck, tail, abdomen) and
those of mastication (jaw) and the eye. The muscles of respiration are
only involved at a late date, causing stertorous breathing and it may be
asphyxia. Peristalsis is impaired so that there is some costiveness and
tardiness in digestion. Urination becomes difficult and infrequent on
account of the difficulty of assuming the normal position for the act,
and spasm of the sphincter vesicæ and dangerous distension of the
bladder may follow. The urine is often albuminous and has a high density
and color. Priapism is not infrequent in the male.
The predominance of the spasm in special groups of muscles has been the
occasion of giving different names to individual cases.
_Trismus_ or _lockjaw_ is that condition in which the muscles of the
jaws are violently contracted so that the incisors can only be separated
slightly or not at all.
_Orthrotonos_ is that condition in which the muscles in tonic spasms
keep the neck, back and loins rigid, straight and unbending, in one
horizontal line.
_Opisthotonos_ is when the muscles of the spine are in rigid spasm, so
that the back and loins are slightly depressed, the tail elevated and
trembling, the neck drawn upward with a concave superior border
(“ewed”), the head extended and the nose elevated.
_Emprosthotonos_ is caused by spasms of the muscles of the ventral
aspect of the body, with arching of the back and tucking up of the
abdomen.
_Pleurosthotonos_ is when the trunk is spasmodically bent to one side,
right or left.
Spasms of the muscles of the eyeball, cause sinking and apparent
diminution of that organ, with the protrusion of the membrana nictitans
over one-third, one-half or even more of its front surface. This is
often referred to by owners as “hooks”.
More striking and pathognomonic than the above is the extreme
hyperæsthesia and irritability which rouse into activity or aggravate
the symptoms under the slightest cause of disturbance. The effort
required to feed from the ground, the stretching of himself to urinate
or defecate, the rustling of straw litter under his feet, loud talking,
or other sudden noise, banging of doors or windows, hammering in the
vicinity, a current of cold air, a flash of light, moving the patient in
the stall, attempts at mastication, simple handling, administering
medicine, or sudden jerking of the head upward promptly brings on a
paroxysm of spasm. Pushing the head suddenly upward or jerking on the
halter, is often resorted to as a means of diagnosis, the sudden
resulting rigidity of the muscles generally, the rolling of the eye, its
retraction toward the depth of the orbit and the protrusion of the
membrana nictitans over one-half, one-third or more of the cornea,
bringing out the diagnostic symptoms in a striking manner. In very
severe cases the head may be drawn upward and backward almost to above
the loins (Henry), or one or more of the dorsal or lumbar vertebræ may
be broken or crushed (Zundel). A sudden loud noise will sometimes cause
the exhausted animal to drop to the ground.
Perspiration is not uncommon. Breathing is usually accelerated, the
encrease being in ratio with the violence of the spasms. Pulse and
temperature are usually normal at first and may be in slight cases
throughout. Even in severe cases the pulse does not rise so much as the
respiration. In violent and fatal cases the temperature often rises
excessively before death (104° to 110° F.).
When the jaws are not absolutely closed, the tongue is often wounded by
the teeth, and, in any case is covered by a tenacious mucus, which may
hang in strings from the lips. If the jaws are still movable,
mastication is still carried on, but slowly, painfully and imperfectly,
and deglutition is more or less difficult. Young animals are unable to
suck.
_Symptoms in the horse._ When the symptoms are fully developed, they are
very characteristic. The neck is raised, often concave along its upper
border, the nose raised and protruded more or less, the nostrils widely
expanded, the eyes sunken, fixed and anxious, with diluted pupils and
protrusion of the haw outward and upward from the inner canthus, the
ears are pricked, rigid, and drawn toward each other at their tips, the
facial muscles may stand out visibly and are firm, the angle of the
mouth is drawn back, the veins of the head are full and prominent,
saliva froths or drivels from the lips, the tail is elevated and during
paroxysms will tremble, and the muscles of the back and limbs are
projecting and hard. The limbs are extended outward to give a wider base
of support. If moved, the general stiffness is at once seen. The patient
cannot be turned round in his stall, he may not even be able to turn the
neck to one side, and if backed he resists, or accomplishes the movement
only with the greatest difficulty. In walking, the limbs are used as
stilts with little or no bending of the joints, and if turned, the body
is not bent but moved around with difficulty as if one rigid mass. The
pulse is small and hard, the breathing slightly hastened, and the mucosæ
congested and reddened. The jaws may be firmly closed, or they may still
part for a time half to one inch. In all severe cases the patient
obstinately stands, and if he should drop, or lie down, the breathing
and spasms are usually encreased and, in the efforts to rise, the
respiratory muscles may become spastic with promptly fatal results.
In _cattle_ the same general symptoms prevail. The stiffness of neck and
back, the habitual elevation of nose and tail, the stiffness of the
legs, propped outward for support, and moved like unbending posts when
made to walk, the hardness of the muscles, standing out under the skin,
the rigidity of the lips, firmly closed or slightly opened, the general
fixity of the erect, retracted ears, and the sunken appearance of the
eyes with marked protrusion of the haw, are largely as in the horse. The
muzzle is usually dry and hot, the jaws clenched, the tongue firmly
compressed against the palate and covered with thick, tenacious mucus,
and the flanks are often flattened by the contraction of the oblique
muscles, so that they descend almost vertically from the lumbar
transverse processes. There is great difficulty in turning and the trunk
moves in rather a rigid mass without bending laterally, and the limbs
are stiff and stilted. Tympany of the rumen sets in early with oppressed
breathing and arrest of defecation and urination, which had been already
difficult. The reflex excitability to noises, or other causes of
disturbance is often less than in the horse. In cases following
metritis, this may be due in part to the depressing poisons absorbed.
_Sheep and Goat._ Show the same general rigidity of trunk and limbs, the
drawing of the head and neck upward and backward, the elevation of nose
and tail and the firm closure of the jaws. As the disease advances they
may lie on the side with legs straitened and rigid and head and tail
raised toward the back. The occlusion of the eye by the haw is the same
as in the horse.
In _swine_ the spasms begin with the jaws and face, and extend to the
neck, back and limbs with the same general symptoms as in other animals.
Champing of the jaws and profuse frothing at the mouth have been noted
and the protrusion of the haw is characteristic. As in sheep, the animal
may lie on its side with head and limbs rigid and an early death may be
looked for. Convulsions are easily distinguished by their transient
character.
_In dogs_ tetanus is rare. Möller had two cases in 50,000 sick dogs,
Friedberger and Fröhner but one out of 70,000. Cadiot saw two cases in
ten years of the Alfort clinic. Labat had several cases in sheep dogs. A
slight transient trismus has been noticed as common in puppies. When
generalized there is stiffness of the trunk and limbs, abduction of the
members. The spine may be straight and rigid or drawn upward and
backward, and the loins depressed. The haw covers the eye more or less,
the lips are rigid, the jaws clenched, and the skin of the forehead
wrinkled. The ears are stiff and drawn toward each other, or backward.
The reflex excitability is as great as in the horse, the slightest touch
or sudden noise producing violent paroxysms. Inability to bark is a
marked feature. Temperature may be normal or up to 107° F.
_In birds_ it is very rare, in keeping with the insusceptibility to
strychnia, ergot and other tetanizing agents. Dreymann gives one case in
a _turkey_, and Babes’ experimental cases in pigeons and chickens from a
specially virulent bacillus obtained from the horse. The pigeons
suffered much more certainly and severely than the chickens, in which
there was a marked power of resistance. Dreymann’s turkey moved with
stiff limbs and body, had the wings clinging firmly to the body, the
head and neck extended and the bill firmly closed. The haw protruded
over the eye, and there was hurried and oppressed breathing.
_Course._ _Duration._ The course of tetanus varies with the genus
affected, with the individual susceptibility and above all with the
length of the incubation, and severity of the attack. Cases that set in
with great violence after an incubation of two or three days or less are
likely to advance to an early death. An early generalization of the
spasms, with high temperature (104° F), hurried breathing, congestion of
the mucosæ and extreme excitability may end fatally in twenty-four hours
or within a week.
If on the other hand the incubation appears to have extended over one,
two or three weeks; if the disease is at first equivocal, with some
stiffness and firmness of the muscles, but with little or no trismus; if
the patient can open the jaws an inch or more and masticate even slowly
for a number of days after the onset of the first symptoms; if the haw
projects only slightly over the eyeball and the excitability is not
extreme the prospect for recovery is much better. Such tardy cases may
seem to stand still for a week and then have a slight aggravation and
this may be repeated, or a slow improvement may set in and go on
gradually to complete convalescence. Improvement may be manifested by a
softer or more relaxed condition of the muscles, by a slightly freer
movement of the limbs and jaws, by a greater ease in swallowing, by
encreasing movements of the ears and eyes, by the lessened projection of
the haw, by the freer breathing and circulation and by the permanent
lowering of temperature to the normal standard. Convalescence is always
slow, but especially slow in severe cases in which time must be allowed
for repair not only of the central nervous lesions but also of the
ruptures and trophic changes in the muscles.
In _cattle_ the disease is usually slow in its progress and improvement
may not set in till the close of the third week. In sheep, goats and
dogs on the other hand it is habitually acute, and death may supervene
from the third to the eighth day. In the horse all forms are met with
and the result will vary according to the severity of the attack.
_Mortality._ Friedberger and Fröhner sets the mortality in sheep and
pigs at nearly 100 per cent.: in horses at 75 to 85 per cent.: and in
cows at 70 to 80 per cent. In tetanus neonatorum in lambs, the deaths
reach about 100 per cent. In this case the disease usually sets in
within forty-eight hours after birth, and with a very high temperature
difficult deglutition becomes a marked feature, so that if the patient
is not speedily killed by dyspnœa, it soon perishes from starvation and
exhaustion.
The _cause of death_ is usually _asphyxia_, _hyperpyrexia_, or
_exhaustion_.
_Lesions._ There are no constant or pathognomonic structural changes in
tetanus. Those that are found are inconstant and as a rule secondary. A
wound (entrance channel) can usually be made out, often in the region of
the foot, or in connection with castration. In the new born there is the
unhealed navel, and in parturient cows the catarrhal, septic or injured
womb. In the seat of such wound may be found the foreign body (nail,
splinter, etc.), and some pus or simple congestion or even necrosis. The
nerve trunks leading from such infected wound may be hyperæmic. The
presence of the bacillus in the wound may be determined by microscopic
examination or inoculation on a small animal.
The changes in the nerve centres may be congestion of the horns of gray
matter, and there may be slight hæmorrhage, exudation, especially shown
in the encrease of the cerebro-spinal fluid, softening, cell
proliferation, and granular invasion of the nervous tissue. In separate
cases the myelon, the corpus striatum and the cerebellum have shown
lesions. The meninges are occasionally hyperæmic. Spinal lesions have
been noted especially in the bulbo-cervical and lumbar regions.
Exceptionally in the horse there are blood extravasations from fractures
or dislocations of the vertebræ.
In subjects dying of asphyxia the lungs and right heart are congested,
and the blood may be black, only loosely coagulable and with free
hæmoglobin. There is congestion of the intestinal as of the respiratory
mucosa, and also of the liver, spleen and kidneys. The congested bladder
usually contains urine contrary to what is the case in rabies.
_Diagnosis._ From _strychnia poisoning_ tetanus is distinguished by the
gradual and progressive approach of the spasms and by the absence of the
intervals of complete relaxation which separate the rapidly recurring
and violent spasms of strychnia. In tetanus the spasms may be modified
but never completely intermitted, and more or less stiffness, trismus
and protrusion of the haw constantly persist. In strychnia too, the
paroxysm is far more intense than in the early stages of tetanus. The
spasms of strychnia are general, while those of tetanus are often most
intense in particular groups of muscles often at first in the vicinity
of the inoculation wound.
From _rabies_, tetanus is easily distinguished by the absence of any
history of a bite; by the persistence of the tonic spasms especially of
the masseters and abdominal muscles during the intervals between the
more violent paroxysms (in rabies there is temporary complete
relaxation); by the absence of clonic spasms which alone occur in
rabies; by the absence of the paralysis which characterizes advanced
rabies; by the mental clearness and the absence of hallucinations or
mischievous disposition which are marked features of rabies; by the
absence of the depraved appetite of rabies; and by the fact that the
brain does not contain the infecting germ as is the case in rabies.
From _rheumatism of the neck_ (torticollis) tetanus is easily
distinguished by the permanent trismus which is not shown in rheumatism,
and by the fact that spasms are easily roused by any artificial
excitement, indicating an extraordinary hyperæsthesia and excitability
which are nearly absent in rheumatism. The steady unmistakable progress
of tetanus is in itself diagnostic.
From _meningitis_ tetanus is to be diagnosed by the presence of trismus
without impairment of the mental faculties or fever. In meningitis the
spasms are usually confined to particular groups of muscles and do not
become generalized under active excitement as in tetanus. Even if the
spasms of meningitis affect the jaws and pharynx they are rarely
paroxysmal or roused by excitement as in tetanus. They may even be
clonic.
_Tetany_ is more commonly localized in particular groups of muscles, and
shows longer and more irregular intervals between paroxysms than does
tetanus. It is improved by thyroid extract, and may be roused at will to
contraction by pressing on the nerve going to the affected muscles.
_Laminitis_ in its most violent form and early stages, may be confounded
at first glance with tetanus, but the high fever, the standing on the
heels, the advance of the hind legs under the body, the great heat and
tenderness of the feet, the impossibility of standing on one fore foot
when the other is lifted and the strong pulsation of the digital
arteries, are sufficiently distinctive.
_Treatment._ For fully developed tetanus no known resort of therapeutics
can be relied on. In slight cases that have shown a long incubation and
a slow increase and extension of spasm and in those having trismus only,
a recovery may be expected. Treatment has been conducted largely on
theoretic lines and may be divided into antispasmodic, eliminating and
antidotal or antiseptic.
Rest, darkness and absolute quiet are the first and main considerations.
A dark stall, with no straw litter, the rustling of which often excites
the patient, but rather a little chaff, saw dust or even earth to
prevent noise from the feet, and the exclusion of all visitors are
essential. As a rule slings should be put under the patient so that he
cannot lie, nor drop down, and this becomes more imperative as the
disease advances. The aggravation of the spasms when down, and the
danger of their extension to the respiratory muscles are far more to be
dreaded than the temporary excitement caused by the application of
slings. Food should be sloppy mashes, of bran, middlings, oat meal,
linseed meal, gruels or milk, or green food may be allowed in moderate
amount if the jaws are still movable. It must not be forgotten that
digestion is impaired and food that is indigestible, especially
fermentescible, or in excess, may arouse fatal colics and bloating, yet
in a protracted exhausting disease like tetanus, the strength must be
sustained by all means in our power. Pure water should always be
accessible. Food and water should be furnished in buckets at a level
which will not necessitate either raising or dropping the head to get to
them (about 4 feet). The food must be given often, in small quantity to
avoid fermentation and spoiling. If noise cannot be wholly excluded it
may be an advantage to put cotton wool in the ears. I have seen a mare
recover when completely covered with cotton wool under blanket and
hoods.
_Local antiseptic treatment._ Theoretically this is of great value since
the microbe is confined to the inoculation wound and by the time the
first symptoms appear, the spores have developed into bacilli and are in
a condition to be easily destroyed by disinfectants. We can, therefore,
by caustics or active disinfectants destroy the infecting microbian
colony, and prevent the further entrance of any toxins into the
circulation and nerve centres. The principle has been shown
experimentally successful in cases of inoculation in the tails of cats
and Guinea pigs, and the amputation of these members as soon as tetanic
symptoms appear (Kitasato, Babes). Unfortunately in too many cases, when
first seen, too much of the marvelously potent toxin has already reached
the nerve centres, and these have already undergone such changes, that
the disease is likely to go on to a fatal issue in spite of the cutting
off of future supplies of toxin. Yet the principle is sound and proves
helpful in proportion as it is applied nearer to the time of infection.
The most thorough method is the amputation of the infected member, if
like the tail or ear it can be excised without ruining the animal. In
1875, Barbillon had success in again amputating the tail, in a case of
tetanus after docking. Next to this comes the excision of the wounded
tissues, but this can too seldom be effectually and certainly
accomplished, and we must fall back on caustics and antiseptics. The
actual cautery if thoroughly applied may be trusted to destroy the
bacillus along with the tissues, but most of the chemical escharotics
unite with the albumen to form an impermeable film, which protects the
tissues in the deeper part of the wound against the antiseptic action.
Of the different antiseptic applications _carbolic acid_ should be
especially recommended as being not only antiseptic, but also an
antidote to the toxins as shown below. It has the further advantage of
acting as a local anæsthetic, and of not coagulating albumen. Creosote,
creolin, lysol or other antiseptic may be used instead and should be
applied thoroughly to all parts of the depth of the wound on a pledget
of surgeon’s cotton or through a tube. When agents so little destructive
are employed they may be continuously applied to the sores for a length
of time.
Recoveries have taken place after neurectomy, and after stretching the
nerve going to the wounded part, the theory being to check the afferent
(sensory) nervous current, and arrest the reflex spasms. The new
irritation, however, caused by the surgical wound is to be dealt with,
and may itself turn the balance against recovery.
Nervous derivation appears to have been beneficial in some advanced, or
partially convalescent cases. One horse after 14 days illness (Taffanel)
and another after 21 days (Prud’homme), were castrated, bled freely and
slowly recovered. Tisserand gives another case without mentioning the
stage of the disease. A horse with advanced tetanus was taken to the
seashore and shot. He fell into deep water, swam ashore and made a
recovery. But whatever virtue may be in elimination of the toxins by
bleeding, in nervous derivation or in the shocking of an unbalanced
nervous system, these can hardly be recommended as regular methods of
treatment. Yet the older veterinary records contain many instances of
alleged benefit from bleeding.
_Internal treatment._ The whole list of antispasmodics have been tried,
with no very satisfactory result. Opium has been extensively employed in
spite of its tendency to encrease constipation, and morphia given
hypodermically has checked spasm and induced sleep. Hydrocyanic acid and
potassium cyanide have shown a decided reducing action on the spasms
with the same drawback of favoring constipation. Potassium and other
bromides are useful in mild and chronic cases, and may be given in full
doses in combination with chloral hydrate. Calabar bean and eserine have
been given for their physiological action on the nerve centres, and
recoveries have followed their use, but they have little effect on the
spasms until the system has been saturated to the point of threatening
collapse. Chloroform has the advantage that it can be easily given by
inhalation, but while it may be pushed to the extent of temporarily
checking the spasms, yet these return at once when the action of the
drug is exhausted. Chloroform is always dangerous to a weak or exhausted
heart and cannot be given for any great length of time continuously. It
is, therefore, very unsatisfactory. Sulphonal and trional have similarly
checked the spasms. Gelsemium has given good results in certain mild
cases, but it must be pushed to the extent of coming just short of
poisonous doses, and the fear of an overdose, together with its failure
in severe cases, have prevented its general acceptance. The same end has
been sought by the use of nauseating antispasmodic agents, as tartar
emetic, tobacco, apomorphia, and lobelia, but though useful in
individual cases, these are on the whole no more successful than other
agents. Phenacetin, antipyrin, acetanilid and cocaine have respectively
received credit for some recoveries.
Chloral hydrate commends itself as being at once a most potent
antispasmodic and hypnotic, and an antiseptic. It can, moreover, be
conveniently given as a rectal injection, thus avoiding the irritation
and excitement of administration by the mouth. Given in this way too, it
tends to relaxation of the bowels, instead of constipation. Carbolic
acid which can be conveniently given by enemata has an anæsthetic
action.
_Antiseptic and Antidotal_ or _Antitoxin treatment_ is more promising,
yet it has failed to come up to the full measure of expectation, mainly
because the nervous changes have already reached a stage which cannot be
undone speedily or at all. Under this heading would come phenic acid (½
oz.) and probably chloral hydrate (1 oz.), already referred to, and the
various compounds of iodine which may be here noted.
_Iodine Terchloride._ _Iodine._ Behring and Kitasato secured immunity of
two months duration, by injecting the animal with a filtrate of a
culture of tetanus bacillus, and then injecting at the same point 3cc.
daily, for five days, of a 1 per cent solution of iodine terchloride.
Roux and Chamberland had similar results by using iodine instead of the
iodine terchloride, and maintained the full measure of immunity by
repeating the inoculation every fortnight. Here it is evident that the
action of the iodine is directly antitoxic or antidotal, when introduced
along with the toxins and before they can reach the nerve centres.
_Iodide of Potassium._ In an experimental case of general tetanus in the
dog, Babes had a recovery in ten days, by injecting subcutem 5cc. of
Lugol’s solution and thereafter for eight days 10 to 30cc. daily. This
suggests the use of this agent along with phenic acid, or as an
alternate, in any case in which phenol appears to be losing its effect
by use. It may be used hypodermically, or in the drinking water or by
rectal injection. It has an advantage over phenic acid in being actively
diuretic and eliminating, while phenic acid has the recommendation that
it tends to lower nervous excitability and moderate the reflex spasm.
Theoretically the combination of the two agents, which do not mutually
decompose each other, should give the best results.
These experiments have been often repeated showing clearly the antidotal
action of the iodine compounds when mixed with the virus before
inoculation, or injected with the virus into the seat of the wound. When
employed later when the symptoms have developed, everything depends on
the changes already accomplished in the nerve centres, and the severity
and generalization of the spasms.
_Serum Antitoxin Orrotherapy._ Babes appears to have been the first
(1889) to use the serum of animals (rat) recovered from tetanus in
mitigating and curing tetanus in experimental cases. An attempt on a
well developed case in man failed. His method of preparing the serum is
as follows: A horse of 900 lbs. (461 kgm.), is inoculated with a mixture
composed of 0.5cc. toxin (of which 0.001 mgm. kills a mouse) and 0.5cc.
iodo-potassium iodide, and then at intervals of four or five days of
2.5cc., 4, 5 and 10cc. of the iodine mixture. Then stronger mixtures are
used: first 2 parts of toxin to 1 part of the iodine mixture; dose
10cc.; then 3:1 dose 10cc.; then 4:1 dose 5cc.; then 15:1 dose 10cc.;
then 30:1 dose 25cc.; and finally virulent cultures in progressively
encreasing doses 10, 20, 30 and 50cc. One week after the last injection
1cc. of the blood serum will antidote 50cc. of toxin. Injection of toxin
is however continued and the dose is gradually raised to 200cc. Eight or
fourteen days after the last injection the blood serum may be taken for
protective purposes. He has prepared antitoxin from cows in the same
way, and Brieger and Ehrlich have prepared it from the goat. Chickens
being naturally refractory to tetanus toxin can bear large doses and a
potent antitoxin is more speedily secured from them. In the case of the
cow the milk is rich in antitoxin.
Other methods of preparing an animal for producing the antitoxin have
been resorted to as injecting it with a mixture of toxin and antitoxin
in increasing doses, or again injecting with a mixture of toxin and
thyroid extract in increasing doses. The extract of the normal thyroid
contains a natural antitoxin.
It may be fairly inferred that the antitoxin is not formed in the nerve
cells alone in their resistance to the toxin, but also in the thyroid,
the liver (bile having an antitoxic action), and perhaps in other organs
or liquids.
The blood of the immunized animal drawn through the sterilized cannula
and aspirating syringe is coagulated in vessels set on ice, and the
serum when separated is mixed with 0.5 per cent. carbolic acid and 1 per
cent. chloroform, and kept in the dark in well closed bottles. It will
usually keep for years.
Early experiments with antitoxins showed that when mixed with the toxin
before injection it could be trusted to neutralize it. Ehrlich, Tizzoni
and Cattani even claimed success in all experimental subjects if
employed as soon as the slightest symptoms of tetanus were shown. They
found, however, that it required 1000 to 2000 times the amount of
antitoxin in such cases than was required when it was mixed with the
toxin prior to injection. They found, moreover, that when the disease is
fully developed the dose must be 150 times more than is required when
the first symptoms are shown. It should be added that when the disease
has developed rapidly, after a short incubation, and is well advanced
the antitoxin treatment is usually of little avail. The changes in the
nerve centres are already too great to allow hope of recovery. In man
the ratio of recoveries are about as follows: After incubation of 10
days or under, 3 to 4.5 per cent. recover. After an incubation of 11 to
15 days 50 per cent. recover (Woodhead). Lambert claims 46 per cent.
recoveries in 114 cases, and 38.71 per cent. recoveries in acute cases
with an incubation of 8 days and under.
On the whole the ratio of recoveries is greater under the antitoxin
treatment than before, though far from sustaining the optimistic views
of Behring and other early experimenters. Babes draws attention to the
fact that spore laden splinters of wood, in the wound render the
antitoxin useless as a continuous succession of fresh spores, bacilli
and toxins are thereby supplied. As this is one of the most common forms
of casual infection it interferes seriously with the success of
antitoxin treatment.
Roux and Borrel found that in animals, intracranial injection of the
antitoxin was the most effective method. Recovery also followed its
injection into the cerebrum of a tetanic boy. Babes had recoveries in
two cases out of three with cerebral or intracranial injections. As the
reflex spasms depend on the spinal centres these would seem to be the
ideal points of injection.
Babes who has done a large amount of subcutaneous and intraperitoneal
injection of antitoxin, employed for man doses of 300 to 500cc., which
would represent 8 to 10 ozs. as the dose for an ordinary horse. As the
antitoxin is rapidly eliminated from the body, these should be repeated
daily or every other day. Nor should this supercede other curative
measures. The leading principles may be thus stated: 1st. Antitoxin
should be used at the earliest possible moment. 2nd. The infected wound
area must be thoroughly disinfected or destroyed by caustics, and that
at once. 3rd. The antidotal treatment by phenol and iodine must not be
omitted. 4th. Palliative treatment by antispasmodics, narcotics or
soporifics must go hand in hand with antitoxic treatment. 5th. Measures
should be taken to secure elimination of the toxins present in the
blood.
_Treatment by brain emulsion._ Wassermann and Takaki (Berlin Klin. Woch.
Jan. 3d, 1898) have in a number of cases, mixed 1cc. of brain substance
of a warm-blooded animal with ten times the lethal dose of tetanus toxin
and injected without producing any symptoms of tetanus. They obtained a
similar immunity by injecting the brain emulsion 24 hours after the
injection of three times, and in other cases of five times the lethal
dose of tetanus toxin. Control cases uniformly died of tetanus. The
brain matter was obtained from Guinea pigs, pigeons, rabbits, horses,
and men. They accordingly advanced the theory that brain matter is a
direct antidote to the tetanus toxin, uniting with it chemically and
rendering it innocuous. The liver, spleen, kidney, bone marrow and blood
serum gave no such protection.
Marie, in a series of experiments, injected the brain emulsion and
tetanus poison at different parts of the body of Guinea pigs and found
that fatal tetanus ensued. It would appear, therefore, that the brain
emulsion acts by direct contact, and that it is only by its meeting and
combining with the toxin before the latter reaches the spinal cord that
tetanus can be prevented.
Roux and Borrel (Ann. de l’Instit. Pasteur, 1898) demonstrated this
union between the poison and brain matter, by making an emulsion of the
two, and putting in a centrifuge, which will separate the brain
substance from the clear liquid. The fluid obtained in this way was
shown by injection on the living animal to contain almost no toxin.
Knorr and Blumenthal reached the same conclusion as to a chemical union
with the brain matter which robbed the toxin of its toxicity.
Knorr, and Tizzoni, and Cattani and Morax showed indeed, that if the
tetanus toxin is injected subdurally or into the surface layers of the
cerebrum, it produces not tetanus, but a characteristic cerebral
disease. A dose of ¹⁄₂₀th or ⅒th cc. of tetanus toxin produces in the
rabbit, in 10 to 12 hours, restlessness, constant change of place, and
signs of great fear like hiding the head, turning rapidly round,
attempting to escape, polyuria, grinding the teeth, epileptoid
convulsions. The toxin in this case had manifestly united with the brain
substance while the cord suffered little.
Metchnikoff (Ann. de l’Inst. Past., April, 1898) holds that the brain
matter is only valuable in holding the toxin until it can be destroyed
by the leucocytes. He showed that the injection of the tetanus toxin in
chickens or Guinea pigs greatly encreased the production of leucocytes.
He injected tetanus toxin into the aqueous humor of the rabbit without
producing much effect, but when the same agent mixed with cerebral
substance was injected, the result was a great accumulation of
leucocytes, and hypopion. If the mixture of brain substance and tetanus
toxins were injected on the brain, little encrease of leucocytes
occurred, but if thrown into the peritoneum, a most remarkable
leucocytosis took place. In twenty minutes after the injection the fluid
withdrawn from the abdomen showed large numbers of leucocytes filled
with brain substance, but no free cerebral matter.
The present status of the treatment by brain substance is therefore
somewhat uncertain. The value of that agent in holding the toxin is
allowed, but like the antitoxin it must be employed before the toxin has
reached the nerve centres and united with the living ganglion cells. Its
use would be called for therefore at the earliest possible moment and it
should be continued so long as there is reason to suspect the production
of fresh toxin in the wound. Its direct action on the toxin would
suggest its injection around an infected wound, or even as a dressing
for the wound in connection with antiseptics. When tetanus has already
set in it cannot be expected to undo the evil already accomplished by
the union of the toxin with the cells of the cord, though it might in
part arrest and hold new supplies of this poison coming from the wound
to the nerve centres.
_Prevention._ In a disease so deadly as tetanus and so refractory to
treatment even by antitoxin when it is once developed, prophylactic
measures are of the greatest importance. With the extensive adoption of
antiseptic surgery there has already been a material diminution in the
number of cases, yet a greater attention is demanded to the prevention
of casual cases which result from ordinary wounds. Dirty, grimy wounds
filled with the dust of stable yard or garden soil, and such as contain
splinters of wood, stones, thorns, straw and the like can only be
considered quite safe after thorough disinfection. It has been shown
that the toxin is easily neutralized at the time of infection, whereas,
after the disease is developed it will require 1,000 or 100,000 times as
much antitoxin to produce the same effect. In the case of soiled wounds,
therefore, in a valuable animal, a harmless injection of antitoxin or of
phenic acid or iodine solution before the development of tetanic
symptoms is not an unwise precaution. A succession of such injections
might be given to ward off the disease until after a lapse of time
exceeding the short and dangerous incubation.
Much more important is the disinfection of the wound itself. All foreign
bodies must be removed, but especially those that like splinters of wood
and straws are likely to harbor the spores of the bacillus. Then the
wound may be thoroughly cauterized thermically or chemically, or it may
be irrigated with a strong antiseptic solution and then dressed with
some agent that will prove destructive to the spores, and antidotal to
the toxin. Strong carbolic acid may be applied to the whole raw surface
including the uttermost recesses of the wound, and after a few seconds
or half a minute this may be neutralized by filling the wound with
dilute acetic acid or alcohol, after which a dressing of Lugol’s
solution may be applied. Lambert advises a combination of hydrochloric
and carbolic acids.
Weaker antiseptics, like a 5 per cent. solution of carbolic acid, do
more harm than good, as they destroy the pus and saprophytic microbes
and even the tetanus bacillus in the wound, without affecting the
tetanus spores, which finding no other microbes to contest with them the
possession of the field may find themselves in a better position than
before to develop into bacilli and cause tetanus.
Tetanus neonatorum may be certainly prevented by the application of a
disinfectant plaster on the navel at birth. Over 50 years ago in
Scotland this desideratum was met by applying on the navel of the
new-born child a soft and immaculately clean piece of cotton cloth which
had just been flamed over a light. On the island of St. Kilda the former
mortality of 67.2 per cent. of new-born infants, was promptly abolished
by dressing the navel daily with iodoform. For new-born animals a cheap
and convenient application may be made by incorporating 1 oz. powdered
iodine and 2 lbs. wood tar, and smearing this on the navel.
Much may be done by disinfection of stables and yards where the victims
of tetanus have been. The anærobic germ soon loses its virulence in free
air and sunshine, and one has to dread especially, filthy stables,
collections of manure, contaminated litter, wood, combs, brushes and
buckets. In unpaved yards remove the infected surface soil and replace
by fresh disinfected earth, or still better, well burned brick.
For horses which are necessarily exposed to manure or contaminated soil,
it is commendable to wash the hoofs and pasterns on returning from work
and then sponge with a weak solution (5 per cent.) of phenic acid.
Another resort is to smear the hoofs daily with an ointment of tar and
lard, equal parts. This cannot protect from infection by splinters of
wood containing the spores, but is to a large extent preventive in the
case of bacilli that might have been otherwise lodged on the surface and
which could have been carried into the wounds inflicted by nails and
other noninfected bodies. Careful shoeing is all important, to avoid the
bruises, suppurating corns and _gravelling_ which make openings for the
ready entrance of the spore.
Roux and Nocard recommend immunization by protective inoculation. This
is not only possible, but would be justified economically in the case of
valuable animals, or in all animals in a district where the bacillus
tetani is universally spread. The method is the same as advised above
for the immunization of animals, for the production of antitoxin.
In districts where tetanus is rare, the cost of universal immunization
against the disease would very far exceed the losses front casual cases.
Under such conditions it would be an economical blunder.
FOOT AND MOUTH DISEASE.
Synonyms. Definition. Susceptible animals: cloven footed, all warm
blooded animals. Historic notes; Geographical distribution; English
invasions in 18th and 19th centuries; North and South American
invasions in 1870; In Asia from immemorial times. Causes: infection in
liquid of vesicles, saliva on pastures, roads, feeding and drinking
places, halters, etc.; from feet on pastures, buildings, yards, roads,
cars, boats, etc.; from teats through milk. Microbe not certainly
known, micrococci, streptococci and bacilli found. Virus inert when
dried 24 hours at 88° F.; survived 9 months at 32° F., attack
immunizes for 5 months; injection of 1 lymph and 2 of blood of immune
renders refractory; filtered lymph still virulent; microbe probably
infinitesimal; accessory causes: movement, mingling of cattle, sheep,
swine, etc., war, trade, common pasturage, infected roads, ships,
yards, halters, etc. Symptoms: incubation 36 hours to 6 days; slight
fever; redness, tenderness of buccal mucosa and teats, grinding teeth,
smacking tongue, tender feet, shaking them backward, bullæ on mouth
and teats, not nodular, nor chambered as in variola, salivation,
bloody, circular or irregular raw sores, vesicles and erosions in
interdigital space, shedding hoofs, sheep walk on knees, gangrenous
mammitis; intestinal eruption and diarrhœa in sucklings. Mortality.
Prognosis; recovery in 15 days, deaths rare if cared for. Losses from
destruction of product and emaciation—occasional abortion. Diagnosis:
based on infection of all exposed bisulcates, localization on mouth,
teats and feet, inoculability on other warm blooded animals,
unchambered vesicles, slight fever, and prompt recovery. Notes of
affection in man. Symptoms in man. Prevention and treatment in man.
Prevention in animals: exclusion of contagion, immediate and mediate;
close infected pastures and roads, stop all movement of bisulcates,
disinfect all boats, cars, places and things exposed, exclude
visitors, guarantees with strange animals, quarantine and disinfect
arrivals, exclude fresh animal products, fodder and litter, wash,
disinfect soiled clothes. Inoculation undesirable. Treatment in
animals: cleanliness, dryness, disinfection, segregate sick and well,
gaseous antiseptics, liquid ointments. Gruels, mashes, sliced, boiled,
or pulped roots. Local dressings for mouth, teats and feet. Evulsion
of hoof. Mammitis.
_Synonyms._ Aphthous fever: Aphtha Epizoötica, Eczema Epizoötica.
_Definition._ An acute infectious disease of the lower animals but
especially of ruminants, characterized by a slight fever and the
eruption of vesicles, or ballæ on the skin and mucosæ, and usually those
of the mouth, feet and teats.
_Susceptible Animals._ The animals that prove the most obnoxious to the
disease are the bisulcates—large and small ruminants and swine. Man
however is susceptible as are also horses, dogs, cats and fowls, when
they are inoculated or fed upon the infected milk or other products. It
is doubtful if any warm-blooded animal enjoys an immunity.
_History, Geographical Distribution._ Toward the middle of the
eighteenth century this disease prevailed in Central Europe and England.
The latter country stamped out both this and the Rinderpest, but it
continued to prevail on the Continent and was re-imported into England
in 1839. It reached America through an importation from England to
Montreal in 1870, but owing to more or less effective quarantine, to the
absence of cattle traffic from east to west, and above all to the
prolonged confinement in yards and stables during our northern winter,
it burnt itself out in the course of the year. In Asia it has prevailed
from time immemorial, and it was imported into South America in 1870.
_Etiology._ This disease has long been known as caused by infection
alone. Excluded from England in the middle of the eighteenth century it
did not appear again until re-imported in the middle of the nineteenth,
and then speedily overran the whole island except the breeding districts
into which strange stock were never taken. In South America it was
unknown until imported from the Old World into the Argentine Republic
and then it made a wide extension and maintained itself where the stock
was kept on unfenced ranches. In our fenced Northeastern states it died
out and has not reappeared.
The infection is especially resident in the vesicles or aphthæ. From the
mouth this is distributed, with the abundant drivelling saliva, on
pastures, roads, feeding and drinking troughs, ponds, streams and
halters, and readily communicates the disease to healthy stock following
in the same places. From the feet and especially the interdigital space,
it is left on the vegetation, buildings, yards, cars, boats and all
other possible media to infect other stock in turn. From the teats it
mingles with the milk so as to infect the young suckling and all animals
and men to whom the milk may be given. It may become dried on litter and
other light objects and carried by the winds, or it may be carried on
the feet of men or animals including birds, but apart from this it is
not readily diffused and oftentimes a broad highway may set a limit to
its propagation.
The infecting microbe is not definitely known. Nosotti found a
micrococcus in the lymph of the vesicle, which stained readily in
aniline colors, was easily cultivated and pathogenic. Klein found a
streptococcus which, similarly tested, presented an equal claim to be
the causative factor. Bassianus and Siegel found in the blood and
tissues of a person who died of foot and mouth disease a small oval
bacillus, which they later obtained from the vesicles of three children
who were suffering from the disease, and from animals attacked in two
successive epizoötics. With this they first successfully inoculated a
calf and from the pure cultures obtained from its blood, inoculated
three calves and a young pig.
Löffler and Frosch, the recent commission on foot and mouth disease in
Germany, report that no organisms could be seen nor cultivated from the
lymph found in recent bullæ of the buccal mucosa, though this lymph
proved virulent when inoculated on calves.
They found that the lymph became inert when dried for 24 hours at 31° C.
(88° F.), while it retained its vitality and virulence after exposure
for 9 months to a temperature of 0° C. They concluded that it could not
penetrate through the unbroken skin nor mucosa, and that it was most
effective when injected into the blood or peritoneal cavity. One attack
conferred immunity for 5 months. Blood from immune animals, injected
into susceptible ones, does not confer immunity, but 75 per cent. could
be rendered immune if injected with a mixture of the lymph from the
vesicle and double the same amount of the blood from the immune animal.
Animals so treated become immune to 100 times the infecting dose.
Filtered lymph was still virulent and the commission suggests that the
microbe may be so small as to pass through the filter, and escape
discovery by the most powerful lenses. An object one fifth the size of
the smallest known bacillus—that of influenza—would be invisible under
our best microscope.
By actual experiment the virus has been found in the nose, larynx,
bronchia, stomach and intestines, but into all these the virulent lymph
of the bullæ can find its way. In the intestines, indeed, in cases
caused by feeding, bullæ have been found on the mucosa.
A most important question would be that of the virulence of the milk,
but inasmuch as the vesicles appear on the teats and even on the
openings of the milk ducts, and in bursting discharge their contents
with the milk into the pail, the milk becomes per force infecting. The
experiment of Hertwig and his students who infected themselves by
drinking the warm milk by way of experiment, has been often repeated
unwittingly by unwilling victims, and the many cases of calves, pigs and
chickens contracting the disease by consuming the otherwise discarded
milk leaves no room for doubt that this product is often infecting.
Among conditions contributing to a spread of infection, nothing is more
potent than a free movement of ruminants, and swine whether determined
by war, trade, or the intermingling of different herds on commons or
unfenced ranges. In infected countries, in which cattle are distributed
through large central markets there is always a wide extension after one
of these fairs, the infection being narrowly circumscribed to herds
receiving cattle from the fair, or those that have travelled on the same
roads or fields after the market cattle. It has repeatedly happened that
cattle shipped from the United States, where this disease has long been
unknown, have been found diseased on their arrival at a British port,
simply because they have been tied upon the passage with halters
formerly used on infected Irish or Continental stock.
_Symptoms in animals._ There is first a period of incubation shorter in
hot than in cold weather and varying from 36 hours to 6 days
(exceptionally 15 days). It is altogether probable that prolonged
incubation is really delayed infection, the virus having been attached
to the feet for some time before it entered the tissues. Cattle usually
show the disease two days after exposure in a public market, building or
conveyance.
There is first moderate hyperthermia (102° to 103° F.), indicated by the
clinical thermometer before there is any outward sign of ill health.
There may be erection of the hair, tremors or distinct shivering,
dryness and heat of the muzzle, redness and even tenderness of the
buccal mucosa and teats, saliva drivels from the mouth or may show as a
frothy mass at the commissures or margins of the lips, and there may be
grinding of the teeth and a peculiar smacking of the tongue and hard
palate which may be heard at a considerable distance. There are greatly
impaired appetite and rumination. Tenderness of the feet is shown by
halting or lameness and by the extension backward and shaking of the
hind feet in turn.
With the appearance of the eruption, usually on the second day of
illness, the fever as a rule moderates, and on examination of the mouth
bullæ of ⅓d. to 1 inch in diameter may be found on the inside of the
lips, and cheeks, or on the palate and tongue, with, in many cases, a
congested areola, but showing no nodule as in variola. These bullæ may
extend to the muzzle, pituitary membrane or pharynx. They burst very
soon after their formation, exposing a red base of inflamed corium, with
a clearly rounded margin, or, at first, with shreds of the torn
epithelial covering. The salivation now becomes more profuse, glairy and
even bloody, and there is more active movement of the tongue. When the
bullæ have been confluent there are formed extensive red patches denuded
of epithelium, and the suffering causes a complete but temporary
dysphagia. The renewal of the epithelium, however, takes place promptly
and may be well advanced in four or five days. Upon the teats the bullæ
appear at about the same time but are usually smaller than the buccal,
and do not show the thickened base of cow pox. They burst in 36 to 48
hours unless broken earlier by the hands of the milker, forming sores
comparable to those of the mouth, which are liable to be kept up by the
necessary manipulations in milking.
Upon the feet the eruption shows especially in the interdigital space,
at first as vesicles smaller than those of the mouth and teats, leaving
erosions and ulcers which extend under the adjacent horn, and upward on
the front and back of the pastern. From exposure to mud and filth these
are liable to be kept up even longer than those of the mouth and teats,
and under neglect the entire hoof is often shed. In sheep and swine the
disease may be localized almost exclusively in the feet. Sheep will even
walk on the knees.
In young animals and those fed on the milk, the eruption may take place
on the intestinal mucosa with violent congestion, diarrhœa and a fatal
issue. Aggravated cases may show gangrenous mammitis or abortions.
_Mortality and Prognosis._ While there are seasons of special pathogenic
severity, yet as a rule, the foot and mouth disease is a mild affection
and unless neglected, the patients entirely recover in about fifteen
days. The pecuniary loss in dairy and feeding cattle has been found to
average in Great Britain about $10 per head, and as few animals escape,
the consequences are usually very serious. In England the losses from
this disease in 1883 reached $5,000,000, in France, those of 1871 were
$7,500,000 and in Switzerland, $2,500,000. In Germany, over 7,000,000
animals suffered from 1889–94.
_Differential Diagnosis._ While a mistake might be made in an isolated
case, such a thing should be absolutely impossible where cattle and
other animals are collected in herds. The rapid infection of the whole
herd, the implication of sheep and swine along with the cattle, and the
eruption of the characteristic bullæ on the mouth, feet and udder or on
two of these locations to the exclusion of the rest of the body, is not
likely to be counterfeited by another disease. An outbreak of gangrenous
ergotism in Kansas, Missouri and Illinois in the spring of 1884, was
pronounced to be foot and mouth disease by a number of veterinarians,
including an expert sent by the Government of Canada. On behalf of the
U. S. Treasury I investigated the disease, which caused in many cases
sores on the mouths and feet, but it spared all sheep and swine, could
not be conveyed to them nor to new born calves by inoculation, and in
many cases it caused gangrene of all the tissues, soft and hard, and
separation of the limb at a given point, often near the tarsus. The
quarantines were raised, the disease made no further extension, and the
existing panic subsided.
_Infection of Man._ The first authentic record of this affection in man
we owe to Valentin, who records that during the outbreak in Hesse in
1695 men suffered from inflammation of the gums, tongue and mouth.
Michel Sagar says, that in 1764 men who drank the milk were affected
with aphtha. In 1828 it was conveyed from animals to men in Bohemia
(Nadberny), in Styria (Levitsky) and Wurtemberg (Kolb). In 1834, three
veterinarians, Hertwig, Mann and Villain, voluntarily drank a quart each
of the warm milk of a cow suffering from this affection. On the second
day Hertwig suffered from fever, headache and itching of the hands and
fingers. Five days later bullæ formed on the hands and fingers, the
tongue, cheeks and lips. In the two others the eruption was confined to
the buccal mucosa. Since that time records of the infection of human
beings have been very numerous. During the American epizoötic of 1870 I
met with the case of a farmer at South Dover, N. Y., who suffered from
sore mouth and blisters along the margin of the tongue from drinking the
milk. The danger is greatest in children on an exclusive milk diet and
who drink it warm. Kolb in 1828, noticed acid vomiting and diarrhœa in
such subjects, Hübner observed that beside the buccal eruption such
children often suffered from inflammation of the stomach and bowels and
that very young children fed on the milk of the diseased cows died.
Balfour, Watson and others have noticed similar results in Scotland.
Allbutt saw the buccal eruption in three children in Yorkshire, England,
during the local prevalence of the English epizoötic in 1883, and
secured information of a number of other cases in the same district.
A number of cases were recorded during 1893 in Germany. A shepherd
infected himself by holding in his mouth the knife with which he had
pared the diseased feet of sheep, and another workman and a veterinarian
had extensive eruptions on the hands after dressing the affected feet. A
number of milk-maids were infected by milking, the eruption appearing on
the hands, and in one case on the breast. A child fed on the milk of
diseased cows, had chill and fever with gastric disturbance, and later
an eruption of vesicles on the lips and tongue and between the fingers
and toes.
Again, in 1895, during the prevalence of foot and mouth disease in the
southern part of Berlin, a considerable number of the milk consumers
suffered from fever with the eruption of bullæ on the tongue and buccal
mucosa generally, which on early bursting left very painful ulcerations.
The acute disease did not last more than five days, but left a sense of
great weakness for a time. Virchow, who made an investigation,
unhesitatingly pronounced it to be foot and mouth disease.
Cases of infection through butter made from infected milk are on record.
A Berlin veterinary student suffered from the buccal eruption and
erysipelatoid swelling of the ear, and a German clergyman had in
addition a period of chilliness, fever, diarrhœa and pruritus. Similarly
Schneider quotes cases determined by infected cheese, and Friedberger
and Fröhner, cases caused by virulent buttermilk.
_Symptoms in Man._ In man there is observed the tendency to localization
on the same points as in animals. As the hands are naturally exposed to
infection by milking or treating the diseased animals, they are
especially obnoxious to the eruption, and the same is true of the mouth
when the infected milk or other dairy products are consumed. The bullæ
on the buccal mucosa are generally confluent, and often extend to the
fauces and pharynx, rendering speech difficult and swallowing painful,
and leaving extensive and painful sores which, however, soon heal up. In
women the bullæ have been seen around the congested nipples, and in
exceptional cases they have been generally diffused over the body.
In cases due to drinking the milk, the early febrile symptoms are liable
to be accompanied or followed by nausea, anorexia, abdominal pain and
diarrhœa, and still later by the cutaneous and buccal eruption.
The duration of the disease is from 10 to 15 days and as a rule no
permanent scars are left on the skin or mucous membranes.
The _diagnosis_ is assisted by the knowledge of the prevalence of the
disease in herds in the district, and that the patient has handled the
diseased animals, or drunk their milk, or eaten their butter or cheese
products. The predilection of the eruption for the fingers, the roots of
the nails and the mouth is very significant. The disease follows an
acute course and convalescence is complete in ten or fifteen days, which
serves to differentiate it from most skin eruptions. From variola which
pursues an equally rapid course it is distinguished by the absence of
the primary nodular swelling, and of the septa or pillars that divide
the mature pock into independent chambers.
_Prophylactics._ The best prevention for man is to exclude the disease
from the country and its herds as is now the case in the United States.
When the disease does exist in herds the attendants should cauterize any
sores on the hands, and wash the hands with an antiseptic, such as a 10
per cent. carbolic acid solution, after handling the diseased. The milk
and its manufactured products—butter and cheese—should be withheld from
consumption until after the herd has recovered. Infection can be
obviated by boiling the milk.
_Treatment._ The disease follows a rapid course and is self-limiting,
and usually benign so that active treatment is not urgently demanded.
The local lesions are best met by non-poisonous antiseptics, such as:
borax in powder or strong solution; boric acid (4:100); sodium
hyposulphite (½ oz. 1 qt.); chlorate of potash (½ oz. to 1 quart);
salicylic acid (1:100); or salicylate of soda. Pounded ice may be used
as a soothing agent. The cutaneous lesions may be wrapped in cloth wet
with one or other of the antiseptic lotions. Any disposition to ulcerate
may be met by the stick of silver nitrate.
Slightly laxative or diuretic agents may be employed for their febrifuge
and eliminating properties and the food should be light, easily
digestible and given cold.
_Prevention in Animals._ When the disease exists in a country or
district this includes all measures preventive of immediate or mediate
contagion. Arrest of all movement of cloven footed animals in infected
districts, disinfection of cars, boats and other conveyances, of
markets, yards, highways, seclusion of infected herds and pastures,
exclusion of visitors, disinfection of products, certificates of
soundness of origin, thorough disinfection after recovery of the herd,
such are the leading points to attend to. Inspection or closure of fairs
and markets is desirable and any exposure of diseased or infected
animals should be visited with heavy penalty, in addition to the cost of
detention and supervision. For a noninfected country a certificate and
guarantee of non-exposure with each cloven-footed animal imported, and
of thorough disinfection of the cars, boats, halters or other objects
used upon them, and of the places, fodder and litter supplied, together
with a quarantine (1 week) and surface disinfection should be required
under penalty. Exclusion of fresh hides, bones, guts, hair, bristles,
wool, horn, as well as of fodder and litter is essential. Cattle
attendants, drivers and others whose clothes are soiled with the
products of the barn, should have the same washed and disinfected.
Inoculation has been proposed, and even practiced to pass a whole herd
promptly through the malady, but as immunity lasts but three months, and
the attendant risks to other herds are greatly encreased it is at once
an economic blunder, and a great injury to adjoining owners. Any
resulting extension to other herds should be an occasion for a verdict
for damages at common law.
_Treatment in Animals._ Provision is first made against extension of the
infection. The floor should be kept clean, dry and covered with sawdust,
tan bark, gypsum or litter sprinkled with these or with phenic acid. The
herd should be divided into two lots—the apparently sound, and unsound
kept strictly apart under separate attendants, above all separate
milkers. As soon as any symptoms are shown by an animal in the sound
enclosure it must be instantly transferred to the other and its stall
disinfected. Antiseptics such as gaseous iodine (two tablespoonful of
tincture of iodine, thrown into a quart of boiling water twice daily),
sulphurous acid, salicylic acid, creolin, lysol or other ointment on the
feet and teats, may also be used. In this way it may be possible to save
a number from an attack, yet most commonly the exposure is common and
universal and the malady develops in all simultaneously. For those
already attacked, gruels, mashes, and cool pulped, finely sliced or
boiled roots may be all that is required, the disease runs its course
and recovery ensues in 15 days. As local dressings the following may
serve as examples: for the mouth, borax, chlorate of potash, salicylate
or sulphite of soda 2 drs. to 1 quart water; phenic acid, creolin, or
lysol, one or two teaspoonfuls to a quart; for the foot, clean the
interdigital space and apply tar and carbolic acid with bandage, or use
solutions of creolin, lysol, pyoktanin or blue-stone; in aggravated
cases strong mineral acids with tar; for the teats, ointments of boric
or salicylic acid, creolin, lysol, naphthalin or napthol. Separation of
the hoof or mammitis will require treatment according to indications.
MILK SICKNESS. “THE TREMBLES.”
Geographical distribution: timbered lands in the United States;
different altitudes, and geological formations; on hills and wooded
bottoms; known to Indians and pioneers; now unknown where formerly
prevailed. Contagion: through milk; no specific microbe found in every
case. Alleged causes: rhus; nickel; spirillum; bacillus. Prevails in
dry seasons; contracted under night exposure; confined to given
enclosures; to late summer and autumn. Not conveyed by contagion,
indefinitely, as are plagues. Men show very varying susceptibility;
young children may be relatively immune. Fatigue, debility, ill
health, predispose. Exertion to fatigue rouses symptoms in animal
affected. Cow in full milk eliminates toxins and does not show
symptoms; the milk infects. Steers, bulls and heifers, show marked
symptoms. Calves suffer through milk; swine through veal; dogs through
pork; buzzard through dead dog. Incubation 8 to 12 days. Symptoms:
tardy, lazy gait, drooping, anorexia, ardent thirst, inactive bowels
and kidneys, milch cows when driven or excited, tremble and may
suddenly die. Muscular debility, constant decubitus, complete apathy,
neither evades nor resents injury. Bloodshot, fixed, glazed, unwinking
eyes, pulse and breathing slow, temperature low, hebetude, torpor,
coma; death 8th to 10th day. Sheep very prostrate. Calves tremble when
sucking, vomit and perhaps die suddenly. Pigs and dogs vomit, and show
costiveness, remarkable debility and weariness. Man is weary,
languorous, weak, apathetic, loathes food, is nauseated, retches. No
fever; but ardent thirst, tremulous tongue, mawkish breath, soft
flabby belly, careless of own or family interests, forgetful of
decency. Nausea, vomiting of blueish liquid, hebetude, inactive
bowels, coma. Lesions: gastro-intestinal congestions; ingesta like
hard balls of sawdust. Treatment: charcoal, mild laxatives, elm bark,
egg nog, potassium permanganate. Prevention: clear timber land, let in
sunshine, cultivate. Insects. Sterilize the milk.
This is an infectious disease which has been found enzoötic in certain
unimproved, timbered lands of North Carolina, Georgia, Tennessee,
Kentucky, W. Pennsylvania, Ohio, Michigan, Indiana and Illinois. Beach
says it has never been reported on any of the Western prairies, at any
point west of the Mississippi River, in New England, in the Canadas, in
any islands, or in any part of the Old World. Altitude appears to have
no effect in its production, nor geological formation; it has been found
in the wooded mountains of the Blue Ridge of N. Carolina and Georgia
(Kerr, Salmon, Phillips); in the hills of Pennsylvania and Kentucky;
(Beach, Phillips); on timbered uplands (Phillips); and on the wooded
bottoms of the Scioto and Miami in Ohio (Phillips, Schmidt); in the
timbered bottom lands of the Wabash and White Rivers in Indiana
(Phillips); and in the wooded bottoms (Beardsley), and Indian Grove in
McLean, Co., Ill. (Beach). The constant conditions are the heavily
timbered and virgin condition of the soil.
It was much more prevalent in the time of the early settlers, than it is
to-day, many infecting localities having become salubrious in connection
with the clearing away of the forests and cultivation of the soil. The
disease was well known to the Indians and often proved disastrous to the
pioneers, whole communities being swept off as recorded of Pigeon Creek,
by Nicolay and Hay in their History of Abraham Lincoln. According to
these writers it was “a malignant form of fever—attributed variously to
malaria, and to the eating of poisonous herbs by the cattle—attacking
cattle as well as human beings, attended with violent retching and a
burning sensation in the stomach, and often terminating fatally on the
third day.” Even in these early days settlers were loathe to acknowledge
the existence of the infection on their lands, doubtless because it
depreciated them, and to-day with a better knowledge of the necessary
precautionary measures, it has literally disappeared in many places, so
that it is now difficult to find a case.
_Contagion._ That the disease has been transmitted through the milk from
animals to man and other animals has been too painfully evident from the
first, but no specific microörganism has been found to be constantly
present, capable of pure culture in artificial media and of causing the
disease when transferred from such media to a new victim. Naturally all
sorts of theories have been advanced, no one of which has been
demonstrably proved. It has been attributed to eating of poison ivy
(Rhus toxicodendron) by the cattle, as this plant was usually found on
the infecting lands, but rhus is also common throughout New England and
the Eastern States where milk sickness is unknown. It has been claimed
that it was due to mineral agents, especially nickel, in the water but
the mineral salts in the water are not removed by culture of the surface
soil, which puts an end to milk sickness. Phillips (1876) claimed to
have found the cause in an actively motile spirillum in the blood, but
he had examined the blood of but one patient, and it has not been found
in other patients by subsequent observers. Bitting found a bacillus but
further research has not determined its constancy.
Beach furnishes a series of observations which should be useful in
seeking to estimate the value of any theory propounded. 1st. Milk
sickness is a disease of dry seasons. 2. In unusually dry seasons it is
dangerous to leave domestic animals out over night in the localities
where the disease is prevalent. 3d. It has never been considered
dangerous for animals to pasture on such lands in the day time. 4th.
Cattle in one field will habitually escape, and in another with
apparently exactly the same conditions and the same flora they are
attacked. 5th. The disease is unknown on the open prairies of the
Western States, where the domestic animals are not allowed to remain
over night in the timber belts. 6th. With occasional exceptions, it is a
disease of late summer and autumn. The dangerous lots can, as a rule, be
safely depastured in winter and spring. 7th. The pioneers found that
they could protect their stock by keeping them corralled on a “tame”
piece of land from before nightfall until the fogs and dews became
dissipated on the following morning.
For the land to become “tame” it was only considered necessary to cut
off the timber and let the sunshine act freely on the surface. Plowing
and cultivation did not seem to be requisite in all cases.
A great drawback to research is the difficulty of securing cases to
study. Many lots, formerly dangerous, are no longer so, and others still
infecting are kept so secluded that casual cases cannot be found,
without much expense for experimental animals. Again, owners do not care
to depreciate their land by acknowledging that it is infecting. The
experiment stations naturally enough look askance, on the proposal to
institute expensive experiments on a disease which dies out when the
soil is improved. Deadly as the disease is to the individual attacked
(man or beast), it is not propagated indefinitely from non-milking
subjects, by simple contact or proximity after the manner of plagues. It
usually comes to an end by the death or recovery of the subject that has
contracted it by consuming meat, milk, butter or cheese, the product of
an infected animal. The demand for sanitary police measures is,
therefore, less urgent. Different observers claim that cases occur in
the large cities, through the consumption of meat, butter or cheese,
sent from infected localities, but that the city physician fails to make
a correct diagnosis. These must, however, be comparatively rare.
In addition to ingestion as a cause, certain accessory causes ought to
be noted. Some men eat the infecting material with impunity, while
others succumb to the deadly disease. As the observations have all been
made in or near the infecting localities, individuals may be immune
through a previous attack and recovery, or there may be a native
immunity through unknown conditions. Young children often suffer less
than adults, possibly because of the greater activity of their
emunctories and consequent elimination of the toxic products and the
comparative absence of exhausting or depressing conditions. Their purely
animal food (milk) may exercise an influence, and this may assist in
explaining the fact that certain adults appear to be refractory.
Fatigue, debility and ill health are said to predispose the system. Milk
sickness attacks most violently those that have been subjected to
overwork or severe exertion of any kind, especially in hot weather,
those suffering from want of sleep (sitting up with the sick), those
having a special cause of mental depression, those suffering from some
illness—constipation, indigestion, malaria, etc.
Milch cows are probably more open to the attacks of the germ because
their systems are reduced by simultaneous milking and breeding through a
number of years. Exertion or fatigue has a potent influence in
developing the symptoms, so that it is a common practice in the vicinity
of infected localities to subject animals to a good run before
purchasing. Paradoxically enough the infected milch cow which is
distributing the infecting element freely in her dairy products usually
shows, in herself, no distinct symptoms of the disease. If she is dry or
farrow she suffers like any other animal, but if in full milk, the
toxins, and even the hypothetical microbe, seem to escape in that
secretion, which proves highly poisonous to other animals, while the cow
retains her spirits, vigor and outward appearance of health. Steers,
bulls and heifers, on the other hand, show violent symptoms.
Calves suffer so long as they suck the milk. The dead calf is eaten by
swine, which suffer in their turn, and the dog contracts the disease by
eating one of these animals, or by taking infected milk or cheese. The
buzzard eats the dead dog and dies as the result.
_Incubation_ is from 8 to 12 days, though it may be reduced to two.
(Beach.)
_Symptoms._ In the domestic animals the first indication of illness is a
lazy, tardy disposition, The subject stands apart from the herd, with
drooping head and ears, listless, indifferent to all around him, and
often without appetite; or, in cattle or sheep, rumination. There is
usually extreme thirst, but without correspondingly free urination or
defecation. Peristalsis is virtually abolished and nothing whatever
passes from the bowels. The patient is likely to be found lying down and
it is difficult to get him up, and when raised he moves stiffly and with
reluctance.
In milking cows there may be no symptoms until the animal is excited or
fatigued by violent or continued exercise, as a hard run, or a drive of
four or five miles. This developes the tremors alike in milch cows and
in the mild cases in dry cattle or sheep. The subject stands still and
trembles in a striking way, the action resembling the muscular
contractions seen after the removal of the hide in an animal newly
killed. The head and ears are drooped, movements are uncertain and
stiff, and the animal may even drop dead on the spot.
As the disease advances the muscular debility becomes so great that the
animal lies down if possible, and if once down he seldom rises again.
The decubitus is extended, the head being stretched on the ground. There
is a most complete apathy, the subject showing no fear, no apprehension,
no disposition to escape or resent injury. The wildest or most timid
steer can be freely handled, and there is no disposition to flight or
retaliation. The eyes are bloodshot and become fixed and glazed, winking
ceases, the breathing is slow, pulse infrequent, and temperature often
subnormal. The extremities and surface of the body are cool, the muzzle
dry, the coat usually stares, the apathy merges into a complete
hebetude, torpor and coma, in which condition the animal often dies on
the eighth or tenth day. Violent exercise precipitates the death at
once. Recoveries are infrequent and attended by no critical discharge
from bowels or kidneys, only by a slow, at first almost imperceptible,
resumption of natural action.
The milder cases, those that show no appreciable symptom when at rest,
are seized with trembling or rigor when made to undergo the slightest
exertion; they appear haggard, stupid and spiritless, drag their limbs
slowly and stiffly and quickly stop from pure weariness and debility.
The prostration is even more marked in _sheep_, which often seem unable
to rise, or lack the nervous energy to do so.
_Calves_ tremble while sucking, and will sometimes leave the teat, vomit
the contents of the stomach, fall down and perish.
In _Vomiting Animals_ (_pig_, _dog_,) emesis usually occurs, and torpor
of the bowels or obstinate constipation is present. _Pigs_ burrow under
the litter and are driven out with difficulty, and _dogs_ when called on
to follow, do so reluctantly, slowly and stiffly and fail to keep pace
with their master (“the Slows”).
In all animals alike active or continued exertion rouses or intensifies
the symptoms.
In _man_ there is at first extreme langour, weariness and weakness, the
patient cannot be troubled to move, he loses appetite, loathes food, and
soon has nausea and retching—often from the first. There is no chill,
rigor nor violent headache as in other fevers; but insatiable thirst;
large, flabby, tremulous, moist tongue, coated a dirty white; cold nose,
ears and general surface; dry skin; sweet, mawkish or offensive breath;
flat, flabby empty belly; without peristalsis or defecation. Respiration
becomes very slow, pulse weak and compressible, heart action tumultuous
and labored, temperature often below normal, and though sometimes 99° or
100° F., never higher. The patient takes to bed in four or five days,
or, after exertion or fatigue, in a few hours becomes profoundly
apathetic, expresses no concern for his business, his own future or that
of his family, is intolerant of bed clothes or other covering and
utterly oblivious of the demands of decency. Nausea continues, but
retching becomes weaker, and comparatively ineffective, or brings up a
little liquid which has been compared to blueing water of the laundry.
The apathy merges into a state of hebetude and this into coma, with
fixed, glazed eyes, absence of all winking, and insensibility to
irritants and death takes place quietly without a moan or struggle.
Recovery is slow, and improvement for a time is almost imperceptible. In
some cases there remains a nervous atony, and in man, a lack of mental
and bodily vigor, and a disposition to relapse under exposure to intense
heat or fatigue has been noted, but in many cases recovery is complete
and permanent without lasting weakness.
_Lesions._ Both in man and animals, congestions of the gastric and
intestinal mucosæ have been noted, usually with a dark firm condition of
the membrane, but in some cases with capillary stasis, and sloughing.
Beach never saw indication of tenderness in the abdomen or elsewhere,
nor did he ever find blood nor stercoraceous matter in the vomited
material. The contents of stomach (paunch in cattle) and bowels formed
hard balls like cemented sawdust, firmly adherent to the dry mucosa.
_Treatment and Prevention._ Treatment by the Indians consisted in giving
large doses of powdered charcoal suspended in milk. The early physicians
attempted to open the bowels by calomel and jalap, olive oil, magnesia
citrate, and even croton oil, but the last generally with fatal results.
Milder and hardly less effective treatment consisted in large doses of
elm bark. Beach believed he got better results with quinine and egg nog.
It might be suggested to try such antiseptics as potassium permanganate,
peristaltic stimulants like eserine or pilocarpin, as an eliminating
agent pure water or weak diuretics, and nerve stimulants nitroglycerine
or ammoniacal preparations.
_Prophylaxis._ The time-honored resort of clearing the timber and brush
land so as to let the sun act freely on the soil, and the putting in of
cultivated crops, is proved reliable and permanent. The other
precautions in use are valuable in protecting the herd, but lack the
merit of thoroughness and permanence and thus fail to strike at the root
of the trouble. They are: 1st. the exclusion of domestic animals from
the infected woods in late summer and autumn and in very dry seasons;
and 2d. the exclusion of stock from such pastures from before nightfall
until after the dews have evaporated on the following morning.
The danger which attends on passing the night in the forest, strongly
suggests the intervention for the transfer of the poison of some
nocturnal animal, perhaps a night-flying insect, like the anopheles,
which transmits the plasmodium of malaria. If the germ and its
intermediate bearer (if any) were demonstrated, probably other and
simpler means of prevention could be adopted.
The fact that the propagation of the disease is not constant and wide
spreading, like a genuine plague, lessens the urgency for a rigid
sanitary police, yet animals kept on such infected farms, should be
tested by long or vigorous driving before they are killed for food, and
all milk devoted to the production of butter and cheese should be
Pasteurized or sterilized before use. It might well be questioned
whether the clearing and exposure of infecting places should not be
undertaken by the state as a sanitary measure.
In view of the fact that a milch cow may not show symptoms of the
disease, and yet yield deadly milk, and considering that the owner
cannot always tell whether she has been in the infecting woods, or
having been in, whether she is infected, it becomes an important public
health question whether such a source of deadly disease should be
perpetuated, where human food is open to contamination.
VARIOLA: POX.
_Definition_: Structure of lesion. Nomenclature. History, smallpox,
sheeppox, cowpox, horsepox. Animals susceptible: Man, sheep, cow,
goat, horse, pig, dog, buffalo, camel, monkey. Microbiology: A pure
contagium, particulate contagium, cocci, sporidium vaccinale.
_Horsepox_: Early history, means of infection. Symptoms: Vesicles on
lips, on heels, concretions, treatment. _Cowpox_: Relation to
horsepox. Causes. Relation to smallpox. Observations of Ceely,
Fletcher, Thiele, Klein, Martin, Reiter, Chauveau, influence of
vaccination, of spring parturitions, of infected stables. Symptoms:
Incubation, seat and nature of vesicle, inoculations for vaccine.
Diagnosis from aphthous fever, rinderpest, eruption of mastfeeding,
false cowpox, streptococcus eruption. Duration. Course. Prognosis.
Treatment. _Sheeppox_: Synonyms. Definition. Pathogenesis: Sheep,
goat, ox, dog, pig, horse. Forms: Discrete, confluent, hæmorrhagic.
Distribution. Causes. Contagion; extends on air; experiments on blood;
wool, hides, litter, buildings, yard, parks, railway cars, boats,
clothes, manure, wine, milk, men, dogs, cats, birds, vermin, flies.
Receptivity. Overcrowding, filth, starvation, neglect, wars, commerce.
Recovered sheep. Disinfectants. Incubation 4 to 7 days; conditions
affecting. Symptoms: Hyperthermia, general disorders, rigors,
anorexia, skin blush on parts devoid of wool, red points, papules,
vesicles, pustules, desiccation. Successive crops. On eye, nasal
mucosa, mouth, pharynx, intestines, lungs. Confluent cases. Lesions.
Prognosis. Mortality. Depreciation. Treatment. Prevention: By
segregation, slaughter and disinfection; by ovination. Technique of
ovination. Resulting immunity. _Sheeppox in Goat_: Danger of infection
to sheep. _Goatpox._ _Swinepox_: From man, sheep, goat. Symptoms.
Forms: Discrete, confluent. Susceptibility of young. Treatment.
Prevention. _Dogpox_: From man; from sheep. Other eruptions in dog.
Symptoms: Fever, flushed skin, red points, papules, vesicles,
pustules. Discrete. Confluent. Treatment. Prevention of infection of
man and sheep.
By the generic name _Variola_ is understood a febrile malady attended by
a characteristic eruption on the skin, at first papular, then becoming
vesicular and finally pustular. The structure of the vesicle is so
characteristic that it may be taken to indicate the variolous eruption
as found in man and a variety of the domestic animals. The first
indication of the lesion is the appearance on the skin of fine points of
congestion like fleabites. This is followed by active diapedesis and
proliferation of cells in the papillary layer and rete mucosum,
constituting the nodule or pimple stage. In smallpox this is so firm and
definitely outlined that it has been compared to the presence of a shot
in the skin. As the proliferation of cells increases these form in
separate clusters or groups, isolated from each other by septa or walls
largely made up of the epidermic cells. In the next stage, therefore,
when exudation takes place the lymph accumulates in the spaces occupied
by the clusters of growing cells, and is found in a series of chambers
more or less perfectly separated from each other, so that to evacuate
the whole vesicle, each minute sac must be punctured independently. The
vesicles thus differ from others caused by ordinary irritants in that
each is chambered, instead of forming one common undivided sac, which
may be emptied by a single puncture. In the next stage, when suppuration
ensues, the septa usually undergo liquefaction, so that the liquid
occupies one individed cavity in each pustule. For this reason the
central depression seen in the larger vesicles (cowpox) in their early
stage tends to disappear in the pustule. It may reappear later in the
resulting scab. Desiccation, scabbing and desquamation complete the
course of the affection, a distinct _pit_ being left as a result of the
destruction of the superficial layer of the dermis.
_Nomenclature._ The term _variola_ is believed to come from the Latin
varius (variegated, spotted) and _pox_ from the Saxon pock (pouch). The
specific names, drawn from these tongues sustain this view: As, _variolæ
vaccinæ_, _cowpox_, _kine-pox_; _variolæ equinæ_, _horsepox_; _variolæ
ovinæ_, _sheeppox_; _variolæ caprinæ_, _goatpox_; _variolæ suillæ_,
_swine pox_; _variolæ caninæ_, _dog pox_. The term _smallpox_, (_petite
verole_) is deduced from the small size of the vesicle as compared with
that of cowpox, just as the same has originated the term _smallpox_ in
sheep.
_History._ Variola has undoubtedly existed from very ancient times.
Moore found it referred to in Chinese records of 1122 years before
Christ, but it was only clearly described early in the tenth century by
Rhazes an Arabian physician. Gregory, however, found the name _variola_
in Latin manuscripts in the British Museum of a much earlier date. The
early epidemics of small pox have usually extended from the east, and
the disposition has been to refer its origin to the crowded communities
of central Asia, but nothing is certainly known as to such origin and
the lack of definite recognition and description cannot be taken as
implying that the disease did not exist. The extension of small pox to
America in 1520 was distinctly traced to a sick negro slave landed in
Mexico, and the way in which it swept the continent killing the Indians
by tens of thousands, speaks strongly for its prior absence and the
extraordinary susceptibility of the hitherto unaffected Indian races.
The variolæ of animals are not recorded until later, the mildness of the
forms attacking cattle and horses, and the lack of close observation of
the diseases of sheep furnishing a reasonable explanation. We must pass
over as uncertain the _lues ovium_ of Thomas Wallsingham, (Historia
Anglicana), imported in a _rotten_ Spanish ewe in 1274, and which
prevailed for 25 years destroying nearly all the sheep of the kingdom,
also the reference to the “pockes” of sheep in Chaucer’s “Pardoners’
tale” as highly uncertain. Laurent Joubert in his work on the “_peste_”
mentions _sheep pox_ as prevailing in 1567, and Rabelais speaks of it as
prevailing in France in 1578. It prevailed in Padua in 1649, in Venice
in 1664, 1672, and 1674 (Bottani), in Italy in 1690 (Ramazini), in
Germany in 1687–8 (Stegman), in England in 1711, in Hungary in 1712, in
France, Italy, etc., in 1714 (Kanold), in Venice and Bohemia in 1719
(Bottani), in Saxony in 1720, in Venice and France in 1723–24 (Bottani,
Astruc), in Thuringia in 1725, in Siberia in 1771 (Pallas), and in
Persia generally at the beginning of the 19th century (Bruce). Great
Britian, long protected by her insular position, was infected by sheep
from Germany in 1847 and again in 1862. Under ovination the first
invasion prevailed for four years causing wide spread destruction; under
strict separation based on thermometry, the second lasted but four
months.
_Cowpox_ has existed in England for centuries, but it has only attracted
general attention since the introduction of vaccination by Jenner in
1796. _Horsepox_ has existed concurrently with cowpox, the infection
being habitually transferred by the hands of the milkers from horse to
cow and vice versa. Jenner found it so common in the Valley of
Gloucester, that he considered it as the habitual source of cowpox.
Sacco recognized it at the beginning of the 19th century, Hertwig in
Berlin in 1830, Röll in Vienna in 1855, and Bouley and others later in
different parts of Europe.
_Animals Susceptible._ Variola in some form affects man, sheep, cattle,
horses, goats, pigs, dogs, buffaloes, camels and monkeys.
_Microbiology and Infection._ It has long been well established that
variola is due to contagion alone. The habitual dread of contact with a
smallpox patient, shows the general appreciation of the danger of
contagion, and the many epidemics, started by the introduction of a
smallpox patient and thereafter spreading from that as a centre,
together with the long continued immunity of certain insular or
trans-oceanic countries illustrate this. One of the most striking
examples is the immemorial immunity of the New World until the landing
of the variolous slave in Mexico in 1520, and the immediate, rapid and
destructive spread of the disease among the native tribes. Sheeppox
offers a no less striking example. Prevailing for centuries in Asia and
Europe, its extension to a new district was always the manifest result
of the movement of infected sheep; England remained immune until her
first invasion in 1847, and the second in 1862, in both cases the source
was easily traced, and the disease completely extinguished by the
destruction of the infection in its circumscribed area; the more distant
sheep raising countries, America, North and South, Australia, Tasmania,
New Zealand, South Africa, in the absence of importation of infected
sheep remain free to the present time. For horsepox and cowpox the
demonstration is more difficult as limited outbreaks, have occurred at
intervals in different localities, traceable more or less clearly to
infection from vaccinated persons, yet often mistakenly attributed to
spontaneous developments of the disease. Before the days of Jenner
however it prevailed habitually in certain dairying districts
(Gloucestershire), and I can point to localities in New York, in which
the infection is manifestly laid up in the stables, and the disease
develops yearly in the heifers coming into milk for the first time and
in newly purchased cows, that have not been previously exposed.
The contagion varies greatly in force in the different forms of variola,
the milder horsepox or cowpox, requiring actual contact (inoculation)
while in smallpox and sheeppox, infection may take place at some
distance from the patient (in sheep over 200 yards).
A particulate infecting material was demonstrated by Chauveau, who
filtered the virus and inoculated the filtered liquid without effect,
while the solids retained on the filter invariably produced the disease.
The identity of the microbe of variola has been much discussed. Guttmann
and Grigorjew found in the lymph a coccus (Staphylococcus albus
variolæ), Ruete a very motile diplococcus, and others streptococcus, but
in cutaneous lesions it is very difficult to exclude such elements.
Pfeiffer, Guarnieri, Van der Loeff, Wasielewski and others have drawn
attention to small protoplasmic bodies (manifestly protozoa) found in
the vaccine lymph, and which appear to be the infecting agents.
Wasielewski cultivated these on a rabbit’s cornea to the 48th
generation, and from the last successfully inoculated a calf and several
children.
Funck finds this _sporidium vaccinale_ constantly in the vaccine lymph
and surrounding tissue, as a refractile, amœboid, spherical organism
(spore) 1 to 3μ in diameter, and, less abundantly, a round or ovoid
spore cyst 25μ. These cysts are either smooth or uneven like a
raspberry, and have a single or double contoured membrane. They are
easily stained with Sudan III. Examined in hanging drops they are seen
just under the cover glass, not on the surface of the drops. Larger
flattened bodies found in the lymph, with many included spores are
manifestly epithelial cells. Copiman cultivated the organism in
glycerinated collodion capsules in the peritoneal cavity of rabbits and
dogs, producing zoöglœea masses staining peripherically with methylene
blue, and which caused typical vaccinia in calves. He found the same
elements in variola of man.
HORSE POX. VARIOLA EQUINÆ.
This was recognized toward the end of the 18th century, in the valley of
the Severn, England, by Jenner, who believed it to be the origin of
cowpox, but failed apparently to distinguish it from ordinary
“_grease_”. To-day, when we must trace each case to a preëxistent one in
some animal, and ignore the question of primary origin, we must still
recognize that it passes readily from horse to cow, and from cow to
horse, through the hands of milkers and stable-men, but that it also has
the source of vaccinated persons in the families of those handling the
horses. Whether it was also often derived from the very prevalent small
pox in past times is doubtful, yet it appears to have been much more
common about the year 1800 than it is to-day. When once started in a
stable it passes readily from horse to horse, through the hands of
shoeing-smiths and grooms, including of course their aprons, brushes,
sponges and rubbers, and also through blankets, bandages, litter and
other things on which the virus has been received. The susceptibility of
the skin in the hollow of the pastern depends mainly on the frequency of
chaps and abrasions, and to a certain extent on contact with the
road-mud infected by other passing animals. At times the suffering
animal licks the affected part, and determines the eruption on the
mouth, lips and nose (see contagious pustular stomatitis). Megnin saw
cases affecting the external generative organs and transmitted between
the sexes by coition. (See vesicular eruption on the genitals). All such
cases should be identified by inoculation.
Hertwig, as early as 1830 recorded the existence of horsepox in Berlin,
where it has been seen frequently since, and noted its transmission to
man. Bouley gave evidence of its special prevalence at Paris, and of the
production of typical vaccine vesicles in man by its inoculation. More
recently it has been frequently observed and studied by inoculation and
otherwise.
_Symptoms._ These, whether seen in horse, cow or man, do not differ from
those of cow pox, with which it may be held to be identical. The
observations of Chauveau, Warlomont, and Pfeiffer that experimental
infection, intravenous, subcutaneous, intratracheal (inhalation), or by
feeding almost always failed to give the general eruption which
characterizes small pox and sheep pox. It remains strictly local except
when inoculated on other parts of the skin or mucosa. It must be added,
however, that small pox or sheep pox, when inoculated successfully on
the horse, as a rule remains confined to the seat of inoculation. The
constitution of the horse, like that of the cow, tends to resist its
virulence.
The affected horse may show preliminary febrile symptoms, but these are
usually too slight to be noticed. They are followed by heat, tenderness
and swelling of some part of the skin, usually in the hollow of the
pastern and perhaps the back part of the metatarsal region, with more or
less (sometimes extreme) lameness. On the swollen skin may be detected
nodules, which may pass early into vesicles and pustules. The eruption
varies, however, as developed on the comparatively hairless lips or
nose, or on the densely pilous pastern.
On the lips, or other part lightly covered with hair, one can easily
follow the successive formation of the round nodule, the distinct
(sometimes umbilicated) vesicle, with its clear translucent
straw-colored contents, and the pustule, which bursts, forming a sore,
or dries up forming a dense scab, like that of cowpox.
On the heels, or on any part thickly covered with hair, the vesicle or
pustule is rarely recognized, the exudate on the contrary takes place
mainly on the surface, which becomes encrusted with an abundant
yellowish concretion, matting the hairs together, and sometimes
literally covering them. This may be very misleading to the practitioner
who expects to see the succession of fully developed vesicle and
pustule, and overlooking the true nature of the malady he may allow it
to spread widely in a stable.
Describing his inoculation cases, Chauveau gives the following
successive phenomena:—
“From the fifth to the eighth day the points of inoculation become
distinctly papular. As far as about the tenth day, the papules encrease,
and become more prominent, taking the form of an extremely wide cone,
with a base of ⅓ to ½ inch. During this period these large conical
papules are resistant and painful on pressure, but show no elevation nor
change in the epidermis, save a slightly reddish reflection in animals
with white skins. Afterward supervenes a new stage which may be called
the _period of secretion_. This commences from the ninth to the twelfth
day. The epidermis, slightly raised upon all the papule, sweats out
numerous drops of a limpid, very slightly yellow serosity. These drops
soon concrete into yellowish, transparent crusts covering the whole
surface of the pustule:—a species of characteristic crystallization,
very different from the crusts that succeed the vaccine pustules in mare
and cow. The secretion, which continues several days, is terminated from
the thirteenth to the seventeenth day after inoculation. If then the
crust is raised there is exposed a humid, pink, granular surface not
projecting beyond the surrounding skin. This surface is hollowed out by
a very deep central cavity, a sort of umbilicus, in which is inserted,
like a nail, a projection from the deep surface of the crust.”
I would add that after recovery the hair in the seats of the nodules has
a lighter color and, on the shanks and higher, remains dappled for the
season.
No _treatment_ is demanded. The application of a solution of sodium
bisulphite once or twice a day, or continuously on a bandage, will
greatly modify the intensity of the inflammation, and ward off complex
infections. If the skin is left tender or with a disposition to crack,
treat it as advised under chapped heels.
COWPOX. VARIOLA VACCINÆ.
This is manifestly the same disease, and due to the same microbe as
horse pox. The disease of the one genus is easily transmitted to the
other and the lesions and symptoms are the same, as if the virus were
derived from an animal of the same species. Differences in the local
manifestations appear to be due rather to the varying conditions of the
skin and hair follicles, than to any material distinction in the virus.
_Causes._ Aside from the germ (Sporidium vaccinale) the conditions which
favor infection are: the milking of susceptible cows with imperfectly
washed hands, after dressing legs, the seat of horse pox eruption; the
milking of healthy cows after those affected with cowpox; and the
milking with hands contaminated with the exudate in cases of vaccination
of man. That susceptible cows may also be inoculated successfully from
smallpox patients, under given conditions appears to be true, but in
Western Europe and America this is very uncommon, and would be much more
so if vaccination were universally carried out. Among those who claim
the identity of small pox and cow pox may be named Ceely, Reiter,
Babcock, Thiele, Voigt and Klein.
Ceely alleges the infection of five cows and one heifer, in 1839, in
England, from chewing the flock of a bed on which a small pox patient
had died. In 12 or 14 days they had tender congested udders, with hard
pimples imbedded in the skin, followed by blisters, and brownish scabs.
The milk diminished, saliva drivelled from the mouth, the cheeks were
inflated and retracted, the coat stared, their feet were drawn together,
and the back was arched. The disease was communicated to the owner. This
was clearly an outbreak of aphthous fever, which invaded England in that
year, and was still an unknown disease to medical men. The implication
of the heifer which would not have been inoculated with variola through
the hands of the milker, and the salivation which is unknown in cow pox,
but points directly to the buccal vesicles of foot and mouth disease,
are conclusive on this point.
Ceely later, after many fruitless attempts to convey smallpox to the
cow, at last met with results which indicated cowpox, and which he
thereafter passed from cow to cow with the characteristic cowpox
eruption.
Fletcher further reports the transmission of smallpox through the horse
to the cow, and thence to the child in the form of cowpox.
In 1836, Thiele, Kasan, S. Russia inoculated some cows on the udder with
smallpox lymph, and conveyed the lymph of the resulting vesicles back to
man, and from man to man for seventy-five generations of the virus
without finding any variation from the type of the true vaccine disease.
He repeated the experiment with equal success in 1838.
Such experiments, made before the days of careful antiseptic, or
aseptic, laboratory methods, by men who were daily engaged in making
vaccinations, cannot be very implicitly relied on, yet the success of
Thiele in Central Asia, the early home of variola, may indicate the
possibility of a transition, under given eastern conditions, which, to
say the least, is exceedingly rare in Western Europe or America.
The experiments of Klein, conducted under modern methods, are more
conclusive, and seem to imply the possibility of smallpox passing into
cowpox, in the bovine system, under some not yet clearly defined
conditions. Until such conditions are sufficiently well known, so that
they can be controlled at will, no one can be justified in attempting to
produce lymph for vaccination by simply passing smallpox virus through
the system of the cow.
It seems important to note one or two instances of the evident
transmission of smallpox from man to man through the bovine system.
In 1860, Martin inoculated variolous matter, from a man who had just
died of smallpox, on a cow’s udder, and subsequently inoculated about
fifty persons from the eruption caused in the cow. Most of those so
inoculated had unmistakable smallpox and three died.
Reiter had a very similar experience.
Chauveau (French Commission) inoculated twelve susceptible cattle with
smallpox virus and produced, in all but one, small conical (smallpox)
papules and vesicles, and in ten of these, on subsequent inoculation
with cowpox, six proved immune, three had rudimentary pustules, and one
had a distinct cowpox eruption.
A milch cow and two heifers were inoculated with smallpox and cowpox on
two sides of the vulva, with the result that each disease appeared in
the seat of its inoculation, with its characteristic vesicles, and the
two developed side by side. The smallpox vesicles were by inoculation
conveyed from ox to ox with steadily decreasing activity. Inoculated
from the cow on a child, it caused great hyperthermia, vomiting, one
large vesicle like vaccinia and a general eruption like varioloid.
Inoculation from this child upon another produced a mixed eruption of
cowpox and varioloid. Inoculation from the second child on a bull and
heifer produced papular eruption only.
Smallpox virus, inoculated on a horse produced a papular eruption, but
failed to affect another horse that had been previously vaccinated.
Cowpox virus inoculated on the first horse which had had the papular
eruption, caused a second papular eruption (not cowpox). The virus from
a vesicle in the first horse caused a similar eruption in another horse,
on which it was inoculated. The lymph from the papular eruption led to a
similar eruption in cattle, on which it was inoculated, but did not
protect against cowpox, subsequently inoculated.
The lymph from the papular eruption in the horse, inoculated on two
children, produced fever, vomiting, a general papular (smallpox)
eruption, in which a few of the pustules only showed a tendency to
umbilication. A child and its mother in the same ward contracted
varioloid. A child inoculated from one of the first named children, had
six large umbilicated vesicles like cowpox and a general papular
(smallpox) eruption. Another child inoculated from the last had six
large umbilicated vesicles, and a general papular (smallpox) eruption.
From the papular eruption of one of these children a horse and seven
cattle were inoculated and in all a varioloid eruption resulted.
The rational conclusion is, that while there is every indication of a
primal identity of the two diseases, and indeed of all forms of variola,
as shown by a disposition of the virus from one genus, when inoculated
upon a totally different genus, to show some indication of the
characteristic eruption of the latter, yet the generic type, which comes
from the long continued growth in the one class of animal, becomes so
fixed, that it cannot be overcome at once, and sometimes apparently not
at all, by transferring it to an animal of another class.
If the unfortunate results obtained by Martin, Reiter, and Chauveau, are
insufficient to deter from the use of smallpox lymph which has been
passed through the cow, the long experience with humanized vaccine,
which in its inoculation from man to man for a century has shown no
tendency to revert to smallpox virus should be a sufficient warning
against such dangerous optimism.
No deduction can be safely drawn from the comparative mildness of most
of the cases caused by reinoculation from cow or horse to man, inasmuch
as that all forms of variola can be rendered less severe by resorting to
inoculation, which was extensively practised to limit the ravages of
smallpox before the days of vaccination, and is still largely resorted
to in the case of sheeppox in Europe. In each of these diseases the
mortality can easily be reduced to 2 per cent. instead of the 20 to 50
per cent. which are lost when the disease is contracted casually.
As occurring casually, cowpox like horsepox is rare. Yet in Denmark, a
dairying country, 1,037 cases were reported in 1877–8, and 878 cases in
1888–9. I have found some outbreaks explainable, through the existence
of vaccinations in the families of the milkers, and Bollinger says that
in Germany, most outbreaks take place in spring, the time when children
are vaccinated. He should have added that this is the usual time of
parturition in the cow, the time when primipara are first subjected to
the danger from the hands of the milker, and when the cow from the
noninfected district is brought into an infected stable for the season’s
milking. In a dairying district in Tompkins Co., N.Y., the affection
appeared every spring, in the same barns, in heifers with their first
calf and in newly bought cows. All older cows, bulls, steers and
unimpregnated heifers escaped.
_Symptoms._ The period of incubation is two days, after inoculation, and
though it may appear to extend to a week when the disease is contracted
accidently, it is impossible in such cases to state the exact date of
infection. The preliminary fever is not always present, or recognized,
yet there may be slight encrease of temperature, partial impairment of
appetite and rumination, extra firmness of the fæces, a higher color of
the urine, and above all a slight diminution of milk, which is a little
more watery and coagulates more readily, than the normal.
This is followed by heat and tenderness of the udder and the appearance
on the teats of small, pale red nodules the size of a pea or larger. In
one or two days more the nodule, largely encreased in size, presents in
the centre a depressed or _umbilicated_ bluish white portion, with a
firm yellowish, reddish or reddish blue margin, and outside this a soft
pink areola, shading off into the white skin. The epidermis is raised at
points by a viscid, yellowish lymph, enclosed in a series of saccules
(multilocular vesicle). The vesicle encreases to 8 or 10 lines in
diameter by the eighth or tenth day, and exceptionally, the umbilication
is effaced by the excessive production of lymph. If left unbroken a
brownish shade appears in the centre and gradually extends toward the
periphery, the contents becoming purulent, and the pustule gradually
drying up to form a crust. The drying and thickening of the crust goes
on until the fourteenth day and the crust is usually detached by the
twentieth, leaving a pale rose colored, smooth, shallow depression,
which forms the permanent pit left after the skin has healed. The
primary scabs usually show the central umbilication, and always the
conical projection in the center of the deep aspect, and corresponding
to the pit.
Vesicles on the mammæ may pass through the above stages, but those on
the teats are usually ruptured by the hands of the milker as soon as the
liquid is thrown out, and this gives rise to troublesome sores, with
complex infections, at times implicating the gland tissue so as to cause
destructive mammitis with loss of one or more quarters, and in any case
abraded and irritated at each milking, so that the animal resists
handling, the milk is drawn off imperfectly, and dries up or the cow
becomes an inveterate kicker. If the milker has not been vaccinated he
is liable to contract the disease.
A succession of vesicles often appear on the same animal, so that they
may be found in all different stages of vesicle, pustule and crust on
the same bag at one time. The later eruptions may be the result of
inoculation from the earlier ones, and tend to prolong the attack
materially.
In inoculation of the bovine animal for the production of lymph for
vaccination, the skin of the abdomen from the symphysis pubis to the
umbilicus is shaved, or in other cases the skin between the thighs, or
in still others the skin on each side over the loins, and the virus
applied in 50 to 200 points, by preference scraped until liquid oozes,
but without any escape of blood. In a warm room the eruption matures in
four or five days, its form taking on an appearance approximating that
seen on the hairy skin of the horse. The individual lesions are somewhat
extended corresponding in form and size to the abrasion on which the
lymph was applied, and usually present the appearance of a raised patch,
covered by a grayish film of epidermis, on the removal of which there is
seen a raw alveolated surface filled with the amber-colored lymph.
_Differential Diagnosis._ From _aphthous fever_, cowpox is clearly
distinguished by (a) the multilocular structure of the vesicle, while
that of aphthous fever is a single undivided cavity which can be drained
completely by a single needle prick; (b) by the pitting or umbilication,
the aphthous vesicle being uniformly rounded and convex; (c) by the
absence of vesicles or sores on the mouth and feet, which are rarely
wanting in the aphthous eruption; (d) by the comparative absence of
hyperthermia and constitutional disturbance, which is better marked
though still slight in aphthous fever, and (e) by the absence of the
intense and subtle infection of aphthous fever, which quickly attacks a
whole herd and extends with equal rapidity over sheep, goats and pigs,
attacking all cloven-footed animals virtually without exception. The
cowpox patient, on the contrary, does not necessarily attack the cow in
the next stall unless milked by the same hands, and spares heifers,
bulls, steers, sheep, goats and pigs.
From the _rinderpest_ cutaneous eruption it is easily distinguished by
the presence of lymph in the lesion, that of rinderpest being a mere
epidermic concretion; by the absence of the intense fever, anorexia and
general constitutional disturbance, and of the early and high mortality
which characterize that disease; by the absence of rapid and uniform
infection of other cattle irrespective of a common milker; by the
immunity of heifers, steers and bulls, which are speedily prostrated by
rinderpest, and by the absence of the congestions and epithelial
concretions of the mucosæ which characterize rinderpest.
From the _leg irruption_ found in animals feeding on distiller’s swill
and grains, or on the mast of beet sugar factories, by the history of
the outbreak, of the dietary, of the seat and nature of the disease, and
by the escape of animals living on a different aliment.
From the _false cowpox_ (varicella) it is distinguished by the
unilocular lesion of the latter, its absence of areola, and its rapid
pustulation and drying, in five or six days into a thin papery crust
instead of a thick, firm, umbilicated scab, as in cowpox. Varicella is
further liable to appear in successive crops and thus last for several
weeks.
The _streptococcus eruption_ on teats and udder, is marked by the
formation of abscesses of various sizes from a simple pustule upward, by
the unilocular condition of the pus sac, by its tendency to invade the
deeper tissues, and by its rupture and granulation without the formation
of the thick umbilicated scab of cowpox.
The _hard warty growths_ on the teats which last for weeks or months
should never be mistaken for cowpox.
_Cowpox_ usually lasts for some weeks in a herd, the duration depending
on the number of susceptible animals and, whether these are habitually
milked by the same person.
_Course. Prognosis._ It is a mild affection, which does not endanger
life, yet it causes considerable loss through diminution of the milk
secretion and, it may be, altered character of the milk, through the
persistent sores and ulcers of the teats, through inflammation of the
mammæ, and through an acquired habit of kicking.
_Treatment_ is rarely needed. Any costiveness should be corrected by a
cooling saline laxative (½ to 1 lb. Epsom salts) or by soft food, and
milking should be done with great care to prevent rupture of the
vesicles and the formation of sores. A teat tube may be used if
necessary. Sores may be dressed with bland ointment. An ounce each of
spermacetti and sweet almond oil with half a dram of gum myrrh. Or the
vesicles or sores may be washed after each milking with a solution of 2
drams hyposulphite of soda in 1 quart water.
SHEEPPOX. VARIOLA OVINA.
_Synonyms._ Pocks; Peltrot; Clavelee, Picotte, (Fr.).
_Definition._ An acute febrile affection, eminently contagious,
prevailing epizoötically in sheep and goats, characterized by early and
marked hyperthermia, and general constitutional disorder, followed by
the appearance on the bare or merely hairy portions of the skin, of
diffuse redness becoming intensified in points, a rounded papular
eruption, passing into vesicles, pustules and scabs, which latter dry up
and drop off in 15 to 20 days.
_Pathogenesis._ Beside sheep and goats which contract the disease by
exposure, the following genera have been successfully inoculated: ox,
dog, pig, horse.
_Forms._ Two typical forms are recognized: (_a_) the _discrete_,
_regular_ or _benign_, in which the vesicles remain relatively few, and
well isolated from each other, and (_b_) the _confluent_, _irregular_ or
_malignant_ in which the vesicles are generally diffused over the body,
even on the parts covered by wool, and set so close together that they
merge into each other forming extensive continuous lesions. Other forms
are the _hæmorrhagic_, _purple_ or _black sheeppox_, the volante or
intermittent kind, etc.
_Geographical Distribution._ Formerly common in Central and Western
Europe, it still prevails continuously in the Balkans, the Danubian
Principalities, Italy, Spain, the South of France and Algiers. Like
other forms of variola, its permanent home is in Asia.
_Causes._ Long before the advent of modern bacteriology, sheeppox was
held to be always and everywhere the result of contagion alone. Whenever
it entered a new locality it was as the result of the importation of an
affected sheep or one of its products; insular places like England
maintained a permanent immunity, though the disease prevailed on the
other side of the narrow straits or channel; yet when imported (1847 and
1862) it demonstrated a general susceptibility of the flocks on exposure
or inoculation; more distant lands (America, Australia, Tasmania, South
Africa, etc.) in the absence of imported infection remain clear to the
present day.
The infection is more intense and diffusible than that of cowpox and
horsepox following in this the smallpox of man. Absolute contact is not
necessary, in either case the infection is carried in the air either on
dust or otherwise, and above all in a confined building, a crowded sheep
fold or a dusty highway.
In all forms of variola the virulence is concentrated in the lymph of
the vesicle, and in horsepox and cowpox it is largely confined to this,
whilst in sheeppox in severe cases it must also at times infect the
blood, as lambs are occasionally born with sheeppox. On this basis the
infection of the secretions generally has been advocated, but it is to
be supposed that in moderate cases these are contaminated after
secretion. Nocard and Roux produced immunity by the transfusion of blood
from the sick to the healthy, but in no case a variolous eruption. Even
the serosity from the swollen lymph glands failed to convey the disease.
In view of the diffusible nature of the germ, however, we must recognize
that all secretions may be quickly contaminated as soon as they are
exposed, and therefore no product of a sick or suspected sheep can be
held to be safe, and all should be treated as presumably infected. The
most dangerous products and those most liable to convey the disease are
wool, hides, litter, buildings, yards, covers, parks, railway cars,
boats, manure, urine and milk.
Living creatures like men, dogs, cats, birds, vermin, flies and other
predacious insects are occasional bearers of infection.
_Receptivity_ must be considered in every case. In countries and
districts habitually immune from sheeppox, all breeds appear to be
equally susceptible, the only refractory specimens being sheep that have
survived a first attack, and lambs born of ewes that had the disease
(naturally or inoculated) during the later stages of gestation. New born
lambs, on an exclusively milk diet, are alleged to be somewhat
refractory. In a country where sheeppox has prevailed long and
extensively, as in Algiers and Brittany, certain breeds of sheep seem to
have attained to a large measure of immunity (Nocard). This is doubtless
largely due to the survival of the more insusceptible strains of blood,
as Algerian sheep carried into France lead to most virulent outbreaks
among the native animals (Galtier).
This relative immunity is still more decided when we come to animals of
other genera. Though the latest results of research seem to identify the
sporidia found in the different forms of variola, yet the long habit of
living in an environment found in the ovine race unfits the germ for
pathogenic life in various other genera that have their own variolæ.
Sacco and Villain reported inoculations from sheep to man, but as the
first was experimenting with variola at the same time, and the second
did not test his pustules by reinoculation the results are not
convincing. Küchenmeister had a general eruption in sheep after
intravenous injection of variola of man, but failed to test it by
reinoculation. Voisin and Nocard on the other hand were uniformly
unsuccessful in attempts to convey sheeppox to man, and the handling of
variolous flocks from time immemorial must have led to many cases in
man, had he been appreciably receptive. It is virtually the same with
cowpox. Huzard vaccinated 2,000 sheep without producing immunity from
sheeppox. Voisin had precisely similar results. He further inoculated
infants with sheeppox, and later, successfully, with vaccine lymph.
It does not follow that these genera would be insusceptible under all
conditions. Yet the failure to immunize against each other would argue a
wider divergence of sheeppox and cowpox, than of smallpox and cowpox, or
than of bovine and avian tuberculosis.
Galtier failed to inoculate sheeppox on rabbits or Guinea pigs, yet
Jourdan, records a destructive outbreak in the Alps, in hares, kept in
the same places with variolous sheep.
_Accessory External Causes._ All unwholesome conditions of life, and
especially overcrowding, filth, starvation, and neglect contribute to
the extension of the infection. Still more so, the importation of sheep,
whether in the parks of armies, or in the channels of trade, by rail, or
steamboat, through stockyards or markets.
The virus is possessed of unusual vitality, and in the dried condition,
secluded from air and light will remain virulent for an indefinite
period. Hence the danger of wool, and dried sheepskins. Even in the
moisture of an ordinary shed it has retained its infectiveness for five
or six months. The sheep that has recovered from the affection may
transmit the disease to others for a period of six weeks. The virulence
is rapidly destroyed by exposure to free air and sunshine, by a high
temperature (140° F.), by dilute HCl (2:100), by carbolic acid (2:100),
by zinc chloride (5:100), by potassæ permanganas (10:100), by lime
chloride (4:100), or indeed by any of the strong antiseptics.
_Incubation._ This extends from four to seven days on an average, with a
minimum of two and a maximum of twenty days. The conditions favoring an
early eruption are youth, high condition, and a hot season, or close
warm building, with overcrowding. Those favoring a tardy eruption are
old age, debility, and above all a cold or wet season with exposure in
the open air. Simonds, who inoculated in England in the cold months
(October and November) never saw it exceed 13 days. In certain cases,
however when the eruption had already commenced in mild weather, the
sudden occurrence of a week of cold and wet, would stop it short to
start anew on the return of warm weather a week later. In inoculated
cases the incubation is shortened, while it is prolonged when the virus
is introduced by the digestive or respiratory passages.
_Symptoms._ During the last two or three days of a prolonged incubation
and especially in old sheep, there may be some impairment of appetite
and rumination, dulness, a stiffness of movement of the hind limbs, and
a disposition to lag behind the flock. The temperature may even have
risen (104.5° F.), yet Simonds has never seen the febrile symptoms
precede the eruption.
There follow, trembling, or rigors, accelerated pulse (80 to 90) and
breathing, arched back, anorexia, suspension of rumination, costiveness,
redness of the eyes, epiphora, a watery discharge from the nose,
gradually becoming more viscid, and a marked hyperthermia (105°, 106° or
107° F.) If the skin is white, a blush, with some heat, is shown in the
seat of the future eruption, usually on the parts uncovered by wool, the
axillæ, sternum, abdomen, udder, inner sides of the thighs, lower
surface of the tail, and the face—especially the eyelids, nostrils and
lips.
In two days more, deep red points, like flea bites, appear more or less
numerously, in the congested parts of the skin, and in twenty-four hours
these have increased to firm rounded papules which are felt to extend
into the true skin. These vary in size from 3 to 12 mm. or more. In two
or three days the papule has become firmer and less tender, and shows in
the centre a paler area where the exudation has resolved it into a
vesicle. The characteristic sheeppox vesicle is rounded or flattened on
its summit, being rarely pointed as in smallpox, or umbilicated as in
cowpox. It is usually surrounded by a pink zone, which is at times
infiltrated, firm and resistant. After about the sixth day, the vesicle
becomes yellowish from the formation of pus. The pustules, with the
surrounding tumefaction, encrease for about three days, when if they
have not become confluent nor infected, they begin to dry up, acquiring
a grayish crust on the surface which gradually encreases to a thick
scab, which in five or six days more is detached leaving a pink, pitted
spot covered by forming epidermis. Sometimes no distinct scab forms, but
the crust dries, cracks up, and falls off in scales.
All the vesicles do not appear at once, but some earlier and some later,
so that the successive stages of the eruption may be often seen together
on the same subject, and the case is thereby materially prolonged.
As in other forms of variola the hyperthermia usually subsides with the
appearance of the eruption, but as often reappears in some measure with
pustulation (secondary fever of reaction), and becomes more severe in
proportion to the extent and confluence of the eruption and the
occurrence of complex infection.
The eruption may invade the conjunctiva, the cornea (inducing
blindness), the nasal mucosa (causing difficult breathing), the mouth
(salivation, difficult mastication), the pharynx (difficult
deglutition), the stomach and intestines (diarrhœa), the bronchia
(cough), or the vulva.
With the occurrence of desiccation, in discrete cases, the fever
subsides, the swelling of the skin and head disappears, the discharges
from the nose and eyes cease, and the animal is restored to health.
A secondary eruption will sometimes take place, but only papules form,
which disappear without reaching maturity.
The duration of discrete sheep pox is usually about three weeks, but it
may reach four in cool weather. It is more rapid and more prone to
dangerous complications in hot weather. As the members of a flock are
usually attacked in succession, it may take three months to pass through
a flock.
In _confluent_ or _complicated cases_ the fever of invasion is very
high, the sheep dull, prostrate, tender to touch along the back and
loins particularly, with hurried, labored, panting, breathing, and
mawkish, fevered breath, the weakness increases rapidly, standing even
may become difficult, the wool is loosened and falls off in patches, the
exposed skin is red, shading, it may be, into a violet hue. The head
droops, the lips and nostrils swell, saliva drivels abundantly, anorexia
is complete, though thirst may be ardent, a yellowish and even reddish,
fœtid discharge may flow from the nose, respiration is difficult, the
eyes are watery and deeply sunken, and the head, limbs, breast and
abdomen are extensively infiltrated and œdematous.
Fever does not subside with the occurrence of eruption, which may appear
thickly over the whole body, the woolly parts as well as the bare or
hairy. The vesicles, which have often a dark, unhealthy look, tend to
become confluent, and instead of proceeding regularly to maturity, they
may remain hard or indolent papules or nodules or blacken and dry up.
The secretion, when it takes place, is liable to be a thick, yellowish,
fœtid pus. The eruption has much more tendency than with the discrete
form to invade mucosæ, and not infrequently the serosæ are involved,
especially those covering the lungs, liver and spleen. In the worst
cases death may result from the fever before any eruption has taken
place, in other cases the extent of the internal lesions tends to hasten
a fatal result. With the amount of care that can be given to a flock,
confluent cases are usually fatal.
In connection with the itching and scratching of the nose, abrasions and
complex infections ensue, resulting in extensive ulceration and gangrene
implicating the nasal cartilages and bones. The eruption around the
pasterns may lead to shedding of the hoofs, and sloughing of the whole
digital structures. Suppurating and gangrenous swellings form
subcutaneously and in the lymph glands with fatal results. Blindness is
especially liable to happen from the formation of the eruption on the
conjunctiva and cornea. Ulcerations and sloughs are common on the
internal mucosæ, and even on the serosæ. In implication of the abdominal
organs, a fœtid diarrhœa is usually present, and in pregnant ewes
abortion is the usual result.
_Lesions._ The cutaneous lesions are in their multilocular structure,
the same as in cowpox, but differ materially in size and form. The
typical vesicle is small (5 to 12 mm.), and neither broad and
umbilicated like cowpox, nor conical and pointed as in smallpox, but
round with a slight flattening on the summit. On the same animal may
often be found all the successive stages at once, red points or
hæmorrhagic spots, vesiculation, pustulation and even desiccation. The
early changes are seen in the papillary layer and rete mucosum, in the
form of swelling and congestion of the papillæ, exudation, active
proliferation of the epidermic and tissue cells, and migration of
leucocytes, (embryonic cells polynuclear) vacuolation of the papule, the
spaces being filled with a straw colored exudate, and finally, the
replacing of this by pus. If the local inflammation is very acute, the
pustule may be resolved into a small abscess. On section of the skin the
affected parts are found to be the seat of congestion and gelatinoid
exudation, extending into the subcutaneous and intermuscular connective
tissue, and even the muscles themselves are blackish and their
capillaries engorged. The exudation is especially abundant in the
dependent parts (head, neck, sternal and abdominal regions, legs). In
proportion to the severity of the attack there are congestion,
exudation, swelling, and blood extravasation in the lymph glands.
The nasal mucosa is congested, thickened or even ulcerated with
abundant, tenacious, muco-purulent secretion and the nasal chambers
narrowed or obstructed, and similar changes may be present in the
larynx, trachea and bronchia. Spots of ecchymosis and even distinct
variolous vesicles are to be expected. The pleuræ are often the seat of
congestion, petechiæ, exudation, and discoloration (red or pale). The
lung may show congestion and hepatisation in circumscribed areas, or
there may be on the surface of such hepatised portions red or grayish
foci, like a lentil, pea or bean, the seat of degeneration or forming
minute abscesses. The pericardium and myocardium may be involved to a
limited extent.
The buccal and pharyngeal mucosæ may be the seats of vesicles, or
erosions or ulcers the result of their destruction, and the
gastro-intestinal mucosa presents ecchymoses, vesicles, abrasions, and
open sores in the midst of inflamed catarrhal patches. The mesenteric
and other lymph glands are congested, swollen, softened and friable.
Congestions and petechiæ are found on the peritoneum, liver, spleen and
kidneys, with, at times, nodular foci. In certain cases congestions and
effusions have been found on the pia mater and arachnoid, in the
cerebral ventricles and the brain substance.
_Prognosis._ _Mortality._ Mortality varies much with the severity of the
special outbreak and the conditions of life, favorable or otherwise, in
which the flock is placed. In the milder forms the mortality may not
exceed seven per cent, while in the more violent the whole flock almost
may perish. A fatality of 20 to 30 per cent is the general average. Yet
the inoculated form kills but 2 per cent.
If at the outset there is great weakness and prostration, complete
anorexia and high fever, the prospect is discouraging. If the fever is
moderate and strength and appetite retained, the case is very hopeful.
On its first advent into a new country it causes a far greater mortality
than after it has been long domiciled there, and frequent outbreaks have
killed off the more susceptible strains of blood. Again very hot
weather, or, still more, the prevalence of cold, drenching rains
aggravates an outbreak and greatly encreases the fatality.
The loss is not to be measured by the deaths alone. The failure of the
crop of lambs, through abortion, the shedding of wool, the loss of
sight, hearing, hoofs, digits, flesh, stamina, etc, render recovery far
from desirable, in the worst cases, as the animal fails to thrive or pay
for its keep. On the contrary it is immune from any future attack, and
if left in a thrifty condition it becomes especially valuable in a
district where sheeppox prevails.
_Treatment._ Once established in the system the disease will follow its
regular course, through all its stages. Yet we can, by dieting, pure
air, cleanliness, shelter and even by medicinal measures, do much to
render that course a safe one. Cool sheds, pure air, clean floor, dry
clean litter and shelter from rain are above all important. The sheep
may be separated in different enclosures in small lots of 5 or 6 to
prevent crowding, heating, and excitement, and in any case the infected
should be removed from the noninfected, and even from each other to
avoid infection and reinfection. This is especially requisite in hot
weather.
For the strong and vigorous, a diet of sliced roots and meal (oat, bran,
linseed, barley, wheat middlings) is good, while for the weak, gruels of
oat meal, barley meal, linseed meal, or the same agents dry, may be
given. Powdered saltpeter may be given in this (1 oz. to 8 or 10 sheep)
and common salt allowed to be licked at will. Drinking water may be
given pure, or slightly acidulated with sulphuric or hydrochloric acid,
or hyposulphite or bisulphite of soda may be used as a substitute for
the latter. The bowels are usually costive, and may be relieved at first
by 3 ozs. of sodic sulphate, and later, if need be, by soapy injections.
Often during the course of the disease a sudden access of fever may be
cut short by a mild laxative, if that is not contra-indicated by
existing diarrhœa.
Avoid giving heating agents to bring out the eruption. The severity of
any case and the danger of complex infection are usually in ratio with
the extent of the eruption.
Lotions of hyposulphite of soda may be applied to the affected parts
from the first, and even weak lotions of chloride of zinc after the
maturation of the pustules. For the eyes, nose and mouth antiseptic
lotions may be called for.
In the advanced stages, in weak subjects, tonics and stimulants may
prove useful. To the mineral acid, quinine (10 grain doses) or gentian
(drachm doses) or other bitter may be added for valuable stock.
Treatment is only permissible in the case of very valuable animals and
when they are surrounded with the most perfect antiseptic precautions,
to prevent the escape of the infection.
_Prevention._ As in all dangerous infections this must be the preëminent
object, and when a new country has been invaded by the disease, no
sentiment nor alleged value of affected or exposed animals should be
made the warrant for treatment, nor stand in the way of the extinction
of the plague by the most rigorous measures. The recovery of an
individual flock is never to be put in the balance with the danger to
which other flocks are thereby exposed. To avoid smuggling away of
exposed animals, and consequent spread of the disease, the loss should
be met by the commonwealth and no foolish idea of administrative
economy, should tempt a stock owner to endanger the flocks of a whole
nation.
Sheep and goats from countries where sheeppox exists should be
absolutely excluded. If, in exceptional cases they are allowed to land
on our shores, they should be guaranteed by a veterinary certificate as
coming from a noninfected district, by a route free of infection, they
should be critically examined by an expert on arrival, and if passed,
should still with all clothing and utensils, be subjected to thorough
disinfection. The clothing of attendants should be similarly dealt with.
If importation is merely across a frontier, a quarantine of 21 days
followed by a disinfectant bath should be enforced.
If sheeppox has gained a footing in a flock in a new country, the flock
should be at once appraised and destroyed, and the place thoroughly
disinfected and shut up for three months. All cars, ships, wharfs,
landings, chutes, yards, buildings, parks, roads, etc., used by them
should be closed and thoroughly disinfected. All flocks exposed to any
such place or thing should be placed in strict quarantine for three
weeks, under official veterinary supervision and disposed of, should
they become affected.
As an alternative each infected and suspected flock should be secluded
in a well fenced place or shed from which all men except the necessary
attendants, all dogs and other mammals, including vermin, all birds and
as far as possible all flies are excluded. They should be divided into
small lots of 5 or 6 placed in separate pens, their temperatures should
be taken 3 or 4 times a day, and any one showing a temperature of 104°
or 105° F. should be instantly removed to a separate pen, and destroyed
as soon as the disease can be identified. In this way a diseased sheep
can usually be removed before it has infected its fellows, and at the
worst the infection will rarely spread beyond the 5 or 6 animals
enclosed in the pen where the first case appeared. It is well to
sprinkle the wool of all the flock with a 5 per cent solution of
carbolic acid, and the floor or ground with chloride of lime. The
diseased carcasses should be thoroughly sterilized by burning, boiling,
or immersion in strong acids, or they should be deeply buried, the
infected pen disinfected on each occasion, and the hands and clothes of
the attendants purified.
Careful treatment in this way will usually cut short the disease with
the loss of those only that were already infected when the outbreak was
taken in hand, but it must be in the hands of men who are at once
experts and vigilant and trustworthy. The English invasion of 1862,
under the direction of the late Professor Gamgee, was completely stamped
out in four weeks on this plan, whereas the invasion of 1847, met by the
expedients of inoculation and quarantine, lasted for four years, with
great losses in a number of flocks, and a very heavy bill for continued
expert supervision. This should be a wholesome lesson to the American
legislators who consider the prompt extinction of infection, by
abolishing this source of its increase in the living body, as a wasteful
outlay.
_Preventive Inoculation, Ovination._ If it were possible to give
immunity against sheeppox by inoculation with the exudate of cowpox, and
without danger to the sheep from fatal cowpox, or from its
transformation into the more destructive sheeppox, it would be a most
desirable resource. But experiment goes to show that vaccination is
useless, in the temperate climates at least. Sacco, Hussan, Buniva and
others in Italy vaccinated sheep extensively and claimed to have
obtained good results, but this has not been endorsed by subsequent
observers. D’Arboval vaccinated 1,523 sheep, of which 1,341 contracted
cowpox, and out of 429 of these exposed to sheeppox later, 308
contracted the latter disease. Ceely vaccinated two sheep, both of which
afterward had mild sheeppox through inoculation. Simonds and Marson
vaccinated 306 sheep, 112 of them successfully, and of these last
two-thirds contracted cowpox a second time on re-vaccination.
Twenty-nine of the successfully vaccinated sheep were inoculated with
sheeppox lymph, and in every case successfully. It is obvious that
vaccination, as a protective measure, is absolutely untrustworthy in
France or in England. Under the warm skies of Italy, as in Persia, there
may be a close relationship between the two diseases, yet in Italy
sheeppox was constantly prevalent, and it is to be feared that the
immunity in a number of cases was due to a previous attack of that
disease rather than to the vaccination. It should be noted that in
Persia sheeppox is said to be communicable to man, while in England,
Ceely failed to transmit it.
Ceely suggested variolisation with human smallpox as a preventive of
sheeppox, but Simonds and Marson failed to convey smallpox to the sheep,
though the same animal readily contracted sheeppox. One can hardly
contemplate Ceely’s proposal with equanimity. Immunity for sheep would
be dearly bought at the cost of a general diffusion of smallpox virus.
_Ovination_ or inoculation with the lymph of sheeppox is the only
available method of immunization. It entails, however, an
extraordinary multiplication of the virus in each inoculated animal,
and considering the numerous loopholes for its possible diffusion it
can only be looked on as a very dangerous and usually, in the long
run, a very expensive resort. The experience of England, above
referred to, is eloquent in witnessing against ovination, and “in
Prussia and Austria the dissemination of sheeppox went hand in hand
with inoculation.”—Friedberger and Fröhner.
On the other hand _ovination_ is not fatal to the flock operated on. The
mortality is often below 1 percent., and virtually never exceeds 4, with
a general average of about 2 per cent. It is this comparative impunity
of the inoculated flock which closes the eyes of most persons to the
great danger to a whole country and the wasteful prodigality of the
operation.
_Ovination_ further shortens the duration of the outbreak in a large
flock, passing all through the disease in 21 days, whereas as contracted
by simple exposure, the duration of the outbreak may last 90 days or
more. It further enables the owner to give such protection, shelter and
care as will guard the flock against exposure and dangerous
complications. But while preferable to the abandoning of the disease to
its natural course, it is always to be strongly condemned, where it is
possible to adopt the method which detects the sick animal in the
incipient stage by thermometry, and does away with the infection by its
removal, followed by disinfection. The only excuse for ovination is the
general prevalence of sheeppox on an island or other secluded district
where there is no great added danger from the further diffusion of the
virus, and when its simultaneous practice over the whole region can be
made the basis for universal disinfection and the definite extinction of
the contagium.
_Technique of Ovination._ The lymph (“ovine”) should be taken from a
mild case of the disease, and from a vesicle at full maturity (about the
6th day), but containing as yet a clear, translucent exudate, without
turbidity or other indication of formation of pus, or other infection.
Inoculation is made by preference on the bare lower surface of the tail
near its tip or 3 to 4 inches behind the anus. If this is unsuitable,
the inner side of the ear, an inch from the tip is usually selected,
though there is here an added element of danger, owing to its proximity
to the eye. The insertion is made with an ordinary suture needle, which
is introduced obliquely under the epidermis about one line, and pressed
upon with the thumb as it is withdrawn. A still better instrument is the
inoculation needle or lancet with a groove or spoonlike hollow on one
side. Or the skin may be scratched or abraded with the lancet, as in
vaccination, until serum oozes, when the virus is rubbed on and the part
is covered with a piece of sticking plaster. On the third or fifth day
the flock is again examined and those that have failed to _take_ are
ovinated anew.
The virus is most conveniently taken direct from the affected sheep, but
it may be preserved in capillary tubes, or on glass or ivory points, or
mixed with glycerine between glass plates, or finally, the first scab
well dried may be preserved and utilized, a minute portion being
inserted with the lancet in a pocket made under the epidermis.
Attempts have been made to secure a mitigated and safer virus, by
diluting the lymph with water or normal salt solution (1:50–150)
(Peuch), by amputating the seat of inoculation (the tip of the ear) on
the 4th or 7th day, when the vesicle is formed (Galtier), by taking a
susceptible sheep and inoculating it with sheeppox virus for ten
consecutive days, and then selecting for use the lymph from the papule
of the sixth inoculation. The inoculations of the seventh day and later
give rise to no papule even (Pourquier). By this means it is claimed
that the inoculated disease remains strictly local, passes through its
successive stages in a shorter time (15 days or less), and is perfectly
harmless to the sheep inoculated. Nocard and Mollereau sought the same
end by mixing the virus with oxygenated water, and Semmer and Raupach by
heating it to 130° F. In view of the facts that it is only under
extraordinary conditions that ovination is permissible at all, and that
the mortality, resulting from it can be kept down to about 1 per cent.,
it seems hardly worth while to attempt to obviate this loss, by any
method which may come short of the full measure of immunity.
Ovination confers immunity for a year or longer.
The care of the flock during eruption is the same as in sheeppox
contracted in the usual way.
SHEEPPOX IN GOAT. VARIOLA CAPRINA.
The goat can be successfully inoculated from the sheep, the resulting
vesicles being smaller and less prominent, and the disease assuming a
milder type. It is alleged to pass naturally from sheep to goat, and
from goat to sheep, as well as from goat to goat but, on the whole, it
is a rare disease and goats have been known to live in flocks of sheep
attacked with sheeppox, without themselves contracting the disease. The
malady seems to be of little account to the goat, yet in sheep
countries, the interests of flockmasters would demand that it should be
stamped out as vigorously as the same disease in sheep.
GOATPOX; VARIOLA CAPRINA.
In Persia according to Bruce goats suffer from a form of variola, having
larger vesicles, umbilicated and approximating to, if not identical with
cowpox. In Algiers there is found a goatpox from which sheep are alleged
to be immune (Nocard, Peuch, Bremond, Galtier) so that further
observations are wanted to put the different forms of variola of the
goat in their proper places. In a country where sheeppox is constantly
present, there is of course the possible source of fallacy of
experimenting with animals that have already had the disease, therefore
it would be expedient to put all forms of goat variola under police
control.
SWINEPOX. VARIOLA SUILLA.
Variola appears to be rather more frequent in swine than in goats.
Ficanus as quoted by Joubert saw it in 1567, contracted it was supposed
from smallpox patients. It was noted by Ramazini in 1690, by Stegman in
1697, and later by Gerlach and others. In 1891 517 cases were reported
in Hungary. It is said to be derived from man by the use of bed straw
for litter and from sheep by occupying the same stall. It can be
transmitted experimentally from pig to pig, from pigs to goats, and from
goats back to pigs (Gerlach). It is also claimed to pass from the pig to
man (Freidberger and Fröhner). Young pigs are especially subject to it
and one attack confers immunity for the future.
_Symptoms._ After a febrile condition of variable length, but usually of
a high intensity, red spots appear on the head, neck, chest, belly or
inside the arms and thighs, at first like flea bites, but passing
through the stage of papule to become vesicular on the sixth day. About
the ninth or tenth day they become purulent, and in two or three days
more a black, concave, circular crust has formed which is soon detached.
The eruption may be _local_ or _general_, _discrete_ or _confluent_ and
the issue of the case will depend much on this character. In exceptional
cases the eruption invades the mouth, eye, throat, stomach, or
intestines. Croker notes the accompaniment of a fatal lobular catarrhal
pneumonia.
It must be carefully distinguished from urticaria, eczema, and eruptions
due to pustulating irritants.
_Treatment_ is in the main the same as for sheep, care being taken to
secure perfect cleanliness, pure air, dry clean litter, easily digested
food, and protection from crowding, undue heat, cold or wet. Buttermilk
and other acidulous and diuretic drinks are recommended, and careful
attention to the state of the bowels throughout.
_Prevention_ is still more important, and better than any treatment
would be the most rigorous measures for its extinction along the lines
laid down for sheep pox. Whether the infection has been derived from man
or sheep it must be looked on as eminently dangerous to the class of
animal from which it originated, and every available means used for its
extinction.
DOG POX: VARIOLA CANINA.
Dog pox is rare, the affection occurring especially in the young. It is
said to be derived in certain cases from smallpox patients (Weiskopf),
and in others from sheep pox (Röll). The latter claims that the dog has
also its own specific form. Dupuis and others claim experimental
transmission from man to dog. At the same time eruptions connected with
gastric or hepatic disorder, distemper, eczema, or aphthous fever are
liable to be mistaken for it.
_Symptoms._ The young animals suffer from fever for a day or two,
followed by heat and redness on the sides and belly, and points of
deeper red, like flea bites, which gradually evolve through papules and
vesicles to pustules, and terminate in crusts, that drop off leaving
round bare spots. The vesicles may appear locally or generally and may
be discrete or confluent. Sucking puppies, when attacked usually perish.
In _treatment_ the same hygienic measures are demanded as for other
animals, special care being required to keep the bowels and kidneys
acting in a healthy manner. Perfect cleanliness must be secured, and
nonstimulating easily digested food. Excessive fever would demand tepid
baths, cold sponging, or acetanilid, and undue warmth, crowding and cold
exposure must be alike guarded against.
In view of the alleged sources of the disease in man and sheep, the
strictest seclusion of the affected dog, in disinfected surroundings
will become absolutely essential and when this cannot be carried out he
should be summarily destroyed.
VESICULAR EXANTHEMA OF HORSES.
_Definition_: Vesicles usually on external genitals, with fever and
infection. Causes: Contagion by coition, clothing or stable utensils;
inoculated on man or cow, resembles cowpox, but a first attack does
not always immunize a stallion; inoculable on sheep, goat and pig.
Symptoms: Incubation one to six days; local redness, heat, swelling,
tenderness, papule, vesicle, pustule, scab, desquamation,
depigmentation on genitals or in sucklings on mouth, lips, nose; may
extend to mammary and inguinal regions, with swelling, stiffness and
constitutional disturbance. Diagnosis from dourine. Treatment:
Cleanliness, astringent, antiseptic lotions; open and disinfect
abscesses; laxatives or diuretics. Prevention: Withhold from breeding.
_Definition._ An acute infectious disease, manifested by hyperthermia,
hyperæmia, and the formation usually on the external generative organs
of a crop of papules rapidly progressing to vesicles, pustules and open
sores, and attended by great local irritation and itching. It runs a
mild course and recovery ensues spontaneously in about fifteen days.
_Causes._ The disease is only known as a contagious affection,
propagated from animal to animal by breeding together, or by using the
same comb, brush or rubber, or by sucking, and in rare cases by other
accidental or experimental inoculations. To make a successful
inoculation the virus must be taken from the vesicles or pustules. When
transferred to man or ox it develops an eruption which is
indistinguishable from cowpox (Trasbot, Peuch, Galtier). Still a first
attack does not always confer immunity, as stallions may have two
successive attacks within a few weeks (Steinhoff). This implies that
either this is not genuine cowpox, as claimed in France, or that two
different exanthematous affections have been classed as one. Inoculation
with the virus has produced a characteristic eruption in sheep, goats
and pigs.
_Symptoms._ After a period of incubation of from one to six days there
appear heat, swelling and tenderness of the affected part, followed by
the formation of papules, gradually passing into vesicles, pustules and
scabs which scale off, leaving a white depigmented surface. In stallions
and mares the usual seat of the eruption is the external generative
organs; in young sucking animals the mouth, lips, nose and quarters, and
in inoculated cases wherever the virus has been implanted.
In the _mare_ there is swelling of the lips of the vulva and redness of
the vaginal and vulvar mucosa with points of a darker red, which become
firm, papular, vesicular and finally pustular. A similar eruption shows
on the skin of the swollen labiæ, on the lower surface of the tail and
on the hips, though on these points the phenomena are obscured somewhat
by the abundance of pigment. The contents of the vesicles are at first
limpid but gradually change to opaque yellowish white, brown, or even
red from slight blood extravasation. It causes not only marked
tenderness but great itching so that the patient rubs the tail and rump,
rupturing the vesicles, causing blood extravasations and retarding
healing. The sores are primarily two or three lines in diameter but may
widen and deepen under the friction. The surface may be red and angry
and covered by a yellowish viscid discharge. When they heal they leave
on the dark skin, round spots white and devoid of pigment. The itching
during the acute stage of the disease, leads to generative excitement,
frequent straining, contractions of the erector clitoris and ejection of
urine. The animal appears to be constantly in heat, yet the absence of
hyperthermia shows that there is no constitutional disorder nor central
nervous affection. The disease appears to be purely local.
In the _stallion_ after a similar incubation, the penis and usually the
sheath become swollen and congested and if free from pigment there are
dark points as described in the vulva. These points become firm,
prominent, and finally vesicular and pustular. If continued in service
the resulting sores may extend and prove protracted. In the absence of
service they tend to heal about the fifteenth day. The eruption may
extend on the scrotum, the inner side of the thighs, the throat, the
lower surface of the neck, and the inside of the forelegs; on any parts
indeed that may become soiled on mounting the mare. The meatus urinarius
is red, swollen and angry, and shows a muco-purulent discharge.
Generative excitement is shown by the more frequent rising and falling
of the testicles, protrusion and retraction of the penis, and the
frequency of urination.
In bad cases in both sexes the eruption encroaches more widely on the
skin, and subcutaneous abscesses may form on the vulva, anus, tail,
between the thighs or on the scrotal, mammary or inguinal regions. These
are attended by extensive local swellings extending on the croup, or
down to the hock, or forward to the hind limbs. In such cases there is
more or less stiffness or lameness, with constitutional disturbance,
hyperthermia, gastric disorder and emaciation.
_Diagnosis._ This disease is distinguished from dourine by the known
absence of the latter from the locality, by the ready transmission, of
the benign exanthema to cattle, by the entire absence of paresis or
mental hebetude, by its rapid progress and early recovery, usually in
fifteen days.
_Treatment_ consists in thorough cleanliness, and the application of
cooling, astringent, antiseptic lotions to the affected parts. Solutions
of borax, boric acid, sulphate or chloride of zinc, permanganate of
potash, corrosive sublimate, chlorine water, creolin, lysol, carbolic
acid, or other such agent with glycerine will act promptly and well. In
the severe cases with secondary abscesses the latter must be opened and
the cavities treated antiseptically. Cooling laxatives and diuretics
with salicylates or hyposulphites may also be desirable.
_Prevention._ No animal having sores nor discharge from the generative
organs should be used for breeding. The owner of the animal infected by
breeding has a good claim for damages.
VESICULAR EXANTHEMA IN CATTLE.
Definition: acute infections, eruptive affection, usually of the
genitals, in cattle, transmitted by breeding, and marked by
congestion, papules, vesicles and pustules. Cause: infection by
coition; by contact, by gutter, by tail, by licking, in sucklings.
Oxen and non-pregnant cows suffer. Symptoms: incubation 1 to 6 days,
cows have swelling, red points, papules, vesicles and pustules on
vulvar mucosa and adjoining skin, with profuse glairy discharge, and
it may be fever: bull has matting of preputial hairs, frequent
micturition, swollen sheath, red penis, vesicles, even necrotic ulcers
and distortion. Immunization short, uncertain. Treatment as in horse.
Prevention: seclusion and disinfection of animals, disinfection of
stalls, gutters, rubbing posts, trees, complete segregation of sick
from healthy.
_Definition._ An acute eruptive affection, attacking particularly the
generative organs of breeding cattle, manifested by congestion, papules,
vesicles and pustules of the mucosa and skin and transmitted largely by
copulation.
_Causes._ The one known cause is infection and the most common mode of
communicating it is by the generative act. In this it agrees with the
mild coital exanthema of horses, and the two affections have been
considered as identical with each other and with cowpox (Trasbot). The
similarity of the symptoms and the duration of the disease sustain this
view, but, if correct, it is probable that the affection has undergone a
distinct modification which adapts the microbe especially to life in the
genital canal, and to the maintenance of its virulence for a longer
period, and finally, robs it of the power of producing any permanent
immunity. Cowpox, though raised on the lips of the vulva, the inner side
of the thighs and the abdomen where it can be easily reached by the tail
does not tend to implicate the genital canal, and it so quickly secures
immunity, that neither male nor female would be likely to long convey
the disease. Yet in both horses and cattle experience shows that the
acquired immunity of vesicular exanthema is very short lived.
Cattle, much more than horses, are liable to transmission of the disease
by other channels than coition. Contact with the same soiled stall and
gutter, the direct transference to adjoining animals by the soiled tail,
and the greater frequency with which they lick themselves and others
doubtless contribute to this. The frequency of non-coital infection is
shown in Numann’s cases affecting the anus and sheath in oxen; also in
Fenner’s long list of cases in 669 non-pregnant cows, in a number of
cows in advanced pregnancy and in calves of a few weeks old (Friedberger
and Fröhner).
_Symptoms. In Cows._ After an incubation of one to six, (or
exceptionally ten) days, there occur swelling and redness of the lips of
the vulva, and the vaginal mucosa with here and there dark red points,
and an abundant clear, glairy discharge. The red points may become firm
and papular, and an exudate beneath the epithelium transforms them into
vesicles at first translucent but later yellow or brown as pus cells
accumulate. The clear mucous discharge meanwhile becomes opaque and, as
the pustules open, forming sores, yellowish and purulent. This discharge
soils the tails and hips, drains out on the back part of the stall and
the gutters and is carried by the tail to the udder and to other stock.
Itching may be severe and the constant rubbing and switching of the
tail, may irritate the sores and cause them to deepen or extend, beside
favoring septic infection and local necrotic processes. In such cases
there may be more or less fever, impairment of appetite, rumination and
digestion, and of the secretion of milk. Abortion is not unknown though
exceptional.
_Symptoms. In Bull._ The matting together of the long hairs of the
prepuce may be the first indication of the disease, attended or followed
by frequent micturition, or by standing with the tail raised and the
accelerator urinæ pulsating over the ischiatic arch as if passing urine.
The sheath appears swollen, the penis red granular, and angry, with red
spots, and even the scrotum may be involved in the enlargement. The red
points advance as in the female through the different forms of papule,
vesicle and pustule to the formation of sores which are more or less red
and angry. There may be an indisposition or even inability to protract
the penis, and the bull may be tardy to serve, or in case the organ is
erected and used, blood may ooze from the respective sores. The disease
usually lasts about two weeks, but may recur a few weeks later in
connection with a new infection. In aggravated and prolonged cases there
may be local septic and necrotic processes, and general fever and
digestive disturbances. Distortions of the penis may render the subject
permanently useless as a sire.
_Treatment_ is essentially the same as in the horse. Antiseptic and
astringent solutions (sulphate of zinc, iron or copper (2:100), nitrate
of silver, carbolic acid, corrosive sublimate, lysol, creolin, etc.) may
be used to advantage. Laxatives and diuretics may be called for.
_Prevention._ This would require the temporary seclusion and final
disinfection of all animals attacked, the thorough cleansing and
disinfection of the stalls and gutters, as well as all posts, trees and
fences on which the animals rub themselves. The attendants should use no
combs, brushes, sponges nor rubbers indiscriminately on the sick and
healthy. They should disinfect their hands and, if necessary, their
clothes after having handled the sick and before handling or milking
sound animals. An obvious precaution is to place the sick and healthy in
separate buildings and yards.
INFECTIOUS GENITAL CATARRH IN RABBITS.
Freidberger and Fröhner record a very contagious catarrhal affection of
the vulva and prepuce in high bred rabbits, and conveyed from animal to
animal by sexual congress. The characteristic symptoms were extensive
swelling of the parts and an abundant muco-purulent discharge.
Injection of the genital passages with a sulphate of copper solution (1
to 2 per cent) for several weeks in succession effected a cure.
INFECTIOUS ULCEROUS STOMATITIS IN LAMBS AND KIDS.
Prevails in France. Predisposing causes, bad hygiene. Specific cause,
streptococcus. Pathogenesis, to lambs and kids through sucking,
drinking, feeding; inoculable on Guinea-pig, not rabbit. Lesions: like
thrush, congested patches, with curd-like concretion; epithelium,
leucocytes, microbe; in bad cases gastro-enteritis, hepatitis, or
pneumonia. Symptoms: hyperthermia, refusal of teat, froth on lips,
dulness, debility, emaciation, death in 15 days; in mouth, concretions
and red raw sores; cough, hurried breathing, diarrhœa; subacute cases
have little fever, or infection. Mortality 8 per cent. in acute cases,
none in subacute. Prevention: separation and disinfection of fold.
Treatment: antiseptics to mouth; borax, sulphites, chlorate of potash,
sodium salicylate, iron chloride, copperas, silver nitrate. Feed
through tube or syringe. Internally, sulphites.
This is found in all parts of France, as described by Besnoit.
_Causes._ The predisposition, as in the case of many other fatal
internal inflammations, depends largely on faulty hygiene, foul, ill
ventilated, hot, close, damp, overcrowded folds, without sunshine,
drainage or free access to the outer air.
The _specific cause_ is a large coccus, isolated or in chains of 2, 3, 4
or more (streptococcus), and found abundantly in the pultaceous buccal
exudate, and in the internal lesions developed by autoinfection. It
grows readily in bouillon in the form of a precipitate in the bottom of
the liquid, in gelatine and glucose in very small, thin colonies, and on
potato in creamy masses. It is stained by anilin and by Gram’s (iodine)
preparation.
_Pathogenesis._ Inoculable on the Guinea pig, it is harmless to the
rabbit. It is readily conveyed to lambs and kids by inoculation, or
through the teats, by licking, drinking, feeding, etc. Acute cases are
very virulent, subacute very little so. Isolated cases of the latter are
not uncommon.
_Lesions._ The buccal lesions are like those of _thrush_ (_muguet_). The
mucosa is more or less congested and reddened with raised patches, of
varying extent, of white, curdy looking concretions, composed of excess
of epithelial cells and leucocytes with an abundant exudate. The
specific coccus is present in great numbers and often in almost pure
cultures. The internal lesions found in the more acute and fatal cases
are mostly in the form of gastro-enteritis, hepatitis and pneumonia,
containing the specific cocci, and due to the inhalation or swallowing
of the virulent buccal products.
_Symptoms._ In the _acute cases_ an intense hyperthermia is the first
symptom, speedily followed by refusal to suck, the accumulation of froth
around the lips, great dulness and lassitude, prostration, rapidly
advancing debility, and emaciation, and death in 15 days in a condition
of marasmus and inanition. When the mouth is opened the curdy white or
yellowish white patches of exudation are seen with an abundant glairy
mucus, and occasionally red, raw, angry patches from which the morbid
growth has been detached. The symptoms of pneumonia or of muco-enteritis
are usually in evidence, with or without diarrhœal or dysenteric
discharges. Acute cases are extremely contagious.
In _subacute cases_ the lesions are confined to the buccal mucosa, as
curdy white, raised concretions with ulcerous surfaces, frothy lips and
refusal of the teat, but without marked hyperthermia or constitutional
disturbance. Contagion is little marked, the disease appearing
enzoötically in flocks, or even as but one case in each of several
flocks.
_Mortality._ Eight per cent. of acute cases may perish, but the subacute
nearly all recover.
_Prevention._ When the disease has appeared in a flock, or in its
vicinity, the mouths of the lambs should be examined daily and affected
subjects and their dams carefully separated. A thorough disinfection of
the fold is imperative.
_Treatment._ Use antiseptics on the mouth, selecting the non-poisonous
articles. Borax may be rubbed freely on the patches. Solutions of
sulphite, bisulphite or hyposulphite of soda (1 oz. to 1 qt.) may be
used at frequent intervals on the mouth; chlorate of potash (5:100),
sodium salicylate (1:100), iron chloride (1:100) may be used. Ulcerous
patches may be cauterized by iron sulphate, silver nitrate, or the
potential cautery. Besnoit advises mercuric chloride (1:1,000) for
cutaneous lesions, but this would be unsuitable for either mouth or
lips. The strength must be sustained by the dam’s milk given through a
tube or syringe. For gastric lesions the sulphites may be given.
CONTAGIOUS ABORTION.
Definition: Premature expulsion of non-viable fœtus. Synonyms.
Susceptible animals: cows, goats, sows, mares. Accessory causes: Ice
cold drinks at periods of ovulation, frozen aliments, ice cold bath or
rain storm, mechanical injuries, unwholesome fermentescible food,
indigestible foods, close stabling, heavy milking, early breeding,
inbreeding, stagnant water, ergot, smut, vegetable irritants or
ecbolics, constitutional diseases, irritation of generative organs,
death of fœtus, urinary calculi, odor of carcass or carrion,
contagion, experimental infection between cows, between mare and cow,
relation to omphalitis. Nocard’s streptococci and bacilli, Bang’s
bacillus with best growth in two distinct grades of oxygenation,
Galtier’s observations, bacterium of the Colon group in America,
infection of the calves (pneumonia). Various kinds of infectious
abortion. Acquired immunity, variable in different forms. Immunized
cow still infecting. Symptoms. Lesions. Abortion in mares.
Therapeutics. Prevention: Protection of a sound herd, guarantee with
purchase, government control, precautions with male or unimpregnated
female, with pregnant. Extinction in a herd, separation, disinfection,
disposal of abortion, manure, urine, disinfection of animal, of
genital organs, precautions as to service, new born, fields, ewes.
Disinfectants, subcutem or in muscles.
_Definition._ The premature expulsion of the product of conception
before it is viable out of the womb. Strictly speaking, a parturition in
which the offspring is so far matured as to be _viable_ is a _premature
parturition_, while if it is _non-viable_ it is an _abortion_. Vulgarly,
however, as applied to herds, the term is used for any early parting
with the fœtus. In this wider sense infectious abortion is _the
premature expulsion of the fœtus owing to an infectious catarrh of the
womb, transmitted from one animal to another by the transference of the
microbe_.
_Synonyms._ Infectious Abortion, Enzoötic Abortion, Epizoötic Abortion.
_Animals Affected._ Abortion is most common in cows, and less frequent
in ewes, goats, sows and mares.
_Forms and Accessory Causes of Abortion._ It was formerly supposed that
abortion in herds was mainly due to mechanical and chemical agencies
acting injuriously on the system, and in adopting the explanation of a
particulate, transferrable, infectious agent for the habitual widespread
forms of the disease, we should not forget these accessory causes, many
of which by themselves cause sporadic abortions without the intervention
of an infectious element.
The free _consumption of ice cold water_ by the healthy dam causes
active gastro-intestinal peristalsis and vigorous movements of the
advanced fœtus, which can be seen or felt in the right flank, so that
this is often resorted to, to determine whether the animal is pregnant
or not. If this is frequently repeated or carried to excess in
susceptible animals it will at times cause abortions. As in all other
cases of mechanical or physiological disturbance, this is most operative
at those periods of constitutional changes, which if the animal had been
unimpregnated would have brought about ovulation and œstrum.
The greedy ingestion of _cold aliments_, like _frozen roots_, or green
vegetation covered with _hoar frost_, may have a similar action, the
more so that such aliments are extremely fermentescible and liable to
cause tympany and undue pressure on the gravid womb.
Even without ingestion, exposure to _cold rain or snow storms_ or the
_plunging in ice cold water_ tends to produce excessive peristalsis and
fœtal movements and thereby prove injurious.
_Mechanical injuries_ to the abdomen as _crushing by a gate_, _kicks_,
_hooking with horns or tusks_, _hounding with dogs_, _riding of each
other when a cow is in heat_, are liable to produce congestions,
detachment of fœtal membranes, and even death of the fœtus.
Very _fermentescible foods_ like those following a wet season or _bad
harvest_, or those made of the leafy albuminous plants like lucerne
(alfalfa), sainfoin and clover, act injuriously in the way of causing
tympanies and compressions, but it must also be recognized that we are
here dealing with fodders abounding in bacterial ferments, and that some
of their products may act physiologically as ecbolics, even if the
bacteria themselves do not colonize the genital passages as infections.
_Insufficient food_ or very _innutritious forage_, too _close stabling_,
_heavy milking_, _early breeding_ (dam or sire), _inbreeding_, are
liable to lower the general stamina and throw the system more open to
the action of other factors.
_Stagnant_, _corrupt drinking water_ has been charged with causing
abortion, and the trouble has ceased when it has been withdrawn, but it
is difficult to estimate its value in different cases—disturbing
digestion, fermentation, poisoning, or introducing of actual infection.
_Ergoted grasses_ and _smut_ in maize, wheat or oats, have been often
charged with wide spread abortions, and though each has in turn been
administered in large and continuous doses without causing abortion,
this does not invalidate the many cases in which it manifestly had that
effect, nor does it show that obstetricians have been mistaken in their
almost immemorial trust in ergot as an ecbolic. It must be recognized,
however, that grown under different conditions, of sunshine and shade,
and harvested at different stages of its development, ergot varies
greatly in its physiological action, as it does also from having been
overkept and thus one specimen is effective or dangerous while another
is absolutely ineffective. The specific action of the alkaloids in
determining contraction of involuntary muscular fibre, is seen alike
when used medicinally and when acting as an accidental toxic agent in
causing spasms, nervous torpor or paralysis, delirium; gangrene of the
feet, tail or tip of the ear; or contraction of the womb and expulsion
of its contents. Like other agents mentioned ergot is at times an active
ecbolic when coöperating with other similarly operating agencies.
_Irritant vegetables_ of various kinds are to be dreaded. Such as act on
the bowels and kidneys, keeping up a constant diarrhœa and diuresis, are
quite liable to cause abortion in susceptible subjects. _Savin_, _tansy_
and _rue_ have obtained a bad reputation in this sense.
_Cotton root bark_ is an active ecbolic, but is not likely to harm
animals unless deliberately administered.
_Impaction of the rumen or manifolds_, and _obstinate constipation_ with
the resulting straining or compression must be named as an accessory
cause.
Severe _constitutional diseases_, especially the infectious fevers,
_aphthous fever_, _lung plague_, _rinderpest_, etc., are occasional
causes of abortion.
It may be brought about by direct irritation of the womb, as in
_ovariotomy_ or _dilatation of the cervix_, or again by _death of the
fœtus_ through _twisting of the umbilical cord_.
Where cattle are subjected to dry winter feeding, in the absence of
ensilage or roots, on the magnesian limestones, small _calculi in the
kidney_ are almost the rule in winter and the irritation caused by these
conduces to abortion.
Nor must mental influence be altogether ignored. Cows and even mares are
exceedingly sensitive to the smells of _decomposing animal matter_, as
seen every day in the vicinity of _abattoirs_, or in case the _carcass_
of one of their fellows has been opened, and not infrequently in
connection with _carrion_, and the occurrence of abortions after such
excitement has been frequently noticed. Cases are on record of specially
susceptible cows having had active labor pains, from being with another
cow at the time of parturition. Shepherds have noticed that violent
thunder storms have been followed by numerous abortions in the flocks.
_The Contagious Form._ Any of the usual causes of sporadic or accidental
abortion may coöperate with the true infectious element and give unusual
energy to it, yet it is of the utmost importance to recognize the
contagion as the essential cause in all cases in which it is present.
This can usually be done by a careful inquiry into the history of the
outbreak.
When a herd has been continuously healthy up to the date of the
introduction of a cow brought from a herd where abortion has been
prevailing, and when following her arrival, one after another of the
original members of the herd abort, without any apparent cause in the
way of change of feed, water, barn, stalls, or general management, the
evidence of the introduction of contagion by the cow in question is very
circumstantial and forcible. If pregnant cows standing next to the new
cow, or near to her, abort, the argument for contagion is still further
corroborated. If the trouble continues in the herd year after year,
attacking fresh animals some months after their purchase, the case
becomes still stronger.
Or if a cow from a healthy herd is sent to a bull, that has been allowed
to serve an aborting cow, and if the resulting pregnancy in the first
cow is terminated by abortion, and if this is followed by successive
abortions in the previously healthy herd, we may reasonably conclude
that we are dealing with the infectious form. If no other appreciable
cause for the trouble can be found we may reasonably conclude that this
was the channel for infection.
Or a bull is brought from a herd where abortions have taken place, and
some time after his arrival, the cows of the previously sound herd begin
to abort, the first cases being in those that the new bull has served.
The occurrence is manifestly the result of contagion.
Or a newly purchased cow aborts, and is disposed of in consequence, and
another cow, placed in the same stall, in due time aborts also, and
others follow in succession, especially those that stood next or near to
the stall in question. Everything points to an introduced infection.
An indefinite number of other exemplary cases might be adduced, each
varying from the last, but all agreeing in this, that the evidence of
infection stands out prominently and unmistakably. The infecting
material may have been carried by the tail, tongue, soiled stall,
gutter, rubbing post, fence or other object, yet the fact of contagion
can be demonstrated with reasonable certainty.
These conclusions have been repeatedly affirmed by actual experimental
transmission. The Scottish abortion committee found that healthy
pregnant cows often escape, though standing near or even next to an
aborting one, but that when a piece of cotton wool was inserted into the
vagina of an aborting cow for twenty minutes and then transferred to
that of a healthy one, the latter invariably aborted. Galtier found that
when the infecting vaginal mucus of the aborting cow was transferred to
the same passage of the healthy pregnant one, abortion took place in the
latter. He succeeded in conveying the disease in this way from cow to
sow, ewe, goat, rabbit and Guinea pig, and found that growth in the body
of the rodent intensified its virulence, so that it could then be
successfully inoculated on the mare, bitch and cat.
Bang subjected two cows, from healthy herds and three months pregnant,
to repeated injections of the products of the culture of his abortion
bacillus in serum glycerine bouillon. Three injections were made on
April 14, May 23 and June 4, and on June 24 one cow aborted. The other
sickened and when killed was found to carry a dead fœtus. Pure cultures
of the abortion bacillus were found in the fœtal membranes and liquids
of both animals.
_Casual Infections._ In a case which came under the observation of the
present writer, a family cow kept in a barn where no abortion had
previously occurred, was taken for service to a bull in a herd where
abortion was prevailing, and though she was only present at the latter
place for a few minutes, she aborted in the sixth month.
Another cow from the same aborting herd, was taken into another herd at
a distance of two miles, where abortion had been unknown up to that
time, and some months later the cow standing in the stall next to her
aborted. The remainder of this herd was sold soon after, so that the
further progress of the disease was not traced.
Tobiassen quotes the case of a cow from an aborting herd, which calved a
fortnight before the regular time. The calf was at once sent to another
farm where no abortion had occurred, and placed in the same building
with the pregnant cows, all of which later aborted. The outbreak thus
started lasted for several years.
Jansen as quoted by Sand, reports the case of a cow from an aborting
herd having been taken into a herd that had been previously quite free
from the disease. Soon after her arrival she aborted, and later, cows in
the same herd aborted. The owner kept the matter secret and sent his
cows to a neighbor’s bull for service, with the result that for two
years abortion prevailed among the cows served by this bull.
J. R. Jansen reports that a cow brought from an infected farm, for
fattening purposes, proved to be pregnant and finally aborted, and that
24 of the pregnant cows on the same farm aborted in the same year.
Mörck relates how a cow that had aborted a fortnight previously was
taken to a farm where abortions had never been known. She aborted during
her next gestation and so did the rest of the herd, 9 in number.
Christensen records the occurrence of a general abortion in a previously
healthy herd, members of which had been sent for service to the bull of
a neighboring aborting herd.
Nygaard reports that a bull from a healthy herd, but which had been
allowed to serve some cows from a neighboring infected herd, was sold to
go on a previously healthy farm, where he was put to 14 cows only. Of
these 12 aborted, and the complement of the herd, beyond the 14 cows,
put to another bull, remained well.
In each of these cases the environment of the animals and the conditions
remained the same, the one appreciable cause of the outbreak being the
contact with an animal from an aborting herd.
_Experimental Infection._ Braüer led the way by transferring in 11
instances the vaginal mucus of aborting cows to the vagina of healthy
ones. The resulting abortions occurred from the 9th to the 21st day
after inoculation. Lehnert repeated this on two cows, the abortions
taking place on the twelfth and twentieth days respectively. Trinchera
transferred the purulent vaginal mucus of an aborting cow to the vaginæ
of healthy ones, determining in the latter, in 9 to 13 days, abortion
attended by suppurating vaginal catarrh. He secured similar results by
using the material scraped from the surface of the chorion of an
immature fœtus.
The Scottish Commission (Woodhead, McFadyean and Aitkin) placed a
healthy pregnant cow in an aborting herd, and on two successive days
lodged in her vagina for twenty minutes a piece of cotton wool soaked in
the vaginal mucus of a recently aborted cow. Within a month abortion
threatened, and on the seventieth day a seven months calf was dropped.
In a second experiment a cow, six months in calf, was taken from a
healthy herd and placed in an aborting dairy herd and a quantity of
vaginal mucus from a cow that had recently aborted was injected under
the skin of the vagina. She calved prematurely at the end of the eighth
month of gestation.
Williamsen, while treating a herd for abortion, took a piece of the
afterbirth of one of the aborting cows and rubbed it on the vagina of a
healthy cow of his own, which had a habit of carrying her calf fourteen
days over time. Five days after she had premature parturition.
He took a fragment of the fœtal membrane from the cow just named and
rubbed it on the vagina of a pregnant cow condemned for tuberculosis. In
seventeen days the cow aborted.
Though not started as an experiment, the writer may name the general
extension of abortion from one or two cows in a tuberculous herd after
they had been tested with tuberculin. Cases of this kind are doubtless
much more common than has been supposed.
Kilborne and Smith developed suppurating vaginal catarrh in cows and
mares by inoculating them with the artificial cultures of bacilli
obtained from the vaginal secretions of aborting mares.
Turner made cultures from the ovaries of aborting mares, and others from
the genital organs of foals suffering from omphalitis, and produced
abortions in pregnant mares by injecting with the same.
_Pathology._ _Bacteriology._ Franck attributed the disease to
_leptothrix vaginalis_, but subsequent observers failed to substantiate
this.
The Scottish Abortion Commission isolated five different bacteria from
the abortion membranes and vaginal mucus, but failed to identify any one
of these as, by itself, capable of causing the disease.
Nocard found in the fibrino-purulent matter between the chorion and womb
in aborting animals a micrococcus occurring singly or in chains, and a
short, delicate bacillus isolated or in pairs. From the absence of evil
effects between pregnancies he opines that the germs grow in the
membranes only, and do not affect the womb nor the general system. He
recognizes, however, that they survive in the womb from one pregnancy to
another in the complete absence of these membranes.
Galtier, on the contrary, conveyed the disease variously by the
inoculation or feeding of the milk or abortion membranes to sheep, goat,
pig, rabbit and Guinea pig, and accordingly claims that the general
system of the pregnant animal is infected, and that the germs can be
conveyed through the blood to the womb. In deducing this from feeding
experiments he appears to make too little account of the ready infection
through proximity of the anus and vulva.
Chester, of Delaware Agri. Experiment Station, found in the fœtal
membranes of aborting cows a bacillus, which in form and habits of
growth closely resembled the bacillus coli commune. In the fermentation
test, however, it showed a marked difference.
Inoculated on rabbits it did not prove fatal. Injected into the vagina
of a healthy pregnant cow it caused slight catarrhal discharge for four
or five days, but the calf was carried to full time six and a half
months later.
Bang found in aborting cows, between the womb and fœtal membranes, a
considerable odorless, gelatinoid, liquid exudate, and some pus cells.
There was active catarrh of the uterine mucosa which often carried the
disease over into the next pregnancy. In the exudate he found a number
of very minute nonmotile bacilli (1 to 3μ), which stained readily with
aniline colors, excepting in a vacuole or nucleus which was less deeply
pigmented. This bacillus grew well in serum glycerine bouillon, and more
sparingly in serum-gelatine agar. In the latter it showed a remarkable
peculiarity which serves to identify it readily from other microbes, in
two successive zones of luxuriant growth at two different depths, with
an intermediate clear zone, in which little or no growth took place. It
seems to prefer a greater or lesser supply of oxygen (21 or 90:100)
without being able to adapt itself to the intermediate condition. As
already stated it produced abortion in the cow in 21 days after
injection into the vagina. It also induced uterine catarrh and abortion
in ewes, goats, rabbits, Guinea pigs and mares when injected into the
vagina. From the vagina it usually reaches the womb, but not always. In
several cases in which it was injected subcutem or intravenously it
caused hyperthermia, and was later found in abundance in the interior of
the womb and fœtal membranes, and in the bowels of the fœtus. The
microbe is, therefore, capable of living in the blood and affecting the
womb by whatever channel it may enter the system.
V. A. Moore and the present writer made a series of experiments at the
New York State Veterinary College. In the fœtal membranes and uterine
mucus of a number of cows, aborting in different parts of the State and
therefore long distances apart, we found a bacillus that in form and
culture-experiments closely resembles bacillus coli commune. This was
nearly always in pure cultures, and in the few cases showing other
microbes, these were only such as inhabit the healthy vagina. Our
bacillus was never found in the womb nor fœtal membranes of cows that
had calved at the full period in healthy herds. It agreed in most
respects with the bacillus found by Chester, but differed somewhat in
fermentation tests. It differed also in proving fatal to rabbits when
inoculated on these animals. Injected in the form of cultures into the
vagina in three old pregnant cows it continued to live on the mucosa,
producing more or less catarrh and muco-purulent discharge in the
different cases, yet all three carried the calf to full time, one having
calved on the 123d day after injection, the second on the 167th, and the
third on the 190th.
The results obtained at the Delaware College Experiment Station and the
New York State Veterinary College, do not differ so seriously, as either
one does from those obtained in Europe, by Nocard, Bang, and the
Scottish Abortion Committee. The facts that the same germs were found,
either in pure cultures, or exceptionally, along with the normal
microbes of the healthy vagina, in the womb, and fœtal membranes of
every aborting cow, that they were never found in the healthy cow which
had calved at full time, and that the generative passages were the seat
of a catarrh, alike in the cows that aborted and in those that were
inoculated with the abortion discharges, but did not themselves abort,
are all but conclusive that this microbe is the essential cause of the
abortion.
The single objection to this view, namely that the inoculated cows did
not abort is explained by the fact that in the New York abortions it is
the rule that the calf is carried six or seven months from the date of
impregnation (the date of the presumptive infection) to that of
abortion. It is to be further borne in mind that our experimental cows
were old, and may have passed through the disease before and become in
some measure immune, that they were dry during the experiment, and were
subjected to no extraneous excitement that would predispose them to
abort. The presumption is that had the experiments been started earlier
in the gestation, the abortion would have come in due time. The microbe
maintained its hold on the mucosa and continued to advance up to and
beyond parturition.
Another distinction of the European abortions, is in the presence of the
microbe in European form in the digestive organs of the calf, and that
the viable calves of infected cows are liable to die of intestinal
disorders a few days after birth. Galtier, the Marquis de Poncius and
Pry insist strongly on this. On a farm on the estate of the Marquis,
where abortion had prevailed for twenty years, the calves of infected
cows show at birth, or very shortly after, symptoms of broncho-pneumonia
and of a complication of nervous disorders. They are breathless, wheeze,
discharge from the nose, cough, scour, have convulsions or other nervous
trouble. A large proportion of such calves die; and their lungs are
found in part red, consolidated and devoid of air and the bronchia
contain a muco-purulent product. Lesions denoting inflammation of the
serosæ of the lungs, liver and intestines are common. This coincidence
of a fatal disease in many of the surviving calves is exceptional among
the aborting herds of New York.
In noting the evidence of a wide difference between the prevalent
American and European forms of abortion in cows, one should be prepared
to go farther, and accept if need be, still other distinctive forms in
each of the two continents. Any catarrhal condition of the uterine
mucous membrane, is a recognized hindrance to conception, and cause of
abortion, and we must recognize that the forms of invasion of the womb
by pus microbes are as numerous as there are irritant germs capable of
living in the membrane. The question as to how many of these can produce
contagious abortion is to be determined by the susceptibility of the
membrane to irritation by each germ, and whether the latter can retain
all its power of survival and virulence in passing from one animal to
another. The presumption is, therefore, in favor of a variety of forms
of contagious abortion, each due to its own specific microbe or
microbes, rather than of a single unvarying type of the disease. In some
the affection appears to be a purely local one (American), the microbe
being confined to the genital or genito-urinary mucosa, whereas in
others the microbes (Bangs’, Galtier’s, etc.) live also in the blood
producing a general infection.
Two great types at least have been demonstrated in Europe and America.
Whether future investigation shall show the presence in one of these
continents of the types as yet only known in the other, remains to be
seen. If the particular forms should turn out to be limited to different
continents we are at once confronted with the necessity of an
international sanitary quarantine, and inspection. Matters are bad
enough now in our dairying districts, but if we are to be open to the
importation of new types of abortion, which do not mutually immunize
against each other, but which may be taken one after another in
succession through a series of years, they may easily become
incomparably worse.
_Acquired Immunity._ The question of persistent abortion year after
year, in the same animal, is most important. If a first contagious
abortion entails a second, a third, a fourth and a fifth in the same
animal, in as many successive years, then manifestly the preservation of
such animal is a most wasteful economy, altogether independently of the
danger of her transmitting the infection to healthy stock. If, however,
she herself becomes immune after a first or second abortion, it may be
profitable to retain her for milk production or breeding, provided that
she can no longer infect susceptible cows with which she must come in
contact.
_Acquired immunity_ of the individual cow is the rule after one or two
abortions caused by the microbes with which we are at present most
familiar. There are exceptions to this rule due to special nervousness
and excitability of given cows, which tend to an indefinite repetition
of the abortion, under the stimulation of pregnancy, of the continued
presence of the microbe, or of some local disease (tubercle, tumor,
parasite, etc.) of the ovary, womb or peritoneum. Yet statistics show
that this only applies to a small proportion of cows and these the most
nervous and excitable. The tendency toward insusceptibility to the
deleterious action of the germ, which may still be present, is in the
cow as a rule greater than the disposition toward a nervous encrease of
the susceptibility. The difficulty of reaching a conclusion on this
point depends on the fact that stockowners very commonly dispose of
aborting cows, and as the freshly bought cows are usually attacked
sooner or later, it is too confidently assumed that the old cows also
would have continued to abort had they been retained. Many years ago,
however, observant New York dairymen had noticed that the same cow
rarely aborted over three years in succession, and in the great majority
of cases not over two. The owner of a large herd, who has had much
experience with the disease, assures me that the rule has been, that a
cow did not abort with him a second time. The continuous abortion in a
herd was mainly among newly purchased cows and others that had not been
previously attacked, including heifers carrying first calf. The same is
in a measure true of the European abortions.
Nocard says that after three to five years there is an acquired
immunity. Only heifers and the cows that have been recently bought in,
abort.
Penberthy, speaking of England, says that in case of repeated abortion
in the same cow, the calf is carried longer each successive year until
it comes to its full term.
Sand, in his symposium of the experience of Danish veterinarians, says
it is quite exceptional that a cow should continue to abort, but
outbreaks of abortion disappear spontaneously if no new cows are brought
in.
Bang refers to a herd of 200 head of which 83 aborted in their first
pregnancy, and of these only 20 aborted in the second, while 7 failed to
breed. Counting the latter as having aborted, this amounts to less than
one-third, while over two-thirds of the cows that aborted in the first
gestation carried the calf to full time.
Paulsen quotes the case of a herd of 16, 7 of which aborted after
service by a bull in an aborting herd. One of the seven was sold, but
the remaining six all went full time in the following year.
Mörck records the case of a herd of 16 cows, the majority of which
aborted in the same year. All the aborting cows were sold and fresh ones
purchased. Next year the new stock aborted together with some of the
cows that had been held over. He continued this course for eight years
without any improvement, and then decided to keep the aborting cows as
well as the others. In two years the affection disappeared from the
herd.
Such small herds, in which all become early infected, and in which there
is no further opportunity for the infection of susceptible animals (cows
not yet infected, heifers in first gestation, new purchases), furnish a
better opportunity than do large herds, to trace the acquirement of
tolerance.
In a question of this kind, one must allow for variations in the
different types of abortion caused by various microbes, but in the forms
with which we are familiar in Europe and America, the acquired tolerance
of the individual can be counted on with great confidence. It has indeed
been largely traded upon by purveyors of antiabortion nostrums who
promise to cure the individual cow, to which alone their drugs are
administered. Two evils result: the stock owner’s money is paid for that
which unaided, nature would have accomplished for him; and attention is
withdrawn from the real necessity of the case, the prevention of the
infection of freshly introduced animals. The nostrum vender thus secures
for himself a growing market, as the yearly production of fresh cases in
the same herds, appears to demand a constant use of the agent which
appeared to work so well in the earlier ones.
_Immunized animal still infecting._ The cow that no longer aborts is
not, therefore, a safe member of a herd. As an individual animal she has
become resistant to the pathogenic influence of the germ, she is
invulnerable to it to the extent that she no longer aborts, but her
system and generative passages have acquired no such active bactericidal
power over the microbe as to lead to its speedy destruction. The genital
passages, once colonized, continue to be a field of growth of the
bacillus long after its power to cause abortion in that particular
animal has passed. Analogous cases can easily be quoted from the field
of pathology. The horse that has apparently recovered from dourine still
conveys the disease to others with which it has sexual congress; the
recovered syphilitic person is by no means eligible for marriage; the
recovered pig continues to carry the infecting swine plague bacillus in
its air passages. In short, it is the rule that the immunized animal can
with safety to itself carry a germ that readily infects its nonimmunized
fellows.
In the case of infectious abortion this is one of the most dangerous
elements, as the apparently healthy recovered cow receives no attention
in the way of separation and disinfection, but is allowed to spread the
infection through the bull that serves her in common with other cows and
by being sold into new and healthy herds.
_Symptoms._ Contagious abortion sometimes takes the form of temporary
sterility, the animal taking the male at frequent intervals, but failing
to conceive. If conception takes place, the abortion is usually deferred
until the fœtus has attained a considerable development—in cows till the
third or seventh month; in mares till the fourth or ninth month; in ewes
or sows till the tenth week.
Often times premonitory symptoms are entirely unobserved. Usually there
may be detected some heat and enlargement of the mammæ, with a decrease
in the milk yield, or a serous modification of the milk as in colostrum.
Still more striking is a muco-purulent discharge from the vulva—opaque,
white or yellow—in marked contrast with the perfectly clear, transparent
mucus which appears in œstrum. The discharge may be densely white (in
mares) or reddish, and may be accompanied by some swelling of the vulva
and redness of its mucosa, which is dull, rough and granular, or even
the seat of a papillary eruption. There is rarely hyperthermia or other
constitutional disturbance, and in some cases the abortion is only
discovered by the finding of the fœtus and its membranes in the gutter
or pasture. The membranes are, however, not unfrequently retained,
becoming offensively putrid. In other cases a muco-purulent discharge
persists for a length of time, insuring sterility so long as it lasts,
and causing ill health and emaciation. The fœtus is usually born dead.
The _lesions_ are confined to the generative organs. Bang, found an
odorless, dirty yellow, flocculent, slimy and more or less watery
exudate between the chorion and uterine mucosa involving the connective
tissue between the chorion and arachnoid so as to render it thick and
friable. These conditions were well marked in the French and English
cases, and perhaps somewhat less so in the American, which are
habitually slower in reaching the abortion. Bang found the uterine
catarrh with the characteristic bacillus in cases in which the calf had
been carried to full term, exemplifying the local presence and culture
of the bacillus without the usual abortion outcome. The bacilli were
occasionally, though not always, found in the body of the fœtus, and in
some cases the dead and mummified fœtus was found in the womb, which had
not been stimulated to its expulsion. He even found the bacillus in the
mummified fœtus, and still virulent, after an apparent seclusion of
seven months.
ABORTION IN MARES.
This follows the same general course as does the disease in cows. In
certain American outbreaks (Kilborne and Th. Smith) it has been traced
to a bacillus like the colon bacillus, propagated in the womb and
genital passages, and which produced suppurating vaginal catarrh in cows
and mares on which it was inoculated. It is liable to occur, without
premonitory symptoms having been observed, and to be followed by no
marked sequelæ, so that, as in most cases in the cow, it may be looked
on as a purely local infection. In England, Penberthy, found it to occur
not earlier than the fourth month of gestation, yet he adduces several
cases in which the first case in a breeding stud occurred in four weeks
after the introduction of an infected mare from an aborting stud. In
America on large breeding farms the introduction of the infection has
proved ruinous, as many as 70 or 80 per cent. of the mares having
aborted in the same season.
The conclusion is inevitable, that as in the case of cattle, the sire
may become the means of transmission, and that the same measures of
prevention are demanded. The fact that the affection is less widely
spread or injurious, than in cattle, is largely due to the usual
presence of but one, two or three breeding mares on a farm, so that
there is little opportunity for a rapid extension of the infection.
Multiply and encrease our studs of breeding horses, as cows have been in
our dairying districts, and abortion, once introduced, would prove
equally infective, spreading and injurious.
_Therapeutics_ are useless in contagious abortion as the disease usually
runs its course before any danger is suspected. If premonitory symptoms
are observed, the abortion may sometimes be warded off for a time by
secluding the animal in a quiet place and seeking to obviate labor pains
by opiates and ounce doses of viburnum prunifolium.
_Prevention._ This is to be sought along two principal lines: 1st. The
protection of a sound herd against the infection: and 2nd. The
extinction of infection in a herd already diseased.
_Protection of a sound herd._ This requires the greatest possible care,
because the infected animal usually presents the general appearance of
perfect health, and there is no ready means of testing the presence or
absence of the abortion bacillus. In purchasing a cow or mare in a
public market the new owner may find her affected with this bacillus,
and a serious danger to his whole herd. To protect the latter he must
learn that the herd from which she came has had no abortions for several
years before, and that the offspring for the different years are present
in numbers corresponding to the dams. In the absence of this a
certificate, and guarantee against infection of other animals by the one
purchased, may well be demanded of the seller. A certificate from the
veterinarian attending the herd furnishing the animal, may also be
sought as evidence of the absence of abortion from the locality.
Imported animals should be safeguarded in the same way but with even
greater care, lest the microbian sources of new types of abortion,
should be brought into the country. A guarantee of this kind might well
be demanded by the Federal Government in the case of all breeding
animals imported.
In case of failure to secure the most perfect guarantee with the
purchased animal it would be worth the purchaser’s while to seclude it
from his valuable herd, and not to breed it with the other animals of
his herd until it has been proved to be entirely free from infection. If
bought for a sire it should be subjected to a course of disinfection of
the sheath and penis: if for a dam and unimpregnated, antiseptic
irrigation of the vagina may be made daily for a week, and the external
parts, hips and tail daily washed with antiseptics. If very important to
have her bred, secure, if possible, a male that is not to be used on
other animals. If this is impracticable, let the sheath and penis, and
surrounding skin be thoroughly disinfected as soon as the service has
been had.
If the newly acquired female is pregnant, keep her by herself until
parturition and, even if this takes place at full term, irrigate the
womb daily for a week with a disinfectant, delay having her served for a
month, and if she must go to the sire of the herd, subject him to
thorough disinfection after service. It may be that she still carries
the germ but has become tolerant of it.
_Extinction of Contagious Abortion in a Herd._ 1. Two separate stables,
or compartments, not having a common gutter should be provided, one for
the sound animals, and one for those that are known to be affected, or
that are open to suspicion.
2. The cow or mare that shows symptoms of abortion, or that has aborted,
should at once be removed to the quarantine stable, and her stall,
including the gutter and drain leading from it thoroughly disinfected.
The whole stable should be whitewashed.
3. The aborted fœtus with its membranes, should be at once removed and
burned, or boiled, or deeply buried after it has been thickly sprinkled
with chloride of lime or other active disinfectant.
4. The manure from the infected stable should be taken into an enclosure
into which no animals have access, and freely watered with a solution of
sulphate of copper (6:100).
5. All in the quarantined stable and even those left in the general
stable, should have the external generative organs, the hips, and the
whole length of the tail washed once or twice a day with an antiseptic
solution. Carbolic acid or creolin (2 or 3:100) makes a very safe and
convenient agent, but copper sulphate (6:100) or mercuric chloride
(2:1000) may be substituted. The colorless mercuric solution though
effective and inodorous, has an element of danger in it, when left in
barns in large quantities.
6. Cows or mares that have just aborted, should have the uterus
irrigated daily for a week with a disinfectant solution. Carbolic acid
(1:100 with 1 sodium carbonate) or creolin (1 to 2:100) or mercuric
chloride (1:1000 with 1 hydrochloric acid) are good examples. Use a long
rubber tube and funnel. They should not be bred until all discharge has
ceased.
7. It is a good practice to keep a separate sire for the aborting and
quarantined suspected animals, but the bull for each herd should, after
each service, have his sheath injected with the disinfectant liquid, the
orifice being held and the liquid pressed into all parts and finally,
the skin around the sheath must be well washed with the same.
8. All cows or mares in an aborting herd, or one from which aborting
animals have been removed within a year, should, after delivery, be
injected with a disinfectant for one week exactly as if they had just
aborted. This will guard against the danger from animals that carry the
germ, but have become so tolerant of it that they no longer themselves
abort.
9. New born animals brought in from other herds should be sponged all
over with one of the above-named disinfectant solutions before being
added to the herd.
10. In case the breeding animals go to pasture, separate fields should
be furnished for the aborting and suspected ones and those supposed to
be sound.
11. Breeding ewes, goats and sows should be excluded from all pastures
occupied by suspected herds or those under treatment. The fields should
further be cleared of rabbits as being susceptible to the infection and
capable of keeping it up and transmitting it.
12. It is important to reserve the herd sires for the exclusive use of
the home herds. Where this cannot be done, disinfection of the sheath
and penis should be practised immediately after each service.
Attempts have been made at different times to destroy the bacillus by
subcutaneous or intermuscular disinfectant injections. Bäuer used in the
cow a 2 per cent. solution of carbolic acid, of which he injected two
Pravaz syringefuls under the skin of the flank every fortnight from the
fifth to the seventh month. It was rather unreasonable to expect much
from 10 minims of carbolic acid once a fortnight, even apart from the
fact that this agent is converted into the inert sulphophenic acid in
the body.
Lignieres followed in the same line by injecting into the bodies of the
cervical or other muscles 10cc. (2½ drams) of a mixture of terpinol one
part, olive oil nine parts. This was injected during pregnancy every
second day for the first three months, every third day for the second
three months, and every fourth day for two months. The claim for success
is based on the alleged prevention of second and third abortions in the
same animals, and this becomes rather shadowy when we consider that the
rule with cows is that they do not abort a second or third time. We have
met with veterinarians who claimed a splendid success with the single
injection of the terpinol. Lignieres claims no such success with his
long continued treatment, as he had a percentage of abortions in every
herd treated, and from first to last almost every animal in each herd
aborted once, or was sold nymphomaniac. It is to be feared that the
apparent immunity depended mainly on that tolerance which comes early in
nearly every case to the aborting cow.
INFECTIOUS ENTERO-HEPATITIS IN TURKEYS.
Blackhead. Definition: Infectious protozoan disease of cæca and liver
and general toxicæmia. Microbiology: Amœba in cæca, liver, etc.
Symptoms: Attacks young, dulness, drooping, ruffling, moping,
anorexia, greenish diarrhœa, icteric or dusky mucosæ, blackening of
gobble, etc. Lesions: Enlarged thickened cæca, epithelial degeneration
and desquamation, exudation, mottled liver, with giant and round cells
and amœbæ, degeneration, necrosis, caseation, no abscess. Diagnosis
from bacteridian typhlitis or diphtheria. Treatment: Intestinal
antisepsis. Prevention: Disinfection of buildings, yards, manure,
seclude from other flocks, birds, flies, breed new flock on fresh
ground from eggs of affected or other flock, set in incubator or under
hens.
_Synonym_: Blackhead.
_Definition._ An infectious disease of turkeys, especially destructive
to the young, due to a protozoön (amœba meleagridis), and characterized
by inflammatory thickening of the walls of the cæca, diarrhœa, brownish,
yellowish or greenish areas of degeneration of the liver, and congestion
with blackish discoloration of those portions of the head which are
uncovered by down or feathers.
_Microbiology._ The microörganism (amœba meleagridis) is found in the
thickened walls of the cæca, in the exudate, in the lumen, and in the
degenerating patches of the liver. The most common and simple form is
that of a rounded body, varying slightly in form, and containing a group
of very minute granules situated somewhat eccentrically. They may be
enclosed in lymph spaces or less frequently in giant cells, or have
portions of broken up cells adherent. Their size varies from 10 to 15μ.
They may be stained by the following process: Harden in 95 per cent.
alcohol saturated with mercuric chloride, then in the same with an equal
amount of a 5 per cent. solution of bichromate of potash, and finally in
Hemming’s solution. After a day in these solutions they are washed for a
day in running water, then treated with ascending strengths of alcohol,
dried by passing through alcohol and chloroform, imbedded in paraffin,
sectioned dry, and stained in Delafield’s hæmatoxylin and eosin. The
spherical or slightly oval amœbæ have a homogeneous, bluish red tint,
feebler and therefore distinct from the tissue nuclei. Near the centre
in most a blue circular line shows the outlines of the nucleus.
Th. Smith compares this affection with the amœbic dysentery affecting
the large intestine and liver of man, and notes these differences, that
amœbic movements have not been observed in amœba meleagridis, and that
hepatic abscess does not occur in the turkey. The indisposition of the
bird to suppuration may perhaps account for the latter distinction.
Smith found rounded organisms in the tubules of the cæca and flagellates
in the lumen of the gut, but did not attach any importance to their
presence. Bacteria were only found in the lesions in the solid tissues
where the subject had not been killed and immediately examined, but left
over night for examination in the morning. There was no constancy in
their species as in the case of the amœbæ, all indicating that their
invasion was post mortem.
_Symptoms._ The disease is most frequent and fatal in the young (1 to 4
months, exceptionally 6 to 10 months), and the symptoms vary much in
different cases, according to the intensity of the disease and the
relatively extensive implication of the different organs. Among the
general symptoms are those of general suffering and ill health, dulness,
spiritlessness, drooping of the head between the wings, a pendent
condition of wings and tail, erection of down or feathers, separation
from the flock, the bird moping alone and sitting much of the time. The
more characteristic phenomena which are rarely sufficient to identify
the disease unless it is known to be prevalent, are loss of appetite, a
greenish diarrhœa, yellowish or brownish discoloration of mucosæ,
emaciation which becomes extreme if the subject survives long enough,
and more or less blackish discoloration of the gobble and bare portions
of the skin covering the head.
_Lesions._ These are characteristic, the cæca being greatly enlarged,
the walls thickened by a yellowish submucous exudate, the epithelium
disintegrated and desquamating, and the mucosa covered by a solid
yellowish gelatinoid exudate arranged in superposed layers, while the
contents are soft, pasty or of a greenish liquid appearance. The
comparative stagnation of the contents as in the appendix of man appears
to favor microbian infection. Amœbæ are especially abundant in the
exudate into the submucosa and in the lymph spaces. The liver changes
show infective inflammation in the spots of mottling, followed by
degeneration, and necrosis, the liver cells disappearing under the
compression of the giant and round cells and the amœbæ, the surface over
the affected parts is depressed, and the mottling may show a variety of
colors, as brown, brownish red, or yellow, pale yellow, grayish or dirty
white. The degenerating tissue may become caseated, but abscess appears
to be unknown, though so common in amœbic dysentery of man. In the skin
of the head the blackish color predominates; there is more or less
congestion, capillary embolism, and tissue degeneration.
_Diagnosis._ Th. Smith notes three cases of diseased cæcæ without great
thickening of their walls, and an exudate in the lumen having the
general appearance of that seen in the amœba disease but with no amœbæ,
only the bacillus coli communis. The odor was strongly feculent. In all
three cases the liver was healthy. In one there was an abundance of
tapeworms in the bowels. Manifestly the absence of liver lesions may be
held to indicate the absence of the protozoan disease. VonRatz
(Budapest) gives two similar cases, with many nematodes, those in the
exudate being 8 to 14 mm. long.
Zurn describes the presence of the diphtheria of fowls in the intestines
of hens, turkeys and palmipeds and sometimes confined to the cæca. It is
characterized by great prostration and debility, and an offensively
smelling diarrhœa at first pultaceous and mucous, later bloody, and
followed by constipation, in which case the cæca and rectum are
ulcerated and blocked with the yellow croupous exudate. It lasts 2 to 3
weeks or even months, is subject to relapse, and sometimes occurs as a
sequel to the diphtheritic affection of the head and throat. The absence
of marked thickening of the cæcal wall, and of the protozoön, the
presence of the diphtheritic exudate in the lumen, and the croupous
condition or congested appearance of the head and throat are
distinctive. Th. Smith, however, refers to two cases, supposed to be of
this kind, in which the walls of the cæca were greatly thickened, the
result of reparatory inflammation following a slough of the mucosa.
Siedamgrotzky also describes thickening of the walls of both cæca in a
hen, the mucosa being covered with a thin pseudo-membranous exudation,
without ulceration.
It would seem that the cæca of birds, like the vermiform appendix of man
is very subject to invasion microbes, bacterian and protozoan, and
should always be carefully examined in case of intestinal or hepatic
disorder.
_Treatment_ would be in the line of intestinal antisepsis with carbolic
acid, salol, sulphurous acid, or the sulphites, with a laxative of
castor oil, to carry these agents unchanged to the cæca, but no success
has attended attempts in this direction, and the danger that comes from
preservation of the infected animal, and consequent multiplication of
the microbe would as a rule far more than counterbalance any probable
recoveries.
_Prevention._ Moore has shown that the amœbæ, passed with the fæces,
contaminate the food and water and thus actively propagate the disease,
so that preventive measures must be mainly directed toward the
purification of these infecting media. To be thorough new ground must be
secured on which no diseased turkeys have been, and through which no
water from contaminated or suspected land can flow; if necessary this
must be closely fenced to prevent all ingress or egress, and on this
ground we can place, as soon as they leave the shell, young turkeys
hatched from eggs obtained in noninfected localities, or the eggs
carefully washed of the turkeys living on infected ground. In this way
the heredity and quality of the flock can be preserved without risk of
contamination from the parents. The amœba is not known as a parasite of
other birds, but if it should eventually be found to be so or to occupy
any other animal body as an intermediate host, the local extermination
of such host will become a necessary precaution.
When a new flock has been started in this way, the birds of the old
flock may be fattened, killed and marketed, and as suggested by Cooper
Curtice the grounds they have occupied may be secluded by fencing for
one or two years, in the hope that the amœba will perish by this break
in the chain of its life history. If this should prove successful with
the land, the infection might be easily exterminated in the whole
infected district or state.
The poultry buildings will require thorough disinfection. All manure and
droppings must be carefully removed and the building whitewashed, using
freshly burned quicklime and ¼ lb. of chloride of lime to the gallon of
the mixture. The litter should be burned, and all nests, roosts,
drinking vessels and troughs soaked with a mixture of sulphuric acid ½
gallon, carbolic acid ½ gallon, and water 20 gallons, (Th. Smith). The
agents are mixed slowly in a vessel set in cold water. The same may be
liberally applied on the surface, fences, etc., of the yards. Or
quicklime, freshly burned, may be used freely on the yards holding the
infected flocks (Moore). Mercuric chloride is dangerous. When the
infected flock has been finally disposed of, the buildings and yards
should be again thoroughly disinfected, and together with the field
runs, abandoned for at least one year.
ASTHENIA IN CHICKENS.
Microbiology: bacillus of colon group. Pathogenesis to Guinea pigs:
rabbits, pigeons and chickens refractory to artificial cultures.
Treatment.
_Synonym._ “Going Light,” Bacterial Infection of the Duodenum.
C. F. Dawson, in investigating a wasting disease of well fed Brahma
fowls in Maryland in which there was no appreciable symptom except the
gradual and extreme loss of flesh and weight found in all cases a
catarrhal duodenitis, with the presence in the contents of a bacterium
in pure cultures, and apparently allied to bacillus coli communis.
_Bacteriology._ The bacterium is 1 to 1.3μ long, by .5μ wide, with
rounded ends, often in pairs. It does not stain in acid nor alkaline
methylene blue, carbol fuchsin, nor alcoholic dyes, but stains easily in
aqueous solutions of the same stains and by Gram’s method. It is ærobic,
facultative anærobic, grows at 50° to 120° F. in acid or alkaline beef
bouillon, with fœtor; in glucose, saccharose, or lactose bouillon with
the production of acid; in milk causing coagulation; on gelatine, agar
and potato. Growth in Bouillon ceased at 131° F. and sterilization took
place at 135° to 140° F. Vitality was not lost under freezing nor
drying. It was killed by a 1 per cent. solution of carbolic acid in five
minutes, or by formaldehyde gas, but not by lime water.
_Pathogenesis._ Inoculated subcutem, in a _Guinea pig_ caused death in
24 hours, with a necrotic œdematous condition of the adjacent tissues
like malignant œdema, and containing the microbe. It was further found
in the liver, spleen, abdominal exudate, heart, blood and lungs, but not
in the kidneys.
It proved harmless to _rabbits_ when injected subcutem, but fatal in 24
hours when thrown into the peritoneum. The lesions were severe
duodenitis and omental inflammation, and the bacterium was found in the
liver and duodenal wall.
Pigeons, rats and mice proved refractory to the artificial cultures,
also chickens. The latter were injected subcutem, intraabdominally and
intravenously. Yet in view of the constancy of the lesion in hens with
the microbe in pure cultures and the absence of all other morbid
conditions, Dawson felt justified in attributing the disease to this
microörganism. It is possible that his experimental hens had become
immune from a previous attack, or failed in some condition of food or
environment which is essential to pathogenesis, or finally there may
possibly be some other infinitesimal microbe present which escaped
observation, but which furnished the occasion for the coincident
development of the colon bacterium.
_Treatment._ The indications are: the expulsion of the offending
bacterium to be followed by nutritious, easily digested food, pure water
and tonics. Dawson advises castor oil in dose of two teaspoonfuls, or
calomel ¼ grain repeated till purgation occurs; and to be followed by
powdered fennel, anise, coriander, cinchona of each 30 grains; powdered
gentian and ginger of each ½ dram; powdered copperas 15 grains. The
addition of bismuth, pepsin, or orexin may be suggested.
APOPLECTIFORM SEPTICÆMIA IN CHICKENS.
Streptococcic infection in hens. Most violent in pullets and hens;
less so in capons and cockerels. Found dead, or sick 24 hours,
ruffled, prostrate, neck limp, head drooped, indisposed or unable to
rise, liquid icteric fæces, blood-stained skin of neck and breast,
death without agony. Lesions: Soiled anal feathers, plump carcass,
skin pallor save neck and breast, extravasation of blood subcutem and
intramuscular, mucosæ anæmic, peritoneal engorgement and effusion,
enlarged, engorged liver, cell proliferation, degeneration,
coagulation necrosis, gall bladder full. Enlarged congested spleen,
degeneration. Congested swollen kidneys, epithelial degeneration,
casts, streptococcus. Congested, consolidated bronchioles, alveoli,
lungs, with microbe. Meningeal congestion, exudate. Bacteriology:
Streptococcus, pure cultures in lesions, size, chains, tetrads,
staining qualities, culture media, colonies, action on sugars, acid,
no gas, on milk no coagulation, on gelatine no liquefaction. History:
Stagnant water; no evident source of infection, buzzards, etc.
Pathogenesis: Inoculation, intravenous or intramuscular, feeding. On
duck, pigeon, rabbits, mice, dogs. Guinea pigs and sheep immune.
Immunization by injection of sterilized cultures.
Under this name Norgaard describes a hæmorrhagic streptococcic infection
which prevailed in 1901 in a flock of 200 to 250 Plymouth Rocks in
Loudon County, Va. Forty birds died within six weeks, and later the
mortality reached 200, death often occurring suddenly while feeding, or
the birds would drop from their roosts in the night and be found dead in
the morning.
_Symptoms._ In the majority, the pullets which died suddenly, no
symptoms whatever were observed, yet a certain number of the capons and
cockerels were noticeably ill for 12 to 24 hours. In these the feathers
were ruffled, the prostration extreme, the head drooped between the
wings, the neck was weak and wobbling (limber neck), the wings and tail
drooped, and the animal lay on its breast often unable to rise.
Sometimes there was a passage per anum of liquid bile-stained mucus.
Close examination of the neck and breast might detect hæmorrhagic
discoloration of the skin, though the skin elsewhere was pale and
smooth. Death takes place without a struggle.
_Lesions._ The anal feathers were usually stained, indicating diarrhœa;
the picked carcass was plump and fat, with pale, healthy looking skin,
except on the neck and breast, where it was discolored by extravasated
blood; at such points the connective tissue and muscles were infiltrated
with blood in areas of an inch in diameter, more or less, and with
irregular outlines. The buccal mucosa was clear, pale and bloodless. The
cavity of the body contained an abundance of sero-sanguinolent exudate,
and the mesenteric veins were engorged. The _liver_ was greatly enlarged
and congested, the greater part of its substance being apparently
composed of the distended blood vessels. The hepatic cells were granular
and fatty, and if death had been delayed over twenty-four hours their
outline became indistinct and the nucleus stained only faintly. In the
foci of disease were clumps of round cells and leucocytes in and between
the acini, and in still more tardy cases points of coagulation necrosis.
The streptococcus was abundant in the necrotic centres, among the clumps
of leucocytes, in the parenchyma and capillaries. The _gall bladder_ was
usually distended with bile. The _spleen_ had the large size and well
developed Malpighian bodies that characterize the well-fed bird, but it
showed still greater enlargement, combined with sanguineous congestion
and circumscribed blood extravasations. With a hand lens were seen
numerous round, semi-transparent points, the size of pin holes, which
the microscope revealed to be centres of coagulation necrosis,
surrounded by embryonic tissue. The centres consisted of a granular
debris with abundance of the streptococcus. The _kidneys_ were congested
and swollen, and in cases that had survived two or three days there was
granular degeneration of the epithelium of the tubules, and the lumen of
the tubes contained casts with leucocytes and streptococci. The organism
was also present in the capillaries. The _lungs_ presented areas of
congestion and consolidation, exudation into the walls of the
bronchioles and the alveoli, and an abundance of streptococci in the
lesions. In the cranium were a subdural exudate and meningeal
congestion. For examination of the tissues they were hardened in
specimens of alcohol of encreasing strengths, embedded in paraffin and
stained with carbol fuchsin with a counterstain of methylene blue.
_Bacteriology._ The streptococcus was found in pure cultures in all the
diseased centres except in the intestinal contents. Smear preparations
were made from the blood, the abdominal exudate, the intestinal
contents, the bone marrow, the cerebral exudate and the sanguineous
effusions into the muscles.
The coccus is .6 to .8μ in diameter, in short chains of 2 to 8 cells, or
in some media much longer. Involution forms are common, and Norgaard
claims to have seen indications of fission in two directions to form
tetrads. The organism stains in the usual aniline dyes, as well as by
Gram’s and Gram-Weigert’s method. It is nonmotile, ærobic, facultative
anærobic, grows in solid and liquid media that is neutral, or slightly
acid or alkaline (not if strongly acid), best at 98.6° F., and slower at
the room temperature. In alkaline peptonized beef bouillon in 24 hours
it forms threads and balls on the sides and bottom of the tube, leaving
the liquid clear. On agar there are formed small shining, grayish
colonies 1.5 mm. in diameter with brownish centre and bluish periphery.
With all the sugars it produces acid, but no gas. It does not coagulate
milk. On gelatine colonies are formed in four days, and there is no
liquefaction.
_History of the Outbreak._ The outbreak commenced early in January,
without any obvious occasion for the introduction of infection. There
had been no chicken disease on the place for 25 years, and no chickens
had been purchased except from a neighboring farm where the stock
remained healthy. They had been fed on corn meal, wheat bran, wheat
tailings and whole corn, together with scorched wheat from a burned
barn. The poultry houses were clean and well aired, and after they had
been closed there was no abatement of the disease. The water was from a
stagnant pool receiving drainage from the stable, but this was no new
condition and January is not the driest month with the foulest water.
The suggestion may be hazarded that the infection may have been
introduced by the usual infection bearer, the buzzard, or by some other
wild bird, or mammal.
_Pathogenesis._ Among the _chickens_ the most rapid and fatal cases were
in pullets, then among the laying hens, while the capons and cockerels
were less severely affected, and some survived from three to seven days.
Those _inoculated intravenously_ as a rule sickened on the second or
third day with a temperature of 110.7° F., and were found dead the
following morning.
Some took injections of .25 to 1cc. in the _pectoral muscles_ with
impunity.
Chickens that had fasted 24 hours, took each daily for 3 days, a few
cubes of bread soaked in a fresh bouillon culture. Death followed in
four out of six, in from four to thirteen days from the beginning of the
experiment. The birds gradually became listless, refused to eat, and
remained quiet in a corner of the cage, with closed eyes and head
drooping until it rested on the ground. Diarrhœa was frequent but not
invariably present.
Chickens fed on the chopped up viscera of rabbits that had died of the
disease perished in 3 to 10 days.
A _white duck_ inoculated intravenously with .5cc. of peptonized beef
bouillon culture, took ill on the 8th day, and died on the 12th. There
was loss of coördination and use of the wings, temperature 109° F., and
necropsy showed valvular endocarditis containing the streptococcus. A
second duck sickened on the 11th day, but recovered after three days’
illness. Killed on 21st day, all cultures from heart, spleen and kidney
remained sterile. Subcutaneous, intramuscular and feeding experiments
failed to produce the disease in ducks.
A _pigeon_ injected with .5cc. bouillon culture intravenously died on
the fourth day with the internal lesions of chickens, and blood
extravasations on head and neck. Intra-muscular injections and feeding
experiments were fruitless.
In _rabbits, intravenous_ injections of 1 to 1.5cc. led in 24 hours, to
temperature of 105.3° F., without impairment of appetite, or other
marked sign of illness, and as a rule the subject is found dead next
morning. _Intra-abdominal_ and _intrapleural_ injections kill in two to
four days, and _subcutaneous_ ones in three days. In addition to the
lesions found in chickens, there is often bloody urine, a sanguineous
lymph on and beneath the cerebral meninges and in the fourth ventricle,
and deep congestion of the cancellated tissue of the vertebræ.
Streptococci are abundant in the lesions.
In _mice intraabdominal_ injection of .01cc. killed in 48 hours, and
_subcutaneous_ injections in 2 to 5 days. The lesions were like those
seen in birds, and streptococci were abundant.
In _dogs_ after _intravenous_ injection there was hyperthermia (103.6°
and 104.1° F.) and lameness of the right fore shoulder joint, followed
in 5 to 8 days by recovery. Feeding on the viscera of the diseased
chickens, was followed by anorexia, and vomiting only.
_Guinea pigs_ and _sheep_ proved refractory.
_Immunization._ The injection into the wing vein of .5 to 2.5cc. of
bouillon culture, sterilized by heat proved protective to the chickens
against inoculations of the virus while the check animals invariably
died.
TUBERCULOSIS.
Synonyms. Definition: infectious disease caused by bacillus, attended
by productive inflammation, tubercles, necrotic degeneration,
caseation, fibroid change, calcification or ulceration. Animals
susceptible: python, salamander, carp, fish, birds, rodents, sheep,
goats, solipeds, cattle, dogs, cats, apes, swine, wild ruminants,
kangaroo, carnivora, cage birds, civilized (housed) man. Geographical
distribution: with dense population, Central Europe, Britain, Eastern
States; little in absence of cattle products—Scottish Western Isles,
Iceland, Newfoundland, Greenland Highlands, Arctic North America,
Northern Norway, Sweden, Lapland: open air life protects. Virulence:
ancient records, modern, early antituberculous legislation, decimation
of herds, researches of Vilemin, Gerlach, Chauveau, Semmer, Parrot,
Tappeiner, etc. Bacillus tuberculosis: evolutionary changes, relation
to actinomyces, 1.5 to 3.5μ by 0.2μ shorter and thicker in ox,
solitary, exceptionally short chains, on blood serum may be
filamentous, staining slow, carbolated fuchsin, technique, sections;
biology, adaptation to environment, to genera, variation in same
genus, experiments showing real identity of variant forms; vitality:
in water human bacillus 50 to 70 days, bovine bacillus indefinitely,
avian 117 days, dried sputa 9 months, cow’s lung 102 days, putrid
material 43 days to years, survives gastric juice, sunlight kills in
some hours, if in thin layer, day light 7 to 18 days, dry heat (212°
F.) for an hour left living bacilli, moist heat 140° F. for 1 hour
kills, low temperatures (−25° F.) fail, after 15 days in salt failed
in rabbit, after 30 in Guinea pig. Chemical disinfectants. Accessory
causes: racial vulnerability, close buildings, dark, foul, damp
stables, poor scanty food, heavy milking, conformation, early
breeding, inbreeding, age, predisposing diseases, traffic in animals,
dairy extension, admission of tuberculous animals from other states,
assorting tuberculous for sale in a given State, sale of sound from
tuberculous herd, lack of indemnity for animals killed, private
testing of herds and sale of tuberculous, accustoming to tuberculin
test, antipyretics during tuberculin test, false certificates of
tuberculin tests, feeding hogs on tuberculous offal, feeding calves
and hogs on tuberculous milk, feeding hogs after tuberculous cattle,
feeding from a common trough, dry, dusty stables, extension through
vermin, flies and other insects carry virus. The tubercle: miliary,
pinhead, conglomerate, proliferation of cells—tissue and leucocytes,
in nests in stroma, giant cells in center, then epithelioid, then
lymphoid, caseation, calcification, fibrosis, pearl disease.
Localization: _Cattle_: pulmonary: miliary tuberculosis, aggregation
into larger tubercles, caseated centres, fibroid, cretified,
abscesses, vomicæ, complex infections, infiltrations, difference from
broncho-pneumonia, lesions of different ages; pleural lesions;
congestion, exudation, fringes, nodules, grapes, adhesions,
caseations: bronchial and mediastinal glands, congestion, swelling,
softening, induration, caseation, cretefaction: cardiac lesions:
lesions of mouth and throat, pharyngeal glands: gastro-intestinal,
peritoneal, mesenteric glandular; œsophagastoma; liver tubercle;
splenic; pancreatic; genito-urinary; mammary; cerebral; spinal;
orbital; skeletal; cutaneous; muscular; glandular; table of
distribution. _Swine_: lesions: pharyngeal, intestinal, mesenteric,
muscular, hepatic, splenic, glandular, pulmonary, skeletal, caseation,
liquefaction. _Horse_: lesions: thoracic, abdominal, glandular, of
serosæ, vertebræ, etc. _Sheep_ and goat: lesions: thoracic, abdominal,
glandular, hepatic, pharyngeal, facial, etc., verminous affections.
_Dog and Cat_: lesions: respiratory, abdominal, pharyngeal, tonsillar,
hepatic, pancreatic, splenic, skeletal, arthritic, cutaneous. _Apes
and Menagerie Animals_: lesions. _Chickens_: lesions: intestines,
liver, spleen, peritoneum: lungs and kidneys often escape. _Pheasant_:
lesions: as in hens, centre zone has epithelioid cells, fibroid,
cretefaction, amyloid degeneration. _Parrot_: lesions: eye, beak,
tongue, palate, larynx, bones, joints, lungs, liver, intestines,
muscles, skin. Primary and secondary infection, extension by
lymphatics, blood channels, tonsils, inhalation, deglutition.
_Synonyms._ Consumption; Tabes; Scrofula; Pining; Grapes; Great White
Plague, etc.
_Definition._ An infectious disease common to man and a large number of
animals, caused by the bacillus tuberculosis, and characterized by a
productive inflammation giving rise to small, rounded bodies
(tubercles), or diffuse infiltration, with a tendency to necrotic
degeneration, and caseation, or to fibroid degeneration (sclerosis),
calcification or ulceration.
_Animals susceptible._ Tuberculosis comes near to being a panzoötic,
since although reptiles, fishes, birds and some mammals do not readily
contract it under normal conditions, yet under abnormal and debilitating
conditions nearly all will succumb to it.
_Reptiles._ Sutton found tuberculosis in a python which was kept so warm
in the London Zoological Gardens that a thermometer between its folds
registered 85° F. Kráhl, Battaillon and Ferre cultivated the bacillus in
frogs, Kráhl in snakes. Blauvelt found tuberculosis in a salamander.
Lechner found it in amphibia.
_Fishes._ Broussais records the prevalence of tuberculosis in carp in a
pond which received the sputa of a consumptive man. Under the skin were
found rounded tumors, containing abundance of bacilli, that infected
rabbits and Guinea pigs on which they were inoculated.
_Birds._ In birds of the farmyard—hens, pheasants, turkeys, ducks and
pigeons—it is very frequent and often occurs as an epizoötic. While the
tuberculosis of barnyard fowl is a manifest variety and not readily
interchangeable with the varieties affecting the mammal, yet, with a
special predisposition, it can be transferred and can then be conveyed
from animal to animal in the new genus in which it has been implanted.
That of cage birds is interchangeable with that of man.
_Rodents._ Guinea pigs have a strong susceptibility to tuberculosis,
whether from human or bovine source, and rabbits for that of birds, and
by continuous transmission through the body of the rodent, all alike
seem to tend toward acquiring common characters. The Guinea-pig,
therefore, has been especially availed of for the experimental
transmission of tuberculosis, and, as the disease in them becomes acute
and rapid in its progress, these subjects permit the multiplying of
experiments in a short period. _Rabbits_ are less vulnerable to the
bovine or human form.
_Sheep and goats_, kept under usual conditions, show a remarkable
immunity from tuberculosis, yet if directly inoculated an inherent
susceptibility is easily shown. Habitual immunity may be in some degree
due to their open air life, to the heavy winter fleece protecting them
against chills, to the comparative absence of the heavy and continuous
milk yield demanded of cows, to the more restricted development of the
lymph plexuses in the lungs and elsewhere, and to the limited
opportunity offered by the small tonsils for infection entrance.
The _horse, ass and mule_ rarely contract tuberculosis casually, the
more spacious stall, outdoor life, hard muscular condition, the very
small tonsils, the exclusive nasal respiration, the paucity of
connective tissue lymph plexuses, and the abundance of red globules,
probably favor immunity. Yet on inoculation by Chauveau, Nocard and
others, the horse readily succumbed to infection, generalization taking
place more certainly than in the ox.
_Cattle._ The bovine races are remarkably subject to tuberculosis. This
is probably due in part to the great amount of connective tissue lymph
plexus in the lungs and elsewhere, the habit of using the mouth in
hurried breathing, the deep, sudden inspiration through the mouth and
over the tonsils that follows a cough, the habitual restricted size of
the cow stables, the absence of individual separated stalls, the habit
of feeding from the same trough with the cattle adjacent, the great
drain of yearly breeding and heavy milking, the retention in the herd of
old, failing cows for their milk product and high priced offspring, and
the bovine habit of licking each other with the infected tongue. In many
European cities and even in country districts the disease is very
prevalent. In Copenhagen a few years ago 17.7 per cent. of all oxen and
cows killed in the abattoirs were tuberculous; in Berlin 15 per cent.;
in Holland 20 per cent.; in Pomerania and Bomberg 50 per cent.; in
Hildesheim, Hanover, 50 per cent.; in Berlin dairies 75 per cent.
(Ostertag): in Leipsic and Edinburgh 20 per cent. The great variation in
the data for the different cities is suggestive of different inspection
standards. American figures as given by the Bureau of Animal Industry
are for Baltimore (mostly cows recently from the country) 2.5 to 3.5 per
cent.; and for the packing centers (among 2,273,547 mostly fat steers,
and therefore selected) 0.02 per cent. It is here largely a matter of
locality and infection, I have seen large herds with 100 per cent.
tuberculous, and extensive districts, in the north and especially in the
south entirely free from the disease.
_Dogs and cats_ in their natural condition rarely show the disease, but
contract it readily on inoculation. Cadiot found 40 cases in 9,000 _post
mortems_ of dogs. The young are apparently more susceptible than the
old, and primary lesions in the abdomen are common and suggest infection
through the food. The majority belonged to consumptive persons, and
gnawed the bones that had been first picked by the owner, and ate from
his plate what he left. Jacobi records the case of a dog, with general
tuberculosis, which habitually licked up the expectorations of his
phthisical master.
_Apes and Monkeys_, in confinement, almost all die of tuberculosis.
_Swine_ contract tuberculosis readily, the large tonsils, the habit of
breathing through the mouth, and the abundance of connective tissue and
lymph plexuses in the lungs and elsewhere contributing to this. Yet in
them the affection is mainly a dietetic disease. Swine kept in the
country and fed on vegetable food are rarely affected. In Saxony, where
17 per cent. of the cattle are tuberculous only a shade over one per
cent. of swine were so, and in Baden only 0.02 per cent. In hogs raised
on our western farms and corn-fed the proportion is much less. Yet in
those fed on uncooked skim milk, kitchen scraps and the refuse of
slaughterhouses in a raw state, tuberculosis becomes very common. In one
case, in a large public institution, where the dairy herd was
universally affected, and where, on their slaughter, their raw offal had
been thrown to the hogs, I found that the latter were almost all
tuberculous. Similarly, in feeding experiments, from the time of
Gerlach, pigs and especially young pigs, have shown themselves to be
very susceptible.
Among the less domesticated animals that contract tuberculosis may be
named _deer_, _elk_, _gazelle_, _antelope_, _camel_, _dromedary_,
_giraffe_, _kangaroo_, _lion_, _tiger_, _jackal_, _jaguar_, _bear_,
_arctic fox_, _rat_, _mouse_ and the _common cage birds_, etc. Fröhner
found 36 per cent. of parrots affected in Berlin.
_Man_ has long been recognized as standing in the front rank of
susceptibility to tuberculosis. Yet even in his case the prevalence of
the affection bears an intimate relation to his indoor life. In large
cities _post mortems_ often show that one-third have suffered, and that
one-seventh and upward of the whole population die of tuberculosis.
Natives of tropical islands and countries, living in the open air and
apart from close association with civilized man, often escape entirely.
In South Africa the herdsmen living in close buildings suffer
encreasingly, while their cattle, kept constantly in the open pasture,
escape.
_Geographical Distribution._ The prevalence of tuberculosis shows a
direct relation to the opportunity for infection rather than to climate,
latitude or altitude. It is the prevailing disease of civilized
communities with dense populations, and especially in large cities where
the general vitality is lowered and the crowded buildings give every
opportunity for infection. It is preëminently the disease of Central
Europe, of Great Britain and of our Eastern States, where there is the
greatest activity in business, manufacture and commerce. Yet in the
Scottish Hebrides, Iceland, Newfoundland, the Greenland Highlands,
Arctic North America, the northern parts of Norway and Sweden, Lapland
and Finland it is hardly known. The absence of commerce and cattle and
the sparse population have much to do with this. The coasts of Greenland
with their Danish stations have two-thirds of the population tuberculous
(Cook); the Indians of Barrow’s Straits, when infected in 1899 by the
frozen-in whalers, suffered from it as from a plague; in Christiana,
Stockholm and St. Petersburg it is as prevalent as in the large cities
of Central Europe. Elevated and dry climates have often been found to be
free from the affection, yet it prevails inside the double windows of
houses in the higher Alps, and has, within a generation established a
notorious prevalence in Minnesota, Dakota and westward, as it has in
Australia, mainly owing to the advent of consumptives who sought for
health in the dry atmosphere. The hills and dry tablelands in North and
South America, Africa and Asia which have acquired a reputation for
salubrity, owe this largely to the sparse population and the absence of
facilities for infection. In South Africa, in spite of the dry and
genial climate, the disease is constantly encreasing in the human
(housed) population. The sea-coasts, which are the seats of large cities
and the centres of population and trade, are also the most extensively
affected with tuberculosis—in the West Indian Islands, Panama,
Nicaragua, Mexico, Yucatan, Columbia, Equador, Peru, Chili, Ceylon,
Guinea coast—while the sparsely peopled highlands of the same countries
are practically free.
What is true of man is equally so of cattle. In the Gulf states of this
country, herds living in the open air are practically free from
tuberculosis, while in New Orleans and other large cities, the cows shut
up in the confined stables and yards, are as tuberculous as those of the
great cities of the north. So in many districts in the northern states
we find no bovine tuberculosis, while in others, differing in no
essential particular as regards geological formation, altitude,
exposure, and industrial use of the animal, a large proportion are
affected.
_Virulence._ Tuberculosis has long been recognized as virulent. “It is
indicated in the Mishna and other Jewish works as rendering the meat
unfit for consumption, but to come to more modern times, we find that
throughout the seventeenth and eighteenth centuries the flesh of
tuberculous animals was excluded from human food, alike by the civil and
ecclesiastical laws of Europe. Tuberculosis in cattle was erroneously
identified with syphilis of man, which made a frightful extension in the
end of the fifteenth century, spreading from the army of Charles VIII
which had been engaged in the siege of Naples. This conviction lasted
until it was disproved about 1782. Though mistaken in the identity of
the two diseases, the fact that for centuries the common people and
physicians both associated tuberculosis with a malady so notoriously
contagious as syphilis, speaks strongly for the forcible evidence of
contagion manifested at that time. Morgagni, who must have begun
practice about 1700 A. D., testifies to the strong conviction of the
contagious element in tuberculosis. Indeed it became a common practice
to isolate the consumptive person from the public, and after his death
to burn his clothes and sometimes even the house, or at least to subject
them to a careful disinfection. It is recorded that in 1750, in Nancy,
the magistrates ordered the burning, in the public square, of the
personal property of a woman who had died of phthisis, from sleeping in
the bed of another consumptive person.
“At Naples, a royal edict of September 20, 1782, prescribed the
sequestration of the phthisical, the disinfection of the rooms,
chattels, movables, books, etc., with vinegar, eau-de-vie, lemon juice,
sea-water, fumigations, etc., under a penalty of three years at the
galleys, or in the case of nobles, of three years imprisonment and a
fine of 300 ducats. A physician who failed to report a case of
consumption was fined 300 ducats for the first offense, and banishment
for ten years in case of a second. Any one assisting in such evasion of
the law was sent to prison for six months.
“Chateaubriand found that, in 1803, he could not sell his carriages in
Rome, because Mme. Beaumont, who had died of consumption, had ridden in
them three or four times. George Sand, who was with the phthisical
Chopin in Minorca in 1839, was refused a lease of the house for the
second month, and the price of repainting and purifying was demanded.
Later, in Barcelona, they were assessed for the bed on which Chopin had
slept, as the police regulations prescribed it should be burned.
“This was not a mere survival of vulgar prejudice. Jacobi tells us of a
dog which died of consumption from eating the sputa of his phthisical
master. Laennec, the discoverer of auscultation, and the great authority
on pulmonary consumption, records that he himself contracted a
tuberculous nodule, through a wound with a saw, while making a necropsy
in a case of phthisis. Laennec died of tuberculosis later, although he
seemed to have checked this lesion by caustics. Andral joins Laennec in
enjoining the greatest caution and cleanliness in taking care of, or
associating with persons having advanced tuberculosis.
“Cullen, who started with a strong prejudice against the doctrine of
contagion, leaves us the following instance of its occurrence: ‘A young
man predisposed to phthisis married a Dutch girl of a sanguine
temperament and good constitution. Some days after the marriage the
woman lost her fresh color and was attacked by a bad cough; a month
later she commenced spitting blood. The physician advised her not to
sleep in the same bed with her husband, but she refused to follow his
advice, and six months later she died of phthisis. The servant who took
care of her and the domestic, who avoided, as far as possible, staying
in the sick chamber, both died of consumption.’
“Wickmann, court physician in Hanover, in 1780, pronounces emphatically
for contagion. In Zurich, at that time, one death in every six was from
phthisis. The contagion of phthisis was slow in its operation, and was,
therefore, less evident than that of plague, smallpox, scarlatina and
other affections attended by a skin eruption, but it was no less real
and deadly. It was also less frequently indirect, or carried from victim
to victim by intermediate agents. He cited instances of the transmission
of consumption from husband to wife and vice versa, and claimed that the
marriage of a phthisical person should be legally prevented. As a means
of preventing the disease, he proposed a strict surveillance of
establishments for the sale of old clothes, and the avoidance of leaving
infants with consumptives.
“Valsalvi and Sarconi refused to make necropsies of persons who had died
of phthisis.
“Dr. Ruhling, of Gottingen, writing in 1774, of the disease in animals,
says: ‘The malady is transmitted to sound animals by direct contact of
animals standing side by side in the stall, and licking each other, and
breathing the expired air direct from the diseased lungs; the
frequenting of the same pastures will also serve to propagate it.’ In
Krunitz’s encyclopedia, published in Berlin, in 1787, is the following:
‘The heifers show an ardent desire for the male, and remarkably enough,
do not become pregnant, but part with the fruit of conception. When
opened these animals show the first stomach, kidneys and surface of the
lungs, covered with pustules like dried mulberries or in suppuration.
The affection is contagious, and communicates itself from one animal to
another by contact.’
“Fromage, in the Dictionaire de Rozier, Article Phthisis, says: ‘Men of
art are very much in accord that this malady is not contagious, but some
stock owners think differently.’
“Huzard, who saw much of tuberculosis in the Parisian dairies in the
concluding decade of the last century, said that most of the
veterinarians looked upon the disease as contagious, and that some of
the physicians believed the same of the phthisis of man.
“Dewar, speaking of his experience in Scotland in 1839, and succeeding
years, in a particular herd, says: ‘The proprietor agreed to remove
partition walls, and to make openings opposite one another in the
outside walls, so that there might be a current of fresh air passing
through. These alterations combined with cod liver oil, tonics and
stimulants, may have prolonged life but yet no cure was effected, and
that herd died out. I resorted to every precaution when new cattle were
purchased to prevent infection; as I had an idea, even at that time,
that the disease might be communicated from one to another when in
immediate contact. The precautions adopted when fresh cattle were
purchased had the desired effect, for in a few years afterward, they
were as good a lot of cattle as any in the district. That herd left an
impression on my mind that never can be effaced, and made me always
dread the evil consequences of tuberculosis. Having practiced in the
same locality, which is an extensive breeding and rearing district, I
have seen several herds decimated. Though I have sometimes foretold the
owner what he might expect, yet he did not believe me until so many were
infected that the byres were infested with the fearful malady, and your
remarks in regard to nose contamination are so true that I do not think
it possible any can escape that are so exposed. I have also seen, as
Grad has, the same stall infecting beast after beast until a thorough
cleaning and disinfecting, with plenty of fresh air had removed all
infection.’
“Spinola, writing in 1858, of bovine tuberculosis, gives contagion as a
possible cause, and Lafosse, in 1867, says: ‘Physicians begin in
imitation of Morgagni to believe in the contagion of phthisis. The facts
published by Villemin appear to support this opinion, which has been
held by our colleague, Dupont, of Bordeaux, for several years.’
“Cruzel in his work of date, 1868, is much more positive; he says: ‘This
fœtid expired air, inhaled immediately by another cow upon a sound lung,
gives the latter tuberculous infection. It is a matter of every day
experience to the veterinarian. Two oxen or cows are kept in the same
stable, take their food from a common rack or manger, lie in the same
stall, and respire nose to nose. The one is, to all appearances,
perfectly sound, the other is in as good a condition, and is vigorous,
but it coughs from time to time, and its breath is foul. Soon we notice
that the animal that does not cough, eats with less appetite, he loses
flesh and soon he is unequivocally affected with the same malady as the
first.’ The foregoing quotations show clearly that in spite of the
misleading teachings of Broussais and others, the doctrine of contagion
in tuberculosis could not be overcome, and that up to the time of the
remarkable experiments of Villemin, in 1865, it maintained its hold upon
the minds of extensive and careful observers. In animals, especially,
the evidence was so frequent and clear, animal following animal in the
same stall, and eating from the same infected manger, only to be
infected in turn, and two animals stalled together, and licking the same
manger with their prehensile tongues, transmitting the infection with
certainty the one to the other, were facts that could not possibly be
ignored. Other cattle in the same building might escape for a length of
time, but the eating in common from the same fatal manger, by a
tuberculous and a healthy animal, quickly sealed the fate of the latter.
“Physicians, too, who were compelled to investigate the causes of the
extraordinary fatality from tuberculosis in the armies and navies, could
not shut their eyes to the fact notwithstanding that they came to the
task strongly prejudiced through education against the acceptance of
contagion. Thus, Dr. Bryson, in his report to the Epidemiological
Society, in 1860, on consumption in the several ships of the English
navy on the Mediterranean station, says distinctly that the disease
appeared to be propagated by contagion. Dr. Parkes, quoting this in his
Practical Hygiene, says: ‘It may be inferred that pus cells were largely
thrown off during coughing, and floating through the air, were received
into the lungs of other persons. The production of phthisis in animals
confirms this view. The case of monkeys in the zoological gardens,
narrated by Dr. Arnot, is a striking instance. Cows in close stables
frequently die of phthisis. But not only phthisis may reasonably be
considered to have one of its modes of origin in the breathing of an
atmosphere contaminated by respiration, but other lung diseases,
bronchitis and pneumonia, appear also to be more common under such
circumstances.’
Villemin in 1865, published his investigations in which he had produced
tuberculosis in a great number of animals, by inserting particles of
fresh tubercle or injecting the tuberculous sputa of man into the
subcutaneous connective tissues, the peritoneum and the trachea. There
resulted in nearly every case a chronic disease, the marked phenomena of
which were caseated centers devolving from firm inflammatory nodules in
the seat of inoculation, in the adjacent lymphatic glands, in the lungs,
serous membrane, liver, spleen and kidneys. The centers of such nodules
were at first transparent and grayish, but soon the center underwent
necrobiosis, forming a soft cheesy mass the size of a pin’s head, and
gradually enlarging to that of a pea, a bean, a hazel nut or larger.
After a period of about 14 days the lymphatic gland nearest the seat of
injection could be felt as a firm pea-like nodule, and in two weeks more
a second gland on the line of the lymph circulation, had become enlarged
and nodular, while the first, now the size of a large bean, had probably
undergone distinct softening. This became adherent to the skin, burst
and discharged continuously or at intervals with little or no tendency
to heal. If killed at this date, the animal showed only the open sore
and a chain of nodular pea-like caseated lymphatic glands leading up
from it. The lungs might be apparently sound, but the spleen and liver
usually showed miliary elevations on the surface, with clear grayish
centers, as viewed under a magnifying glass, opaque patches were found
on the omentum, and the lymphatic glands of the mesentery, of the portal
fissures of the liver and of the Hilus of the spleen were distinctly
enlarged and resistant. If not killed, the subject usually died 100 to
120 days after inoculation, and then the lungs were found studded with
tubercles miliary or larger and more or less caseated; the bronchial
mediastinal, subdorsal, pectoral, prepectoral, phrenic, mesenteric,
hepatic, and splenic lymphatic glands were more or less enlarged and
caseated, while the liver and spleen were enlarged and studded with
multiple tubercles. Guinea pigs give the most extensive and intensive
lesions, rabbits much less so, but in both emaciation and wasting are
very marked. In short the lesions are essentially and unmistakably those
of generalized tuberculosis.
“At first, however, incredulity prevailed and experiments on a large
scale were inaugurated all over Europe and America to put the question
to crucial test. Martin, Conheim, Burdon-Sanderson, Simon, Wilson, Fox,
Lebert and Wyss, Fraënkel, Waldenbourg, and others inoculated with all
sorts of non-tuberculous organic materials (bronchial mucus, foul pus,
cancer juice, diseased liver, simple cotton setons, etc.) and from these
in Guinea pigs there resulted local caseated foci, and implication of
the adjacent lymphatic glands. It was found that the liquids from low
types of pneumonia produced these apparently tubercular deposits, while
that from acute sthenic pneumonia did not; that the cotton thread seton
failed to produce the disease if it were first steeped in carbolic acid,
and that the lesion caused by breaking a bone without injury to the skin
failed to produce the characteristic lesions even in the very
susceptible Guinea pig. It became evident, therefore, that the morbid
results in these cases, were due to accidental inoculations with the
poison of the tubercle, which is widely distributed, or with some pyæmic
or other germs.
“Gradually the truth triumphed, and those who had at first been loudest
in their opposition were led by their own experiments to become the
firmest supporters of the new truth.
“As early as 1874, Gerlach had experimented largely in feeding the milk
of tuberculous cows, and had infected calves, pigs, sheep and rabbits in
this way. Chauveau in (1874), Klebs (1873), Semmer (1880) and Parrot
(1870) fed calves, cats, Guinea pigs, pigs, sheep and a variety of other
species of animals with tuberculous flesh or lungs, or saliva, producing
tuberculosis in a large proportion of cases. In this manner they escaped
the charge of the operation of a wound and of ærial bacteria, and yet
succeeded in producing infection. The lesions in this case began in the
intestinal mucous membranes and mesenteric glands.
“Another essay in the same direction was made by Tappeiner (1878), who
infected rabbits, Guinea pigs and dogs, by enclosing them in boxes and
compelling them to breathe tuberculous liquids intimately mixed with the
air atomization. In these cases lesions began in the lungs and bronchial
and mediastinal glands.[1]”
Footnote 1:
(From Report to the N. Y. Legislature, 1895. James Law.)
_Bacteriology._ The _bacillus tuberculosis_, the essential cause of
tubercle, was demonstrated by Koch in 1882. It was at first supposed to
be peculiar in its indisposition and tardiness to take a stain, and in
its retention of the stain once imparted, even when it is treated with
acids. Later observations have shown that these characteristics are
common to certain other bacilli, notably to those of leprosy, smegma,
and to specimens found in timothy hay and other grasses, cow dung, milk
and butter. These furnish sources of fallacy in the milk and butter
especially, but when the specimens examined are taken from the interior
of a tubercle, lymph gland or serous cavity the danger of error may be
practically ignored. What is quite as important is the fact that the
tubercle bacillus is subject to evolutionary changes in adapting itself
to a habitat in different genera of animals, and to a lesser extent in
different parts of the same animal, by which its pathogenesis is
modified, but these variations do not materially affect the staining
qualities. Still more striking variations have been found in old
cultures, ovoid forms (Metchinkoff), club-shaped microbes and filaments
(Metchinkoff, Klein, etc.), branching filaments (Fischl, Coppen Jones),
divergent club-shaped groups, like actinomyces (Babes and Levaditi). The
last named, seen in inoculated rabbits, have been held to establish a
relationship between the microbes of tuberculosis and actinomycosis, as
the club-shaped cells do not take the usual Ziehl-Neelsen stain for
tubercle bacilli, but the Birsch-Hirshfeld’s actinomyces stain. Apart
from the rabbit such variations are not likely to prove sources of
fallacy in identification of the microbe.
_Morphology._ As met with in the tubercle of man or ox the bacillus is a
minute rod with rounded ends, 1.5 to 3.5μ long, by 0.2μ in thickness. In
the ox it is shorter and thicker on an average than in man. They are
usually solitary, but two and exceptionally even three or four elements
may be united. In stained specimens unstained portions are frequently
seen (spores?). When cultivated on blood serum there is a tendency to
form elongated rope-like colonies having a waving outline. Other
evolution forms have been already noted.
_Staining._ The resistance to staining is overcome by a heated alkaline
watery solution of methylene blue (Koch), or better by a carbolated
solution of fuchsin (Ziehl-Neelsen). To a 5 per cent. watery solution of
carbolic acid add one tenth of its volume of saturated alcoholic
solution of fuchsin. The suspected sputum or scraping from a section of
a lesion is spread in a thin layer on a cover glass by drawing over it
the straight edge of a second cover glass, dried in the air, and passed
three times through an alcohol flame with the smeared side up. It may
then be floated on the surface of the staining fluid with the specimen
side down, then gently heated for three or four minutes almost to
ebulition, drying being prevented by the addition of more of the
carbol-fuchsin solution as required. It is then washed in water to
remove excess of the staining fluid and treated with a bleaching acid
solution (sulphuric acid 5 per cent. or nitric acid 15 per cent.) When
decolorized it is well rinsed in two or more portions of a 60 or 70 per
cent. alcohol and then in water. Next stain with a 1 or 2 per cent.
aqueous solution of methylene blue for one minute and wash off the
excess with water. The tubercle bacilli will appear of a deep red and
other bacteria blue.
_Gabbett’s_ counter-staining and decolorizing solution is especially
useful in economizing time. After staining, as above directed, in the
carbol-fuchsin solution for one minute, wash in water, then cover with a
solution of 2 grams methylene blue (powder) in 100cc. of 10 per cent.
sulphuric acid, until the film has a faintly bluish tint: then wash
thoroughly in water and examine. Tubercle bacilli come out red, others
blue.
In _examination of tissues_ the microscopic sections are steeped for
twenty-four hours in the carbol-fuchsin solution (or 1 hour at a
temperature of 45° to 50° C.), then decolorized in a 5 per cent.
sulphuric acid for a few seconds, then in a 70 per cent. alcohol: they
are then counter-stained in an aqueous solution of methylene blue,
washed in water dehydrated with absolute alcohol, cleared up in xyol or
oil of cedar, and mounted in Canada balsam.
_Biology._ The _bacillus tuberculosis_ is notorious for its variant
forms, assumed in adapting itself to given environments, and which it
retains with considerable tenacity for a time, even when placed in a new
and different medium. It is largely held to be an obligatory parasite,
and incapable of survival as a saprophyte, yet Straus, Nocard and
others, have shown that the form obtained from the tuberculosis of birds
can easily be made to live in suitable dead mixtures of organic matter.
It is also notorious that the bacillus taken direct from the tubercle of
the mammal, and which, as a rule, fails to grow at once in glycerined
bouillon, yet, after a first successful culture in the new medium, often
adapts itself completely, and thereafter it can in many cases be
transferred from bouillon to bouillon, with as great certainty as it
could formerly be inoculated from ox to ox. The difference is one of
habit and adaptability, rather than any primary and permanent
distinction of species. There is every reason to believe that the
microbe has lived, and under given conditions can still be made to live
as a saprophyte, with a greatly reduced adaptability to parasitic life
in the animal, just as we see to-day that it is only with great
difficulty transferred from certain genera of animals to certain other
genera (from bird to ox and vice versa). Trudeau tells us of a culture
of a bacillus tuberculosis from man, inoculated on the rabbit and then
cultivated _in vitro_ in successive generations for six years, that was
in this way robbed of its pathogenesis for Guinea pigs, which, after
inoculation, lived for many months, some two and a half years, and some
even recovered. The average duration of life in the Guinea pig, after
tuberculosis inoculation from man, rabbit, Guinea pig or recent culture
is but seventeen days. The bacillus of human sputum often produces only
localized tuberculosis in the ox. Even in the same species and
individual the pathogenesis often varies materially. Nothing is more
familiar than the slow progress of tuberculosis in the bones and lymph
glands of man, on the one hand, and its frequently rapid progress in the
lungs, liver and brain, on the other. As inoculated on the lower animals
bacilli from the lungs of man are usually more virulent than those from
the lymph glands (Creighton, Arloing, F. Craven Moore, Courmont and
Denis). Among seven specimens of human sputum, the bacilli in six cases
showed a fair average vitality, whereas those of the seventh failed to
grow on blood serum of the dog (Theobald Smith). In both man and cow a
large proportion of cases of tuberculosis remain localized, the disease
lasting for years with little or no appreciable advancement, and not a
few subjects appear to make a permanent recovery.
On every hand this evolutionary tendency of the bacillus tuberculosis
places itself in evidence, demanding a recognition of the fact, that
more or less transient or lasting variations in accordance with previous
or existing environment, control to a large extent the transmissibility
of the disease among different genera and even among individuals of the
same genera and species, and also the fatal progress, or the mild and
evanescent issue of the infection.
Even the most widely divergent of these evolutionary forms can often be
made to approach each other and apparently merge into one type.
Profiting by the example of Metchnikoff, Nocard enclosed in collodion
capsules the bacilli of the human sputum and inserted the capsules into
the peritoneal cavity of chickens which had proved refractory to their
direct inoculation. This excluded the direct action of the leucocytes
from the encapsuled bacilli, but allowed the endosmosis of the serum of
the fowl for their nourishment. After a sojourn of four months or more
they were transferred to other capsules and again enclosed in the
peritoneum and after a second and third transference of this kind it was
found that the bacillus had become actively pathogenic for the chicken,
having acquired the infecting potencies of the bacillus of avian
tuberculosis.
In keeping with the above is the fact that both rabbit and horse are
easily infected by the bacillus obtained from birds, and that after a
certain number of transmissions through the rabbit the issue of the
bacilli of bird and mammal appear to become identical. No less
instructive are the cases of the infection of carp by human sputa and
the conveyance of tuberculosis to rabbits and Guinea pigs by inoculation
with the nodules of the infected carp.
The _vitality_ of bacillus tuberculosis is strong but variable. In
sterilized water at 46° to 64° F. the human bacillus survived for fifty
to seventy days (Chantemesse and Vidal), the bovine indefinitely
(Galtier) and the avian bacillus at a higher temperature one hundred and
seventeen days (Straus and DeBarry). In dried expectoration the bacillus
of man still infects after nine or ten months (Koch, Schill, Fischer, De
Thoma). In infected cow’s lung, dried and pulverized, it infected Guinea
pigs at 102 days (Cadeac and Malet). In putrid matter it infected after
43 days (Schill, Fischer), 167 days (Cadeac and Malet), several years in
a grave (Schottelius).
It is not destroyed by gastric juice (Fischer, Falk). The bacillus from
tubercle of birds has a much greater vitality than that of mammals.
Marfucci successfully seeded new media from a culture of two years old,
and cultures in artificial media can be started more successfully.
Full _sunlight_ renders sputum on a solid nonabsorbent surface
noninfecting in several hours, varying according to the thickness of the
layer (Koch, Straus). When sputum is mixed in soil it may survive until
the 137th day (Feltz). On woolen cloth it may live five hours (Migneco).
_Diffuse daylight_, with shading from the sun, killed in seven days
(Koch), to eighteen days (Lucibelli).
_X-Rays_ do not arrest the growth of cultures (Blaikie, Pott, Ausset).
A _dry temperature_ of 212° F. for an hour left some of the bacilli
still infecting to Guinea pigs (Lartigan).
A _moist heat_ of 140° F. for one hour sterilizes (De Man, Th. Smith,
etc.). The scum formed on the milk may still prove infecting (Th.
Smith). Half an hour of a moist temperature of 212° F. is sterilizing.
Yet in the case of steaks, roasts and boiled meats the size of the piece
often prevents the reaching of this temperature throughout, and it
becomes unsafe to use any meat in which the redness of the juice shows,
that the albumen has not all been fully coagulated (162° F.).
A _freezing temperature_, −16° to −26° F., does not devitalize the
bacilli, even when alternated with thawing at intervals for several
weeks (Galtier, Cadeac and Malet).
_Heavy salting_ of meats has been thought to kill the bacillus in a
month. After 15 days in salt the microbe failed to kill rabbits, but
still killed the Guinea pig, whereas after 30 days it killed neither
(Galtier). The fact that salted meats are always unequally impregnated
in different parts, renders this extremely unreliable and more of a
snare than a guide.
The action of chemical disinfectants varies not only with the agent but
also with the medium in which the bacillus is found. In simple liquid
media (bouillon) the following results were obtained:
_Parts per 1000._ _Killed in._
Carbolic Acid 50:1000 30″ (Yersin)
„ „ 10:1000 1′ „
Alcohol (absolute) 1000:1000 5′ „
Ether 1000:1000 10′ „
Iodoform ether 10:1000 5′ „
Mercuric chloride 1:1000 10′ „
Salicylic acid 2.5:1000 6 hrs. „
Anilin water Saturated ———————— ——————— ————————
Thymol 3:1000 3 hrs. (Yersin)
Formalin vapor 60:1000 40 hrs. (Murray)
Sulphurous Acid (Sulphur 1 oz.
to cubic metre) ————————— 14 hrs. (Vallin).
The following agents proved ineffective: Saturated aqueous solution of
creosote, or of B-naphthol, of naphthalin, of potassium iodide, of
potassium bromide:—bromine water, iodine water (1:500), iodoform
solution or vapor, vapor of oil of turpentine.
ACCESSORY CAUSES OF TUBERCULOSIS IN ANIMALS.
While recognizing that in the absence of the tubercle bacillus there can
be no tuberculosis yet we must not ignore the fact that many conditions
of the animal system and its environment contribute largely to the
propagation of the disease on the one hand, or to hinder its progress on
the other. None of these conditions can call the germ into being _de
novo_, but in its presence, they greatly favor its diffusion or even its
malignancy. Like any other seed, this bacillus requires a suitable soil
and favorable climate, to bring out its most destructive development. In
striking the balance, we have to guard against the error of so many, who
would attribute to the germ alone the deadly results and who assume that
these should be the same under all conditions, and the opposite error no
less prevalent, that ascribes the evil to the conditions, and holds that
without these the germ would be harmless.
_Hereditary Predisposition. Racial Vulnerability._ Before the discovery
of the specific bacillus, when as yet tuberculosis was held to result
from a constitutional weakness, or cachexia in which deterioration of
cells was held to be the main factor, the disease was held to be mainly
hereditary, and its every day transmission in the line of descent, and
the increasing mortality to extinction of given families were
confidently appealed to in support of the doctrine. Now, however, we
recognize that congenital tuberculosis in man or beast is very
exceptional, and that the morbid process almost invariably takes its
start from the germ implanted after birth. In Saxony when the
tuberculous cows were 16.5 per cent. tuberculous calves were but .2 per
cent., though the latter had been fattened on the milk of the former. In
Munich but two calves were found tuberculous in 400,000 killed, and in
Lyons but five in a similar number. Up to the present the number of
calves recorded as tuberculous at birth does not exceed seventy.
That the young almost always contracted the disease, only after birth,
virtually disposes of the alleged heredity of the tuberculosis but it by
no means antagonizes the heredity of the racial vulnerability. As man,
cattle, swine and Guinea pigs show a much greater vulnerability than the
carnivora in general, so certain families in each of these genera show a
more decided susceptibility to tuberculosis under similar conditions
than do certain other families. This goes far to explain the appearance
of tuberculosis, in certain lines of blood, and its advance to the
extinction of the family, while under no better environment, other
families can count on a practical immunity. In the Burden herd of
Jerseys in 1877, I condemned eleven animals, verifying my diagnosis by
necropsies, and found to my surprise that I had taken every
representative, even the grades, of a given family, and left all the
pure bred members of a second family untouched. Both families had
mingled freely in the pastures and yards, yet the second family
furnished no cases of tuberculosis then nor for many years afterward.
The case is all the more striking that the non-tuberculous family gave
the largest yield of milk and might have been expected to run down
rather than the other on account of this drain.
_Close Buildings. Lack of Ventilation._ Air rendered impure by being
breathed again and again, predisposes strongly to tuberculosis, and has
been even looked upon as the sole cause (Macormac). Everywhere city
dairy cows, kept in confined, close buildings, suffer severely (6 to 20
per cent. and upward); in Berlin 75 per cent. (Ostertag); in Denmark 61
per cent. (Bang), while in the same districts country cows are
comparatively immune (often 1 to 2 per cent.), and steers raised in the
open air still less (0.02 per cent. for our Plains cattle). For the
slighter cases of tuberculosis in man and beast, life in a pure open
air, day and night, in a genial climate, gives the best hope of
improvement or recovery. In the Burden Jersey herd above referred to,
animals condemned in spring as tuberculous, were turned out to pasture
during the summer where they maintained an appearance of robust health,
yet when returned to the barns in fall they fell off rapidly, so that
some had to be helped to rise in the stall. “The stabled cow, the tame
rabbit, the monkey, the caged lion, tiger or elephant are almost
invariably cut off by scrofulous affection” (Aitken). It has long been
noticed that sailors sleeping in close spaces (Bryson, Parkes), soldiers
confined to close stone barracks even in the tropics (Parkes), suffer
much more than the officers in more spacious rooms (Clark). Monks and
nuns (two-thirds of the deaths, Leudet) occupying confined cells, and
the inmates of prisons (four times the average outside, Baer) have shown
an extraordinary prevalence of tuberculosis and attendant mortality.
While this can be attributed mainly to the preservation and
concentration of the bacillus in such places, a considerable allowance
must be made for the impure and rebreathed air.
_Dark, Foul, Damp Stables._ Dark stables are usually close, dirty and
damp as well, and all these conditions alike conduce to tuberculosis.
Darkness hinders the development of organic coloring matter in living
bodies, whether chlorophyll in plants or hæmoglobin in the blood of
animals. Hæmoglobin is the main oxygen carrier in the blood, and in case
of its deficiency the tissues are not properly ærated. The result is as
if the inhaled air contained little oxygen, so that darkness further
intensifies the evil of rebreathed, deoxygenated air. The extraordinary
mortality from tubercle among prisoners, monks, nuns and miners serves
to further accentuate this conclusion.
Trudeau’s experiment with rabbits is instructive in this connection. Of
a number inoculated with the same number of tubercle bacilli, one half
were kept in the open air and the rest in a dark, damp, underground
place deprived of sunlight. When killed on the same day, it was found
that the open air rabbits showed only slight lesions or none, while the
underground lot had extensive tuberculosis.
The impure stable air lowers the vital tone of the animal, especially if
the impurity has come from animal exhalations.
The same is true of damp air, “a damp ship is an unhealthy one,” and
Bowditch and Buchanan pointed out the especial prevalence of tubercle in
cold, damp, undrained, foggy localities. This does not hold for all damp
lands, yet damp, fog, and cold are especially hurtful in presence of the
germ.
INSUFFICIENT OR UNWHOLESOME FOOD.
Starvation and indigestible or innutritious food contribute to debility,
and lessen the power of resistance. Hence in the poor, half starved
denizens of city slums, and among neglected herds of cattle,
tuberculosis, once introduced, makes rapid and extensive ravages.
Conversely overfeeding often acts in the same way, developing
indigestion and thereby robbing the tissues of their proper nourishment.
HEAVY MILKING.
In dairy cows, of milking breeds, the drain on the system is liable to
prove too great, under a ration-for-milk, warm sloppy mashes of grains,
bran, middlings, roots, distillery swill, exclusive diet of silage,
saccharine roots, or marc, warm drinking water, a warm atmosphere,
liberal salting, and enforced idleness in the stall, with careful
stripping of the bag. The butter cows, (Jerseys, Guernseys, Alderneys,
etc.) are especially liable to suffer, as the greater the yield the more
the system is robbed of the adipose material which is so needful to a
vigorous health. When the cow has been reduced to a high-pressure milk
factory her physical size reduced to obviate the need of a large
sustaining ration, and her milking capacity stimulated to the highest
degree, the presence of the tubercle bacillus is especially dangerous.
CONFORMATION.
It was formerly held that cows with heads narrow between the horns,
small thin necks, narrow chests defective also in depth and length,
loose projecting shoulders and elbows, pendent, pot bellies, with hollow
flanks, and a general laxity of the frame were especially predisposed to
tubercle. In many such cases the suspected animal was already the victim
of the affection, which had brought out these characteristic features of
weakness and emaciation. In other cases the unthrifty appearance was due
to poor feeding and care or to chronic disease, which in robbing the
system of vigor and hardihood laid it open to the attack of the tubercle
bacillus whenever it was introduced. Even when there was no such
depressing influence affecting the individual, the inheritance of such a
frame, betokened a constitution lacking in vigor, and with little power
of resistance to the invading microbe. Some milking breeds which tend to
the above conformation, show an unusual development of the lymph glands
and plexuses, and as tuberculosis attacks the lymphatic system
preëminently, the bacillus finds an especially favorable field for
development in such systems. It would, however, be an error to assume
that the compact, rounded frame, with circular chest and abdomen, and
full, firm neck and shoulders, with a great disposition to fat and
little to milk, is in any degree immune. Under the presence of the
tubercle bacillus, and close stabling, they often succumb quite as
rapidly as the most susceptible milking breeds. The meat producing
breeds with a strong propensity to fatten, have an extraordinary
development of lymph spaces and plexus in the intermuscular and
subcutaneous connective tissue, and the microbe finds a welcome home in
their sluggish, inactive and atonic systems as well as in the typical
dairy cows.
BREEDING TOO YOUNG.
Breeding from immature animals undermines the vitality as the system is
overtaxed to sustain at once the demands for further growth, for the
nourishment of the unborn offspring, and for the yield of milk. Some
families of Jerseys have been undoubtedly injured in this way, through
the desire to diminish the size of the cow, and yet retain the highest
milk and butter yield.
CLOSE BREEDING.
Inbred families are proverbially subject to tuberculosis. By pairing
individuals that show in a marked degree the desired qualities of early
maturity, heavy milking, or fattening, the greatest stimulus is given to
the enhancement of such qualities, and with this there is the
correspondingly ready receptiveness to the tubercle bacillus. To this is
added a degree of constitutional delicacy which comes from too close
breeding, and which otherwise shows itself in an encreasing infertility,
when bred with an animal that is nearly related. In addition, the high
bred animal is kept much indoors, where the bacillus, once introduced,
is easily preserved and propagated, and is denied the free outdoor life
and exercise which might develop muscle and vigor. This is no valid
argument for introducing inferior blood to the deterioration of the
economic value of a race, but rather for the complete exclusion of the
bacillus which may find in our treasured herd an especially inviting
field for its ravages.
AGE.
In both man and beast, age appears to have a predisposing effect, but
apart from debility or trauma, this may be fully explained on the ground
of often repeated infection, an indoor life, and, in dairy cows, the
excessive drain upon the system. In thoroughbred herds of cattle, in
which the cows are preserved as long as they will breed, and in dairies
where they are kept as long as the milk yield is satisfactory, the
oldest show by far the largest percentage tuberculous. In secluded
individual dairies we have found 100 per cent. affected, Ostertag gives
the average for Berlin at 75 per cent., and Bang for Denmark at 69 per
cent.
PREDISPONENT DISEASES.
As already noted all diseases which undermine the health tend to
diminish the powers of resistance to the tubercle bacillus. To be
especially dreaded, are long standing diseases which produce emaciation
and debility, fevers that for a length of time impair sanguification,
metabolism and nutrition, diseases of the digestive organs which cut off
the requisite supply of nutritive material, and, above all, diseases of
the lungs and air passages that impair the tone of the tissues and
invite the attack of the invading microbe. Bronchitis, laryngitis,
pharyngitis and tonsilitis in all their varied forms are to be
particularly noted. Even in man it is believed that one of the most
common channels of infection entrance is through the open tonsillar
crypts, and the same doubtless is true of animals. Pigs, with their
large tonsils and frequent infection through feeding, are probable
examples of this, and when, in addition to the detention of the microbe
in the cavities, there is an inflammation and debility of the tissues,
the opportunity for infection is greatly enhanced.
ENCREASED TRAFFIC IN (TUBERCULOUS) ANIMALS. DAIRY EXTENSION.
In common with all infectious diseases, tuberculosis owes its great
extensions to the sale and purchase of animals. Where an indigenous race
of cattle is raised and sold, without any additions from without,
tuberculosis is usually rare and confined to the one herd, or to those
having intimate intercommunication with it. Where, on the other hand, a
large stock is kept up, as in milk dairies, and few or no calves are
raised, but the bulk of the cows are sold off yearly and replaced by new
purchases, tuberculosis, sooner or later, finds admittance through the
body of an infected animal, and once implanted in the herd, it goes on
encreasing, without limitation, except by the sale or death of the more
seriously affected. The larger the herd and the greater the number of
yearly changes, the greater the number of opportunities for the
introduction of an infecting animal. Where a great part of the herd is
turned off yearly, and the new animals are drawn from any or every
source indiscriminately, it would border on the miraculous if such a
herd were to remain free from the infection for any great length of
time. The recent extension of tuberculosis in herds has been coincident
with the great development of commerce in live stock, and the rapid
transit on land and water by steam. Before the days of the steam engine,
animal plagues advanced slowly and uncertainly, excepting in the
presence of a great European war, which drew animals from all available
sources, congregating them in large mutually infecting droves in
commisariat parks, and marching them in the wake of the army for its
daily supply. Inevitably every country invaded was infected, and the
plagues spread from the line of march in all directions. The more deadly
plagues, like rinderpest and lung plague, were the first to appear, and
in this lay a certain measure of palliation of the evil, as the exposed
and often weaker animals were killed off, so that the slower contagion
like that of tuberculosis had not time to develop. This mitigating
influence held good so long as the deadly plagues were not placed under
effective control. When, however, a nation successfully extirpated and
excluded lung plague and rinderpest, the way was opened for a freer
extension of tardily developing plagues like tuberculosis. The great
development of beet sugar factories and the accumulation of herds to
consume the marc; the extraordinary extension of manufactures which have
made England and certain countries of Western Europe consuming rather
than agricultural lands, and the wonderful modern expansion of dairy
husbandry have combined to encrease and concentrate the cattle industry
in ratio with the manufacturing and commercial progress of the nations,
and as the live stock are kept under a milk-stimulating regimen and a
life passed largely indoors, the way has been open for an ever-advancing
encrease of tuberculosis. In the United States the centralization of
population in the Eastern States and in all great centres of industry
and the concentration of cows for the milk supply, and in certain
districts in connection with butter and cheese factories, have
contributed to wide local extensions of consumption. Hence it has been
no uncommon thing to find herds in the vicinity of cities with 20 to 100
per cent. affected, in striking contrast with the 0.02 per cent. found
in the fat cattle from the plains.
The modern railway traffic brings to all these swarming centres of
animal industry, live cattle from long distances to supply the constant
depletion through deaths and the disposal of dry cows, and thus the
whole Atlantic slope is drawn upon to fill the eastern stalls. Infected
animals thus shipped from Ohio, Indiana, Illinois, Wisconsin and
Michigan for the good of the herds in those states find new homes in New
York, or New England, where they have four to twelve mouths to propagate
the infection before they are themselves disposed of. As in the days of
the lung plague in America, the eastward trend of bovine traffic,
becomes to a certain extent a protection and benefit to the herds of the
west, but in equal ratio it operates to the detriment of our eastern
stock. What is true of the planting of new centres of infection in the
busy dairy districts of the east, and of the steady increase of disease
in already infected herds, through the constant addition of new cases
purchased, is no less true of the corresponding districts devoted to
dairying interests in the west. It is the natural order of things, that,
everywhere, the new accessions of infection, coming in the lines of
trade, into large dairy herds, kept to a great extent indoors for months
at a time, must hasten the general infection of such herds. When,
therefore, no intelligent measures are interposed to check the evil, we
must expect that the marked increase in the prevalence of tuberculosis,
which we have witnessed of late years, shall become more and more
evident year by year. Journals have claimed credit for befriending the
stockman, in opposing all control of the cattle traffic, dealers have
denounced all control as ruinously oppressive and injurious, and
legislators have turned a deaf ear to the warnings of science and
experience, but time, in this as in all other plagues, will justify the
demand for an intelligent control, and the increasing losses will one
day open the eyes of the stockowners to the fact that their truest
friends are those that would exclude the baneful seed, and kill it ere
it has had time to germinate and bring forth its ever increasing
harvests.
In the absence of any systematic and efficient government protection in
this line, the stock owner can only protect his sound herd by the rigid
exclusion of all animals that are not of his own breeding, or in case of
purchase, by an exhaustive inquiry as to the occurrence of sickness or
deaths in the herd from which he buys, and by the professional
examination and test of every animal to be bought. Even then he must
promptly separate, test, and, if necessary destroy any animal that
proves unthrifty, or which by cough, diarrhœa, wheezing or other sign
gives evidence of probable tuberculosis.
_Unregulated Traffic in Tuberculous Animals from Other States._ The
danger of buying animals untested is in no degree lessened when they are
sent in from other states. While some make a business of supplying the
store market with what they believe to be good stock, there is always
the temptation to turn off animals that are unthrifty or poor milkers
and which have proved less profitable than the others. Some even have
the herd tested and sell off those that show evidence of tuberculosis.
Unless, therefore, it is held in check by the tuberculin test, the
traffic is made to the extent of such sales a direct means of
disseminating tuberculosis.
ASSORTING THE TUBERCULOUS ANIMALS FOR SALE IN A GIVEN STATE.
A still more injurious result comes from the order of given States, that
the admission of store cattle shall be guarded by the tuberculin test of
each animal, and the supineness or worse, of adjacent states in
establishing no effective safe guard against the disposal of the
tuberculous culls in the unprotected State. Cattle from the west or
elsewhere in the United States, arrive in a great public market as, for
example, New York, they are here tested, those that stand the test are
shipped into one of the States requiring the test (Massachusetts,
Pennsylvania, New Jersey, Canada), and those that have shown the
reaction of tuberculosis are sold into the herds of the State in which
they were tested. The most malicious enemy of the New York stock owners,
could not devise a surer means of stocking the herds of the State with
tuberculosis than this atrocious system. Yet when the present writer had
a bill introduced into the legislature to correct the evil the opposing
interest proved strong enough to prevent it from coming to a vote. The
legislative committee on tuberculosis which sat later, and upon whose
attention the subject was pressed, also practically ignored it and the
statute which this commission inspired leaves the matter as bad as
before. Under the present law the New York purchaser must secure his own
interests by having every animal he buys tested by a trustworthy
veterinarian.
_Sale of Sound Animals Concentrates the Tuberculosis._ The action of one
or more States in admitting store cattle only after a tuberculin test,
acts directly in encreasing the relative number of tuberculous animals
in adjacent States. The purchaser from Pennsylvania for instance, goes
into a New York herd and purchases all the best animals on the condition
that they pass the tuberculin test uncondemned. It follows that the New
York herd is left with the tuberculous cattle only, and those that,
aside from tuberculosis, are of low value or profitless to keep. Further
as the advance of tuberculosis is proportionate to the relative number
of tuberculous subjects in the herd or building, and the concentration
of the poison, the depreciated herd is almost certain to become rapidly
and generally affected by the disease.
_The Denial of Indemnity for Tuberculous Animals Killed._ Several
American States (and notoriously New York in the recently enacted
statute) forbid compensation to the owner for any animal killed because
it is affected with a contagious disease, and to prevent the extension
of such contagion. All history attests, and any consideration of human
nature might teach, that such a measure is only calculated to spread the
infection. The owner of an animal, affected with a contagious disease,
who can get little salvage by turning it into beef, and none at all if
he hands it over to the State for slaughter, will naturally think of
putting it on the market, where he can secure a good price. How much
more is he tempted to do this when the disease is an occult one, and the
animal shows the outward appearance of health, as is the case in
nine-tenths of many tuberculous herds! Crime cannot be fixed on the
seller, for he is not an expert, and cannot be expected to diagnose the
disease. If the infected cow is of little value for the dairy, she is
passed on, from hand to hand, leaving infection in every herd she has
entered. The ultimate owner (in whose hands the State finds her and
diagnoses her disease), though he may have bought her in good faith as a
sound animal and paid a correspondingly high market price, is made to
lose the whole value of the cow. The real offender who knew her to be a
tuberculous animal, and sold her in consequence at the price of a sound
cow is shrewd enough to keep himself out of the clutches of the law,
while the honest purchaser who has been already swindled, has his income
and property cut off without compensation. Such a law is self-evidently
unjust; it plays into the hands of the swindler at the expense of the
just man; with the object of protecting the community against infection,
it refuses to call on the public for any contribution toward its own
protection. The system is a direct bid for extensive and encreasing
violation of the law and diffusion of the infection and must be accorded
a prominent place in the list of causes. It would be surprising to find
that any country ever extirpated an animal plague by working on such a
system. As a matter of fact no country ever did; all such sanitary
successes from the extinction of sheeppox or rinderpest in Western
Europe, to the recent _stamping out_ of lung plague in the United
States, were based on a just compensation to the owners of the stock.
When, therefore, veterinary sanitary principles and experience have been
so far ignored as to allow the passage of a law, which at once favors
the diffusion of infection by the crafty sale of the infected, the
expatriation of the healthy animals from the home herds, leaving only
the diseased, and finally the selection from herds in transit of the
tuberculous ones to be scattered widely among the herds of the State, we
must not wonder at the continuance or encrease of tuberculosis in the
commonwealth. Until a more rational and common sense legislation can be
secured, the unfortunate stock owner must defend himself by the
expensive alternative of testing every animal he buys.
_Private Testing of Herds and Sale of the Tuberculous._ A most
reprehensible practice is the private testing of herds and the sale as
store animals of those that react. In this way a herd may be cleared of
infection, but at tenfold expense to the public at large, as every
animal sold may convey the infection into a separate herd. It is,
however, a natural outcome of the unwise system of refusing indemnity
for the infected.
_Habituating to Tuberculin Testing and then Selling under Test._ Many
(not all) cattle, when injected with tuberculin repeatedly at short
intervals, acquire a tolerance of the agent and fail to react as at the
first test. We have in such cases examined the animals _post mortem_ and
found active tuberculosis. Unscrupulous owners, aware of the fact, have
their diseased cattle injected repeatedly every few weeks, and as soon
as they fail to respond, sell them under the guarantee of the tuberculin
test. The cattle, of course, carry the infection into other herds. This
swindle could be obviated if it could be made a misdemeanor to have or
use tuberculin except as a State or Federal official acting for the
government. This would imply the corollary that the State should test
the herds when called upon.
_Antipyretics During Tuberculin Test._ Another method of undoing the
tuberculin test is to feed large doses of antithermic agents to depress
the temperature at the time the rise from tuberculin would take place.
Tuberculous cattle may thus be sold as sound animals, with a certificate
of having successfully passed the tuberculin test, the operator having
given such certificate in perfect good faith. It suggests the importance
of withholding tuberculin from public use, or of securing an absolute
control of the feeding and watering of the animals during the test.
_False Certificates of Tuberculin Tests._ Stock owners have reported to
the writer alleged tuberculin tests of their herds which were completed
in three hours, and others have named instances of marking animals for
shipment and giving certificates of testing where no tuberculin had been
used and no examination beyond the most cursory glance had been made.
This might be expected of some non-graduates, registered on a basis of
alleged practice, shamefully ignorant of veterinary medicine and
conscious of their false position, and some educated veterinarians thus
placed at a disadvantage may have been tempted to follow suit, but it
can only end in personal disgrace and an inevitable extension of
tuberculosis. Begotten in a legislative wrong and nourished by moral
weakness, it can only grow into greater evil. Unfortunately such
unworthy actions throw discredit on the very name of sanitary police. To
avoid the evil every one aspiring to the responsible work of testing
cattle should be thoroughly examined as to fitness and licensed to
practice under a heavy penalty for neglect or malpractice.
_Feeding Hogs on Fresh Offal from Abattoirs._ It has been a common
practice, especially in country districts, to turn the raw offal of
slaughterhouses to pigs, and as the tubercle is usually concentrated in
internal organs, the hogs become infected in large numbers. In public
institutions which slaughtered their own meat I have found the hogs all
but universally tuberculous. The danger is only slightly lessened when
the hogs are fed raw butcher and kitchen scraps in swill. It suggests
the compulsory boiling of all swill or garbage containing raw meat.
_Feeding Calves and Hogs on infected Milk._ Though it has been
repeatedly shown that the majority of moderately tuberculous cows do not
yield infected milk, yet in every tuberculous herd, at irregular
intervals, one or more are attacked with tuberculosis of the mammæ, and
the drinkers of the milk take in the tubercle bacilli. This will happen
in the most strictly supervised tuberculous herds, while in those that
are less carefully managed, the milk that is considered unfit for human
consumption is fed to pigs or calves. In one dairy, I found that the
calves, all fed in this way afterward reacted under the tuberculin test,
while the following year the crop of calves, though fed on the milk of
the same diseased cows, with this difference that the milk had been
first heated to 180° F., without exception grew up healthy, and not one
reacted under the tuberculin test.
_Feeding hogs after Tuberculous Cattle._ Where cattle and hogs are kept
on the same place, it is a common practice to let the swine clean up all
food left by the satiated cattle. If there are tuberculous cattle,
affected either in the air passages or alimentary tract, the pigs become
infected by taking in the expectoration by which the food is soiled, or
by rooting around where the cow manure has fallen.
_Feeding from a Common Trough._ In an infected herd, a common cause of
extension is found in the use by the whole herd of a common feeding
trough, in which the food soiled by virulent discharges, is taken by
healthy animals. The habit of tying a cow in different stalls in
succession as she happens to strike one, in place of keeping each cow by
its own stall is a fruitful source of infection. Even when each cow is
kept by its own stall, she often becomes infected by reaching into the
feeding trough in front of the next cow on the left or right and taking
in soiled and infected fodder. In swill stables the evil reaches its
maximum, as the feeding trough for 50 or 60 animals is slightly inclined
so that the liquid food runs from the supply end to the other, and
infecting expectorations are carried in front of all in turn.
_Dry, Dusty Stables._ Tubercle bacilli are not carried out on the
expired air, unless there is forced expulsion as in coughing, snorting
or sniffing. In such cases the solid particles are thrown off in masses
or fine spray and lodged on surrounding objects. These, together with
infecting discharges from bowels, urinary or generative organs, open
sores, etc., dry up, and rise on the dust, and, as sterilization occurs
slowly indoors, they cause more or less infection of the animal inmates.
Cornet, Tappenier and others have thoroughly established this as a
common form of transmission, and shown the great importance of
cleanliness, disinfection and the removal of infecting materials without
raising dust. In an establishment in Paris, a consumptive had served for
3 years. In the following 10 years, 15 of the 20 employés died of
phthisis.
_Extension through Vermin._ As rats and mice (and other rodents) are
susceptible to tuberculosis by ingestion (Galtier) it follows that they
may become the media for extension of the infection through fodder in
which their droppings are scattered, or from their feeding in the same
troughs as the cattle or swine. For swine in particular the danger is
greater because of their carnivorous habits; the rat acquires
tuberculosis through eating the offal of the abattoir, or the scraps of
the butcher’s stall, or kitchen, and the sick rat is thereafter easily
caught and devoured by the pig to its own undoing. To block this channel
of infection the destruction of vermin about slaughter houses, stables
and pig pens is a most important consideration.
_Flies and Other Insects as Carriers of Tuberculosis._ These
congregating on tubercular sores, around the nares or lips, on the skin
contaminated by the virulent bowel discharges, on dishes holding
infecting milk, on objects soiled by infecting discharges, on diseased
carcasses at abattoirs, rendering works and elsewhere, (Spillman,
Hoffmann, Lartigan, etc.,) and on graves where the earth worms have
brought the bacillus to the surface, (Lortet, etc.) become more or less
active agents in disseminating the virus. In this way food and water are
contaminated, and exceptionally, infection may even be implanted on
sores. As the excreta of the flies contain the virulent bacilli, the
latter are deposited on windows, walls, furniture, etc., and may be
later disseminated in the dust of the apartment.
Dewevre found tubercle bacilli in the bedbugs infesting a bed in which
successive cases of consumption had developed, showing that other
parasitic or rapacious insects besides flies must be looked on as
possible propagators of the bacilli. There is reason to suspect, lice,
fleas, ticks and acari especially. The same is true of leeches and other
rapacious invertebrates.
LESIONS. THE TUBERCLE.
The characteristic lesion in tuberculosis is the tubercle, taking its
name from the small rounded nodule which, at first virtually invisible,
encreases often to the size of a millet seed, or a pinhead or even
larger, and which by confluence with others, forms conglomerate masses
of all sizes to which the term tubercle is still applied. Where the
bacillus tuberculosis is implanted, the fixed tissue cells are
stimulated to an undue proliferation, and a diapedesis of leucocytes
takes place from the neighboring capillary blood vessels, the whole
eventuating in the formation of a rounded cluster or nest of epithelioid
and giant and later small rounded lymphoid cells in a fine fibrous
stroma. Baumgarten and his followers claim that the larger epithelioid
and giant cells result from the karyokinesis and proliferation of the
fixed tissue cells, epithelial and endothelial cells, and that the
lymphoid cells which later (often after the eighth day in experimental
cases) invade the lesions, are alone the product of the migrating
leucocytes. Metchnikoff, Yersin and others contend, on the other hand,
that epithelioid and giant cells are directly derived from the
leucocytes and endothelial cells and like these are possessed of
actively phagocytic qualities. As the final outcome before caseous
degeneration, is the great predominance of the small lymphoid cell, it
may well be questioned whether this is not the result of active encrease
in both kinds of cells, as appears to happen in many other
inflammations. For our present purpose it is well to note the early
characters: _Centrally_ often a large (giant) cell with a number of
peripheral nuclei and at times, branching processes; around this as a
_second zone_ epithelioid cells of large size, with round or oval
nuclei, and sometimes giant cells; outside this a _third zone_ of small
rounded lymphoid cells with large nuclei. There is a delicate fibrous
network between the cells, but no indication of capillary blood vessels,
the absence of which may partly explain the constant tendency to
degeneration, necrosis, and caseation. The tissue around the miliary
tubercle is red and congested.
_Caseation._ A striking characteristic of tubercle is the occurrence of
coagulation necrosis, beginning in the centre of the specific nodule as
a whitish or pale softening and degeneration of the cell elements and
gradually extending toward the circumference. The cells, and even the
proximate tissue elements, die and disintegrate passing into a
structureless, granular or hyaline debris, which has been named from its
supposed resemblance to old, ripe, soft cheese. Baumgarten has observed
that the small lymphoid cells are the first to degenerate, followed by
the epithelioid and giant ones.
While the formation of tubercle is at first a productive inflammation of
which the cell clusters and nodules are the result, yet the tendency to
necrosis, and caseation is so great that it must be looked upon as one
of its most prominent features, and is rarely absent, whether the lesion
exists in the connective tissue of the lungs, liver or other organ, in
the lymph glands, in the respiratory or intestinal mucosa or submucosa,
in the osseous cancelli, brain or skin. It is, therefore, largely
pathognomonic, yet it is not peculiar to tubercle, being common in
glanders, and other infective inflammations. Its presence should always
lead to a search for the primary tubercle nodule, with its nonvascular
cluster of lymphoid and giant cells and above all for the specific
bacillus resistant to staining.
The tendency to extensive degeneration and caseation is especially
marked in swine, in which the resulting debris is often so liquid that
the tubercles bear a strong resemblance to abscesses.
_Calcification._ The deposition of lime salts (mainly phosphates) in the
tubercle is a common feature of advanced cases in man and pig, but
especially in cattle. It is unknown in rabbits and Guinea pigs. The
tubercle assumes a hard cretaceous aspect and feeling, grates under the
knife and crepitates when pressed. This is always an evidence of
chronicity, but it has been observed in swine in 3½ months.
_Fibroid Degeneration. Fibrosis._ In this case a productive fibroid
inflammation takes place in the tissue of the tubercle, and it is
resolved more or less extensively into a hard, white, resistant body.
This is the pearly mass which has given rise to the name of the _pearl
disease_ (perl-zucht) in Germany. It may be fibrous throughout, but
usually a number of the nodules show a caseated centre while the
external zone, that nearest to healthy tissue, has alone taken on the
conservative fibroid development. Like cretifaction, fibrosis is an
indication of chronicity in the lesion. It is often seen in man, but
still more so in cattle, in which it affects particularly the abdominal
cavity, but also to a lesser extent the chest and other parts. It is
remarkable for the paucity of bacilli to be found in its substance,
often requiring many sections and infinite patience to reveal the
presence of the microbe. This comparative lack of actively multiplying
bacilli is doubtless one factor, operating in the direction of
conservative processes, chronicity and even partial recovery. In
experimental tuberculosis the extent and rapidity of development of
tubercle, as also of the degeneration are found to be closely allied to
the number of bacilli introduced.
_Cattle: Pulmonary Tuberculosis._ One of the most frequent seats of
tuberculosis, the lung, may in acute cases show a diffuse miliary
tuberculosis, a considerable part of a lobe or of several lobes being
congested, infiltrated, and filled with small individual tubercles,
grayish or transparent in the midst of the general redness. A second
form, often of old standing, is in the shape of hard masses, often
circumscribed or isolated, and easily felt when the soft lung tissue is
manipulated. They are respectively formed by the local aggregation, and
confluence of the small miliary nodules and may vary in size from a pea
to a mass of ten or twelve inches in diameter. On section the miliary
tubercle may not yet show central caseation, but the larger ones do so
as a rule. The caseated nucleus may be soft, cheesy and somewhat
homogeneous; it may be dry, granular and yellow, resembling damp farina
of maize; it may be calcified in its outer portion and invested by a
firm fibrous envelope. The tubercle may be the seat of general fibroid
degeneration, constituting the pearl nodules (perl-knoten) dense as
cartilage and either with or without a soft caseated centre; it may show
an agglomeration of nodules in all stages from the early congested
nodule to advanced caseation or cretefaction, the whole embedded in a
solid congested and infiltrated tissue, largely fibroid. There may be
extensive abscesses, the seats of complex infections, having thick
uneven walls, often showing _grape like_ tuberculous outgrowths, and
containing thick, caseopurulent, viscous, granular, yellowish or
greenish and comparatively odorless contents; in other cases the
abscesses have burst into the bronchia, leaving _vomicæ_ and with the
new resultant infections the contents have acquired an offensive putrid
odor; finally, there may be extensive inflammatory infiltrations,
affecting lobules or lobes, and interspersed with tubercles in the form
of the early grayish or transparent nodule, or even more advanced
caseous or cretaceous centres. These latter serve to distinguish the
condition from broncho-pneumonia, the grayish centres of which might
suggest miliary tubercle. The broncho-pneumonia, however, has the
whitish centres confined to the bronchioles and their terminal air sacs,
and represent their thickened walls and muco-fibrinous contents; they do
not show the same tendency to caseation, nor necrosis of the tissue, nor
to caseation of the dependent lymph glands, and, above all, they do not
contain the bacillus tuberculosis.
A noticeable feature in the tuberculous lung is the great frequency of
tubercles of all different ages from the initial transparent nodule to
the caseated or calcified mass side by side. A tuberculous bronchitis is
a familiar accompaniment, with lines of miliary tubercles, ulcers and a
flocculent (sometimes gritty) muco-purulent discharge, containing
elements of the necrotic tissue and bacilli. Emphysema and interlobular
œdema are also met with.
The _Pleuræ_ often suffer by continuity of tissue from the diseased
lung, but they may be affected primarily through infection of the
circulating blood. The earliest pleural lesions may be congestion,
exudation and the formation of false membranes in fringes, but soon
these become the seats of minute nodules or forming tubercles which
steadily encrease to form pale red cauliflower-like growths—which have
been spoken of as _grapes_, from their supposed resemblance to bunches
of that fruit. Extensive areas of the mediastinal, costal or pulmonic
pleuræ are often completely covered by these productions. Dense, and
thick adhesions sometimes form, holding in their substance
characteristic tubercles.
The _bronchial and mediastinal lymph glands_ receiving as they do the
afferent trunks from the lungs and the great lymph sac of the pleura,
offer in their sluggish currents the most favorable culture vessels, and
almost always become affected in consequence. Not unfrequently they are
found to be tuberculous when the tissues which they drain appear to be
sound, and we must therefore, conclude that the primary slight lesions
in the latter have recovered, or that the bacilli have passed through
the tissues and lymph channels without establishing any centre of
disease. The glandular lesions are primarily congestion and redness,
with more or less infiltration and swelling, followed by a nodular
induration, with enlargement or exceptionally shrinking. When bisected
they may show all stages of the tubercle from the miliary granule to the
caseous, dry, yellow, granular or cretaceous necrosis. By aggregation
these often grow to a large size, a long diameter of 6 to 12 inches
being not uncommon.
_Pericardial and Cardiac Lesions._ The pericardium may be implicated
from the pleuræ or independently, and though tuberculosis of the heart
is rare, it may be the seat of primary tuberculosis or of extension from
the pericardium or endocardium. In the N. Y. State Veterinary College
Museum is a cow’s heart, greatly enlarged, and completely invested and
invaded by tubercle several inches thick.
_Tuberculosis of the Mouth and Throat._ Tubercles sometimes form in the
_tongue_ causing nodular swelling, with a caseated centre. Much more
frequently they attack the _pharynx_ or _larynx_ with the formation of
nodular necrotic swellings, followed by ulcers and the implication of
the adjacent lymph glands. The glands are liable to be invaded through
the tonsillar and other follicles of the faucial and pharyngeal regions,
which like the solitary and agminated glands of the intestines form
excellent culture vessels. The glands most frequently attacked are the
_retro-pharyngeal_, but the _lateral pharyngeal_, the _intra-parotidean_
and _submaxillary_ lymph glands occasionally suffer. They often become
indurated, yet the formation of abscess-like sacs is not uncommon
especially in the retro-pharyngeal.
_Gastro-Intestinal_, _Peritoneal_ and _Mesenteric Tubercles_. Tubercles
of the interior of the stomachs are rare, though they are frequent on
the peritoneal surface of the first three stomachs, as rounded,
subserous nodules varying in size from a pea upward. The _mucosa of the
small and large intestines_ may suffer, by preference in the seats of
the solitary or agminated glands, and the resulting ulcers may extend in
the lines of the lymph vessels from the convex to the attached border of
the gut. The small greenish caseated and calcified nodules on the
intestines, which are so often mistaken for tubercles, are the
degenerated cysts of the œsophagastoma. Tuberculosis of the mesenteric
lymph glands is much more common, the successive stages being
essentially like that seen in the bronchial glands. Beside these the
surface of the mesentery, omentum and abdominal parietes often becomes
the seat of congestion, exudation and cauliflower-like neoplasms or
grapes, as already stated of the pleuræ. In a certain number caseation
or cretefaction may be detected.
_Liver Tuberculosis._ The liver is greatly exposed to tuberculosis as
the single destination of all the blood from the gastro-intestinal
tract. Tubercles also form on its surface by direct infection from the
peritoneum. The hepatic tubercles are often very large and numerous,
adding greatly to the bulk and weight of the viscus. There is usually
coincident tuberculosis of the lymph glands of the porta.
_Tubercle of the Spleen._ This is also a favorite seat of the morbid
process, exposed as it is to the reflux of infected blood in the portal
vein, and to access of the bacillus from the peritoneum and omental
lymphatics.
The _pancreas_ is less exposed to the channels of the circulation and is
less frequently affected.
_Genito-Urinary Tubercles._ The _kidneys_ are always liable to suffer in
generalized tuberculosis, in accordance with their function of
elimination and the great quantity of blood that passes through them.
The tubercles may be numerous, encroaching upon and destroying the
glandular tissue, and determining congestion, nephritis and hæmorrhage
(Schütz). The _ovaries_, when tuberculous, lead to nymphomania and
sterility; they become swollen, with rounded projections, indurated, and
on section show all stages of infiltration, caseation and calcification.
They may encrease to a great size. Tubercles are found on the _Fallopian
tubes_, the _serous and mucous surfaces of the womb_, and in the _broad
ligaments_, in all their characteristic forms. The _bladder_ and
_vagina_ are less frequently involved. In the male the _testicle_,
_epididymus_, _tunica vaginalis_ and _prostate vesicles_ are sometimes
affected. The swelling and induration of the affected organ, or the
existence of hydrocele, may be noted.
_Tubercle of the Udder._ From the mass of blood passed through the udder
it is specially exposed to infection whenever the bacilli enter the
circulation. It may also be directly infected by the entrance through
the teat, or a trauma, of the bacillus of the stable dust. There may be
for a time only a slight general swelling which leads to no suspicion on
the part of the milker, and as the secretion is not arrested, a
dangerous product may be distributed. At this stage the lobules on
section appear swollen, gray, with paler or yellowish points and minute
hæmorrhages. The milk ducts contain coagula and bacilli (Bang). In other
cases, usually more advanced, the gland is hard, nodular, enlarged, and
shows a marked thickening of the walls of the smaller milk ducts and
secreting follicles, with yellowish and even caseous and calcified
centres. The gland is often greatly enlarged, the milk suppressed or
completely altered, and tubercular neoplasms or ulcers exist in the
larger ducts.
_Tuberculosis of the Brain and Spinal Cord._ As noted in Volume III.
this occurs in young cattle especially in the form of tubercles of all
ages attached to the pia or arachnoid, on the brain, or cerebellum, or
in the ventricles, also in the cerebral matter, in or on the lumbar
enlargement of the cord or on its pia. Several cases have come under my
notice in the mature cow.
_Tuberculosis of the Eye._ This has been seen mainly as a result of
experimental inoculation, yet casual cases also occur in the cornea,
sclerotic, iris or choroid, the product undergoing early necrosis and
softening into a yellow mass filling the different chambers.
_Tuberculosis of the Bones._ Though less frequent than that of internal
organs this is not rare. It usually attacks the spongy tissue, near the
articular extremities, or the vascular line between epiphysis and
diaphysis, giving rise to considerable exudate, thickening of the bone
and arthritis. The vertebræ, ribs, sternum, petrous temporal, frontal
and occipital also suffer. Sections of the bone show dilatations of the
cancelli, filled with the characteristic nonvascular groups of giant,
epithelioid and lymphoid cells with, at times, softened and caseated
centres. The adjacent bone is congested and softened, so that the
detachment of epiphysis and apophyses is not uncommon. In case of
invasion of the joints the cartilages and ligaments are the seat of
tubercular deposits, softening, fibroid change and caseation, and there
is general synovitis. The cartilages of the ear (concha) and nose
(septum) may also be invaded.
_Tubercles of the Skin._ These are not very uncommon in cattle being the
counterpart of the tuberculous warts and ulcers of the hands of
butchers, tanners and others that handle the products of diseased
animals. They may show as little pea-like nodules in the substance of
the skin, or immediately beneath, very commonly on the side of the
abdomen, where their presence in life furnishes a useful suggestion, as
enlarged masses forming raw, warty projections with centres of
caseation, or as clusters of warty-like growths of this kind (grapes).
_Tuberculosis of the Muscles._ This is comparatively rare in cattle,
though by no means unknown, appearing as tubercles of the size of a pea
and upward, in or between the muscular masses, often showing a caseated
centre.
_Tubercle of Lymph Glands._ No organs in the body suffer more than the
lymph glands as they receive through their afferent trunks and develop
the bacilli coming from any adjacent tissue to which they are
subsidiary. There is also evidence to show that bacilli entering from
the lungs or bowels may pass through these without apparent effect to
develop in the connected lymph glands. The frequent infection of the
pharyngeal, bronchial, mediastinal and mesenteric lymph glands has been
already sufficiently noticed, and if the other groups suffer less it is
mainly because the tissues from which they derive their lymph are less
frequently infected. An intimate knowledge of the different groups of
lymph glands is a most essential prerequisite to the diagnosis of
tuberculosis in life, and no less to a satisfactory _post mortem_
examination. The order of relative susceptibility and importance is
somewhat as follows: Bronchial, mediastinal, mesenteric, hepatic,
sublumbar, mammary inguinal, subdorsal, phrenic, intercostal (especially
the first and second), pharyngeal, parotid, submaxillary, prescapular,
prefemoral (stifle), prepectoral, axillary, cubital and popliteal.
_Relative Frequency of Tubercle in Different Parts in Cattle._ The
following table gives the seat of tubercle as noted by a number of
observers. It is open to the objection that it is the result of
examination for diagnosis, and therefore gives the most obvious rather
than the complete list of lesions. Examination of the brain, bones, deep
muscles and intermuscular glands, etc., was usually omitted. Again, as
the animals were often steers, the indications as regards the generative
organs are unreliable. The œsophagostoma nodules on the bowels have been
so often mistaken for tubercles that I have omitted all reference to
intestinal tubercle.
DISTRIBUTION OF TUBERCLES IN DIFFERENT ORGANS OF CATTLE: PER CENT OF
AFFECTED CATTLE.
────────────┬─────┬───────────┬────────┬──────────┬──────┬───────
│ % │ │ │ │ │
│Right│ % │% Costal│ │ │
│Lung.│Mediastinal│Pleura. │ │ │
│ % │ Glands. │ % │ % │ │
│Left │% Bronchial│Visceral│Mesenteric│ % │ %
│Lung.│ Glands. │Pleura. │ Glands. │Liver.│Spleen.
────────────┼─────┼───────────┼────────┼──────────┼──────┼───────
German │ │ │ │ │ │
Abattoirs,│ 75 │ 29 │ 47–55 │ │ 28 │ 19
Pearson, │ │ │ │ │ │
(Penna), │63–57│ 60.7–33.8 │ 22 │ 23.25 │ 20.7 │ 5.7
Bryce │ │ │ │ │ │
(Canada), │77.27│ 56.8 │ 11.36 │ 11.36 │ 40.9 │
Reynolds │ │ │ │ │ │
(Minn. │ │ │ │ │ │
Agr. Ex. │ │ │ │ │ │
Station), │89.4 │ 33.3–64.9 │ 79 │ 12.5 │ 35.4 │ 27
Law (N.Y. │ │ │ │ │ │
Grade │ │ │ │ │ │
Herds), │34.8 │ 64 │ 6.4 │ 9.6 │ 1.6 │
Nelson (N. │ │ │ │ │ │
J. Exp. │ │ │ │ │ │
Station │ │ │ │ │ │
Cows), │33.9 │ │ │ │ 28 │
Russell │ │ │ │ │ │
(Wis. Exp.│ │ │ │ │ │
Station), │ 55 │ 72.4 │ │ 24 │ 10 │
Stalker & │ │ │ │ │ │
Niles (Ia.│ │ │ │ │ │
Exp. │ │ │ │ │ │
Sta.), │ 36 │ 61 │ │ │ 8.3 │
Reick │ │ │ │ │ │
(Leipsic),│ 100 │ │ [2]57 │ │ 83 │ 18
────────────┴─────┴───────────┴────────┴──────────┴──────┴───────
────────────┬───────┬───────┬───────┬───────────┬──────────┬──────────
│ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
│ │ % │% Liver│ │ % │
│ % │Lumbar │ Lymph │ % │Pharyngeal│ %
│Uterus.│Glands.│Glands.│Peritoneum.│ Glands. │Diaphragm.
────────────┼───────┼───────┼───────┼───────────┼──────────┼──────────
German │ │ │ │ │ │
Abattoirs,│ 10 │ 5 │ 1 │ │ 4 │ 0.2
Pearson, │ │ │ │ │ │
(Penna), │ 5.5 │ │ 10.3 │ 14 │ 15.15 │ 11.4
Bryce │ │ │ │ │ │
(Canada), │ │ │ │ 45 │ │ 2.27
Reynolds │ │ │ │ │ │
(Minn. │ │ │ │ │ │
Agr. Ex. │ │ │ │ │ │
Station), │ │ │ 8.3 │ │ 18.7 │
Law (N.Y. │ │ │ │ │ │
Grade │ │ │ │ │ │
Herds), │ │ │ │ 17.7 │ 6.4 │
Nelson (N. │ │ │ │ │ │
J. Exp. │ │ │ │ │ │
Station │ │ │ │ │ │
Cows), │ │ │ │ │ │
Russell │ │ │ │ │ │
(Wis. Exp.│ │ │ │ │ │
Station), │ │ │ │ │ 31 │
Stalker & │ │ │ │ │ │
Niles (Ia.│ │ │ │ │ │
Exp. │ │ │ │ │ │
Sta.), │ │ │ │ │ 5 │
Reick │ │ │ │ │ │
(Leipsic),│ │ │ │ [2]57 │ │
────────────┴───────┴───────┴───────┴───────────┴──────────┴──────────
────────────┬────────┬──────┬────────┬──────┬──────┬─────────
│ │ │ │ │ │
│ │ │ │ % │ % │
│ │ │% Iliac │Lymph │Lymph │
│ │ │ and │Glands│Glands│ % Lymph
│ % │ % │Inguinal│ of │ of │Glands of
│Stomach.│Udder.│Glands. │Udder.│Flank.│Shoulder.
────────────┼────────┼──────┼────────┼──────┼──────┼─────────
German │ │ │ │ │ │
Abattoirs,│ 0.16 │ 1 │ 0.06 │ │ │
Pearson, │ │ │ │ │ │
(Penna), │ 7.2 │ 8.75 │ │ 13.5 │ 9 │ 7.75
Bryce │ │ │ │ │ │
(Canada), │ │ │ │ │ │
Reynolds │ │ │ │ │ │
(Minn. │ │ │ │ │ │
Agr. Ex. │ │ │ │ │ │
Station), │ │ 16.6 │ │ │ │
Law (N.Y. │ │ │ │ │ │
Grade │ │ │ │ │ │
Herds), │ │ 6.4 │ │ │ │
Nelson (N. │ │ │ │ │ │
J. Exp. │ │ │ │ │ │
Station │ │ │ │ │ │
Cows), │ │ │ │ │ │
Russell │ │ │ │ │ │
(Wis. Exp.│ │ │ │ │ │
Station), │ │ 6.9 │ │ │ │
Stalker & │ │ │ │ │ │
Niles (Ia.│ │ │ │ │ │
Exp. │ │ │ │ │ │
Sta.), │ │ │ │ │ │
Reick │ │ │ │ │ │
(Leipsic),│ │ 17 │ │ │ │
────────────┴────────┴──────┴────────┴──────┴──────┴─────────
────────────┬────────────┬──────┬────────┬──────┬────────┬───────
│ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
│ % │ % │ % │ % │ % │ %
│Pericardium.│Heart.│Kidneys.│Bones.│Muscles.│Larynx.
────────────┼────────────┼──────┼────────┼──────┼────────┼───────
German │ │ │ │ │ │
Abattoirs,│ 0.9 │ │ 0.7 │ │ 0.1 │ 0.13
Pearson, │ │ │ │ │ │
(Penna), │ 8.2 │ │ 2.1 │ 0.4 │ │
Bryce │ │ │ │ │ │
(Canada), │ │ │ │ │ │
Reynolds │ │ │ │ │ │
(Minn. │ │ │ │ │ │
Agr. Ex. │ │ │ │ │ │
Station), │ │ │ 2 │ │ │
Law (N.Y. │ │ │ │ │ │
Grade │ │ │ │ │ │
Herds), │ │ │ │ │ │
Nelson (N. │ │ │ │ │ │
J. Exp. │ │ │ │ │ │
Station │ │ │ │ │ │
Cows), │ │ │ │ │ │
Russell │ │ │ │ │ │
(Wis. Exp.│ │ │ │ │ │
Station), │ │ │ │ │ │
Stalker & │ │ │ │ │ │
Niles (Ia.│ │ │ │ │ │
Exp. │ │ │ │ │ │
Sta.), │ │ │ │ │ │
Reick │ │ │ │ │ │
(Leipsic),│ │ │ 52 │ 9 │ 49 │
────────────┴────────────┴──────┴────────┴──────┴────────┴───────
Footnote 2:
All serosæ.
_Swine._ The _lesions_ in swine, though essentially like those in
cattle, differ in some particulars. The primary tubercles are more
commonly pharyngeal or intestinal and mesenteric, in keeping with
infection by ingestion; caseation will often proceed to liquefaction, so
that the tubercles appear like grumous abscesses with irregular outlines
and vascular growths on their walls; there is less tendency to
cretefaction than in cattle; the muscular and intermuscular tissues and
the lymph glands are far more frequently affected; ulceration of the
pharyngeal and intestinal mucosæ is more common. The lungs, liver,
spleen and visceral lymph glands are very subject to tubercle, the
kidneys, uterus and testicles somewhat less so, and the nerve centres
least of all. The serosæ are often involved and the seat of clusters of
vascular or caseated neoplasms (grapes). The bones and joints also
suffer, particularly in young growing animals.
_Horse._ The horse suffers much less frequently than cattle or swine,
probably largely because of his outdoor life, his better tone as the
result of muscular work, and the absence of the excessive milk secretion
which is secured from cows and of the dangers from ingestion that attend
on swine. Yet, according to Nocard, it is even more susceptible, and the
disease once established is liable to advance more rapidly to a diffuse
generalization. The _lesions_ in the lungs and abdominal cavity resemble
those of cattle, both in nature and abundance; tuberculous polypi and
ulcers are more common; the visceral lymph glands (bronchial and
mesenteric) are early and severely attacked; the liver and spleen suffer
extensively, the serosæ somewhat less so; lesions have been noted in the
vertebræ, skin and muscles (Cadiot). In rare instances tubercles have
been seen in the heart, and the aorta has been atheromatous (Cadiot).
Necrotic degeneration, caseation and cretefaction occur as in cattle.
_Sheep and Goat._ Tuberculosis is infrequent in the goat and especially
so in the sheep, owing perhaps largely to open air life and their
predilection for high, airy pastures. When inoculated they show a marked
susceptibility, and under favorable conditions they contract the
infection casually. The tubercles may be found in all parts of the
body,—lungs, thoracic lymph glands, intestines, mesenteric and sublumbar
glands liver, spleen, serosæ, lymph glands at large, vertebræ, etc.
There is less tendency to calcification than in the ox, the older
tubercles remaining in the caseated condition or bursting and forming
vomicæ. A common seat of casual tubercle in sheep is around the throat
or on the sides of the cranium or face.
More frequently than in cattle, verminous affections (œsophagostoma
columbiana, and venulosum in the bowels, stongylus filaria and rufescens
in the lungs, linguatula denticula in the mesenteric glands) are
mistaken for tuberculosis, hence the necessity for a careful
investigation into the nature of the neoplasm, the presence of the
tubercle bacillus, and the absence of the worms and their eggs. Except
in the case of the linguatula the lymph glands are little affected by
the worms.
_Dog and Cat._ The _lesions_ are often concentrated on the respiratory
or alimentary tract, but they have been noted also in the pharyngeal
glands, tonsils, posterior nares, serosæ, liver, pancreas, spleen, nerve
centres, ovary, uterus, testicle, epididymus, tunica vaginalis,
prostate, heart, aorta, bones and joints. They follow the regular
development of bovine tubercle, and caseation and cretefaction are
prominent features. These animals are especially liable to infection by
eating the left victuals from the plate of a consumptive owner, as well
as by devouring consumptive prey, and the primary lesions are to be
looked for along the line of the throat, bowels, liver and lungs. For
the dog Cadiot records caseating polypi and ulcers on the mucosa of the
larynx, trachea and bronchia, and Müller and Cadiot several cases of
pharyngeal caseating adenitis in the _dog_ bursting externally and
developing intractable fistulæ, having abundance of bacilli in the
discharge. These he attributes to expectorated virus from old standing
tubercles in the chest infecting the pharyngeal mucosa and indirectly
the lymph glands. The infection entering with the food and lodging in
the follicles of the tonsils would act in the same way, and infected
wounds received in fighting must also be quoted. _Cats_ suffer from
similar intractable sores, some of which may be traced to a tuberculous
origin. The lungs are often extensively hepatized and of a general pale
grayish color, but the early miliary lesions, the caseating and
cutaneous centres, the vomicæ often intercommunicating, the tuberculous
bronchial and mediastinal glands and the bacilli show the true nature.
Intestinal ulcers are common, especially on the agminated glands, and
small tubercles, in all stages of degeneration are met with in the
enlarged liver, the spleen, pancreas, kidney, etc.
_Apes and Menagerie Animals._ In these tuberculosis is common alike in
the thoracic and abdominal forms, and the lesions in the main are those
of domestic cattle.
_Chickens._ The _lesions_ are common in the abdominal cavity, the
intestines, liver and spleen being the most frequently attacked, while
the subcutaneous connective tissue, bones and joints also suffer. The
lungs and kidneys usually escape. The intestinal mucosa shows small
nodules, often caseated, or ulcers; the enlarged and friable liver is
studded with tubercles from the size of a hemp seed upward, gray or
translucid, homogeneous or with central necrosis, simply or in
conglomerate masses, with congested or hæmorrhagic periphery; the spleen
is swollen and permeated by similar deposits; fibrinous ascitis is not
uncommon; the abdominal lymph glands are enlarged and congested.
The early tubercle shows a central, necrotic, hyaline area, consisting
of the debris of disintegrated cells, which is colored brown by picro
carmine, unlike the nucleus of the pheasant tubercle (Cadiot). Around
the hyaline centre is a zone of large epithelioid cells, the nuclei of
which stain strongly in carmine. Outside this is the usual zone of
small, round, lymphoid cells. In the whole the tubercle bacilli can be
made manifest by the carbol-fuchsin (Ziehl-Neelsen) stain. In the older
and larger tubercles the central necrotic mass has encroached in part or
in whole on the epithelio-lymphoid zone.
_Pheasant._ The _lesions_ have the same seats and naked-eye aspect as
the chicken tubercle, but under the microscope the smallest and most
recent tubercles show epithelioid cells to the centre, or later, the
central zone presents a dense fibrous network enclosing open spaces and
giving a mahogany stain with Lugol’s solution (iodine and potassium
iodide). (Cadiot). There has been an organisation of connective tissue
which has submitted to amyloid degeneration, making a clear distinction
from the tubercle of chicken.
_Parrot._ The _lesions_ were thus located by Eberlein and Cadiot:
│ Cadiot.│Eberlein.
Eye and periocular region, │ 12│ 14
Commissure of the beak, │ 7│ 11
Tongue, │ 8│ 9
Palate, │ 4│ —
Larynx, │ —│ 2
──────────────────────────────┼──────────────────────────────┼─────────
Bones and Articulations, │Upper limbs (wings), 7│ 14
„ │Claws, 3│ —
„ │Cervical, Dorsal and 5│ —
│ Caudal, │
──────────────────────────────┼──────────────────────────────┼─────────
Lungs, │ │ 7
Liver, │ │ 4
Intestine, │ │ 3
Muscles, │ │ 1
Heart, │ │ 1
The _skin lesions_ are vascular neoplasms containing bacilli and usually
invested with a covering of horn, but sometimes, on the legs and feet
raw. The morbid growth may be rounded or conical, narrowing to a point.
The _lesions of the buccal mucosa_ begin as small, grayish swellings on
the angle of the mouth, palate, tongue or larynx which grow out into
more or less rounded vegetations. The _lesions of the liver and lungs_
are mostly miliary with the usual tubercular features, but they may grow
to larger size, as a pea or bean. In the _cancelli of bones_ and on
their surface, the lesions resemble those of the mammal.
The cutaneous form has been held to be the counterpart of warty lupus of
man, the more plausibly that the disease is developed by inoculation
from tuberculous men. The arthritic type represents what is described as
gout in parrots.
In any case the recent miliary lesion presents the true tubercular type
of a central giant cell or cells with bacilli, surrounded by epithelioid
cells, and they in turn by small, rounded lymphoid globules.
PRIMARY AND SECONDARY INFECTION.
The estimate of the relative, early or late infection of two organs or
tissues may often be made with reasonable accuracy from the fact that
the lesions in one organ are old, caseated, calcified or sclerosed,
while those in the other organ are all recent, with vascular environment
and almost devoid of caseation or other degenerative process. We cannot
safely predicate our decision on the greater number of old lesions in
one organ rather than another, as the disease may have advanced much
more rapidly in the one tissue. Still less can we state with certainty
that the disease has not entered by a given channel because no lesions
are left to show the transit of the bacillus along its supposed course.
We frequently find tuberculosis of the bronchial or mesenteric glands,
when we can detect no lesion in the lung, nor intestine. The bacillus
has been passed on without establishing any lasting lesion in transit.
It is often too confidently asserted that the infected dust inhaled,
falls directly on the air cells and determines the extensive pulmonary
tuberculosis that ensues. So, on the other hand, it is often too
arrogantly assumed that tubercle bacilli ingested with food, must
necessarily show their results mainly in the intestines, mesenteric
glands and liver. That solid particles can find their way directly into
the lungs, has long been demonstrated by the pulmonary anthracosis of
the miner, and the deadly phthisis of the stone hewer and cutler. The
experiments of Cornet, Tappeiner and others in producing pulmonary
tuberculosis, by compelling the inhalation of infected spray,
corroborate this experience very satisfactorily. Yet it does not follow
that all of the offensive matter penetrated the air cells at once on the
air inhaled. The heavy particles of steel, quartz and even of coal dust
must be mainly arrested on the surface of the moist air passages, yet,
under the irritation caused by their presence and the consequent arrest
of the ciliary motion, they would slowly gravitate downward to the
pulmonary cells. In the case of the inspired tubercular spray or dust,
we must recognize the possibility of the approach of the bacillus to the
lungs through the lymph and blood channels as well. The bacilli lodged
in the pharynx, and, above all, in the tonsillar follicles, can readily
enter the lymph vessels, and are finally poured into the lower end of
the jugular vein, but a few inches from the right heart, by which they
are instantly propelled into the lungs. If then the lung is the most
receptive and least resistant organ, it may easily be that this is the
first point where the bacillus can establish a strong and effective
colony. Apart from this the colonization of the tonsillar follicles may
determine a constant supply of fresh bacilli, which may gravitate down
with the abundant mucus toward the lungs.
This tuberculous colonization of the tonsillar follicles is doubtless
the main source of the infection of the pharyngeal lymph glands, which
is so common in ox, pig and dog. It tends further to intestinal
tuberculosis through the frequent swallowing of the products of the
infected follicles. Then the infection of the pharynx and tonsils,
whether established by inhalation or deglutition, may be the first step
toward a secondary infection of the intestines.
Again the bowels can be infected by the frequent swallowing of the
expectorations brought up from the diseased lungs or bronchia.
Conversely the lungs may be easily infected secondarily from preëxisting
disease of the abdominal organs, and again primarily through the lymph
channels. With tuberculosis of the cardia or liver the bacilli can
follow the lymph vessels of the œsophagus or vena cava so as to reach
the mediastinal glands, and from these glands in a state of disease they
can easily pass into the adjacent pleural cavity and reach the lung. Or
by following the mesenteric lymphatics they reach the thoracic duct and
enjoy what is virtually for them a culture fluid, until discharged into
the jugular, which, as already stated, is but a few inches from the
right heart and lung.
Extension through the general blood stream usually takes place only when
tubercles have already become numerous and extensive in a given region
of the body, and its occurrence is the signal for a generalized
tuberculosis.
The extension from the gastro-intestinal organs, pancreas and spleen may
be considered as a partial exception. Here the infecting blood is not
the general blood stream, but has to run the gauntlet of the liver
capillaries by which the bacilli may be sifted out and delayed. This
arrest subjects the liver to secondary tuberculosis in almost all cases
of abdominal tuberculosis, and goes far to explain the extraordinary
frequency of the disease in this organ. Ingestion tuberculosis almost
necessarily leads to hepatic tuberculosis, and this notwithstanding that
the primary lesion may have been very circumscribed.
The tuberculization of such a large vascular organ as the liver,
however, paves the way for further extension, and if once extensively
diseased, the early generalization of the infection is to be dreaded.
TUBERCULOSIS CONTINUED.
SYMPTOMS OF TUBERCULOSIS IN CATTLE.
Microscope and staining; by centrifuge; by agglutination test; by
inoculation; by tuberculin test; tuberculin; reaction; precautions,
temperature before injection, exclusive of other illness, of
parturition, abortion, heat, isolation, of hot building, of cold
draughts, of hard floor, of faulty milking, privation of water, of
change of food, of journey, of rude handling, of previous recent
tests, of antipyretics, make special examination in unthrifty, test
excluded animals later, danger of infecting through thermometer;
technique; dose; time of injecting; identification and record of
subjects; seat of injection; sterilization of syringe and skin;
temperatures hourly or every second hour from 8th to 16th or later;
typical reaction; accurate record of feeding, watering, milking or
other occasion of hyperthermia or hypothermia; passing on the value of
a rise; local swellings; chills; tremors; effect of test on general
health of reacting and nonreacting animal; action on parturient cows;
reliability of test. Relation of human to bovine bacillus; varying
character of microbes generally, of tubercle bacillus in man; bacillus
of man and bird interchangeable; tuberculosis in man and ox,
similarity, coextensive, apparent exceptions, direct infection—man to
cattle—cattle to man; encrease of tabes; experiments of Adami, Ravenel
and Garnault; experiments on cold blooded animals; bearing of
variations of susceptibility on sanitary work. Treatment: When
admissible; hygiene; rich feeding; oleaginous seeds: cod liver oil;
pneumatic cabinet; grooming; warm bath; medicated inhalations;
sulphurous acid; chlorine; formaline; calmatives; carbonate of
creosote; derivatives; streptococcic serum; air or oxygen in
peritoneum; excision of tubercle; Prevention; Extinction in cattle;
expense, supply of tuberculin and efficient veterinarians;
appraisment; indemnities; vermin; disinfection; scheduling; control of
purchases. Breeding healthy stock from infected; raising healthy
offspring without sterilizing the milk. Removal of unthrifty and
suspicious animals. Removal of animals showing objective symptoms, or,
tuberculin reaction. Generally applicable measures. Hygiene of milk,
butter, cheese, whey, oleomargarine. Hygiene of meat.
Tuberculosis may be acute or chronic, yet as seen in cattle, from casual
infection, it usually comes on very slowly and insidiously and follows a
chronic course. As the symptoms vary according to the organs involved it
will be convenient to consider these in turn beginning with such as show
the most diagnostic phenomena.
_Pulmonary Tuberculosis._ Though one of the most common and dangerous
forms of the disease this may last for months or years without any
suspicion on the part of the owner or caretaker of anything amiss. There
may be an occasional cough, short, weak, dry, wheezing, perhaps repeated
and roused by opening the stable door in cold weather, by leaving the
stable for the cold outer air, by rising suddenly in the stall, by being
driven on a run for a short distance, by drinking cold water or by
eating dusty food. If driven for some distance, or put to draught work
(ox) the subject blows more than the others. Sometimes even at rest,
breathing is slightly accelerated. Yet the spirits may be as good, the
eye as clear and full, the coat as smooth and sleek and the skin as soft
and mellow as in health. Some such animals give as much milk, of as rich
a quality, or, when put up to fatten, lay on flesh apparently as well as
their healthy fellows. In favorable cases percussion may elicit
circumscribed areas of dulness, and wincing or other sign of tenderness,
and auscultation may detect crepitation or wheezing over the same
points. By covering the nose and mouth with a sac or blanket the
breathing is rendered more labored and the morbid sounds become clearer
and more definite. The use of a stethoscope or phonendoscope may also
render them more distinct. The morbid râles are more significant of
tuberculosis if found in a number of isolated and circumscribed spots,
with healthy respiratory murmur between, than if simply surrounding a
single extended area of flatness as is usual in pneumonia. Much,
however, stands in the way of success at this early stage. The heavy
muscular and bony mass of the shoulder covers the anterior lobe and
partially muffles the auscultation sound, while it renders percussion
useless. The thick covering of the ribs in fat animals proves a serious
barrier to successful auscultation and percussion. The varying plenitude
of the abdominal viscera, and the rumbling, trickling, gurgling, and in
the case of the rumen the crepitation of the contents, tend to
complicate, obscure or cover up the pulmonary sounds. There is usually
no appreciable elevation of temperature, or a slight rise of about one
degree takes place at distant and uncertain intervals so as to render it
useless for purposes of diagnosis.
When the disease is more advanced and the pulmonary lesions more
extensive, the animals usually appear less thrifty on the same feeding,
yet fat animals are habitually killed for food that show quite extensive
pulmonary tuberculosis. With loss of condition, the coat loses its
lustre somewhat, the hair becomes dry and stares in patches, and the
skin loses its mobility and mellowness. The cough may be more frequent,
perhaps paroxysmal under excitement, harsher, more short and broken, and
either dry and husky or moist and gurgling, with a succeeding deep
inspiration perhaps a moist râle. When the skin on the last ribs is
pinched up between the fingers and thumb it is slower in flattening down
to its normal smoothness, pinching of the spine at the shoulder or back,
or it may be of the sternum, may cause wincing and even moaning, and the
same may come of percussing the ribs smartly with the closed fist. There
is now more decided evidence of flatness on percussion on the various
affected points, and of abolition or lessening of the respiratory
murmur, which is replaced by wheezing, or by bronchial blowing sound,
heart beats and abdominal crepitation or gurgling, conveyed to the ear
more clearly through the intervening consolidated tissue. The breathing
may be slightly accelerated even at rest, and becomes distinctly so on
exertion. The appetite fails somewhat and the secretion of milk lessens,
or it may become more pale and watery. Chronic tympany occurring after
meals occasionally appears, usually indicating tuberculosis of the
glands along the œsophagus with pressure on that organ impairing
eructation, and on the vagus nerve so as to impair nervous control. In
connection with this there come on signs of generalization of the
tubercle, as irregularity of the bowels, or enlargement or nodular
induration of some of the superficial lymph glands, as the pharyngeal,
prescapular, prepectoral, axillary, prefemoral, inguinal or mammary.
Expectoration is usually abundant but it is difficult to secure it for
diagnostic purposes since the moment it reaches the pharynx it is
instantly swallowed, while any that may have been projected into the
anterior nares is licked out by the pointed tongue. Nocard tried to
secure this through a cannula passed in between the tracheal rings but
with very little success. Others have introduced the hand into the
pharynx, rousing the cough by tickling the larynx, and attempting to
bring out the expectoration in the hand. When it can be secured its
solid and opaque flocculi may be stained and examined for the bacillus,
or it may be inoculated on a Guinea pig, intraperitoneally, to test its
virulence. If there are open vomicæ or complex infection the breath is
usually heavy and mawkish.
In the most advanced stages the symptoms are very characteristic. The
subject is miserably thin and wastes visibly from day to day, the hair
is dry and erect, most marked along the spine, the skin is scurfy,
rigid, lousy, and clings firmly to the bones, the eyes are pale, deeply
sunken in their sockets and bleary, the tears running over the cheeks,
while a yellowish, granular, fœtid, and often gritty discharge flows
from the nose, and dries in masses around the alæ. The cough is weak,
painful, paroxysmal, and easily roused by pinching the back or breast or
percussing the ribs. The breathing is liable to be hurried, even
panting, and the animal may stand most of its time with nose extended to
obviate the oppression that comes of recumbency. All the visible mucosæ
are pale and blanched, and the pulse weak and rapid with every
indication of anæmia. The temperature is usually raised to 104° or 105°
F. and the milk secretion is completely arrested. Indications of
generalized tuberculosis become more marked in the enlarged glands,
diarrhœa, and clouded (purulent), or blood stained urine with
microscopic casts, and even anasarca. The morbid sounds in the lungs
have become a complex variety according to the nature of the lesion,
blowing, wheezing, amphoric, friction, creaking, mucous, with the other
bruits conveyed from adjacent organs. Death usually occurs in a state of
complete marasmus, after months or years of illness.
_Tuberculosis of the Abdomen._ This usually affects the intestines,
mesenteric glands, peritoneum, liver, spleen and pancreas, and has been
known as _tabes mesenterica_. The generative organs also occasionally
suffer, in which case, an early and rather persistent symptom is
sterility, with a too frequent or it may be persistent desire for the
bull (nymphomania). There is usually a steady loss of condition in spite
of good feeding, the impaired functions of the intestinal mucosa, but
especially of the mesenteric glands, liver and pancreas, interfering
seriously with absorption and assimilation. The victims are therefore
known as piners. While there may be more or less fever, highest in the
evening, this is by no means marked, and cough and respiratory trouble
may be entirely absent. Indications are not lacking, however, of
digestive trouble. Slight tympany may follow meals, and the bowels are
irregular, costiveness alternating with diarrhœa. If heavy feeding is
resorted to, diarrhœa is the usual result, accompanied, it may be, by
colic and tympany. There is a tendency to formation of pea or nut-like
nodes under the skin of the flank, and Kleinpaul claims that the
tubercles or vegetations on the rumen can be felt by manipulation of the
left flank. Clearer evidence can often be had by rectal exploration, the
tubercles and enlarged glands being felt on the rumen, in the knotted
mesentery and in the sublumbar and subsacral region.
In case of _uterine tuberculosis_, the nymphomania may be supplemented
by a purulent discharge, and rectal exploration may detect the tubercles
on its surface, in the broad ligaments or even in the enlarged ovaries.
Great fœtor of the fæces may indicate ulceration of the mucosa,
indigestion or impaired hepatic function.
For a great length of time the disease may be virtually confined to the
mesenteric or portal glands, or even to the spleen, while the animal
enjoys fairly good health. Again, in some instances, the subject may be
fat and sleek, though the rumen, omentum or mesentery is to a large
extent literally covered with tuberculous vegetations. The
tuberculization of the intestines, mesenteric glands, liver or pancreas
interferes far more with the general health than does even extensive
peritoneal tuberculosis.
As the case advances it tends to generalization and winds up with the
general symptoms predicated above of pulmonary tuberculosis.
_Genital Tuberculosis_ in the bull is associated with nodular swelling
of the testicle, epididymus or cord, hydrocele, and exceptionally
tubercle on the penis, or in the prostatic sac.
_Mammary Tuberculosis._ This may be primary and circumscribed under
direct infection through a trauma or by the milk ducts, but more
commonly it is secondary to generalized tuberculosis. It may be a rather
firm, uniform, painless swelling of one or two quarters (usually hind
ones) without at first serious interference with milk secretion. As the
disease advances, the follicles and ducts being invaded, an irregular
knotted condition is developed, the milk becomes pale, watery,
semi-coagulated and filled with bacilli, and the climax is reached in a
densely indurated condition of the gland. From the first the mammary
lymph glands, behind and it may be in front of the organ, become
swollen, and they are finally indurated as caseation or calcification
ensues. The superficial inguinal glands often participate.
_Pharyngeal Tuberculosis._ In this rather common localisation the
retro-pharyngeal glands and those on the side of the pharynx especially
suffer, though the parotidean lymphatic gland and the submaxillary often
participate. Enlargement and induration of the tonsils and ulceration of
the mucosa may be present. There is distinct swelling of the throat or
displacement downward of the larynx, and the enlarged or hard nodular,
perhaps even shrunken, glands may often be detected by manipulation. The
nose is carried slightly protruded and a stertor or wheeze accompanies
the breathing. A glairy liquid may run from the mouth or nose, and in
this, bacilli may often be detected under the microscope. The
retro-pharyngeal glands are very subject to softening and liquefaction,
and in such a case an obscurely fluctuating swelling may be detected
above the pharynx when the hand is introduced through the mouth.
This usually terminates in generalized tuberculosis, though it will
often remain for a length of time the one appreciable localization.
_Cutaneous Tuberculosis._ The counterpart of _tuberculosis verrucosa_ of
man, this probably usually occurs by direct inoculation in a sore, yet
the infection may reach the seat of lesion through the blood. It is
usually represented by an irregular clustering warty growth, hanging
more or less loosely from the skin and showing at points caseating
centres. Bacilli may be recognized under the microscope.
_Glandular Tuberculosis._ Aside from the tuberculosis of the internal
lymph glands already referred to, tubercles may form in any group of
lymph glands, causing swelling, induration, fibroid degeneration or
tuberculous abscess. Among these may be named the glands in front of the
stifle or shoulder, at the root of the ear, beneath the zigoma, in the
jugular furrow, the prepectoral, axillary, inguinal, etc.
_Tuberculosis of the Brain and Meninges._ Disorder of the cerebral
functions occurring in generalized tuberculosis may be held to point to
this disease. The earlier meningeal symptoms are often those of
excitability, timidity, spasms, visual troubles, etc., merging later
into vertigo, hebetude, paresis, unsteady gait, local paralysis and
coma.
_Tuberculosis of the Eye._ This has been seen mostly as the result of
experimental inoculation, with conjunctival and sclerotic congestion,
corneal opacity, and the development of yellowish centres in the iris
and choroid, from which the tubercle extends into the chambers.
_Tuberculosis of the Heart, Pericardium or Pleura._ Tuberculosis of the
pleura is usually a concomitant of pulmonary phthisis, yet it may exist
for a time independently, and its diagnosis presents serious
difficulties. There may be tenderness of the intercostal spaces, a
friction sound in case of raw granular surface or vegetations, creaking
from false membranes or even flatness low down on percussion. If these
escape notice, a short painful cough and slightly hurried breathing
under exertion, in the absence of objective symptoms of lung disease,
may lead to suspicion, but the true nature of the affection must remain
in suspense. It usually leads to pulmonary or glandular (bronchial), and
finally generalized tuberculosis.
_Pericardial or Cardiac Tuberculosis_ is usually secondary and may be
suspected when friction is synchronous with the heart sounds, when the
heart beats or sounds are irregular or intermittent, or when the area of
cardiac dulness is greatly encreased.
_Tuberculosis of Bones and Joints._ This is more common in calves and
growing cattle, but may be present at any age. As affecting the vertebræ
it causes stiffness and unsteady gait, perhaps what was looked on as a
simple sprain causes persistent lameness in spite of treatment, and a
point or area of tenderness on pinching is manifest. In the large bones
and joints of the limbs, the cancellated extremities, or it may be a
simple process with its inserted tendon or ligament, shows a firm,
persistent swelling, and there is acute synovitis of the joint. In acute
cases in calves the epiphysis may become detached from the diaphysis so
as to make the limb useless. In the mature animal the enlargement and
lameness may last for years without material change. The condition may
be difficult to diagnose, in the absence of signs of tuberculosis
elsewhere in the body, or unless the synovia, withdrawn through a
sterilized nozzle, with antiseptic precautions, should show the presence
of bacilli.
SYMPTOMS OF TUBERCULOSIS IN SWINE.
In young pigs, infected by the milk of the dam, there are general
unthriftiness, stunted growth, emaciation and unhealthy skin, encrusted
with a dark unctuous matter or scurf, as in chronic hog cholera.
Temperature is variable on successive days, or times of the same day.
Digestive disorder is manifested by slight colics, diarrhœa, vomiting,
tympany and abdominal tenderness. The pig becomes pot bellied, with
hollowness of the flanks in front of the iliac bones, and manipulation
may detect the tuberculous bowels and mesentery in the form of a knotted
mass.
Roloff describes a caseous colitis with ulceration of the mucosa, which
is probably tuberculous.
Enlargement of the superficial lymph glands (pharyngeal, inguinal,
prescapular) may be present. Traumatic infection of the castration sore
and inguinal glands has been noted. As the disease becomes generalized,
implicating the lungs, there is a dry paroxysmal cough and hurried
breathing, becoming more oppressed on the slightest exertion. If quiet
and thin enough for auscultation and percussion the usual morbid lung
sounds can be heard. Unlike cattle, pigs are very subject to muscular
and intermuscular tubercles, and as there is a general tendency to
caseation, these are usually to be found as saccular cavities with soft,
sometimes liquid, caseated contents. The bones and joints may suffer, as
in cattle. The tonsils are usually enlarged and even caseous. The outer
auditory meatus and the interior of the eye have been found affected.
Cases affecting the brain were manifested by nervous disorder, rearing
up on the fence, turning in a circle, spasms, rolling of the eyes,
paresis and paralysis, often hemiplegic. When one or other of these
indications of local disease is found associated with the general
disorder of the lungs or bowels, in a herd fed on raw meat scraps, milk,
or the soiled food of tuberculous animals, the evidence is strongly in
favor of the local tubercle corresponding to the symptoms. It is
noticeable that diagnosis by microscopic examination is difficult and
uncertain because of the relatively very small number of the bacilli. In
the mature pig the disease may be difficult of diagnosis without
tuberculin, and a _post mortem_ examination may be necessary to identify
the disease in the herd.
SYMPTOMS OF TUBERCULOSIS IN THE HORSE.
Though not a common disease in the horse yet a large number of cases are
on record, and accidental and experimental cases alike show that this
animal is peculiarly receptive to the disease. The early symptoms depend
on the location of the primary lesions, yet the general phenomena of
debility, languor, early fatigue, unfitness for violent efforts,
perspiration on slight exertion, irregular appetite, occasional rises of
temperature and emaciation may usually be noted. The advance is usually
slow, almost imperceptible, with periods of improvement and aggravation.
Some cases have appeared in the submaxillary and pharyngeal lymph glands
with sore throat and were for a time mistaken for glanders (Ehrhardt,
McFadyean). Others show a swelling of the appearance of cold abscess in
the seat of the prepectoral glands (Johne, Röbert). One showed widely
distributed lymph nodes and enlarged and indurated lymph glands
(prepectoral, inguinal, etc.) with thickening of the intervening lymph
vessels (Cadiot). This last suffered from bronchitis two months before.
A number of cases reported by McFadyean showed special stiffness of the
neck, with swelling and distortion of the vertebral joints, due to a
tubercular osteitis and periostitis, and associated as necropsy showed
with internal tuberculosis. Cases of this kind occurred in the practice
of McConnell, Dawes, Insall, Malcolm and Hill, so that tuberculosis may
well be suspected in cases of disease of the cervical vertebræ. In all
of these cases post mortem examination, performed at once, or after a
long delay, showed generalized internal tuberculosis.
When the chest is extensively affected, the symptoms are those of
broncho-pneumonia or heaves (broken wind), there is hurried breathing
with paroxysmal cough sometimes dry and wheezy, at others moist or
mucous, a double lift of the flank in expiration, and a muco-purulent
discharge from the nose, sometimes streaked with blood. Auscultation
detects a varying force of the respiratory murmur at different points,
with more or less wheezing. Blowing and other sounds conveyed to the ear
through the solidified lung tissues are more rare or less marked.
Percussion may show general resonance, encreased at emphysematous
points, and diminished in small circumscribed areas, the seats of
tubercle or consolidation. There are of course the attendant debility,
inappetence, fever and steadily advancing emaciation. In some cases the
enlarged tracheo-bronchial glands are seen to bulge forward between the
two first ribs, and by the sides of the trachea. Stocking of the limbs
is frequent.
Abdominal tuberculosis is most common in the young foal and when not
secondary, may be due to feeding on tuberculous milk, especially in
those brought up by hand on cow’s milk. There is debility, emaciation,
anæmia, irregular appetite, digestive disorder, constipation alternating
with diarrhœa, colics, pot-belly, falling in beneath the lumbar
transverse processes, dry, harsh, scurfy skin and advancing marasmus.
Rectal exploration will usually detect the enlarged sublumbar and
mesenteric glands, and the simultaneous manifestations of disease of the
lungs, superficial lymph glands, throat, or bones serve to identify the
disease.
In the advanced stages of tuberculosis in solipeds polyuria is a
frequent phenomenon (Nocard) tending to hasten the general anæmia and
marasmus.
The patient often works for months or years but with gradually
encreasing debility, which is soon fatal after the occurrence of
generalized tuberculosis.
In estimating the nature of the disease, indications may often be drawn
from the environment, feeding, etc. Nocard as the result of a careful
study of the morphology and habits of the bacilli has shown that the
more purely abdominal form of equine tuberculosis is near akin to that
of the chicken, while the pronouncedly pulmonary form resembles the
human type. McFadyean on his part adduces a number of cases of
tuberculosis in horses that had been fed largely on cows’ milk, a most
significant fact considering that such a ration is rare for this animal,
and that few horses contract tuberculosis casually. Exposure therefore
to the sputa of man, of the nasal or bowel products of birds or to the
milk of cows, may suggest the probability of tuberculosis in a horse
with chronic anæmia, debility and wasting.
The discharges from the nose of the affected horse are more available
than those of cattle for examination and experimental inoculation, yet
in many occult cases the diagnosis by tuberculin is the only reliable
resort.
SYMPTOMS OF TUBERCULOSIS IN SHEEP AND GOATS.
The tubercles have been usually found post mortem in these animals or as
the result of experimental inoculation, and symptoms have not been well
recorded. They follow the same order as in the ox, weak husky cough,
wheezing and other râles in the lungs, disorders of the digestive
organs, swollen lymph nodes and glands, and caseated products in those
that were of some standing. I have found these latter especially, in the
region of the throat in high bred rams kept in confined buildings or
yards and highly fed to prepare for _letting_ or sale. These lose in
vigor and activity and _scrofulous_ swellings form on the neck, head or
elsewhere and become rapidly caseated. In German abattoirs tuberculous
sheep proved 0.1 to 0.15 per cent. In Saxon goats the percentage was
0.6.
SYMPTOMS OF TUBERCULOSIS IN DOGS AND CATS.
These follow in the main those of consumptive cattle. As the infection
generally enters with food, the early symptoms often point to disease of
the throat and alimentary tract, while the later ones involve those of
the respiratory organs as well. Impaired and capricious appetite,
debility, early exhaustion under exertion, emaciation, sunken pallid
eyes, apathetic expression of the face, lack of life and gaiety, a
knotted feeling of the abdomen if the region is flaccid, and a tense
fluctuating sensation if ascitic, with usually enlargement of the
superficial lymph glands are noticeable.
When the chest becomes affected there is the hurried breathing, quickly
encreased by exertion, panting, paroxysmal cough, wheezing, and the
various morbid râles in the chest, crepitant, friction, creaking,
blowing, cavernous, mucous, etc. On percussion, flatness is detected in
limited areas in a number of centres. Expectoration is usually promptly
swallowed and can only be secured with difficulty for examination.
When tuberculous sores and fistulæ occur in the region of the throat or
elsewhere, the evidence is patent and the bacilli can easily be found in
the discharges.
In _cats_ the course and symptoms do not materially differ. In both
animals the history usually shows the connection of house life and the
habit of eating after tuberculous persons.
SYMPTOMS OF TUBERCULOSIS IN BIRDS.
In the gallinaceæ there may be inappetence, vomiting, diarrhœa, with
hurried breathing, sneezing, and the general phenomena of debility,
weakness, advancing emaciation and anæmia, the comb and wattles becoming
pale and flaccid and the visible mucosæ bloodless. The eyes are sunken
and lack lustre, the head sinks, the wings and tail droop, and weight is
steadily lost. When the bones and joints of the legs and wings are
involved the local swellings and distortions are visible indications of
the trouble.
In _parrots_ these local swellings and particularly the horn-covered
vegetations on the face and around the beak are characteristic.
_Canary._ Tuberculosis is common in the canary, contracted, as in the
parrot, from man, with whom alone the caged bird comes into dangerous
contact. The interchange of the disease between pet birds and their
owners would demand the exclusion of such from the rooms of
consumptives, and a careful watch for indications of disease of the air
passages with marasmus, that the bird may be disposed of before it has
become a source of danger.
DIAGNOSIS OF TUBERCULOSIS.
It is needless to repeat the various symptoms of tuberculosis according
to its different seats and the degree of its extension in the animal
body. In cases in which the indications are slight, greater importance
may be given to them through the knowledge of the existence of more
advanced or decided cases in the same herd, or the necropsies of animals
taken from it. Yet in the average herd it is safely within bounds to say
that three fourths of the affected cattle will escape condemnation if we
employ objective symptoms alone. In one herd of seventy head, in which
the tuberculin test condemned twenty-four head (being 50 per cent. of
the mature animals), I left the examination after slaughter to the
veterinarian of the A. J. C. C. who was at the time skeptical as to the
value of the tuberculin test. He wrote me afterward of his surprise at
finding every one of the twenty-four condemned animals tuberculous, when
not one of them had shown symptoms by which he could recognize the
disease in life. This is no exceptional case, and may be advanced rather
as a typical example of the ordinary infected country herd.
_Microscopic_ detection of the bacillus in the expectoration may be
successful in the horse with pharyngeal or pulmonary tuberculosis, but
fails in those forms that affect the other internal organs. It is all
but useless for the expectoration of cattle and dogs. When there is
cutaneous tuberculosis or a tuberculous fistula this is much more
valuable, and it is especially useful in dogs and parrots.
The precipitate in the centrifuge will often show the bacilli that are
present in milk, but in very many cases of tuberculosis the bacilli are
not present in the milk.
The centrifuge used on the _urine_ may also succeed when kidneys,
bladder or prostate are affected, but the bacilli are rarely found in
the absence of disease of these organs. The smegma bacillus is a source
of fallacy.
The serous effusions in the affected _serosæ_ (pleura, peritoneum,
pericardium, synovial cavities) may also be centrifuged and the presence
of the bacilli revealed.
The _agglutination test_ of Arloing and Courmont though often giving
positive results, (95.5 per cent. in pulmonary tuberculosis, 50 per
cent. in surgical, Arloing and Courmont; 40 per cent., Knopf; 25 to 50
per cent., Lartigan); yet proved too unreliable, and frequently gave
positive results when tuberculosis was absent. The best medium for
cultures to be so used is 6 per cent. glycerine bouillon, and the age of
the tuberculosis culture 8 to 12 days. One part of fresh blood serum of
the suspected animal in a sterilized capillary tube is added to ten
parts of the bacillus culture, and the tube placed in an oblique
position. In 2 to 24 hours a fine sand-like material precipitates along
the sides of the tube, and the microscope shows the bacilli in clumps,
absolutely still without even Brownian movements. Gallemaerts found that
it proved very satisfactory with the serum of Guinea pigs after three
days from intraperitoneal inoculation, was less marked after
inoculations subcutem, and that in man the agglutination appeared in
influenza and pneumonia in the entire absence of tuberculosis. Such an
uncertain test cannot be utilized in veterinary sanitary work.
_Experimental inoculation_ with milk, expectoration, morbid discharges,
the scraping of nodules, etc., is much more searching, and will detect
more cases than the microscopic examination. But it fails entirely in
cases in which the milk of unquestionably tuberculous animals is free
from bacilli, or in which the local nodule or discharge tested is itself
free from tubercle. It is a test of the local lesion and not of the
entire animal system.
In choosing a subject for inoculation, the first consideration is that
it must come from a healthy stock and be itself free from tuberculosis.
Next, it must be of a species actively susceptible to the habitual
tuberculosis of the animal from which the inoculated matter is taken.
Thus for man, ox, dog and parrot, the Guinea pig is especially
appropriate, while for gallinaceæ and horses, the rabbit is to be
preferred. Inoculation is usually made into the peritoneal cavity.
As a period of two or three weeks is usually necessary to allow of an
extensive development of tuberculosis, the method must be too often
discarded on account of the delay in obtaining results.
_Tuberculin test._ Many stock owners still entertain an ignorant and
unwarranted dread of the tuberculin test. It is quite true that, when
recklessly used by ignorant or careless people it may be made a root of
evil, yet as employed by the intelligent and careful expert it is not
only perfectly safe, but it is the only known means of ascertaining
approximately the actual number affected in a given herd. In most
infected herds, living under what are in other respects, good hygienic
conditions, ⅔ or ¾ are not to be detected without its aid, so that in
clearing a herd from tuberculosis and placing both herd and products
above suspicion the test becomes essential.
_Tuberculin_ is the bouillon in which the tubercle bacillus has been
grown, charged with the toxic products of its growth, but which has been
raised to a boiling temperature to destroy all germ life, and from which
the dead germs have been removed by passing it through a porcelain
filter. When a physiological dose of this has been injected, subcutem,
into the suspected animal, it has no effect on the non-tuberculous,
while in the tuberculous it produces, in the course of the next 24 hours
(usually from the 8th to the 16th), a steady rise of temperature by 2°
F. or more, followed by a slow subsidence to the normal. This may last
for from three to ten hours in different cases.
Among the precautions may be named:
1. The temperature of the animal is best taken at intervals, or at
least, morning, noon and night, on the day preceding the injection to
see that the animal shows no habitual rise at any time of the day. Yet
in busy field work the one night temperature taken just before injecting
will rarely fail to give a satisfactory normal as a standard for the
animal. Any quotidian rise almost invariably reaches its climax at
night.
2. _The subject must be in good general health._ If there is present in
the system any concurrent disease it may undergo an aggravation within
twenty-four hours and give a rise of temperature that will be mistakenly
set down for tuberculosis. At the very start, therefore, it is important
that the general health of the subject should be first assured by a
critical professional examination. If some other disease is present the
tuberculin test had best, as a rule, be delayed until that has subsided,
while if tuberculosis is found the test will be superfluous.
3. _The subject must not be within three weeks of parturition, nor about
to abort._ In many cases, though not in all, as preparations are made
for calving, the system becomes unduly susceptible to the presence of
tuberculin and that agent will cause a rise of temperature, though no
tuberculosis is present. Unless this source of error is carefully
guarded against the most valuable cows in the herd may be condemned
unjustly.
4. _The cow must not be within three days of the period at which “heat”
would naturally occur._ Under the excitement of œstrum the body
temperature usually rises two or three degrees, and if tuberculin has
been used this rise may be attributed to tuberculosis and a sound animal
may be condemned. Nor is it always enough that the animal is supposed to
be pregnant. Abortions sometimes take place unexpectedly and unknown to
the owner. If, therefore, a cow under the test and which is not well
advanced in pregnancy should show a rise of temperature it should be at
once ascertained whether the animal is not in “heat.” If symptoms of
“heat” are found she should be set aside along with any calving cows to
be tested again when such a source of error is no longer present.
5. _The tested animal must not be exposed to a hot sun in a closed
area._ In excess this will cause heat apoplexy, and the fever heat which
ushers this in, may easily be mistaken for the indications of
tuberculosis.
6. _Cattle taken from pastures must not be enclosed in a hot, stuffy
stable._ While they must be tied up to allow of the temperature being
taken at short intervals, coolness and ventilation should be secured in
summer by a sufficient air space and the requisite ventilating openings.
7. _Exposure to cold draughts between open doors and windows, or to wet
or chilly blasts out of doors should be carefully guarded against._ A
chill proceeding from any source and alike in the presence or absence of
tuberculin causes a rise of the internal body temperature.
8. _Heavy cows unaccustomed to stand on hard boards may have a rise of
temperature in connection with resulting tenderness of the feet._ One
must avoid hard floors on the day of the test or make examination of
feet and allow for attendant fever.
9. _Omission of the previous milking or a change of milker and
consequent retention of part of the milk_ will raise the temperature of
a nervous cow, and in careless hands secure an erroneous condemnation.
10. _Privation of water at the regular time will often cause rise of
temperature_ especially when on the dry feeding of winter. I have seen a
general rise of two degrees and upward from the delay of watering for a
single hour, while after watering the temperature went down to the
normal and remained so. Water always tends to a temporary lowering of
temperature but in the presence of tuberculosis it soon rises again.
11. _Change of food is liable to produce a slight indigestion and rise
of temperature._ This should be avoided as far as possible, and when a
herd is taken up from pasture for the test, it should have grass,
ensilage or other succulent food.
12. Cattle just from a long journey by road or rail, or other cause of
violent exertion are liable to have an elevated temperature from the
leucomain poisoning. Such should be left at rest until the transient
fever shall have subsided.
13. Violent handling of nervous cows in taking the temperature must be
carefully avoided. The operator who cannot handle them gently is not fit
for this work.
14. There must be evidence that the animals have not been repeatedly
tested at short intervals shortly before. In a number of instances I
have found a proportion of the cattle irresponsive to tuberculin, though
a _post mortem_ proved the presence of tuberculosis. Unscrupulous men,
wishing to sell on a guarantee, can avail of this in animals so
unaffected by the test.
15. The operator must have absolute control, even of the feeding and
watering of the animals on the day of testing. Otherwise the rise of
temperature may be prevented by a liberal use of antipyretics and a
false guarantee may be secured.
16. An unthrifty animal, having general symptoms suggesting
tuberculosis, must be subjected to the most critical examination in
addition to the tuberculin which in such animals often fails to cause
hyperthermia. Fortunately in such animals the tubercles are usually
numerous and extensive enough to be discovered through objective
symptoms.
17. Animals excluded from the test by reason of some individual
unfitness at the time (parturition, œstrum, abortion or any other
disease) must be marked and held for the test later after such
disqualification shall have passed.
18. The operator must bear in mind the possibility of transferring other
diseases from animal to animal, by contact, by the use of the same
hypodermic needle on two in succession, and above all by the clinical
thermometer. Diseases like contagious abortion, which present no obvious
symptoms in the intervals, are especially liable to be carried in this
way, and instances of the active extension of this after a test, have
come under my notice. The operator should always enquire carefully as to
the existence of abortions and sterility in the herd, put the aborting
animals by themselves, using a special thermometer upon them, and
carefully washing the hands before going to other cattle. It is well
further to clean the thermometer after each animal and disinfect it with
carbolic acid solution (5:100).
_Dose of Tuberculin._ Of the usual American preparation 2cc. (30 drops)
is adapted to a cow or ox of 1,000 to 1,200 pounds. For larger and
smaller animals a moderate encrease or reduction must be made, yet a
considerable latitude is allowable. The new-born calf will take five
drops and the animal of 700 pounds 25 drops.
_Technique of the Operation._ Lapses are so easily made when dealing
with a large herd and are so dangerous that a regular plan should be
systematically followed. The following will be found simple and
convenient:
1. Inject the herd at 10 or 11 P. M. to secure a good rest and be fresh
for the rise of temperature early next morning.
2. Before injecting have the subjects arranged in order and record them
by name or other means of identification, with age, sex, breed, weight,
pregnant or not, past or prospective date of calving, abortion,
indications of disease, temperature taken just before injection and
appropriate dose.
3. Inject into the loose connective tissue on the side of the neck, the
animal being held by the nose, if necessary, by an assistant.
4. Use a syringe which has not been employed for any infectious
products, and see that it is thoroughly cleansed and disinfected by
boiling or by filling it with a carbolic acid solution (5:100).
5. After drawing the appropriate dose into the syringe, wipe the nozzle
and dip it in strong carbolic acid before inserting it into the skin.
This safely disinfects any virulent matter that may be lodged on the
surface of the skin, and obviates those infected swellings and abscesses
that have been a cause of complaint by stock owners.
6. When the nozzle is withdrawn from the skin, wipe it and dip it again
into the strong carbolic acid to prevent any risk of infecting the
tuberculin into which it is to be plunged.
7. The nozzle is much more easily inserted in the skin if the latter is
pinched up so that the needle will transfix it at a right angle, instead
of passing through a greater amount of the dense tissue because of the
oblique direction. An excited animal with a thick, tense hide and a
contracted panniculus muscle will offer serious obstruction which
lessens greatly as the subject gets over its excitement and the muscle
relaxes.
8. Temperature should be taken at 6 or 7 A. M., eight hours after
injection of tuberculin, and every two hours thereafter, until the
sixteenth hour.
9. If any subject shows no rise of temperature until the 16th hour after
injection, its examination may be discontinued, but if it shows a slight
rise toward the 16th hour it should be continued until it has shown a
distinct reaction with steady rise and fall, or until, without such
distinct reaction, the temperature descends to the normal.
10. If one has shown a distinct reaction but is still rising at the 16th
hour, it should be continued till it begins to fall. The typical
reaction is one in which the rise and fall are both gradual, and extend
over a number of hours.
11. In recording the temperatures, there should be noted the exact time
of each feeding, watering and milking, or any other condition (change of
weather), which may in any way affect the heat production or radiation.
12. In old, emaciated animals and in second or third tests, Pearson uses
twice the usual dose of tuberculin or more.
_Tuberculosis Reaction._ With slight variations different operators make
their estimate of tuberculosis reaction on nearly the same general
basis. A rise of 2° F. over the highest temperature of the day or days
before, in the absence of any other appreciable cause, and provided that
the elevation has followed the tuberculosis type of gradual rise and
fall, is held to condemn. If, however, this rise does not exceed the
normal average, if the temperature before injection did not exceed 100°
and that after injection 102°, the case may well be held in doubt and
reserved for re-testing. If, on the contrary, the initial temperature of
the animal was 103°, and there was, between the 8th and 16th hours, a
gradual typical rise and fall, reaching 104° or a little over, in the
absence of any other cause for this, the subject would be condemned.
Cattle having an initial temperature of 103° or above are not favorable
subjects for the test, except in the case of calves in which the
temperature is normally higher and the reaction must reach a higher
point. In all cases of doubt it is well to hold for a second test,
unless urgent sanitary considerations demand that a herd should be freed
from the infection in short order. Then it may be better to risk a
single error, with the concurrence of the owner, than to leave a
possible centre of infection in the herd.
Local swelling in the seat of injection may be charged to lack of
antiseptic care, or the presence of septic germs in the system of the
animal prior to injection.
A chill during the period of reaction is not uncommon, especially in
cold weather, or in a draught of cold air. The coat may stare along the
spine in patches, or generally, tremors may be seen on the body or
limbs, and a clammy coldness invades the ears and horns, and especially
the points of the hocks and ischia. The back is sometimes arched and the
feet drawn together somewhat.
In the absence of any source of excitement the head may be less
elevated, the ears lopped forward or drawn back, and even the eyelids
may droop somewhat. These phenomena may last for a few minutes or for an
hour or two.
In testing other genera consideration must be had of the different
normal temperature (horse 99.5°, dog 98.5°, sheep or pig 103°, bird
106°), and the varying susceptibility to tuberculin, the Guinea pig
requiring a maximum dose relatively to its size and man or horse a
minimum.
_Effect of Tuberculin Test on the Later Average Health of the Animal
Reacting._ The transient fever and reaction on the day after injection
modifies the milk secretion temporarily to a certain extent in ratio
with the hyperthermia. The consensus of veterinarians of the largest
experience, and the voice of the International Veterinary Congress at
Berne in 1895, oppose the doctrine of any continuous effect on the
health even of the tuberculous. Yet in the case of Governor Morton’s
large herd of Guernseys a careful record of temperatures showed that for
weeks after the test the reacting animals presented oscillations which
were not shown before, and which were not found to occur in the sound
animals. In the activities of sanitary work such indications are easily
missed.
_Effect of Tuberculin Test on Sound Animals._ In 1894 I tested this on a
number of thoroughbred Jersey and grade cows, injecting them six times
at intervals of from five to fourteen days. It led to no appreciable
change of the general health as shown by the temperature, breathing,
pulse, yield of milk or its quality. Careful analysis was made of the
milk at each milking, and in two animals soundness was attested by _post
mortem_ examination. Similar tests made by the Bureau of Animal Industry
and others led to the same results. Cows in which the yield of milk was
on the gain continued to encrease in the same ratio as those that had
not been injected, and those in which it was on the wane showed no more
rapid decrease. The butter fats and total solids showed no variation
more than appeared in the healthy.
_Action of Tuberculin on Parturient Cows._ The testimony of Bang, Eber
and Pearson, based on a very extensive experience, would indicate that
the tuberculin test is not forbidden by the parturient condition. Eber
concludes that unless the initial temperature materially exceeds 39.5°
C. (103° F.) the parturient state is no barrier to successful testing.
My own experience, on the contrary, is that a considerable proportion of
parturient cows give a reaction when the initial temperature did not
exceed 103° F., and when no sign of tuberculosis could be found. As an
example, a cow in high condition, with an initial temperature of 102.8°
F., rose gradually from the eleventh hour after injection and reached
106.3° by the eighteenth, a rise of 3.5°. From the record she was not
due to calve for three months, but a fortnight later, when already
killed and laid open, she showed all the signs of parturition, a fully
matured calf, and not a trace of tubercle. This is far from unusual, and
I am convinced that many errors will be avoided by refusing to condemn
parturient animals or those within a couple of weeks before or after
parturition on the tuberculin test alone.
_Reliability of the Tuberculin Test._ Even in the most careful hands the
tuberculin test cannot be held to be infallible. A certain very small
proportion of cows react without the recognition of any tubercle post
mortem, some because of other bodily conditions, like parturition or
abortion, but in skilled hands these may be ignored in ordinary sanitary
work. Pearson claims to have had but 8 such cases in 4400 cows that gave
a typical reaction. He suspects that some of these even had undiscovered
tubercle, and Nocard thinks that all such cases are to be explained in
this way. On the other hand a very few really tuberculous animals fail
to react, some in connection with advanced disease, some because of
repeated previous testing, and some because of the introduction of
antipyretic agents into the system, but such cases can either be
detected and controlled or are so infinitesimal in numbers, that they
can be safely ignored in sanitary work. In skilled hands, the tuberculin
test will show at least ⁹⁄₁₀ths of all cases of tuberculosis, when other
methods of diagnosis will not detect ⅒th. See above case of herd where
objective symptoms showed nothing, yet tuberculin condemned half the
mature cattle, and post mortem confirmed this, the skeptical
veterinarian being judge.
_The Relation of the Bacillus Tuberculosis of Man to that of Cattle._ On
the discovery of the bacillus tuberculosis it was largely assumed that
it was the same in all tuberculous animals, in all organs and in all
circumstances. But it was soon found that the bacillus of chicken
tuberculosis differed materially from that of the mammalian, that it
could be inoculated only with difficulty on cattle or Guinea pig, as
could that of the latter on the bird. The bacillus of the chicken found
a most receptive home in the rabbit and horse, and was more easily
started in artificial culture in glycerine bouillon, than was that of
man or ox. But presently it appeared that the affinities and disparities
did not end here. The bacillus from man or ox led to much more
pronounced lesions in Guinea pigs than in rabbits, and the abdominal
bacillus of the horse was inoculable on the chicken. Both horse and
parrot proved receptive to the bacillus from man. Swine, like Guinea
pigs showed a receptiveness to the bacillus of man or ox. The bacilli
from the sputum, open tuberculous sore, or bones of man showed less
virulence for Guinea pigs and rabbits than did those from tubercles in
the human lungs and liver. The bacillus from the ox showed a greater
virulence toward rodents and other small animals than did the bacillus
from man. The bacillus of human sputum inoculated on the ox did not
habitually cause generalized tuberculosis, but oftentimes a local
tubercle or group of tubercles, and sometimes the inoculation wound
healed without permanent lesion. These last points were seized upon to
sustain a doctrine of probable duality for the microbe of tuberculosis,
but if duality it was quite evident it could not end there, but must be
extended to multiplicity, each small group of genera having a tubercle
bacillus peculiar to itself. Those who thought their interest lay in
arresting all sanitary control of tuberculous cattle and their products,
became urgent in opposition to active government measures, demanding
mathematical proof of the infection of man from cattle, under conditions
that would exclude the remotest possibility of the introduction of
infection from another source. The clearest and most abundant
circumstantial evidence would not suffice, they must have direct
experimental inoculation under conditions of precaution against outside
germs, which were practically impossible in any community, conveniently
ignoring that such inoculation, if successful, would have amounted to
manslaughter, and that no such experimental evidence has been had, or
can be had, of any of the deadly diseases of man. Infection by exposure
and accidental inoculations can be had in abundance, just as they can in
tuberculosis, but never under the rigid precautions which would exclude
the possibility of extraneous infection.
The subject has assumed such importance that I may be excused for
introducing a portion of my paper read before the New York State Medical
Society in 1900.
1. _This Variability is Common to Microbes Generally._ Certain bacilli,
like those of anthrax, grow in the living body as rods only, but become
long filaments in given artificial media. They produce no spores in the
living tissue, but do so readily in the carcass or soil. Transferred
from ox to ox they are generally fatal, but if grown for several
generations in Guinea pigs, and then transferred to cattle, the
resulting disease is slight (Burdon-Sanderson, Duguid, Greenfield).
Rabies passed from dog to dog is almost constantly fatal, but if passed
through the ape and then back to the dog it is comparatively harmless
(Pasteur). In both these cases the inoculated animals become immune from
the more virulent germs, showing that they have passed through the
actual disease in an unusually mild form. The later system of Pasteur is
founded on this same general truth, as are also the methods of lessening
the pathogenesis of germs by subjecting them to compressed oxygen, to
graduated heating, to an altered chemical condition of the culture
medium, to antisepsis, etc. For a time such weakened cultures often
retain their lessened pathogenesis, even through a succession of
cultures in a susceptible animal body, acting as if the germ were indeed
a distinct species. But it might well have been considered that a
microbe which had changed its aptitudes in a given environment could
presumably revert to its original habits under the incentive of a
suitable medium. And this is precisely what does take place. Pasteur has
shown that the less potent rabic virus becomes more potent when passed
several times through the body of a rabbit, and that the weakened
anthrax germ acquires greater force when passed through a series of
small birds or newly-born mammals.
To come to tuberculosis, Trudeau tells us that a culture of bacillus
tuberculosis from man inoculated on the rabbit, and then cultivated for
two years _in vitro_, becomes much less destructive to Guinea pigs, and
that after six years of such artificial culture all the Guinea pigs
inoculated with it live for many months, some for two and a half years,
and some even recover. The usual life of the Guinea-pig after
inoculation is seventeen days.[3] All of our zymotic diseases have in a
similar way cycles of malignancy and benignancy. For a series of years
measles, scarlatina, diphtheria, smallpox, or grippe have an unwonted
mildness, and, again, one or another merges into a cycle of extreme and
fatal malignancy. Rinderpest on the steppes of Asia is comparatively
harmless to the native stock, but among outside cattle imported into the
steppes or attacked in their native lands it is habitually fatal. Texas
fever is mild among the indigenous cattle in the Gulf States, but very
deadly to Northern stock. Glanders is not at all fatal to horses of the
plains, the Rockies, or the Sierras; but it becomes redoubtable when
these horses carry it to the Eastern seaboard, and still more so in
Western Europe. It is a common experience to see a malady transformed
through the effects of heredity or acquired immunity, through
environment or the temporary mitigation of virulence in the germ; and
again we see the same disease, no longer restrained by such inhibitory
conditions, bursting forth as a malignant and deadly plague. We have,
therefore, no warrant for the hypothesis that a pathogenic germ which,
under given conditions of life, has lost in pathogenesis, but not in
vitality, should continue forever to exist as a harmless microbe.
Footnote 3:
Johns Hopkins Hospital Reports, Bulletin 100.
2. _Varying Malignancy of the Tubercle Bacillus in Man._ Nothing is more
familiar to physicians than the slow progress of tuberculosis of the
lymph-glands and bones, on the one hand, and its frequent rapid progress
in pulmonary, abdominal, or encephalic organs on the other. It has on
this account been rather difficult to persuade many of the etiological
identity of scrofula and consumption. In experimental tuberculosis the
same truth constantly crops up. Arloing and his followers found that the
tubercle bacillus from the lymph-glands of man proved less virulent and
deadly than that from the human lungs (_Lecons sur la Tuberculose_). As
early as 1880, Creighton drew attention to this in his work on _Bovine
Tuberculosis in Man_.
But the bacillus from the lungs is subject to variations of this kind.
Among seven specimens of human sputum, cultivated by Theobald Smith, six
had a fair average vitality, while the seventh failed to perpetuate
itself on dog serum.[4]
Footnote 4:
Journal of Experimental Medicine, 1898, No. 111.
It should be strongly emphasized in this connection that the failure of
extension and generalization of the sputum germ when transferred to
cattle does not distinguish it from the tubercle bacillus as conveyed
from ox to ox. Everyone at all experienced with the tuberculin test well
knows that in most herds the majority of the tuberculous animals show no
generalization, but only a localized tuberculosis. There is reason to
believe that even recoveries take place after slight infection, and it
is certain that many tuberculous cattle continue for years in what
appears to be good general health. Unless in particularly susceptible
subjects or under specially poor hygienic conditions, or unless in case
of reinfection, the average bacillus of bovine origin habitually fails
to produce in other cattle a rapid extension and generalization.
3. _Interchangeability of Bacillus of Man and Bird._ Of all known forms
of tubercle bacillus that of birds is the most distant from that of man
or ox, and yet the beautiful experiments of Nocard[5] serve to establish
their essential identity. Taking the bacillus of human sputum, which
would not infect the fowl, he enclosed it in collodion capsules, which
confined the bacilli while allowing transudation of the animal fluids,
and left these in the abdomen of the chicken for not less than four
months. He repeated this three times in succession with the product of
the original sputum germ, and obtained a bacillus which was actively
pathogenic for the chicken, though it had been harmless after the
sojourn of four and eight months respectively.
Footnote 5:
Annales de l’Institut Pasteur, September, 1898.
This may explain the reported cases in which a flock of poultry have
developed tuberculosis a few months after they were placed in the hands
of a consumptive caretaker. That such transmission does not always occur
is not surprising, considering that transmission between man and man is
infrequent in comparison with the number of exposures. So in cattle the
majority of exposed animals usually escape, although in such a case
there can be no plausible explanation on the ground of a difference of
germ. We have in every case to consider the necessity for receptivity as
well as infectivity, and the lack of either is a bar to infection. When,
however, we assume that the most diverse tubercle bacilli are
descendent’s of one original stock, that a large herd must furnish some
animals of more than usual susceptibility, and that such animals are
subjected to continuous accessions of both bacilli and toxins, we can
easily understand how some of the more adaptable germs will in time
accommodate themselves to the new medium. A Pettinkoffer, with an immune
constitution or a specially vigorous gastric digestion, may with
impunity drink a culture of cholera spirillum, but the same is not true
of the drunkard fresh from a spree and with seriously impaired
digestion.
_Bacillus Tuberculosis in Man and Ox. Points of Similarity._ The
bacillus tuberculosis of cattle is in general shorter and thicker than
those of man, but many in both subjects are morphologically
indistinguishable. Such differences are often far exceeded by different
specimens of one stock of germ seeded on different media. There is no
great difference in the thermal death point, and the viability in light,
dryness, cold and putrefaction. The tendency is in all cases to colonize
the lymph plexus or glands and to develop the specific lesions, with
slight variation in detail. The slow development of the lesions from
both forms of bacilli and their histological similarity is another
argument for their essential identity. The slow growth of both on
artificial media, the demand of each for a medium having the same
approximate composition, and the similar pathogenic and diagnostic
characters of the toxic matters elaborated by both germs bespeak a
primary identity. The very remarkable staining qualities of tubercle
bacillus, from whatever source it may be drawn, are no less remarkable.
_Tuberculosis of Man and Ox Coextensive._ The prevalence of tuberculosis
in man and ox in the same country and district is so frequent that it
may be safely set down as the rule. Among ichthyophagists and great
fishing communities, like the people of the Hebrides, Iceland,
Newfoundland, Greenland, and the coasts of Hudson Bay, tuberculosis is
rare. In these countries cattle are few or absent, or, like the hardy
highland kyloes of the Hebrides, they are kept in the open air. The
immunity of the people is not due to insusceptibility, since they fall
ready victims to tuberculosis when removed to infected countries and
cities.
In Northern Sweden, Norway, Lapland and Finland, where cattle are scarce
and reindeer plentiful, tuberculosis is said to be rare, though the
inhabitants live in the closest of dwellings through the long winter. In
most of the Pacific islands there are no cattle, and the natives are
comparatively free from consumption. In Hawaii, since the introduction
of cattle, consumption has increased. Australia and Tasmania, which
forty years ago were the great resorts for English consumptives, have
become increasingly the homes of infection since the development of the
cattle industry and the influx of phthisical subjects. Minnesota and
Dakota, in the early days, were held to be incompatible with
tuberculosis, but since the advent of the white man and his stabled
herds they have largely lost their sanitary reputation. The highest
known mortality from tuberculosis to-day is that of the reservation
Indians of these States, who feed on raw, diseased beef. In the Kighiz
steppes the Tartars subsist on the flesh and milk of their solipeds, and
largely escape consumption. In Japan, Dr. Ashmead tells us that the
common people escape tuberculosis, while the aristocracy suffer
severely. He attributes this mainly to the debauchery of the ruling
class; but it must not be overlooked that they eat freely of beef and
dairy products, which the rice-eating poorer population do not. The same
remarks apply in measure to the mandarin and plebian classes in China.
Holden tells us that tuberculosis is rare in Columbia, Ecuador and on
the eastern slopes of the Andes, where little or no milk or butter is
used. It must be further borne in mind that in these countries all herds
live in the open air, and practically escape infection.
These examples must be contrasted with the consumers of beef and milk in
civilized temperate countries, where the stock are largely kept indoors.
A general average mortality of 7 or 8 per cent. from tuberculosis, and
the _post mortem_ evidence in European and American hospitals of 33 to
50 per cent. which show tubercular lesions, recent or remote, cannot be
lightly passed over. The contrast with our reservation Indians is still
more striking. Holden and Treon testify that the meat furnished to the
Indians is always poor and often diseased, and that when the stock
arrives our hungry wards devour the internal organs raw, or, later, the
flesh as pounded preserved meat, and still uncooked. The deaths of these
Indians from tuberculosis is 50 per cent. of the total mortality.[6] Dr.
Washington Matthews, who spent twenty-one years among the Indians, gives
their food as the main cause of the disease, and states that when the
supply of fresh meat is liberal the death rate from tuberculosis is
highest (Census of 1880).
Footnote 6:
Medical Record, August 13, 1883.
If we now contrast this fearful mortality with the immunity of the
Indians of Hudson Bay, Great Slave Lake, Alaska, and the North
generally, we have a most suggestive picture. It may be conceded that
the extreme Northern Indians, being beyond the cereal region, have a
slight measure of protection in their meat diet; but the recent spread
of tuberculosis, like a plague, among the inhabitants of Barrow Straits,
when introduced by the frozen-in whalers and the relief party, is
sufficient disproof of any claim of special insusceptibility. There can
be no doubt that in this, as in other virulent diseases, the rule holds
that the long absence of the infection secures the preservation of the
susceptible lines of blood, so that when the contagion does come it
finds a more inviting field than in countries in which the more
susceptible strains have been killed off and the comparatively immune
have survived. Toward the Arctic circle the Indian must crowd into
closer quarters in winter than his brother further south; but, in spite
of all, the beef-eating Indian is being rapidly exterminated by
tuberculosis, to which his brother of the north is a comparative
stranger.
_Exceptions: Their Explanation._ This statement would be incomplete
without a notice of exceptions to the rule. The Cape Town branch of the
British Medical Association reports “that tuberculosis is rapidly
increasing there in the human population, while tubercle in cattle is
almost nonexistent.” This finds an abundant explanation in the different
conditions of life. The men live indoors and concentrate the infection,
whereas the cattle enjoy an outdoor life and escape. In a latitude of
30° south, where frost is rare, and with a dry climate (12 to 30 inches
of rain per annum), the colonists find no occasion for housing their
cattle, so that the conditions for the prevention of tuberculosis are
ideal. It may be added that cattle are far less numerous in Cape Colony
than they formerly were. The destruction first by lung plague and later
by rinderpest has made the cattle industry extremely hazardous, and even
before the advent of the rinderpest many had abandoned cattle and taken
to sheep.
Parallel cases can be found in other countries. In Egypt, the great
resort of consumptives, cattle are almost immune, the abattoirs
furnishing about one tuberculous ox in ten thousand killed.[7] From
Tunis (Alix), Algiers (Sarciron, Plaise), and Senegambia (Lenoir) a
similar testimony comes. Cattle imported from Europe may die of
tuberculosis, which is liable to assume a rapidly fatal type; but the
native cattle, kept in the open air, are practically exempt.
Footnote 7:
Danzon. Études Expérimentale et Cliniques sur la Tuberculose, vol. i.
p. 350.
Jersey cattle in their native island, staked out at pasture all the year
round, show little or no tuberculosis, whereas the housed Jerseys of
England and America suffer severely. The cattle of our Gulf Coast
States, kept on ranches in the open air, are largely immune, and the
cattle of Columbia, Ecuador, Peru, and the Argentine Republic largely
escape; but the housed dairy cows of our Southern cities show a very
high ratio of consumptives. Consumption becomes more and more deadly in
the Southern negro even in the country localities, while the outdoor
cattle of the same districts escape.
The absence of tuberculosis from the sanitarium herd at Saranac requires
to be explained on a different basis. This herd is housed in winter, and
infection, once introduced, would have opportunity to spread. The
absence of tuberculosis is highly complimentary to the management of the
establishment. But a similar immunity is the rule for all well-managed
sanitariums, and not as regards cattle only, but man as well. At Argeles
no case of tuberculosis contagion to attendants occurred in ten years
(Ferrand). At Soden baths, in a village of 1500, there were in
thirty-four years 65 deaths, 15 from consumption (Hopt). At Falkenstein,
in fifteen years, one attendant became tuberculous (Jousset). At
Görbersdorf the cases of consumption in the village and environs
decreased (Knopf). At Brompton, London, in thirty-six years, among 150
attendants, but one became consumptive, though they individually served
for from fifteen to twenty-four years, and nearly 40,000 patients had
been received.[8] A well-conducted sanitarium is and should be a safer
place than the average community, in which 15 per cent. and upward are
tuberculous. The educational influence of such an institution should
decrease tuberculosis in the surrounding districts.
Footnote 8:
Études Expérimentale et Cliniques sur la Tuberculose, vol. iii. p.
408.
_Cases of Direct Infection from Man to Ox._ Chauveau induced
tuberculosis in cattle by feeding the tubercle from the lungs of man.[9]
Footnote 9:
Arloing. Tuberculosis Congress of 1891.
Nocard relates that a Beauce farmer, with a finely appointed stable and
healthy herd, in 1883 employed a dairyman who had cough, profuse
expectoration, and occasional hæmoptysis, and who had been several times
in the hospital in consequence. He slept in the cow stable directly over
the cows. In 1886 two cows, stalled immediately beneath him, showed ill
health and were put up to fatten, but did badly and showed extensive
tuberculosis when butchered. The dairyman stayed until 1891, having to
go to the hospital several times in the interval. In 1892 the tuberculin
test was applied and seven more cows were found to be tuberculous.
Huon tells of a cow bought to furnish milk for calves used to raise
vaccine. She stood the tuberculin test, and was carefully secluded from
all other cattle, but soon began to fall off, and in six months was very
much emaciated, responded to the tuberculin test, and when killed showed
extensive tuberculosis. Her caretaker at the vaccine establishment had
what was believed to be chronic bronchitis, but when he died, soon
after, this was found to be extensive pulmonary tuberculosis.
Bollinger inoculated a three-months’ calf with liquid from human
tubercle and killed it seven months later. Fibroid pedunculated tumors,
from a pea to a walnut in size, hung from the mesentery and spleen, and
the mesenteric and retroperitoneal glands were tubercular.[10]
Footnote 10:
Münchener medicinische Wochenschrift, 1894.
Sidney Martin furnishes the following: Four calves were fed 70 c.c. of
sputum containing a large number of bacilli. Three were killed after
four, eight, and twelve months respectively, and had severally 53, 63
and 13 nodules on the small intestine, mostly on Peyers’ patches. Two
calves received at one dose 440 c.c. of tuberculous sputum, and were
severally killed after eight and nineteen weeks. The first had
tubercular nodules in the intestine and mesenteric glands.[11]
Footnote 11:
Report of Royal Commission of 1895.
Frothingham injected into the peritoneum of two calves, three and
thirteen weeks old, a culture of tubercle bacilli isolated one year
before from the liver of a child. Slight local nodules were produced,
some like spontaneous tubercle, others granulation tissue.
Theobald Smith inoculated sputum into the chest and abdomen of the
following:
1. A yearling heifer, which was killed two months later and showed on
the pleura near the seat of infection a mass of tubercles, one by one
and a half inch in diameter, with partly caseated centres; also a nodule
one-eighth of an inch on the right lung, and small tubercles attached to
the diaphragm and omentum.
2. A yearling injected in the same way showed in two months on the
diaphragm a mass of tubercles two inches in diameter, and a second mass
one inch in diameter on the ribs near the seat of infection.
Microscopical examination failed to detect bacilli, but there is no
evidence that they were sought by culture or inoculation.
3. A cow injected in the chest and killed after two months showed
tubercles of the lungs, pleura, and mediastinal glands, partly caseated
and containing bacilli. Vascular fringes hung from the pleura.
4. A cow receiving a chest injection of sputum culture and killed in two
months showed fringes and pendulous masses on the pleura, with small
tubercles containing cheesy matter and a few bacilli.[12]
Footnote 12:
Journal of Experimental Medicine, 1898, vol. iii. p. 482.
Crookshank injected tubercular sputum into the peritoneum of a calf,
which died of streptococcus infection on the forty-second day. It showed
extensive tubercular deposits in the seat of injection and an abscess
the size of a walnut. Nodular fleshy neoplasms in hundreds studded the
mesentery, omentum, liver, spleen, and diaphragm, and small tubercles
disseminated through the lungs and liver contained tubercle bacilli.
Three abscesses contained streptococci.[13]
Footnote 13:
Transactions of the Pathological Society of London, 1891, p. 332.
The experimental inoculations of cattle with sputum by T. Smith, Kruse,
and Adami showed a decided lack of potency in the bovine system, but (1)
they do not show that the germ at once perishes in the system of cattle;
(2) they do not prove that this germ, if returned from the ox to man,
would prove less pathogenic than if carried from man to man without the
intervention of the ox. (3) The observations of Bollinger, Baumgarten,
and Crookshank show that under certain conditions the sputum bacillus
can and does produce generalized tuberculosis in cattle. (4) Diminished
pathogenesis of the germ when passed from man to cattle is no guarantee
that this germ, or the slightly modified germ of casual bovine
tuberculosis will prove equally mild if transferred from the bovine to
the human patient.
_Cases of Infection of Man from Ox._ Tscherning, of Copenhagen, attended
a young veterinarian who had cut his finger in dissecting a tuberculous
cow. The skin wound healed in three weeks, but a subcutaneous swelling
persisted, an ulcer formed, and a tuberculous mass containing bacilli
was removed. No secondary tubercles formed.[14] A parallel case occurred
to a prominent American veterinarian. The diseased tissue was excised
and the bacilli identified by the bacteriologist of the university with
which the patient was connected, and a permanent recovery ensued.
Footnote 14:
Nocard. Dictionnaire de Med. Veterinaire. Article, Tuberculosis.
Pfeiffer, of Weimar, attended a veterinarian who had been similarly
inoculated from a tuberculous cow. The patient, aged thirty-four years,
had a good constitution and no tuberculous taint. The cutaneous lesion
healed, but six months later there was tuberculosis in the cicatrix;
pulmonary tuberculosis followed, and the patient died of this two years
later. At the necropsy were found tubercular arthritis of the wounded
thumb and many vomicæ in the lungs.[15]
Footnote 15:
Zeitschrift für Hygiene, Band iii.
The post-mortem wart (tuberculosis verrucosa cutis) is familiar to
surgeons as occurring in butchers and tanners, and there is every
presumption that in many cases this is of bovine origin (Martin du
Magny, Hanot, Senn, Riehl, Paltauf, Osier). Gerber testifies that in
exceptional cases this extends to the lymph-glands and becomes
generalized.
Dr. Stang, of Amorbach, had a five-year-old, finely developed boy
patient, of healthy parents, destitute of hereditary taint. He died
after a few weeks’ illness with miliary tuberculosis of the lungs and
enormously enlarged tubercular mesenteric glands. The cow which supplied
his milk had been killed a short time before with pulmonary
tuberculosis.[16]
Footnote 16:
Lydtin. Veterinary Congress, Brussels, 1883.
Dr. Demme, of the Children’s Hospital, Berne, had four infants, the
offspring of sound parents, with no hereditary taint of tubercle, die of
intestinal and mesenteric tuberculosis, having been fed on the milk of
tuberculous cows. Among 2,000 tuberculous infants treated in twenty
years these were the only ones in which he could exclude the probability
of hereditary and other causes.[17]
Footnote 17:
Nocard. Dictionnaire de Med. Veterinaire. Article, Tuberculosis.
Mr. Howe, of North Hadley, Mass., lost a son, aged twenty months, from
abdominal tuberculosis, three months after he had paid a week’s visit to
his uncle and had been fed the milk of the uncle’s tuberculous cow. The
cow showed at death generalized tuberculosis. The child had been strong
and well, as were his parents.
The four-year-old son of Colonel Beecher, of Yonkers, died March, 1894,
of tubercular meningitis, and the two Alderney cows which had supplied
him with milk were then proved consumptive by the tuberculin test and
post-mortem examination.[18]
Footnote 18:
New York Sun, March 29, 1894.
The child of Dr. Brown, U. S. A., and now of Cornell University Medical
School, was similarly cut off by tuberculosis, having been fed on the
milk of a tuberculous cow.
Dr. C. H. Peabody had a child patient die of tubercular meningitis three
months after the family cow had been killed for generalized
tuberculosis. There had been previously no tuberculosis in the family
(Ernst, _Infectiousness of Milk_).
A. H. Rose, of Littleton, Mass., gives the case of a child which was fed
for three years on the milk of a tuberculous cow and died with abdominal
tuberculosis (Ernst).
Gordon, of Quincy, Mass., records the case of a ten months old child of
healthy parents and ancestry which had been fed on the milk of a cow
with advanced tuberculosis, and which died after a few weeks with acute
tuberculosis (Ernst).
Gage, of Lowell, Mass., had an infant patient of healthy parents and
surroundings, but which subsisted exclusively on a cow’s milk that
contained bacilli and infected Guinea pigs. The child died of tubercular
meningitis. A second child fed the same milk suffered in a similar way
(Ernst).
Andersen, of Seeland, reports the death from tuberculosis of a six
months old child which had fed on the milk of a cow having tuberculosis
of the udder. The mother developed symptoms of tuberculosis after the
death of the child.[19]
Footnote 19:
Hatch Experiment Station, Massachusetts Agricultural College, Bulletin
No. 3.
Dr. Gosse, of Geneva, Switzerland, spent his Sundays with his family on
an estate in the hills, and his daughter, aged seventeen years, took
great pleasure in drinking milk warm from the cows. Early in 1893 she
sickened with an obscure illness, and after ten months died, revealing
at the necropsy intestinal and mesenteric tuberculosis. The five cows on
the estate were tested with tuberculin; four reacted and were killed;
two showed tuberculous udders (Nocard).
Dr. H. M. Pond reports four cases of tuberculosis in one family, three
of them fatal. The cows supplying the family with milk were
tuberculous.[20]
Footnote 20:
Pacific Medical and Surgical Journal, 1888.
Dr. Faust, veterinarian, of Poughkeepsie, records the case of a family
on Long Island that lost from tuberculosis 139 cows. A three-year-old
child and two grown sons died of tuberculosis. Tuberculosis was unknown
in the parents’ families.[21]
Footnote 21:
Report to the Board of Health.
Dr. Kelly, veterinarian, Albany, gives the following: In a family of
five a son, aged nineteen years, was very fond of milk and drank it
fresh from the cow, and contracted tuberculosis. Some months later the
farm herd of seventeen registered Jerseys were tested with tuberculin,
and thirteen reacted and showed extensive tuberculosis when killed.
Dr. Cooper, veterinarian, Paterson, N. J., furnishes this: A child, fed
on the milk of a cow, contracted tabes mesenterica. Examination revealed
the presence of tubercle bacilli in the milk. The milk was then fed to
ten kittens, all of which became ill and emaciated, and when killed
showed tuberculosis.
Such cases, in connection with the experimental inoculations, furnish
more than mere circumstantial evidence. They are corroborated and
strengthened by the very uniform diffusion of tuberculosis in man and
stalled cattle in practically all civilized countries. Of the closer
connection in individual cases one or two instances may here be added as
drawn from personal observation:
1. In one case a family cow and the owner’s wife had both advanced
tuberculosis. The lady consumed a good deal of the cow’s milk, but when
she gave up its use she felt decidedly better.
2. The owner of a thoroughbred herd of sixty head had suffered for years
from consumption, and attributed the poor condition of the animals to
lack of care since he had been laid aside. Without the tuberculin test,
I diagnosed tuberculosis in fifty-nine of the animals.
3. In a second thoroughbred herd there never lacked one or two cases of
advanced tuberculosis, two of the family suffered, and the eldest son,
who was fond of milk and vegetable food, died of pulmonary tuberculosis.
4. A dairy of common cows had seventeen out of twenty-six destroyed for
tuberculosis, and the farmer’s wife, father-in-law, and two
brothers-in-law had shortly before died of consumption. The wife felt
ill in the close house air, and with her father occupied herself much
about the cattle.
5. A veterinary professor, who was meat inspector of the city abattoir,
died a few years ago of tuberculosis, which he handled so constantly in
his daily duties.
Stalker and Niles report that 5 persons, 20 to 30 years of age, of
healthy ancestry, died of tuberculosis within two years, on a farm where
17 tuberculous cattle were found, and others had died in previous years,
(Bull. Ia. Agr. Exp. Stat., 29).
Leonhardt reports the death from tuberculosis, abdominal and meningeal,
of two children, fed on the milk of a tuberculous cow, (Rep. N. H. Bd.
of Health, 1892).
Sontag reports the death by tuberculosis of a six months old child of
healthy parents, that had been fed the milk of a tuberculous cow, (Rep.
N. H. Board of Health, 1892).
Dr. E. Pearson quotes the following:
“A well known veterinarian wounded in the hand in opening a tuberculous
cow, had a tumid, intractable sore, the tissues of which when excised
showed tubercle bacilli.
A veterinarian, of Chester Co., Pa., in opening a tuberculous cow, cut
his knuckle, which healed tardily, remained swollen and when excised,
showed typical tubercular lesions including giant cells.”
He quotes from Hartzell the cases of two men wounded in cleaning cattle
cars, both of whom had resulting tubercle, arrested in one case by
excision, but in the other advanced to generalized tuberculosis and
death.
Bang gives the following Danish cases:
A merchant having two chlorotic daughters secured a fine cow to feed
them fresh milk. The cow was killed tuberculous and was replaced by
another which also showed tuberculosis, this time affecting the udder.
The girls died of tuberculosis at 16 and 18 years. Two younger children
fed on the milk of sound cows grew up healthy.
A healthy cow became tubercular, after having been placed in the same
stall in which another had died of tuberculosis. A child fed almost
exclusively on the milk of these two cows died of tuberculosis.
A peasant at Silkeborg drank freely of milk freshly drawn. He died of
tuberculosis, as did also a cow, and later in the same stable, a pig.
A peasant had an 11 year old cow with generalized tuberculosis,
implicating the udder. The wife of the peasant, formerly healthy, became
tuberculous shortly after the udder became affected and died at 45. A
daughter who, like her mother, used the milk of this cow, died
consumptive in the same year. The husband who drank beer, and not milk,
remained well.
A physician fed his two children on the milk of his tubercular cow, and
lost both from tuberculosis. Neither parents nor grand-parents were
tuberculous. (L. Pearson in Bull. 75, Tuberculosis of Cattle).
Thorne had reports from twenty-two Ohio physicians to the effect that
they had traced tuberculosis in their patients to the use of the milk of
tuberculous cows, and thirty-three who believed they had reason to
suspect the meat and milk supply as the source of cases of consumption.
(Ohio Exp. Stat. Bull. 108).
To these may be added the cutaneous forms of tuberculosis (tuberculosis
verrucosa cutis), which occur on the hands of persons (butchers,
tanners, coachmen, cooks, etc.), who handle infected products of
animals. These have been described by Riehl and Paltauf, Senn, and a
number of surgeons and dermatologists and the relation of the occupation
to the seat of the disease is conclusive as to the source of the
infection. It is the exact counterpart of the verrucosa necrogenica of
the hands of persons working in the dissecting rooms of medical schools,
and the source of infection is equally well established in both cases.
A strong argument for the appreciable influence of the bovine bacillus
upon man (acting directly or indirectly through the pig) is that the
relative death rate of Jews from tuberculosis is materially less than
that of other races. It is constantly claimed that orthodox Jews who eat
only kosher (rabbi inspected) beef and no pork, suffer least of all the
population from tuberculosis. Dr. Gerster, judging by the burial returns
of the United Synagogue and the English Registrar General’s returns,
concludes that only about half the relative proportion of Hebrews suffer
from consumption as do other races in the same country. Some remarkable
facts come out in the report of the Royal Commission on tuberculosis in
England. In England and Wales the disease had decreased 39.1 per cent,
in thirty-five years, but this decrease has been mainly in pulmonary
cases, while the abdominal forms decreased only 8.5 per cent. Sir
Richard Thorne, indeed says, that in children of the first year there
had been an actual encrease of 27.7 per cent. Northrup and Still, on the
contrary, present statistics showing that in children the pulmonary form
of tuberculosis is the most common (Brit. Med. Jour. 1898). If in the
face of this there has been a very material encrease of the abdominal
form, coincident with the notorious encrease of the disease in dairy
cows and of the bottle-feeding of infants, may we not enquire how much
of this is due to the greater prevalence of bottle-feeding and the
infected cow’s milk? It is not for a moment supposed that the majority
of infections in children come from the cow. The question is whether
this encrease in the minority is not in measure chargeable on the cow.
The impaired nutrition resulting in some instances from the use of cow’s
milk cannot well be charged with a marked encrease of cases in which the
mesenteric tubercles point so directly to infection through the food. If
it is held that the tubercle bacilli in the milk are harmless, we wait
for evidence of the real cause of such encrease and localization.
The experiments of Adami show that tubercle is directly transmissible
from man to ox though usually with decreased virulence. More recently,
Ravenel using the bacillus derived from the mesenteric glands of a
child, injected intravenously two tuberculin-tested calves, with 5cc.
each of the culture producing exalted hyperthermia, miliary tuberculosis
of the lungs, tuberculosis and caseation of the bronchial and
mediastinal glands, and death in 17 days. Dr. Garnault’s experiment on
himself, now in progress, has already shown the great danger to a
susceptible man, of the bovine bacillus.
As showing accommodation to environment, Battaillon and Ferre found that
the bacillus (mammalian and avian) grown in frogs, Dubard that grown in
fishes, Kráhl that grown in frogs, snakes, fishes and lizards, and
Müeller that grown in the glow worm, thereafter grew at summer
temperature (68° F.) and grew poorly or not at all in the bodies of
mammalia.
The tubercle bacillus is primarily and essentially one, but this must
not close our eyes to the fact that in different hosts and environments
it takes on very different habits, so that for the time and in these
surroundings, it is materially modified in its pathogenic attitude
toward different races. Yet its ready variability when conditions are
favorable to change, renders it desirable to destroy it in all its
forms, and especially in those which approximate most closely to those
that prey on man and animals.
An impartial review of the whole field warrants the conclusion that the
nineteen young (and therefore comparatively insusceptible) cattle which
in Koch’s hands failed to develop generalized tuberculosis after
inoculation with the virulent sputum of man, and the smaller numbers
that resulted in the same way under similar treatment in the hands of
Th. Smith, Dinwiddie and Adami, while showing a very marked limitation
in the susceptibility of the sound bovine system to weak bacilli from
man, cannot disprove the many well authenticated cases of the
transmission of tuberculosis from cow to man and the reverse. The
greater potency of the bovine bacillus over that of man, in its action
on the small rodents and pigs, utterly forbids the unproved assumption
that it is on the contrary harmless to man.
If the object of the sanitarian were merely to delay a fatal result in
his tuberculous patient, while he accepted the prevalence of
tuberculosis as inevitable for all future time, the acknowledged
lessened receptivity of the ox for the bacillus from man would mean more
and would be at least worthy of a hearing, but as the extinction of a
disease germ and its representative plague must ever be the first
object, any movement toward the preservation in cattle of a germ which
is deadly to man and much more so to cattle, must be held as subversive
of the prime purpose of sanitary work. This is true even if we allow,
for the sake of argument, that only a few of the bovine bacilli are
capable of dangerously colonizing the human body, and that special
environment is needful to allow of such successful colonization. On the
other hand the limited receptivity of the ox for the bacillus from man
is the greatest encouragement to active work to exterminate tuberculosis
from our herds. It is impossible to adopt in man the summary measures
that are so successful in the speedy _stamping out_ of the plagues of
the lower animals, so that tuberculosis in the human family can only be
eradicated by slow degrees, and therefore there will long continue for
our herds the danger from the human side, but just so far as the
susceptibility of cattle to human tuberculosis is limited, in the same
ratio are our hands strengthened in effective work for the extinction of
consumption in our herds and for preserving their soundness after they
have once been purified. If they were to be reinfected by the presence
of any consumptive person we might well despair of success in face of a
wide prevalence of tuberculosis in man, but since it is only
exceptionally that cattle suffer from man, outbreaks coming from this
source can the more easily be taken care of. In this view tuberculosis
is approximated somewhat more closely to the other bovine plagues (lung
plague, rinderpest) which can be stamped out with the greatest ease and
certainty, so that as a purely economic measure the argument for the
speedy extinction of tuberculosis in our herds is reinforced.
TREATMENT OF TUBERCULOSIS.
Like all deadly infectious diseases in the lower animals, tuberculosis
is not to be profitably treated as a rule. In the case of specially
valuable breeding animals, in which the prospective progeny will pay for
large outlay, and when the disease is in its incipient stage, treatment
may be warranted. The patient should be thoroughly separated from other
animals, kept in the open air, or, in our northern winters, in roomy,
well ventilated buildings facing the south, well lighted, kept
immaculately clean, frequently whitewashed, and well drained. If there
are more than one case every precaution named under the head of
prevention must be adopted. Exercise to keep the muscular system in good
tone is called for, but never to fatigue. Hence, a sheltered pasturage
is ideal. Feeding must be liberal including a ration of grain or seeds,
and oil bearing seeds like linseed, rape seed or cotton seed may be
specially named. Cod liver oil alone, or etherized is often of great
value, with iron and bitters continued for weeks or months. In the case
of specially valuable animals one may use a pneumatic cabinet the
principle of which is to diminish the air pressure on the body at large
by an exhaust, while pure air for breathing, at the ordinary atmospheric
pressure, is introduced through a tube furnished with a face piece
fitting around closely beneath the eyes. This serves the purpose of
attracting (sucking) the blood toward the skin and other tissues from
the lungs, which in their turn are compressed by the air at the
atmospheric pressure. Pulmonary congestion is in this way lessened,
exudates are absorbed, necrotic tissue removed, sepsis counteracted,
hæmatosis encreased, circulation of both blood and lymph stimulated,
digestion and nutrition improved, and general health invigorated.
Active grooming and even the stimulating effect of cold douches may be
invoked, the skin being rubbed actively until dry and warm.
If the circulation is poor, a stimulating steam or hot water bath of
fifteen minutes followed by a cold sponge and rubbing till dry may be
profitably substituted. In such cases it is well to put a cold sponge on
the head while in the bath.
Medicated inhalation is often valuable especially when the lesions are
on, or near the bronchial mucosa. In 1868, Dewar met with most
successful results from inhalation of sulphurous acid gas impregnating
the atmosphere as strongly as the patient can breath without discomfort.
His own groom who had given up work because of advanced phthisis, under
treatment of half an hour three times a day, became ruddy, gained
weight, and betook himself to work again. In rabbits which I inoculated
with human sputa, the same year, all died tuberculous excepting one
which I fumigated three times a day for weeks. This rabbit remained
plump and well.
As an example of a still more irritating inhalant, I watched the case of
a phthisical man who secured employment on the government disinfecting
corps, in Chicago, in purifying the lung-plague-infected stables with
chloride of lime solution, and who very soon began to improve, gaining
weight and strength, his cough meanwhile subsiding.
Cervello’s use of formalina by inhalation though well spoken of by its
inventor would seem too irritating on the delicate lungs, however good
it is as an antiseptic.
Inhalants may be conjoined with the pneumatic cabinet.
Among agents used to moderate the cough may be named codeine, morphia,
cherry laurel water, wild cherry bark, guaiacol, menthol, syrup of Tolu,
or chloroform, or alcohol inhalation.
As an internal antiseptic, carbonate of creosote has often proved
beneficial.
Mustard blisters on the skin covering the tubercle is claimed by Knopf
to act beneficially by attracting the microbes from the delicate lungs
to the more robust skin and connective tissue, where they can be better
disposed of by the more abundant leucocytes.
He has also found excellent results in complex infections in animals
from the use of Marmorek’s streptococcic serum in doses of 10cc.,
followed after the second dose by 5cc. every 24 hours. In other cases it
failed of the effect (reduction to normal temperature) evidently
indicating that the hyperthermia was maintained by other microbes than
the streptococcus. The principle is good, and perhaps at some time in
the future a bacteriological examination of the sputum may reveal the
microbes present and suggest the sera for such complications.
The introduction of air into the peritoneum has long been known to
exercise a retarding and curative action on abdominal tuberculosis. At
the present writing my colleague, V. A. Moore, is experimenting by
pumping air and oxygen into the peritoneum and pleuræ in cattle slightly
affected, with encouraging results.
I should add that isolated superficial tubercles may often be excised to
advantage, and the part dressed antiseptically.
It is only in exceptional cases, however, that one is warranted in
preserving and running the danger of spreading the tubercle bacillus for
the advantage that can be secured to individual animals from treatment.
EXTINCTION OF TUBERCULOSIS IN CATTLE.
As cattle are the great propagators of tuberculosis on the farm, the
question of extinction necessarily centres around this race. As in all
other dangerous infections, the most prompt and successful method would
be in the time honored one of destroying the infected and thoroughly
disinfecting all their products. The only barrier to success in such a
case would be the conveyance of infection anew from man to cattle after
the herd had been purified. The demonstration that cattle are less
susceptible to infection by the human sputa than many had supposed does
away largely with this objection, as in a generally purified bovine
race, the few primary cases contracted from man could be easily taken
care of. Then, if tuberculous persons were interdicted from attendance
on cattle, the danger in this direction would become very nearly a
negligible quantity.
There remains the question of expense and many honestly consider this as
absolutely prohibitory. The estimate of 5 per cent. of our 68,000,000
head to be killed and paid for at $25 per head, would be $85,000,000.
But there is no necessity for this. Our fat steers at the packing houses
are tuberculous only to the extent of 0.02 per cent., speaking well for
their dams and nurses. The estimate of 5 per cent., based upon the
testing of those few herds that have been taken because they were
already known to be tuberculous, is unquestionably far above the actual
ratio for the United States. It may apply to dairy cattle in some
infected districts, but, for the bovine race of the whole country, it is
absurdly high. If we had 10, 20 or 50 per cent. infected, as in some
countries of Europe, the objection of expense might be a formidable one,
but when the ratio of the infected is but 2:10000, we have every
encouragement on the score of expense to enter on a campaign of
extinction. But again, we do not need to deal with 68,000,000 cattle as
we can omit the steers which are so little affected and which will all
come to the slaughter house in two or three years. The source of their
infection (a few cases excepted) is in the older cows and bulls of the
dairy and breeding herds, and this brings down our total to a little
over 17,000,000. The average census price for dairy cows is $29 and, as
the condemned cows are depreciated by their condition, it would be a
high average to estimate them at $20. Again, the average infected ratio
of cows for the entire country would be set high at 2 per cent., and on
this basis it might well be that the required indemnity would not
aggregate much over $6,000,000. Five or even ten times that amount would
be a mere trifle in comparison with the $3,000,000,000 value, constantly
encreasing, of our domestic animals, with the $99,210,272, representing
our yearly product of beef and beef products, with our annual dairy
products, worth $500,000,000, (Alford), or with our yearly loss of
100,000 of our population in the very prime of life when they are of the
greatest value to the country, representing a yearly drain of
$100,000,000, beside all the suffering and loss entailed by their
prolonged and too often helpless idleness. Though this last item is
doomed to continue for a length of time after the disease has been
extinguished in our herds, it is receiving constant accessions from the
latter, and can never be entirely done away with until our cattle are
above suspicion.
An even more serious problem is the demand for tuberculin and above all
for accomplished, experienced and honorable veterinarians fitted to
conduct the sanitary campaign over the entire country. The tuberculin
cannot be produced in a week or a month, yet the problem of its
production in any required amount in a few months is merely one of the
encrease of existing plants under the management of the same careful
hands now engaged upon it. As to veterinarians it would be impossible to
secure at once the required staff of men capable of carrying out the
work over the whole country. But this is not essential. The work can be
begun in the counties supplying the large cities with milk, and in the
great butter and cheese producing areas where it is so urgently needed,
and it must be made to include all thoroughbred herds, which are so
constantly drawn upon to improve the blood elsewhere, and each herd,
county and district, as freed from infection must be scheduled and no
additions made to it from outside, except under the guarantee of the
tuberculin test, repeated in six months. The reacting animals, must be
appraised, excluded from the herd, and disposed of, it may be to the
butcher to be killed under official expert inspection, and the salvage,
if any, to be deducted from the appraised value; or to be rendered and
the salvage estimated; or to be buried as the case may be. In all such
cases the other animals (horses, pigs) that occupy the same buildings
and yards should be tested, although the risk of the infection of cattle
from these animals is comparatively small. Unless in badly infected
herds, steers and young cattle, which can be kept in a separate herd
need not be tested. Vermin must be killed. Thorough disinfection must be
applied to buildings and yards, and the dairy herd must be retested at
the end of every six months until no more reactions are met with.
In this way the campaign in any State can be begun with a small staff,
which may be steadily encreased as men are trained to the work, and in
no great length of time the dairying and breeding herds can be purified
and the investigation carried into the more purely agricultural fields,
where herds are small and usually free from infection. Many minor points
would require the attention of a competent superintendent of the work.
My object here is to make a plea for the approved and attested method
which has never failed in the case of other animal infections on
enclosed farms, and which is based on the absolute destruction of every
seed of the disease in the area under sanitary control. The method has
the apparent drawback, that it demands a greater relative outlay at the
start, than do others proposed, but in view of its certainty, and the
confident hope of an early abolition of all infection, loss, and
expensive expert control, it must, in my opinion, be looked upon here,
as it has always proved in the past, the course of the truest economy.
It may be compared to the treatment of a field of thistles by removing
the offensive weeds, root and branch, before they have advanced to seed,
instead of merely cutting them down with a mower, and leaving the roots,
to grow anew, to leaf, to blossom and seed, in spite of the temporary
partial drawback. But as the prospect of early legislation along this
line is not a bright one, the expert must accommodate his aims and
efforts to what can be done under the existing laws.
_Breeding Healthy Stock from Parents with Latent Tuberculosis._ When a
State is not pledged to exterminate tuberculosis by prompt and radical
measures, it is quite possible to raise healthy stock from sires and
dams that have the disease in a latent form. It is very exceptional that
calves are born tuberculous. If, then, they are kept in a pure
environment and furnished with the milk of sound nurses, or even with
the milk of their own tuberculous dams, after it has been heated for
one-quarter of an hour to 180° F. or 212° F. they can be preserved in
perfect health.
This is especially adapted to herds of valuable thoroughbreds, the
destruction of which would be a serious loss, and the preservation of
the strain of blood a most desirable object.
The whole herd should be tested with tuberculin, and the advanced and
generalized cases, that can be detected by objective symptoms, should be
at once destroyed and safely disposed of. The animals in good condition
and that have not reacted should be placed in a new barn and yard, or
where no tubercle has been, or in places that have been thoroughly
disinfected, under special attendants. There will remain the animals in
good condition with no objective symptom, but that have reacted, and
these are placed in separate barn, yard and pasture well away from other
stock, under their own attendants, for breeding purposes. They should
have the best of food and air, clean, well lighted, roomy buildings with
shelter from storms, clean sheltered yards, and in summer, pasturage.
Any cow showing indication of active advance or generalization of the
disease (cough, wheezing, dyspnœa under exertion, excessive pallor of
mucosæ, unthriftiness) should be at once separated and destroyed as
endangering the reinfection of others, and the stable subjected to
disinfection. The calf, as soon as born, must be removed to a special
building or park, where it shall get milk from a sound cow or that of
its own dam after it has been carefully sterilized. After sterilization
the milk cannot safely be returned to the unscalded pail into which it
was drawn from the cow, and it should be fed by separate attendants who
have not milked nor handled the affected animal. Any loss of condition,
unthriftiness, cough or scouring on the part of any of the calves should
be the signal for its separation from its fellows, subjection to the
tuberculin test, and, if it reacts, for its destruction and the
disinfection of the building where it was. It is well to test each calf
at six weeks old and to remove the reacting ones. The success of this
method is now well established.
Goodman, of Dorpat, applied it largely as early as 1891, rearing the
healthy calves of reacting cows on the milk of cows that had stood the
test. Bang, of Denmark, raised such calves to sound maturity on
sterilized milk. Reynolds, of Minnesota, reports the raising of
twenty-four healthy calves from infected cows on the milk of tested
cows, while three fed on milk of reacting cows, which was supposed to be
sterilized, all became tuberculous. McEachran (1899) in an extended
experiment succeeded perfectly with the milk of tested cows only. I have
now in hand a Jersey herd in which the progeny, fed on the milk of their
reacting dams, became tuberculous without exception, and in the years
following, those fed on the milk of the same reacting cows after it had
been kept at 180° F. for half an hour all grew up healthy.
Under this method, inasmuch as the infection is not at once
extinguished, but temporized with for the benefit of the stock owner,
State indemnities are not necessarily called for. Yet the State can
profitably test the cattle at public expense, mark indelibly those that
react, schedule them and control them, so that they will not be allowed
to change hands nor to mingle with sound animals until finally
butchered, dead or recovered. The State should see to the thoroughness
of the seclusion, disinfection, the safe disposal of all products from
milk to manure, and the testing at intervals of three or six months of
both cows and calves.
_Raising Healthy Offspring Without Sterilizing the Milk._ In the
northwest territories cows and heifers that have reacted to tuberculin,
but which otherwise appear to be in good health, are made into a herd by
themselves and placed on a special range apart from all other cattle.
They live in the open air, slight shelter being allowed in winter only,
and their calves are allowed to suck the dams until winter. The wide
range, the open air life, and the early destruction by oxygen and
sunshine of the discharged bacilli, tend in the main to ward off
infection, except such as comes in the milk, and the majority of the
calves grow up in apparent health and are fattened for market. A small
minority are born tuberculous or contract the infection from the milk,
but this does not seriously impair the financial success, and living in
the open air they bring little danger to others. The loss is
infinitesimal as compared with the expense of milking a large herd,
sterilizing the milk and feeding it by hand. Advanced cases, with
objective symptoms, should always be removed, and the cows may be tested
at intervals if compatible with profit. The seclusion of the herd should
be complete, by distance, by the configuration of the country, or by
fence.
For this system the climate of our Southern States, where stock can
remain out of doors all the year, offers a better field than the
semi-arctic northwest.
_Removal of all Unthrifty Animals and Those Showing Physical Symptoms of
Tuberculosis._ Before the days of tuberculin testing I succeeded in
extinguishing tuberculosis in several herds by the prompt removal of all
unthrifty animals and such as showed objective symptoms of tuberculosis,
the disinfection of the buildings, the restocking from sound herds, and
the strict separation of the new stock from the old. In one herd of 200
this entailed the final destruction of the whole original herd; in
others the destruction was in the main limited to particular
(susceptible) families. But in these days, with the tuberculin test
available, a resort to a method of this kind would produce an
unnecessarily slow, uncertain and expensive result.
_Removal of Animals Showing Objective Symptoms or Reaction under
Tuberculin._ The Bang (Danish) method is the chief example of this, and
is so considerate of both state outlay and stock owner’s interests that
it is deserving of high praise. Under it the State usually waits for the
stock owner to take the initiative, but to encourage applications from
the owners, it furnishes tuberculin testing without expense, and even
allows a small indemnity for animals killed because of advanced
tuberculosis. In return for this the stock owner agrees to furnish
separate buildings (or enclosures), yards and pasturages, new or, when
necessary, disinfected, one set for the high conditioned, nonreacting,
healthy herd, and a second for the animals that reacted but which show
no further sign of tuberculosis, with separate attendants, utensils and
other appointments for each. This reacting herd is furnished with the
best of food, air, accommodation and hygiene generally, and the milk is
sterilized before it is allowed to pass into consumption by man or for
calves or pigs or for the production of butter. The quarantined herd is
marked, registered, and kept under government surveillance; it cannot be
parted with for stock uses, but it is at the disposal of the owner to
keep it for milk, or fatten at once for the butcher. Finally every
member of this herd is slaughtered under government inspection, and the
beef put on the market or sent to the rendering works as may be decided.
The system secures the hearty coöperation of dairyman, dealer and
government, and while it comes short of the speed and efficiency of a
generally applied method of extinction, it is accomplishing a great work
for Denmark, putting an immediate stop to the advance of the disease in
the worst infected herds, and placing the latent cases of such herds in
a safe seclusion for the rest of their lives. At first the tested herds
showed 40 per cent. affected; now less than 20 per cent.
The feature which would be likely to work the least satisfactorily in
the United States, is the disposal of the sterilized milk as such. It is
to be feared that this milk would find but a poor market with us, and if
it proved unsalable, the preservation of the reacting herd would be no
longer an economic success.
In Pennsylvania where practically the same method is in force, leaving
it in the option of the owner to keep the reacting latent cases and
sterilize their milk, or to abandon them to the State, have them
appraised and slaughtered with indemnity, the uniform practice has been
to accept the latter alternative. Not a single owner, I believe, has
elected to keep a herd in quarantine and sell the milk sterilized. The
result has been that four times the number of applications come in that
the appropriation will warrant the officials to take in hand.
A special feature of the Pennsylvania method is the provision that a
stockowner can have his herd examined, and tested with tuberculin, at
his expense, the State to furnish a certificate setting forth the
condition of the animals. In case of infection, the owner has the option
of abandoning the reacting ones to the State, to be secluded, or
appraised and slaughtered, he meanwhile guaranteeing that he shall
introduce no new animals into the herd except by tuberculin test under
the direction of the State Board.
The usual provision is in force that no indemnity is allowed for any
animal that entered the state not more than three months before, and
without the tuberculin test demanded of all such stock animals.
Indemnities are restricted to $25 per head and under for non-registered
animals and grades, and $50 for registered thoroughbreds. The average
appraised price has been $23.
On the whole an excellent work is being done in Pennsylvania, and herds
now tested are found to contain not more than half as many infected
animals as did those tested a few years ago. A better showing would
doubtless have been made if the State appropriation had permitted the
board to give attention to all applications made.
The good results may be attributed to the adoption of a system which
secured the confidence and trust of the stockowner: he sees that the
State has no desire to oppress nor injure him; he is in no dread of a
high-handed confiscation of his remunerative property without indemnity;
while advanced cases are destroyed he is left the option of segregating
his latent cases and marketing their products under the precaution of
sterilization; he can raise the progeny of these animals if he will,
under similar precautions; he can sell his stock and its product under
government certificate if they prove sound; he can avail of government
assistance in protecting his herd against reinfection, by the testing of
animals to be purchased. Under such a system there is no object in
secreting infection, and in underhanded sale of tuberculous animals,
with the spread of the disease into new centres. Even the tardy or
inimical stockowner is roused to action by public opinion, when he finds
the market for his suspected product growing more and more uncertain,
and feels the daily encreasing pressure of opinion among neighboring
owners, that he is exceeding his rights in maintaining an infected herd
in the very midst of their purified ones.
A most important item of the system of Pennsylvania, and of sixteen
other states, is the compulsory testing of all stock cattle introduced
into the State. This has the further support of the Federal Government
which demands a tuberculin test of every stock bovine animal imported
into the United States. This is a natural corollary of every attempt to
restrict or extirpate tuberculosis from a State, but when through
willful blindness a great State like New York, repudiates a measure of
this kind, it but makes its dairy and breeding herds the depository of
the reacting animals that other states wisely exclude. The sifting
process goes on at Buffalo and other centres and the New York herds are
loaded with the rejected, diseased animals. Under the operation of this,
and the denial of indemnity for animals slaughtered, it will be
wonderful, if the New York stock owner is not soon roused up from his
idle dream of fancied security, by a great extension of the infection.
_Generally Applicable Measures._ Under any system many special rules
will be demanded in individual cases, which it will require the skill of
the expert sanitarian to apply, and which cannot be referred to here.
The following are generally applicable whether by the owner in his
particular herd, or by the State or other authority dealing with the
subject.
1st. On discovery of a case of tuberculosis, test the whole herd with
tuberculin. (See Tuberculin Testing.)
2d. Remove all animals that show a typical reaction.
3d. Destroy and burn, boil or deeply bury all cases of the disease,
unless it is decided to form an isolated herd of latent cases which are
in good condition and apparent good health.
4th. In case of doubt or disturbing influence which may have caused rise
of temperature (calving, heat, exposure, concurrent disease, changes in
management, etc.), keep the suspected animal apart for four weeks and
test again.
5th. Repeat the test every six months, and if two successive tests show
no indication of tuberculosis, the herd may be accounted sound.
6th. As soon as tuberculous animals have been removed from a stable, let
it be vacated and thoroughly disinfected with chloride of lime, 4 ozs.
to 1 gallon of water, and enough quick lime to make a good whitewash
which will show if even a square inch is missed. When chloride of lime
is objectionable because of its tainting the milk, use mercuric chloride
1 dr. to 1 gallon water, with enough sal ammoniac to make it freely
soluble. The roof, walls, and especially the floor, gutter and feeding
trough must be first thoroughly scraped, washed and cleaned, all rotten
wood work must be removed, and, in case of double boarded walls, the
boards must be removed on one side to permit of a thorough application.
Utensils should be scalded and dressed with carbolic acid, 1:20. A
stable incapable of disinfection should be abandoned for a length of
time or burned.
7th. In making new purchases, avoid any herd in which tuberculosis has
appeared, or that has had sickness or deaths in recent years.
8th. Do not purchase from city, suburban nor swill stables.
9th. Do not take a cow that is in ill health or low condition,
especially one with cough, nasal discharge, foul breath, wheezing
breathing, hard nodules under the skin, diseased udder, swollen bones or
joints, or a tendency to scour or bloat.
10th. Test every animal with tuberculin before admitting it into the
herd.
11th. Do not admit strange cattle to house, field or yard. Keep apart
from the herd until tested.
12th. Keep each animal strictly to its own stall and manger.
13th. Board up between the stalls in front so that no two cows can feed
from the same manger.
14th. Be especially watchful of the older cows and on the slightest sign
of ill health, separate and subject to the tuberculin test.
15th. In case a herd of cattle is found to be tuberculous, subject to
the tuberculin test all domestic animals that have mingled with them
freely and fed from the same troughs. Remove those that show a reaction.
16th. Exterminate the vermin (rats, mice, sparrows) in a building where
tuberculosis has prevailed.
17th. Let no consumptive person attend on cattle nor prepare their food.
HYGIENE OF MILK AND MEAT. SANITARY POLICE MEASURES.
This has a reference to both man and beast and involves measures of
private and public hygiene alike. In man, as we have seen, milk is the
source of greatest danger, being habitually taken uncooked, whereas meat
has been usually subjected to a high temperature before it comes to the
table.
_Milk._ The unsterilized milk of the tuberculous cow must always be
regarded with grave suspicion. Especially is the drinking of milk warm
from the cow to be strongly condemned. The feeding experiments of
Vilemin, Gerlach and others, in 1866 to 1869, demonstrated the virulence
on the lower animals of the milk of infected cows, and many accidental
infections have shown the same for man. (See relation of the bacillus of
man to that of animals). This conceded, the question arose as to the
virulence of milk drawn from the sound udders of tuberculous cows. Many
experiments of Nocard, Galtier, McFadyean and others seemed to decide
against such infection. Others have had a different experience, and
especially when the test was made by inoculation. Ernst found tubercle
in 30 per cent. of the cows he examined, though no affection of the
udder could be made out. Theobald Smith, Hirschberger, Bang and others
found tubercle bacilli in milk from sound udders. Pearson, injecting the
milk from sound udders intraperitoneally into Guinea pigs had ten in
sixty-three affected. Rabinowitsch and Kemper found tubercle bacilli in
ten out of fifteen cows with sound udders. While it must be allowed that
often a very small proportion of tuberculous cows with sound udders pass
the bacilli in the milk yet a sufficient number of exceptions are found
to deter one from endorsing such milk as safe. Much more is this
conclusion justified by the consideration that commencing mammary
tuberculosis is in many cases unrecognizable by ordinary examination
intravitam or post mortem. Again when the bacilli are circulating in the
blood (generalized tuberculosis) they can escape from such a vascular
tissue as the mamma without the formation of a local lesion, as they can
pass through the intestinal walls or lungs and colonize the adjacent
lymph glands. Nocard’s injections of the bacilli into the veins seem to
show that they disappear from the blood in 4 to 6 days, but with a
generalization of the infection from within, the presumption is against
a single isolated entrance of bacilli, and in favor of a continuous
introduction. In such generalization therefore the bacilli circulate in
all vascular tissues, and are liable to escape with any normal
secretion, but especially with the milk or urine on account of the great
vascularity of the glands.
When the udder is itself tuberculous the case is incomparably worse. The
milk can scarcely fail to be infecting, and the bacilli, grown in these
highly vascular tissues, apart from the air, are usually of a very
virulent type. Of these Martin writes in the report of the Royal
Commission (England): “The milk of cows with tuberculosis of the udder
possesses a virulence which can only be described as extraordinary. All
animals inoculated showed tuberculosis in its most rapid form.” Woodhead
is equally positive in this position. Galtier says “we should absolutely
avoid the consumption of milk from cows in which the udder is
tuberculous, and boil before using, the milk of all cows affected with,
or suspected of tuberculosis in any form.” Finally we should never
consume without boiling, milk of which we do not certainly know the
origin, and especially in cities, we ought not to omit this precaution
in the case of milk furnished by milkmen.” Rabinowitsch and Kemper add:
“Milk from cows that react to tuberculin must be suspected of being
tuberculous in every case.”
It may well be allowed that the mixed milk from a large dairy,
containing but one or two tuberculous cows, is much less infecting than
that of the tubercular cow herself, and that skim milk that has been
passed through the separator has been robbed of many bacilli which have
been precipitated in the albuminoid material that collects on the inner
side of the bowl. But these mean dilution not purification: they reduce
the danger but do not altogether remove it, and sanitary police should
aim at sterilization in every case where available.
_Butter_, _cheese_, _whey_, and other dairy products have been proved
virulent in different cases (Galtier, Heim, Lasar, Bang, Obermüller,
Roth, Groëning, Gasperimi, Petri, Rabinowitsch). This was true for
butter 120 days old, and cheese 330 days. In a number of cases
Rabinowitsch found a bacillus, similar to the tubercle bacillus and
producing tubercle-like lesions, but differing in its staining,
morphology and culture, and she supposed that other observers had
mistaken this for the tubercle bacillus. Petri, Morgenroth and Hormann,
found the bacillus of Rabinowitsch in company with the real tubercle
bacillus in butter, and Rabinowitsch, later, in fifteen samples of
butter found the bacillus tuberculosis in two.
Bacilli coming from the mouth, bowels, or lungs, are also liable to get
into the milk, through the floating dust of the stable, or from the
teats, udder, tail, etc., (Gaffky).
_Oleomargarine_ cannot be considered as free from this indictment, for
though the tuberculous glands, etc., from the mesentery, may be
sterilized in the preliminary heating process, yet the subsequent mixing
with milk is liable to convey the infection.
The ideal course with milk, if the herds cannot be purified from
tuberculosis, would be to compulsorily remove from the herd every cow
that shows objective symptoms of tuberculosis, or any internal disease
of the udder, and to subject all the milk of the remainder to
Pasteurization at a temperature of 155° F. for twenty to thirty minutes.
This, however, requires skilled and faithful management to avoid renewed
contamination from the lips of the vessel which may have escaped the
heat, or from hands, vessels and objects that were in contact with the
milk before. The boiling temperature for fifteen minutes would be a
safer resort, as requiring less careful handling, yet even this may be
contaminated afterward under poor management. It has the further
drawback of the boiled milk taste and the coagulation of the albumen.
But the outlay for such careful sterilization will soon amount to more
than will the tuberculin test.
_Meat._ For various reasons meat must be held less virulent than milk,
but mainly because it is less frequently the seat of tubercle than the
udder, and because it is usually cooked before being eaten. The muscular
tissue of the ox appears to be unfavorable to colonization by the
bacillus, and although the intermuscular lymph glands do not partake of
this inherent resistance, yet as the glands are very frequently affected
from the tissues which they drain, they necessarily partake in some
degree of the comparative immunity of the muscles. This immunity is,
however, far from complete, as the frequent implication of the
intermuscular glands (prescapular, axillary, prefemoral, etc.),
sufficiently show. Again in estimating the virulence of meat we must
never forget that in the great majority of cases, in ordinary infected
herds, the tubercle is still essentially local; no generalization has
taken place. The muscle is vascular throughout, and in cases of
generalized tuberculosis is infecting, yet a single transient escape of
tubercle bacilli into the blood does not ensure permanent infection of
that fluid, which can usually purify itself in six days or less
(Nocard). On the contrary, when the escape of bacilli into the blood is
constant, so becomes of necessity the virulence of the blood and a rapid
generalization ensues. Such continuous escape may occur in actively
advancing tuberculosis at any point, but it is more certain if the
degenerating tubercle has opened through the walls of the vessels
(capillaries), so that the infecting bacilli can pass into the blood in
a continuous stream. The pus and other microbes, in complex infections,
hasten this degeneration and contribute to generalization of the
tubercle and emaciation. The transient infection of the blood with the
pure tubercle bacillus does not, however, lead to emaciation and
marasmus, and hence the frequency of high condition in spite of
extensive tuberculosis.
Ostertag gives the following as indicating blood infection: “When with
emaciation there is evidence of recent blood infection, enlargement of
spleen and all lymph glands, miliary tubercles of the lungs, liver,
spleen and kidneys.” In the absence of these indications, though there
may be numerous old standing tubercles, caseated, calcified or
sclerosed, he considers that there is no reason to dread infection of
the blood and carcass. Even a tuberculous intermuscular gland does not,
in his opinion, condemn the adjacent muscle. When vomicæ (caverns) are
present in the lungs and internal organs the flesh may still be used “if
embolic tubercles of different ages, indicating repeated eruptions of
tubercle bacilli into the blood stream are absent from the spleen and
kidneys.” This meat is, however, to be sterilized before marketing
(Ostertag).
The United States Bureau of Animal Industry orders the destruction of
all cases of “extensive or generalized tuberculosis;” “any disease or
injury causing elevation of temperature or affecting the system of the
animal to a degree which would make the flesh unfit for human food;”
also “any organ or part of a carcass which is * * * affected by
tuberculosis * *.”
In most countries of Europe even emaciated animals are used for food for
animals or even man, provided the wasting is not too extreme. The
carcass must, however, first be subjected to a temperature of 230° F.
for a period of three hours. This is sold in a special market as low
priced meat and labelled as such. Ordinary cooking does not always
sterilize, as Martin and Woodhead, like Vilemin, found living bacilli in
the centre of a cooked six-pound roast.
TREMBLING IN SHEEP. LOUPING-ILL. INFECTIVE MYELO-MENINGITIS. IXODIC
TOXÆMIA.
Definition: infective, tick-borne disease, characterized by
meningo-myelitis. Animals susceptible: sheep, and possibly swine
(Meek, Greig-Smith) and cattle (Williams). Known in North Britain only
in spring (in Skye also in autumn), on rough pasture with much brush,
and wood ticks, (Ixodes ricinus, erinaceous, marginatus or other).
Experimental infection. Bacteriology: Bacterium fluorescens β and γ
found in exudate and infecting. Accessory causes: dried grass of
previous year, brush, low condition, cold, youth. Symptoms: incubation
10 to 30 days; impaired innervation, hyperæsthesia, timidity,
excitability, trembling, jerking, lack of coördination and balance,
falling, convulsive struggling, jumping, rolling of eyes, stiffness,
opisthotonos, paresis, paralysis of hind—later of fore limbs, apathy.
Wry neck, arched back, stiff joints. Diagnosis from _myelo-meningitis_
by its enzoötic appearance, in spring, on tick infested ground: from
_paralytic rabies_, also by absence of that disease locally; from
_tetanus_ by its general prevalence, the absence of tonic spasm, and
presence of palsy; from _braxy_ by the lack of emphysematous
swellings, and of speedy sepsis; from _anthrax_ by usually healthy
spleen and its confinement to sheep. Lesions: cerebral meningitis with
encrease of subarachnoid fluid, of myelon, reddened, softened, also of
other serosæ, stomach, bowels, liver and kidneys. Prevention: destroy
ticks in winter by burning grass and brush, by ploughing and cropping;
or fence off ½ the pasture one year and the other half next; or lime
soil; or dip repeatedly in April, May and June to keep off ticks;
avoid moving sheep in these months: Give liberal feeding. Mortality 10
to 20 per cent.
_Definition._ All infective disease of sheep, inoculated by ticks, and
producing a meningo-myelitis, with drowsiness, hyperæsthesia,
irritability, paresis and other nervous disorders.
_Animals susceptible._ This is almost exclusively a disease of sheep,
yet Meek and Greig-Smith claim to have seen it in swine that have eaten
the raw carcasses of _louping-ill_ sheep, or that have ranged the tick
infested pastures, and in rabbits inoculated with the microbe from the
wound caused by the tick. W. Williams claims to have seen well marked
cases in cattle, and heard of cases in horses and swine. He speaks,
however, rather obscurely of “_the tick disease_” and seemingly includes
in this all affections inoculated by ticks.
_Geographical Distribution._ This disease has been hitherto described as
existing in the northern part of Great Britain only, but given the
presence of the tick, and of the infection which it carries and the
malady might easily be extended indefinitely. It is known to prevail in
Northumberland north of the Tyne, in Kirkcudbright, Dumfries, Ayrshire,
Lanark, Peebles, Roxburgh, Berwick, Argyle, Inverness, and Ross. In
Berwick it is less prevalent than in the other countries named, while in
the Western Isles it is not only widely spread rising on the hills 2000
feet or as high as the sheep range, but in Skye there are two distinct
outbreaks, in spring and autumn respectively, apparently coinciding with
the appearance of two successive generations of ticks. This may be due
to the prevalence of warm winds from the Gulf Stream. Further
investigation will doubtless show a much wider distribution—the author
has seen an affection bearing the same general characters on the spurs
of the Lammermoors in East Lothian, and the supposed adaptation of the
Norse word _hloupa_ (staggering) suggests that it is probably not
unknown in Scandinavia. W. Williams notes its prevalence on the Silurian
formation, but ticks confine themselves to no geologic stratum, and the
tick is the main agent in carrying infection.
_Causes. 1st, Sheep Ticks._ The sheep tick is not the _ked_ (Melophagus
ovinus) which is common on long wooled sheep everywhere and is an
example of a wingless, degraded dipterous insect.
The sheep ticks, on the other hand, are true ixodes, and of the same
family with our common wood tick and of the cattle tick (boöphilus
bovis) of the Southern States and the West Indies. The ticks collected
from the sheep by W. Williams were identified by Mr. Moore, of the
British Museum, as ixodes ricinus, ixodes erinaceous and ixodes
marginatus. Those obtained by Meek and Greig-Smith showed the following
characters: The male is 2.48 mm. long, by 1.30 mm. broad; the female is
5 to 5.5 mm. long, by 3 mm. broad, or when gorged with blood, 10 mm.
long, by 7 mm. broad. The fasting female is yellowish green, and when
full of blood, blue. Following the rule of their genus, the mature tick
has eight legs, the larva but six. The fasting larva has head, legs and
dorsal plate (scutellum) brown, the remainder of the body yellow.
Scattered hairs appear on the body, legs and maxillæ.
In all ticks the rostrum is a characteristic feature. It consists
centrally and interiorly of a dart covered below and on each side by
rows of teeth turned backward, which, when imbedded in the skin, hold so
firmly that the parasite may be pulled in two in any attempt to pull it
out. Above this dart and on the two sides lie the cheliferæ (horns),
each furnished with three or four teeth turned outwardly and more or
less recurved, by which the dart is worked into the skin. Finally, on
the lateral sides of this central apparatus, are the two maxillary
palpi, which are not inserted into the skin, but applied against it and
operate as feelers prior to and during the insertion of the dart and
cheliferæ. The maxillary palpi are club-shaped and soft.
Ticks pass through three moultings before they attain to the sexually
mature eight-legged form, and though the hexapod larvæ attach themselves
to animals and irritate the skin by their bites, it is only the mature,
impregnated egg-bearing female that lives exclusively on blood and sucks
this to excess.
While given species of ticks show a preference for particular genera of
animals, yet ticks generally in their vagabond life will leave the long
grass and brush where they have been hatched to become temporarily the
guests of any passing animal. It is, therefore, premature to seek to
identify any single species of tick as the only bearer of the infection,
and it is quite possible that any one of several species may contribute
to its propagation.
_Experimental Infection by the Tick._ W. Williams muzzled four sheep
from a healthy district and turned them for several hours a day on a
tick-infested field, and two sickened—one on the eighth day and one on
the sixteenth. Twelve ticks sent out of the district and put on a
healthy sheep caused illness on the tenth day. In a second experiment
with ten sheep, during a colder spring, when there were fewer ticks, no
deaths occurred.
Meek and Greig-Smith turned twenty sheep on a tick-infested louping-ill
pasture, six of the number wearing muzzles to prevent grazing, seven
having been dressed with a mixture of sweet oil, 2 quarts; castor oil, 1
quart; train oil, 1 quart; pitch oil, 3 gills, and cade oil, 1 gill,
while the remaining seven were unmuzzled and undressed. The muzzled
sheep were regularly taken out and fed on food from a healthy locality.
At the end of a fortnight oils were reapplied on the second lot (seven
sheep). No ticks appeared on these sheep, while many were found on the
undressed ones. On the fifteenth one of the unmuzzled and untreated
sheep sickened and died with lesions of louping-ill. On the
twenty-second day one of the muzzled sheep sickened, and died of
louping-ill next morning. On the thirty-first day another of the muzzled
sheep took ill and on the thirty-eighth was killed. It showed
characteristic symptoms and lesions. The seven salved sheep, on which no
ticks could at any time be found, remained healthy throughout.
_Bacteriology._ W. Williams describes a bacillus which he figures as
forming filaments of very uneven breadth, with frequent branching
(contrary to the habit of bacilli), and forming spores in clusters.
These were obtained from the coagulum of the cerebro-spinal fluid and
Meek and Greig-Smith conclude that the alleged mycelium was but the
filaments of fibrin.
McFadyean found pus microbes.
Meek and Greig-Smith (Veterinarian, 1896–7) found in the black bloody
swellings under the skin, where the ticks had inserted their
proboscides, a variety of microbes which in pure cultures did not
provoke louping-ill. These included staphylococcus cereus albus, sarcina
lutea, bacterium putridum, bacterium coli commune, micrococcus
sulphurous, micrococcus bicolor, and micrococcus caudicans. He also
found penicillium glaucum. Two organisms allied to the bacterium
fluorescens and designated as β and γ (G) respectively, were found in
these sores and produced in rabbits and sheep nervous disorders and
lesions which could be fairly identified with louping-ill. These are
about 1.5 to 1.7μ long by 0.7μ broad, and chromogenic with a special
fluorescent appearance. Microbe β inoculated on a rabbit caused on the
second day rhythmic movements of the head downward and to one side, the
eyelids closing as the head dropped, as if the animal were constantly
falling asleep. In another rabbit it caused stiffness of the legs only
and in a third it had no effect. Microbe γ when cultivated ærobically
was harmless to rabbits, but when grown anærobically on mutton bouillon
to which a drop of blood had been added, it caused on the second day
general paralysis of the neck and limbs, spasmodic twitching of the
muscles, dyspnœa and feeble heart action. Two rabbits which survived the
early effects developed large axillary and inguinal abscesses four
months later.
A lamb inoculated with the bouillon culture of γ showed after thirteen
days, lameness of one hind limb, with paresis, and a disposition to fall
to one side or the other. Two months later, when it had greatly
improved, a second inoculation of microbe γ grown anærobically in
bouillon and blood, caused, on the third day, a severe aggravation of
the lameness.
_Accessory Causes._ Much depends on the abundance of old dried grasses
of the previous year in which the larval ticks may hibernate. Land that
has been burnt over in winter, that is cleared of brush, or in which the
aftermath has been killed by free salting or liming will be largely
cleared of the ticks.
Whatever disturbs or undermines the general health lays the system open
to the disease and many flockmasters in tick-infested districts have
succeeded in greatly reducing the mortality by feeding sound hay and
oats in winter. Sudden changes of weather have long been noticed to
coincide with outbreaks of the disease. A change to cold and wet is
especially dangerous as causing a chill and robbing the system of its
tone and vigor. But a sudden access of warm spring weather, especially
if at the same time moist, may have a decidedly predisposing effect by
lowering the general tone. A fatal paresis common in the flocks of New
York, in the absence of ticks, shows a similar tendency to select the
atonic animal. This occurs mainly in spring, when the sheep have been
shut up in close confinement for weeks or months, with flaccid muscles
and fatty livers, and above all if they are in advanced pregnancy with
twin lambs, and if their fleeces are extra heavy. In both affections the
majority of the flock escape, while those that are specially predisposed
succumb. Lambs suffer most, doubtless because of relative weakness, and
on account of their innate and unexhausted susceptibility.
_Symptoms._ After an incubation varying from ten days to thirty some
impairment or disorder of the innervation is shown, varying widely,
however, in different cases.
The two names “trembling” and “louping-ill” long used by shepherds as
characteristic of the disease indicate spasmodic disorder of a clonic
kind, the paresis which is essentially passive having been very
naturally overlooked, or held to be subordinate. There is hyperthermia
the temperature rising at times to 105° or higher, and often marked
hyperæsthesia and excitability at the outset. On approaching the patient
it is very much frightened, and when caught, struggles and twitches in a
remarkable manner or trembles violently. If merely raised or disturbed
the trembling or clonic spasms are very marked, the nose is jerked
forward and upward from the contraction of the muscles attached to the
occiput; the legs may be lifted jerkingly as in stringhalt; when raised
they are moved stiffly or sway uncertainly before the foot is once more
planted; or the sheep loses its balance, falls to the ground and
struggles convulsively in its efforts to get up and escape. As the
result, it will in certain cases jump to its feet, rising meanwhile to
an undue height in the air. In other cases there is squinting or rolling
of the eyes, and movements of the jaws with frothing from the mouth. Or
the spasms may be tonic affecting especially the muscles of the back and
loins, and causing extreme stiffness or rigidity or even opisthotonos.
Lambs are unable to suck.
But whether the early spastic symptoms are well marked or not, paresis
and even paralysis set in sooner or later. This usually begins as
paraplegia, or exceptionally one limb only may be affected at first,
causing the animal to walk on three legs. For a time the fore limbs may
be free, and the patient attempts to move by dragging the hind limbs,
which are extended backward. When the fore limbs become involved the
animal remains down helpless and after awhile apathetic. Temperature and
sensibility are both greatly lowered in the paralyzed limbs. Sometimes
the spasms are lateral and the head may be drawn to one side.
In the animals that survive the early attack, there is likely to remain
some lasting deformity, such as wry neck, arched back, stiff or swollen
joints. Abscesses, which appeared in the inoculated rabbits after a
lapse of four months, are a not uncommon sequel in sheep, the pus
collecting in the neighborhood of a joint, or of the lymph glands of the
axilla, inguinal region, breast or shoulder.
The succession of symptoms are in the main such as are observed in other
cases of myelo-meningitis, first exalted function and later depressed
and abolished.
_Diagnosis._ From other forms of myelo-meningitis it may be
distinguished by its enzoötic occurrence on tick-infested pastures,
which already have a reputation for causing this malady, by its
appearance only in the season of the development of the tick, by the
presence of the tick or of its sores on the skin, and by its entire
absence from adjacent fields which are free from ticks. From paralytic
rabies it is differentiated by the same conditions, and as a rule by the
absence of rabies from the district and of any evidence of a bite. In
tetanus the tonic persistent nature of the spasms, the absence of
paralysis, the marked spasms of the muscles of the eye, and the usually
isolated condition of the case should prevent any confusion. Braxy is to
be distinguished by its emphysematous swellings near the surface of the
body, and by the comparative absence of hyperæsthesia, spasm, or
paralysis. The carcass in braxy undergoes much more rapid decomposition.
Anthrax is more rapidly fatal, shows no such marked nervous disorder,
has a dark, nonoxygenated and often incoagulable blood, an enlarged
sanguineous spleen, and the characteristic anthrax bacilli. It attacks
the larger herbivora as readily as the small.
_Lesions._ The most constant and striking lesions are found in the nerve
centres. In many cases there have been found cerebral meningitis,
involving the choroid plexus (Fair, Hamilton, Klein, Murray, McFadyean)
with an encrease of the ventricular and subarachnoid fluid (Murray,
Hamilton, Williams). The exudate may be yellow or rosy from contained
blood globules (Klein). The meninges are thickened and the seat of
ramified redness. In the region of the spine inflammation is found not
only in the meninges but also in the cord, which may be blood-stained,
softened (Mathewson, Goodwin, Robertson), or in older cases indurated
(Robertson, Hamilton, Williams, Young). In this last condition there is
a sclerotic condition of the neuroglia, and it may be a distinct
atrophy. The exudate is usually abundant and more or less coagulated
into a soft, diffluent jelly.
In many cases there is inflammation of the serous membranes of the chest
(pleura, pericardium, endocardium), and even of the lungs (Fair,
Hamilton, Klein). In some instances there has been inflammation of the
stomach and intestines (McFadyean), liver and kidneys (Klein), and
enlargement of the spleen has been noted. The most constant lesions
appear to be those of the nerve centres, but the wide variety of organs
involved in different cases sufficiently accounts for the variability of
symptoms.
_Prevention._ As the ticks are the chief media of infection, the disease
may be eradicated by their destruction. The burning of all withered
grass and brush during the winter months will do much in this direction.
Their destruction is rendered even more complete by ploughing and
putting the land under a series of cultivated crops. By this means not
only is the winter shelter of the tick removed, but the animal host
which it requires for its complete development is denied it, and it must
perish before the land is again seeded to grass. When the land is
unsuited to cultivation, the same end may be in some measure secured by
fencing off half the pasture, and leaving it unpastured for a season,
meanwhile burning the dry grass or temporarily suppressing it by a
liberal application of salt. The following year the pasture so treated
may be restored to pasturage, and the other half subjected to the same
course of treatment. In the absence of such thorough treatment, a
liberal application of lime to a virgin soil will often bring a growth
so fresh and appetizing that the stock keeps it closely cropped and thus
removes the shelter for the offensive ticks. Finally, the ticks may be
prevented from attacking the animals, by repeated use during April, May
and June of a dip in which tar oil, cade oil, heavy petroleum or other
odorous insecticide forms a component part (see the dip of Meek and
Greig-Smith).
A very obvious precaution is to avoid the movement of sheep during
April, May and June, from tick-infested pastures to others which furnish
rank grass, brush or other suitable shelter for the preservation of the
parasite.
It has been noticed that sheep indigenous to the tick-infested and
louping-ill pastures are less susceptible than those that have been
introduced from outside, but, as yet, no attempt appears to have been
made to secure immunity by the use of sterilized products of the
microbe, nor therapy by the resort to antitoxin. A liberal and tonic
diet is an important element in prevention. Grain and hay should
therefore be allowed whenever necessary to bring the sheep to early
summer in good condition.
_Treatment_ can hardly be said to have been attempted, though mild cases
are allowed by the shepherds to recover. According to Meek, the deaths
often average 10 to 20 per cent. of the flock.
BRAXY, BRADSOT, GASTRO-MYCOSIS OVIS.
Definition: Acute, infectious, bacteridian disease of sheep, with
colic, enteritis, emphysematous swellings, dark, diffluent blood, and
after death rapid putrefaction. Geographical distribution: Iceland,
Norway, Faroe Islands, Scotland. Causes: inclement weather, exposed
localities, low condition, winter food, chill, frosted grass.
Bacteriology: Bacillus gastromycosis ovis: 2 to 6 μ by 1 μ, in pairs
or filaments, sporogenous, polar staining, anærobic liquefying,
gasogenic, found in the gastro-intestinal congested mucosa, serosa,
liver, kidneys, blood. Pure cultures by boiling five minutes.
Pathogenic to sheep, Guinea pig, mice, pigeons, hens and less
certainly rabbits. Symptoms: resemble blackquarter, sudden, rapid,
fatal, back arched, stiff hind parts, crepitating swellings on hind
parts or elsewhere, colics, tympany, anorexia, pulse and breathing
hurried, separation from flock, lying, drooping head, ears and eyelid.
Usually found dead in morning when apparently well previous night.
Lesions: early putrefaction, slight, transient rigor mortis, tympany,
fœtor, sero-sanguineous exudates under skin, on fourth stomach and
bowels, and elsewhere. Contents of large intestine dry, hard.
Effusions in serosa. Spleen enlarged or not. Liver and kidneys
congested, softened, small, pale necrotic areas containing bacillus.
Prevention: drainage and cultivation, winter feeding, abandon infected
pastures in late fall and winter as pasture for young, avoid
overstocking, burn old fibrous heather. Immunization by sterilized
kidney extract. Treatment.
_Definition._ An acute infectious disease of sheep, manifested by sudden
attack, colicy pains, inflammatory and sero-hæmorrhagic lesions of the
bowels, and sanguino-emphysematous swellings occurring subcutaneously
and especially in the hind quarters. The blood is dark, tarry and
comparatively incoagulable and after death putrefaction advances with
extraordinary rapidity.
_Geographical Distribution._ Braxy is generally prevalent in Iceland
where it was described over a century ago (1778) by Ketilson as
“vinstrarfár” or “vinstrarplága” (“Omasum disease”). In Norway it
prevails on the whole Atlantic border to as far north apparently as the
sheep industry extends (Stavanger to Tromso Amt). The Faroe Islands are
said to be affected throughout. In Scotland it prevails like louping-ill
along the west coast especially, and embraces Caithness, Ross, Cromarty,
Banff, Inverness, Aberdeen, Argyle, Bute, Ayrshire, Lanark, Galloway,
Dumfries, Peebles, Selkirk and Roxburgh.
_Causes._ Like louping-ill this affection is associated with inclement
seasons, exposed localities, and insufficient or indigestible food, but
it differs in being an affection of autumn and winter rather than
spring. It is rarely seen in summer. At a time when it was looked upon
as an acute indigestion, its coincidence with hard frost or deep snow,
was explained on the basis that the victim had been driven to eat dry,
fibrous, indigestible grasses, brakens and heather. W. Williams who
formerly identified the disease with anthrax, seemed to go back to this
theory of indigestion. Though that is no longer tenable, yet it would be
wrong to ignore the effect of inclement weather and unwholesome food in
predisposing the animal system, and robbing it of the healthy tone which
would otherwise have successfully resisted the infection in many cases.
The occurrence of deaths after frosty mornings more than during mild
weather, suggests at once the chill effected in the animal, the chilling
of the paunch by the frosted grass eaten producing a subsequent
congestive reaction, and the known facility with which frozen vegetables
undergo rapid fermentation.
Cowan and Borthwick, (Transactions of Highland Society 1863) agree that
the disease is especially prevalent when the land has been overstocked
in summer, or when there has been a drought which withered up the
pastures, and later a free growth of green herbage from the autumn
rains. This they attribute to the “foul and unwholesome” character of
the autumn growth, but it suggests no less the low condition of the
sheep on the overstocked lands and the soft, aqueous character of the
herbage grown rapidly in a comparatively cold season. Cowan quotes cases
in which the lambs, weaned early and put in a separate pasture (hogg
hirsel), suffered a mortality of 50 per cent., while in later years when
allowed to remain with the ewes until winter, the deaths were reduced to
10 or 15 per cent. Here the more rugged health and vigor were manifestly
strong prophylactic factors.
Both Cowan and Borthwick incriminate the withered heather and the dry,
fibrous (“tathy”) and innutritious tufts of grass which make up a large
proportion of many hill pastures in autumn and winter.
Cowan strongly condemns heavy smearing with tar, which he believes to
encrease the mortality, by lowering the general tone of the system:
“Hoggs are very dull and listless for some time after being smeared with
tar, more especially if heavily smeared; ... when the skin is taken off,
every shed or opening in the wool where the tar has been laid on, is as
distinctly visible upon the flesh as the stripes upon a piece of printed
calico.”
It has been further alleged that the deaths are especially common during
the full of the moon, the usual explanation being that the sheep are
tempted to feed in the night and overload the stomach. It may be added
that at such times the grass is taken in a cold—(often frosted)
condition so as to chill the stomach and cause a congestive reaction,
and that short of this, under the night dews the microbian ferments are
moist and ready to start into full activity, while the herbage if it has
been partly frosted is particularly susceptible to bacteridian attack.
_Bacteriology of Braxy._ The essential cause of braxy was revealed by
Ivar Nielson in 1888, who demonstrated on the local lesions of the
alimentary canal and the capillaries of various internal organs a
bacillus which he named _bacillus gastromycosis ovis_. This is 2 to 6μ
long by 1μ broad, occurring in pairs or filaments. The organism has an
elliptical form and stains deeply at the extremities, while the central,
bulging portion fails to take the color, is highly refrangent, and
represents the spore. The non-spore-bearing bacilli are long, uniform
rods with rounded ends. The germ is anærobic, grows readily in serum
glycerine agar, and is gas producing and foul smelling. Liquefies
gelatine. It is found abundantly in the congested parts of the abomasum
and to a less extent in the bowels, in the mucosa, and in the submucous
and subserous tissues. It was also found in the blood and in the small
areas of degeneration in the liver and kidneys. Jensen obtained pure
cultures through the survival of the spores when impure cultures were
boiled for a few minutes.
_Animals Susceptible._ Inoculation of the cultures subcutem produces an
affection resembling malignant œdema, or braxy, in sheep, Guinea pigs,
mice, pigeons and hens, and less certainly in rabbits. Inoculation of a
calf had no deleterious effect, while a second succumbed in forty-eight
hours. In its pathogenesis this microbe appears to be more closely
allied to that of malignant œdema than that of black quarter, as the
latter attacks cattle very readily and has little effect on rabbits,
pigeons and chickens.
_Symptoms._ The more obvious manifestations of braxy bear a resemblance
to those of black quarter, so that the two affections have been often
confounded. In both the attack is sudden, the course rapid and fatal,
the back arched, the step short, especially with the hind limbs, and
there are swellings which crepitate on pressure on the hind quarters or
some other part of the body. Symptoms of colic soon appear, the sheep
lying down and rising frequently and moving the hind limbs uneasily, and
the abdomen becomes distended, tympanitic and tender. Rumination and
feeding are promptly suspended, and as a rule defecation as well. Urine
may be passed frequently in small amounts and of a high color. The pulse
is rapid and often irregular and the breathing hurried and labored. In
some cases the abdominal pain is less acute, the animal standing apart
with drooping head, ears and eyelids and frothy lips, or lying by itself
at a distance from the flock. Sooner or later emphysematous swellings
appear on some part of the body, but most commonly on the hind quarter,
which have a soft, doughy feeling and crackle or gurgle on pressure. In
the great majority of cases, however, the disease runs a rapid course
and ends in death in a few hours, and as the attacks are mostly in the
cold of the night, the victim, which appeared well at night, is found
dead in the morning. Cowan has often noticed that those that stepped
short at night were dead next morning. In certain cases the sheep stood
obstinately to the end and fell dead as if shot. When death was deferred
for several days a common result was shedding of the wool.
_Pathological Anatomy._ A marked feature of braxy is the early
putrefaction of the carcass. The rigor mortis quickly passes and the
carcass bloats up and exhales a putrid odor. On removing the skin one
sees extensive sero-sanguineous exudations, mixed with bubbles of gas of
an offensive odor. The abdomen is tense and tympanitic and the anus
protrudes. Visceral lesions are especially marked in the fourth stomach,
the walls of which are thickened in patches or throughout by a
hæmorrhagic or sero-hæmorrhagic exudation of a dark purplish color. If
killed in the early stages this may be very restricted in area, but
becomes general in animals that have died of the disease. Similar
exudations are found on the walls of the first three stomachs, or on the
small or large intestines. The fourth stomach and duodenum are, as a
rule, empty of food, though containing a sanguineous liquid. The
contents of the large intestines are usually dry and hard. Some serous
exudate is usually present in the peritoneum, pleura and pericardium.
The spleen may be normal or slightly enlarged. The liver is pale, soft
and friable. The kidneys may be congested and swollen and usually show
brownish areas of necrosis in which the bacillus is readily found. The
blood is dark, and though it may be coagulated, the clot is usually soft
and diffluent.
_Prevention._ Much may be done in the way of drainage and above all
cultivation and liming of the braxy pastures, and again laying them down
in grass. Cowan found that braxy diminished largely in ratio with the
improvement and cultivation of the soil. A rotation of crops and the
free æration of the soil tends to destroy an anærobic microbe or to
render it non-virulent. Winter feeding is another well attested source
of protection. Hay with turnips, oats, linseed cake or oil cake seems to
encrease the tone and vigor, and to counteract the fermentations in the
digestive organs which lay the system open to attack. Wholesome and
nutritious food then must be a main stay whenever the health threatens
to be undermined by insufficient or unwholesome pasture, by dried or
withered grass, ferns or heather, by the watery grass of recent and
rapid growth, by frosted and partially decayed herbage, or by pasture
exhausted by overstocking or drought.
Fields and hills known to be infecting must be abandoned especially in
late fall and winter and in the case of the younger and more susceptible
sheep. Understocking is always better than overstocking as the flock is
kept better nourished, stronger and with a greater measure of tolerance
and resistance. Upon land covered with old, fibrous, astringent heather,
burning is often of great value. The new growth of young heather is much
more digestible and nutritious, and destitute of injurious astringency,
and maintains a stronger and healthier flock.
Finally the question of _immunization_ arises. Nielsen attempted this
by drying and heating to sterilization the diseased kidney and
injected small quantities of this suspended in water. Sheep treated in
this way in Norway and Iceland have had a circumscribed inflammatory
swelling and afterward appeared to resist casual infection when placed
on the braxy fields. Jensen carried the experiment a step farther and
inoculated his artificially immunized sheep with 2½ cc. of a virulent
serum-gelatine-agar culture. It was rather unwell for half a day and
walked lame but soon recovered. A dose of ¹⁄₃₀ cc. of the same culture
killed in fifteen hours a larger sheep that had not been artificially
immunized.
_Treatment._ Though some cases of braxy recover yet the treatment of the
disease can hardly be seriously considered as yet. A disorder which is
so rapid in its progress, so early associated with such great and
rapidly extending lesions of the most vital organs, and which proves
fatal so early and almost invariably, leaves little room for a
successful treatment. In the milder cases, likely to recover of their
own accord, this may be hastened by the internal use of antiseptics and
purgatives, and perhaps even by antitoxic serum from the blood of an
immunized animal.
SOUTH AFRICAN HORSE SICKNESS. ŒDEMA MYCOSIS. DUNPAARDZIEKTE.
DIKKOPZIEKTE.
Definition: Geographical distribution: S. Africa; enzoötic or
epizoötic on damp soils; damp, humid atmosphere. Pathogenesis: horses,
and more mildly mules and asses, quagga; (cattle and goats?). Causes:
green forage, from rich, damp lands, eaten dewy; cut and fed with dew
on; dried in sun safe; so of horses stabled or corralled; in hot
summer only; inoculable; penicillium; cultures cause the disease;
debility. Forms: lung sickness—head sickness—blue tongue. Symptoms:
incubation 8 days. Fulminant form asphyxiates in an hour. Acute lung
form has rigor; remittent hyperthermia; prostration; dyspnœa;
cyanosis; serous nasal discharge; frothing; gurgling breathing; cough;
death in 3 or 4 days. Head œdema; general swelling and oozing of
serum. Blue tongue: great lingual swelling; cyanosis; coldness;
projection from mouth; salivation; stertor; asphyxia. Three forms
combined. Mortality. Lesions: serous exudate coagulates with heat or
blood; intermuscular exudates; whole head densely infiltrated;
excessive bloody pleural effusion; punctiform petechiæ; lungs pale,
yellow, great interlobular infiltration; or, if worked, hepatization;
dark, congested mucosæ; blood diffluent; heart pale; spleen enlarged,
blood-gorged; kidneys infiltrated; gastro-intestinal congestions;
cerebro-spinal effusion. Prevention: keep indoors during summer and
autumn; allow no fresh damp forage; or cut only after dew is off;
check rein or muzzle; pastured horses must be stabled at night or in
damp weather. Immunization: by protective inoculations; recovered
horse is re-inoculated until a high grade of resistance is secured and
his blood used to immunize.
_Definition._ An ectogenous, infective disease of solipeds in South
Africa, characterized by intense vascular congestions, destructive
changes in the blood and the profuse exudation of liquor sanguinis into
the tissues of the affected parts.
_Geographical Distribution._ The affection is not known out of South
Africa, where it has been observed since 1780. It appears yearly in
certain areas in the Transvaal, Orange River Colony, Natal, and adjacent
States, but only in certain years in Cape Colony and especially in its
southern portion. In certain years it makes wide extensions so that it
has appeared to become epizoötic instead of enzoötic. The habitual
enzoötic prevalence is in the areas that are relatively lower, damper
and richer than the surrounding country, where the vegetation is
luxuriant and the surface of the ground moist. Thus it is a disease of
low meadows, basins, river bottoms, drying marshes or ponds, and the
Boers have been in the habit of protecting their horses by sending them
to high, dry tablelands, from the first appearance of the disease until
the first frost. Yet elevation in itself is no protection, thus
Johannisburg, 6000 feet above the sea, is habitually ravaged and
Rhodesia loses 90 per cent. annually. A humid atmosphere, mist, or rain
with a high temperature are directly connected with the outbreaks.
_Animals susceptible._ Horses take the disease in its most fatal form.
Mules suffer like horses, while in asses the disease is relatively
somewhat more benign, and the virus after having passed through the ass,
has lost part of its potency. A disease of a similar nature is seen in
cattle and goats. The quagga is also alleged to suffer (Edington).
_Causes._ The disease has been traced to the green forage, grown in
damp, hot seasons on the rich moist bottom lands, in basins, gullies,
etc., and which has been consumed while damp with night dews or fog. Few
suffer that are only turned out to pasture after the sun has dried up
the dew, and that are shut in the stable or kraal before sunset. Coley
who witnessed a loss of 60 per cent. of the stabled horses at Eshowe,
Zululand, found that the deaths were among horses that had been allowed
to eat their fodder wet. The Guinea or Ubaaba grass and Indian corn were
cut at night and fed to the horses next day. The horses that ate this
wet from the bundles were attacked, while those that had it only after
it had been opened and dried in the sun escaped. Race horses that
receive no green fodder very rarely suffer. Horses that are corralled
(in kraal) at night escape.
The hot season is the season of greatest prevalence, the disease
beginning in November and proving especially fatal from the end of
December to the first of March. It appears in a modified form until May
when the first frosts appear.
Though the disease can be fatally inoculated by transferring the blood
from one horse to another, it is the rarest possible occurrence to have
it propagated in this way. It can be absolutely prevented therefore by
attention to the diet.
The real cause of _horse sickness_ is a mold having the general
characters of a penicillium, and which enters the system with the moist,
dewy food. Edington, who discovered this cryptogam, has found it in the
blood in all his necropsies of horses dying of horse sickness. Why this
should be no longer infecting when dried does not clearly appear. It has
been alleged that the disease has gradually extended to the higher
grounds which were formerly free from it, and the introduction of
diseased or infected horses has been advanced as the cause, but in the
unfenced state of the veldt and the former abundance of wild animals
this should have ensured such extension long ago, if it is really a
permanent one. The deadly prevalence of the malady in particular areas
in given years, and its entire absence from such localities in others
may explain the instances of apparent extension. The dryness and cold of
winter is the factor which usually extinguishes the poison in a given
district. We have as yet no absolute proof of a progressive
acclimatisation of the germ in a colder and drier region. Wittshire
observes that it will prevail on one side of a narrow river, while the
other at an equal elevation is practically free from it. There is no
mention of shade which might have explained such a difference in the
growth of cryptogams on the right and left banks.
Such limitations, together with the activity of the infection in damp
seasons, and during damp hours of the day, and its inactivity in dry air
and vegetation, would strongly suggest a microbe which is conveyed in
the body of some invertebrate, but this appears to be nonessential
because Edington has cultivated his mold in vitro and inoculated its
products on horses so as to secure immunity.
Debility doubtless renders an animal more susceptible, yet the disease
usually kills nearly all horses attacked, excepting such as have been
immunized. This is the same for casual and inoculated cases. When,
however, the virulence has been lessened by culture or by passing
through the body of an unsuitable animal the results are very uncertain;
some horses it will kill, while in others it produces a slight and
harmless fever.
_Forms._ Two leading forms of the disease are known: 1st, the _lung
sickness_ (_Dunpaardziekte_), and 2nd, the _head sickness_
(_Dikkopziekte_). A variety of this last is _blue tongue_ (Blautong),
which has been confounded with gloss-anthrax.
_Symptoms._ The _lung sickness_ may appear as a fulminant affection
following on the usual _incubation_ of about eight days. Suddenly, in
the midst of apparently full health and vigor, the breathing becomes
accelerated and dyspnœic; this encreases for about an hour, then the
patient staggers, falls, ejects a mass of white froth from mouth and
nostrils and dies. When death is more delayed, there may be noted a
rigor, and in the evening a rise of temperature to 103° F., lowering a
little next morning and rising again toward night, yet making an
encrease day by day until near the end, when it becomes subnormal. Death
in such cases occurs on the third or fourth day, preceded by great
prostration, hurried, labored breathing, dark red or cyanosed mucosæ,
loud rattling over the large bronchia or lower end of the trachea,
coughing and dropping of a serous fluid from the nose, or accumulation
of white froth around nostrils and mouth. The froth soon condenses in
part into a straw-colored liquid, which collects in considerable
quantity. The abundance of froth blocking the air passages produces
death by suffocation.
In the _head œdema_, the muzzle, lips, head and neck become the seat of
excessive exudation, the swelling of the face drawing back the lips so
as to expose the teeth of the lower jaw. The skin is rendered tense and
exudes the straw-colored serum, as do also the buccal and pituitary
mucosæ.
In _blue tongue_ the exudate is concentrated in the lingual organ, which
swells to an enormous size, forcing the jaws and lips apart, and hanging
out as a dark blue, cold mass. A foul, liquid mixture of saliva and
exudate drivels from the mouth. The pressure on the larynx may cause
marked stertor, advancing to asphyxia.
While these three types may seem to be distinct and uncomplicated in
some cases, more commonly the exudation appears to a slight extent in
all three situations, and it is only the predominance of the symptoms in
one particular part that assigns the attack to one type rather than
another. All are very fatal, but the lung sickness is preëminently so,
very few such surviving.
_Lesions._ There is usually a mass of white froth around the mouth and
nostrils. The serous exudate coagulates readily in the presence of
minute traces of blood, and forms a solid mass of clot when heated. A
yellow gelatinoid exudate is found in streaks or patches, subcutaneously
and between the muscles, but especially along the jugular furrow. In the
_head sickness_ the whole subcutaneous and intermuscular tissue in the
head and neck are infiltrated, and the straw-colored liquid escapes
abundantly when the part is scarified. The same is true of the tongue,
which is stained throughout with blood that has gravitated into it.
The pleuræ contain an abundant exudate more or less deeply stained with
blood. The same is true of the pericardium. In the latter Edington has
found 140 fluid ounces. On the surface of the lungs and pericardium are
extensive yellowish exudates. They are covered with petechiæ mostly
small or punctiform. If the horse has stood at rest throughout the
illness the lungs seem pale, yellowish, yet swollen and indisposed to
collapse. The interlobular tissue especially is infiltrated with serum
so that toward the free margin the lobules may be separated by intervals
of half an inch in breadth as in lung plague of cattle. In horses that
have been worked during the illness the whole organ is congested and
firm, resembling the condition of croupous pneumonia. The trachea and
bronchia show dark congestion of the mucosæ and a mixture of froth and
serous exudate. The large blood vessels contain diffluent blood clots of
an intensely dark color. In the vascular furrows of the heart and along
the large vessels are yellow exudates or blood extravasations. The
muscular tissue of the heart appears normal or rather pale, and under
the microscope the striæ are found to be obscured by cloudy swelling,
and minute blood extravasations and hæmatin are met with. The
endocardium is cloudy, with blood extravasations, and exceptionally
ante-mortem clots are found. The spleen is usually swollen, very dark,
blood gorged and covered with petechiæ. On section there are found
extensive extravasations, with masses of blood pigment and crystals. The
kidneys are enlarged, the capsule easily detached, the epithelium of the
glomeruli and convoluted tubes swollen and their nuclei multiplied. A
gelatinoid exudate is usually present in the renal pelvis. Congestions
have been found in the right gastric _cul-de-sac_ and less frequently in
the intestines. Exudations have also been found in the cerebro-spinal
nervous system, the laryngeal mucosa and the conjunctiva. The latter is
usually cyanosed.
_Prevention._ The first consideration is to keep work horses indoors or
in a kraal during the summer or sickly season. Here they must be fed on
dry hay and grain only, grass being strictly withheld. If it becomes
absolutely necessary to feed green fodder of any kind it should not be
cut until all dew or rain has completely dried off in the heat of the
sun, and if kept over night should be kept under cover and again dried
before feeding. When taken out to work the animal should wear a check
rein or muzzle so that he cannot by any chance reach the green
vegetation. This rule must be most strictly adhered to at night or
during damp weather.
For horses turned to pasture a fair amount of protection may be secured
by shutting them in a stable or kraal before sundown, and until the
vegetation has been thoroughly dried by the sun the next morning.
_Immunization._ A horse that has recovered from the _sickness_ has been
long held to be immune and will bring from six to ten times its former
price. As any disease is liable to be called the sickness this enhanced
value is too often insubstantial. Wiltshire even says that all “salted”
horses eventually die of _horse sickness_ if allowed to live long
enough. Be this as it may Edington appears to have established a
reasonable measure of immunity by his protective inoculations. He takes
a recovered (‘salted’) animal and reinoculates it at intervals with
encreased doses of virulent blood. After the last of these inoculations
the subject is allowed to rest for a long period of time, and is then
re-inoculated with a small dose of virulent blood. A definite amount of
this horse’s virulent blood is mixed with 50cc. of serum and injected
subcutaneously; some days later 30cc. of the same serum with the same
dose of blood is injected; at a later date the procedure is repeated,
with a reduced dose of serum, and fourteen days later pure virulent
blood is injected.” The result has been perfectly satisfactory.
DOURINE.
Synonyms. Definition: Contagious disease of breeding solipeds, with
special lesions in generative and nervous system, and skin, and caused
by a trypanosoma. Susceptible animals: horse, dog, rabbit, rat, mouse,
ass. History: in Europe and America. Causes: contagion; coition;
microbiology; trypanosoma equiperdum; its successive stages: 1.
granules and refrangent spherules; 2; chromatin bodies with two
prolongations; 3. fusiform body with nucleus and nucleolus and two
flagella; 4. pyriform bodies with flagella; 5. fusiform body with
nucleus, nucleolus and undulating membrane: in blood, sperm, milk,
vaginal mucus, sores; disappears from blood in intermissions and
rapidly after death. Lesions: phlegmons of generative organs, papules,
vesicles, mottling, swollen inguinal glands, penis, testicles,
caseation or atrophy, thickened lymphatics, nervous lesions, friable
bones, arthritis, liver, spleen, kidneys, lungs, lack of red globules,
anæmia, muscular atrophy; in mare, in dog. Symptoms: _Horse_:
incubation 11 days, variable; preputial, scrotal, sub-abdominal
swelling, catarrh of genital mucosa, vesicles, sores, swollen penis,
semierections; paraphymosis, slight fever, tender loins, frequent
micturition, paresis, swollen joints, tendons, emaciation marked
anæmia, apathy, dementia, nasal ulcers, submaxillary swellings.
_Mare_: vulvar swelling, distortion, leucorrhœa, eruption, spots of
depigmentation, erection of clitoris, urine in driblets often,
inguinal swellings, sterility or abortion, lameness, trembling, great
anæmia and emaciation. Diagnosis: from urticaria: from glanders,
generative lesions, no response to mallein, paresis: from chronic
paraplegia, by its coition cause, and in horses only; from vesicular
exanthema by gravity and nervous phenomena. Prognosis: Mortality 70
per cent. and upwards. Symptoms in ass slight: in dog severe and
fatal; in rabbits severe. Treatment: prevent copulation, castration,
local antiseptics early. Prevention: prevent copulation of infected
and suspected animals, castrate, import only on certificate and on
long quarantine.
_Synonyms._ _Venereal Disease of Solipeds_; _Equine Syphilis_; _Maladie
du Coit_; _Chancrous Epizoötic_; _Breeding Paralysis_; _Epizoötic
Paraplegia_.
_Definition._ A contagious affection of solipeds, transmitted by
copulation, and attended by specific lesions in the generative organs
and nervous system, such as local venereal swellings, chancrous ulcers
and cicatrices, dementia and paralysis.
_Susceptibility._ As occurring casually the disease is essentially an
equine one, yet the following species are susceptible to experimental
inoculation in the order named: dogs, rabbits, rats, mice, asses. While
the horse shows the greatest susceptibility, the ass is comparatively
very resistant to the poison.
_History._ The malady has probably long prevailed in the east, yet it
was first clearly distinguished in 1796 when described by Ammon as
prevailing in the royal stud at Trakehnen in Northern Prussia. We have
later descriptions of the disease in the same locality in 1801
(Hertwig), and 1807 (Ammon). It was found in Bromberg in 1817 to 1820
(Waltersdorf), also in Hanover (Haveman), in Austria and Bohemia in
1821–8 (Fischer), in Styria in 1821, in Switzerland in 1830, in France
in 1830–2 (Lautour), in Silesia and Pomerania in 1833–40 (Fischer), in
Italy in 1836, in Russia in 1843, (Fischer), in Silesia and Poland in
1830–40 (Freidberger and Fröhner), in Algiers in 1847–55, and in Syria
and Asia generally and perennially (Daumas and Signol).
It appeared at Bloomington, Ill., in 1882, the first affected animal
being a brown stallion that had been imported from France and which bore
on his neck a brand like the letter D. In this locality it extended to a
considerable number of breeding mares and stallions, and having been
recognized by Dr. W. L. Williams, was largely stamped out by a rigid
quarantine of diseased and exposed animals. Some exposed animals had,
however, left the district, and isolated centres of infection have been
since found in Nebraska and elsewhere in the United States.
It is not known to have invaded Belgium, Scandinavia, England, South
America nor Australasia.
All indications point to Asia or North Africa as the primal home of the
disease, as they still prove its perennial one.
_Causes._ The disease is transmitted by contagion and almost exclusively
in the act of coition. Hayne has seen the affection in geldings, and
Haxthausen in mares that had never been served. Schneider, Buffard,
Nocard, Blaise and others have transmitted it freely by inoculation of
blood and nervous matter, so that the possibility of infection through
other channels than the generative organs must be admitted. But such
irregular means of casual infection are so rare, and the probability of
transmission of the virus from a non-breeding animal is so remote that
in the practical measures of sanitary police, the breeding horses alone
need be taken into account.
The extra vascularity of the male and female generative organs at the
period of coition undoubtedly favors infection, as a latent or
apparently recovered case will relapse under its frequent repetition.
The abrasion of the epithelial surface also forms infection atria and
favors new multiple points of infection.
The disease has occurred congenitally (Rodolff, Jessen). It has been
claimed that the higher bred horses with lighter frames are the more
susceptible (Fischer), but this is probably a delusion, the disease
having been often introduced by the Barb and Arabian and propagated
among their grade descendants. The heavy Percheron shows a very ready
susceptibility and a virulent and fatal form of the affection.
_Microbiology._ That the affection was due to a microbe was clearly
shown by its absence from every part of the world into which infected
horses had not been brought. The secluded countries, Belgium, England,
Scandinavia, that breed their own horses, the distant Australia, New
Zealand and South America remained free in face of the constant presence
of the infection in different parts of Central and Southern Europe, in
Africa and Asia. The horses of America and South Africa showed a ready
susceptibility to the virus brought by infected horses, and rigorous
sanitary police control speedily cleared a district of the trouble.
Thanhoffer found in the blood, vaginal mucous, testicle, semen, spinal
fluid, myelon, and roots of the dorsal and lumbar nerves cocci,
especially streptococci and less constantly bacilli, to which he
attributed the malady. More recently Schneider and Buffard have
apparently demonstrated that an infusorian, the _trypanosoma of
dourine_, is the essential pathogenic agent.
The _Trypanosoma Equiperdum_ varies greatly in form at different stages
of its growth or in different media. In the exudate of the slight early
tumefaction, without as yet other symptoms, it is found as minute
granules in groups, as larger spherical very refrangent bodies like very
large cocci, each having a strongly staining nucleus, and as larger
bodies in which a delicate membranous covering encloses one, two or
three masses of chromatin and extends to form one or more points
(club-shaped or fusiform). Each chromatin mass has a nucleolus on its
outer surface or slightly apart from it. Twenty-four hours later there
may be added: First, short, thick chromatin bodies, with two slightly
undulating, pointed, membranous prolongations. Second, more delicate,
fusiform bodies, each with one chromatin nucleus, a detached nucleolus,
and the membrane prolonged into two actively moving flagella. Third,
larger pyriform bodies with chromatin nuclei and nucleoli and the
membrane prolonged into one or several flagella. Fourth, fusiform
bodies, thick or delicate, each having a chromatin nucleus and
nucleolus, and arranged singly or in groups of two, four, six or more,
united together at one end and diverging at the other to form a stellate
mass. These last, 20 to 30μ long by 1.5 to 2μ broad, may perhaps be the
adult form of the parasite from which the small granular or spore forms
found in the most recent lesions are derived. The fusiform outline, the
deep staining central mass, with its adjacent nucleolus, and the pointed
or flagellate membranous prolongations, more or less motile or
undulating, are characteristic features.
In its morphology and evolutionary forms the trypanosoma of dourine has
not been shown to differ from that of surra, nor the nagana or Tsétsé
disease, the granule form, the spherical, the club-shaped or pyriform,
the fusiform with more or less stellate grouping, are characteristic of
all (Lydia Rabinowitsch, Kemper, Schneider, Buffard). The distinction is
found in the pathogenesis of the two diseases.
With active cutaneous or mucous lesions, the parasite is usually found
abundantly in the blood, sperm, milk, vaginal secretions, and the
erosions of the vaginal mucosa or penis. During intermissions, however,
and in the absence of local lesions, examination of the blood may fail
to detect it, yet its inoculation on a dog will usually produce the
affection. It disappears from the blood and tissues with great rapidity
after death, so that, to prove successful, inoculations should be made
before death or immediately after. They are ineffective after 48 hours.
Schneider and Buffard, Nocard and others found the trypanosoma in the
blood and exudates of horses, asses and dogs, suffering from dourine,
and failed to find it, in the same localities, in animals of the same
species which were free from dourine. The infected blood, preserved for
24 hours in sealed glass tubes, and then inoculated on two dogs produced
characteristic dourine, with the extensive production of trypanosoma in
the blood, the destruction of blood globules, and the pathognomonic
local lesions. Inoculation of two other dogs, with the same material, at
the end of 48 hours produced a slight transient hyperthermia only,
without local lesions or propagation of the parasite in the blood. The
same blood inoculated after 15 days produced neither local lesion nor
fever.
_Lesions._ _Horse._ In the early stages are found a phlegmonous or
œdematous swelling of the _sheath_, _scrotum_, _penis_ and _inguinal
glands_ and a yellowish liquid effusion into the scrotal cavity. The
skin covering these parts may show a papular or vesicular eruption or if
this has passed, a mottling with white spots shows where the lesions
have been. Later still the _inguinal glands_ are shrunken and have
undergone fibroid degeneration and induration and the testicles, swollen
or shrunken, contain centres of caseation. The connective tissue of the
epididymus and cord is the seat of a gelatinoid exudation. The _walls of
the scrotum_ may be greatly thickened and the seat of abscess or of
caseous degenerated hyperplasia. In advanced cases the _testicles_ are
usually abnormally small even if the scrotal mass is enormously
distended. The _sheath_ and _penis_ may be the seat of more or less
numerous ulcers, and swellings, contractions and distortions of the
latter organ are not uncommon. The penis may, however, retain its normal
dimensions. The walls of the _lymphatics_ in the inguinal region may be
the seat of hyperplasia, the thickening causing them to stand out like
cords as in glanders. In the advanced stages the _muscles_, especially
those of the hind limbs, become pale and atrophied.
The _nerve centres_ undergo profound changes which have been studied by
Thanhoffer. The _pia mater_ in the affected parts of the spinal cord is
the seat of active congestion and thickening. The central canal of the
cord is dilated (syringomyelia) more at one point than another, contains
more than the normal amount of liquid, and the neuroglia around it is
thickened and fibrous (sclerosed). The _substance of the cord_, both
white and gray, shows congestion, blood staining, at points foci of
softening, and at others induration (hyperplasia of the neuroglia). The
_nerve cells_ are modified in various ways, some being granular, some
discolored by fine granular pigment, some having enlarged and multiplied
nuclei, and some show vacuoles. The _nerve filaments_ often show a
granular degeneration extending from the nerve cell into the axis
cylinder, and the latter is liable to be varicose or uneven in size. In
the affected portion of the cord leucocytes are numerous and hyperplasia
is often present. The neuroglia especially tends to encrease, and apart
from the foci of softening tends to give a special firmness to the
substance. At intervals, in the perivascular spaces, may often be found
minute (microscopic or macroscopic) blood clots. The subarachnoid and
subdural fluid is encreased and may be pinkish. At the roots of spinal
nerves, especially in the dorsal and lumbar regions, a gelatinoid
exudate may invest the nerve, distending the connective tissue beneath
the neurilemma and even occupying the interval between the nerve
filaments. Sometimes large corpuscular bodies are found between the
nerve fibres.
The _cerebral meninges_, especially the _pia mater_, are congested and
opaque. Foci of softening are by no means uncommon and the cerebral
ventricles contain an abnormal quantity of fluid.
The _bony tissue_ generally has lost its consistency and the medullary
matter may be unduly reddened. The large joints contain an excess of
synovia somewhat pinkish in color, and the ligaments of the hip joints
are often congested, thickened and softened. The articular cartilage may
even show patches of blood staining.
The _intestines_ are usually nearly empty, soft, pale and flaccid, and
Ruthe has in one case observed rounded ulcers on the mucosa. Fibroid
thickening on the peritoneal surface may indicate a previous exudate.
The _mesentery_ is thickened, with infiltration and has a yellowish
discoloration and the _mesenteric glands_ are usually enlarged, softened
and friable, though sometimes firm and contracted. The _lymph glands_
adjoining the generative organs are often swollen, pigmented and studded
with foci of caseation, varying in size from a pea upward.
The _liver_ is softened and congested or fatty. The _spleen_ is small.
The _kidneys_ are usually large, but flaccid, pale and bleached.
The _thoracic organs_ may show little change, though hypostatic
inflammation and foci of caseation or suppuration may be present.
The _blood_ is pale and watery and forms a loose, pale, diffluent clot,
while there is an extraordinary diminution of red globules and a
relatively great encrease of leucocytes.
In advanced stages the _muscles_ are pale, anæmic and shrunken
especially those of the hind limbs.
_Mare._ In the mare in addition to the lesions of the internal organs
and blood, the following may be noted in connection with the generative
system. Phlegmonous or œdematous swellings, sores or ulcers on the lips
of the vulva, and on the vulvar and vaginal mucosæ. The parts become
variously distorted, and the vulva, habitually open may expose the
swollen and ulcerated clitoris. A crop of papules or vesicles, running
into sores or ulcers may appear on the urethral orifice, the vulva and
adjacent skin, and even though overlooked, their seats are marked later
by loss of cutaneous pigment and the formation of small white spots. The
mammæ are sometimes inflamed, œdematous and tender, with suppurative or
necrotic foci and the adjacent lymph glands are enlarged by infiltration
or contracted by sclerosis.
_Dog._ These resemble those in horses. In the bitch genito-urinary
congestion, inflammation and catarrh, subcutaneous infiltration under
the belly and inside the thighs, swelling of the inguinal lymph glands,
emaciation, and pallor and atrophy of the voluntary muscles are marked
features.
_Symptoms._ _Horse._ Incubation may last from one to eight weeks
(Maresch), but is usually 11 days from the infecting service. It may be
abridged by a special susceptibility, and by repeated infections and
hence the more acute cases are especially seen in the male in daily
service. In some such subjects local genital infiltrations are speedily
followed by paralysis or vertigo which cuts off the patient in a few
days.
More commonly the malady is _chronic_ though varying in different
countries, epizoötics or even in particular cases.
The first _symptom_ is slight swelling of the anterior border and raphe
of the sheath, which gradually extends backward to the scrotum and
inguinal region and forward on the abdomen it may be as far as the
brisket. This may be hot and painful, but is usually œdematous, cool and
painless. The infiltration affects the end of the penis, the meatus may
be red and angry with a slight muco-purulent discharge, and red spots
vesicles and ulcers may stand out clearly on the pigmented surface.
Williams never saw such eruptions in the American cases and doubts their
existence except as the result of injuries. There are frequent
semierections and service is still possible. Later the engorgement
extends to the specially pendent testicles, inguinal glands and others
adjacent. Paraphymosis is occasionally seen or, more commonly, the penis
hangs out of the sheath soft and flaccid and erection seems impossible.
The local swelling may become excessive, pressing the testicles up
against the inguinal ring, or suppuration and extensive abscess may
follow. Appetite is retained and the temperature remains moderate (100°
to 102° F.).
The local swellings may almost completely subside, except a slight
tumefaction of the end of the penis, hence some (Fischer) have held that
the cutaneous lesions are the primary ones, yet the start of infection
at the generative organs and the fact that a stallion often infects a
number of mares before there is any suspicion of his own infirmity is
evidence enough of the genital seat of the earliest lesions.
The cutaneous lesions, which are essentially secondary, but highly
characteristic, appear from forty to sixty days after the infection
(Schneider and Buffard). They are from a quarter of a dollar and upward
in size (in some old horses much smaller), and rise abruptly from the
healthy skin, becoming the more marked that the hairs upon them stand
erect. These may arise suddenly and subside again in one day, or give
out a serous exudate which mats the hairs into a tuft. They may,
however, last four or five days. These are more patent after a full
drink of water, or after sprinkling or sponging with water. Even when
they have been overlooked these results may often be seen later on
colored skins, in the presence of many circular white spots entirely
devoid of pigment. The most common seat of these cutaneous lesions is
the hind parts (anus, tail, croup, quarters), but they may appear on the
sides, neck, shoulder or thighs.
Tenderness of the loins may now be shown, with frequent, painful
micturition, but the penis becomes more and more paretic, so that
coition becomes encreasingly difficult or impossible. Paresis also shows
in the hind limbs, the animal remains recumbent a great part of the
time, rises with difficulty, starts suddenly forward at the fetlock, and
drags the toe on the ground in walking. Swelling of the joints and
tendinous sheaths, with attendant lameness, is not uncommon. The
appetite remains good, yet emaciation and weakness make marked progress.
The advanced stages are characterised by marked anæmia, paraplegia and
dementia. The visible mucosæ are pale, emaciation advanced, the patient
stubs his toes and sways in walking, and finally drops unable to rise;
or he stands with hind legs straddled and semi-bent, and largely
oblivious of all around him. He may be too stupid to eat unless the food
is placed in his mouth, and yet the neigh of another horse or a mare may
draw forth a feeble retort, as if the deranged generic instincts
remained. Swelling, or even abscess of the lymph glands, axillary,
submaxillary or inguinal, is usually present, and muco-purulent
discharge with ulceration of the nose or eyes is not uncommon. The
joints crack when moved and fractures are common.
The duration of the disease is two or three months, the progress being
more rapid in winter.
_Mare._ Vulvar swelling eight or nine days after service, with ejection
of urine in jets, contraction of the vulva, redness, swelling and
erection of the clitoris, and a muco-purulent discharge are marked
symptoms. European observers note nodules, vesicles and ulcers on the
mucosa and adjacent skin, but these were not observed in the American
cases (Williams). Yet later they showed the characteristic white spots.
Switching of the tail, stamping of the hind feet and painful straining
to urinate are followed in certain cases by ejection of the urine
forcibly in jets or in small dribblets. The catarrhal discharge is at
first watery, but later becomes viscid, sticky and white, yellow or
grayish, or even red. It mats together the hair of the tail and thighs,
and putrefies, exhaling a repulsive odor. The swelling involves the
space between the thighs and often implicates the mammary glands and
even the floor of the abdomen. The inguinal glands are often involved,
and hyperplasias with degenerations and even abscesses may appear in
this region. As in the stallions the local lesions may have periods of
advance and subsidence, and in favorable cases, that are not again
served, there may seem to be a temporary recovery. The mare, however,
remains infecting, and if served the local disease is at once roused
into activity. The button-like skin eruptions appears on the quarter as
already noticed of the horse and in grave cases may caseate or suppurate
and burst, forming an indolent and intractable sore. The dark skin of
the vulva and perineum becomes marked by white spots or by irregular
patches caused by the confluence of several such spots, which for
ordinary breeds of horses are highly characteristic of this disease.
Many Arabian horses naturally acquire such white spots on the dark skin,
and in pure Arabs and grades this appearance need not be held as
evidence of dourine.
Infected mares rarely conceive, and any that do so are likely to abort
before the sixth month.
The systemic symptoms, nervous, paralytic, tremulous, dyspeptic,
atrophic, cerebral and cachectic follow a similar course as in the
stallion.
In grave and progressive cases the lesions of the generative organs
become very marked. The lips of the vulva become rigid and distorted so
that it remains constantly open and the erect clitoris continually
exposed. The skin of the vulva is tense, dry and shining. Lameness is
shown in one or both hind limbs, knuckling over at the fetlock,
shortening of the step, planting the toe first and the heel later with a
jerk, lack of balance, paresis and even inability to rise.
A disposition to trembling is common to both sexes, as is also an
intolerable itching of the skin which may make the animals tear the
lower parts of the limbs with the teeth. In either there may be a local
paralysis of a lip, an ear, an eyelid, or some other part of the body.
In both sexes the disease tends to extreme anæmia, debility and
emaciation, and to infective internal inflammations (lungs, bronchia) or
septic or purulent infections.
_Diagnosis._ From _urticaria_ this disease is to be distinguished by the
absence of lesions of the generative organs in the former, by its
association with change of food and digestive disorder and by the
absence of all evidence of contagion.
From _glanders_ it is to be distinguished in the same way by its casual
transmission by sexual connection only, by its restriction to breeding
animals, and by the irresponsiveness of the victim to the mallein test.
The progressive paresis and hebetude are valuable diagnostic phenomena.
From _chronic paraplegia_ it is distinguished by the same prevalence in
breeding solipeds only, and by its mode of transmission.
The greatest difficulty is experienced with the slight and comparatively
occult cases, and in some of these the history of the infection of a
number of breeding animals, which have been served by the same horse may
be the one guiding point for a number of the cases. For sanitary
purposes it is well to treat as suspicious animals all mares that have
been served by a stallion which is in the line of infection. This
suspicion would attach also to any stallion that had served a mare which
had been to a diseased or suspected stallion, and to all mares that have
been served by the suspected stallion after he had been to the suspected
mare.
From _simple vesicular exanthema_ dourine is to be distinguished by its
comparatively slow progress, and by the uniformity of the lesions of the
generative organs and nervous system, which are lacking in the vesicular
affection.
_Prognosis._ A certain number of animals recover from the milder attacks
which have not become complicated by the grave trophic and nervous
lesions, but as in glanders, recovery from severe attacks and in the
advanced stages is practically unknown. The mortality is set at 70 per
cent. and upward.
_Symptoms in the Ass and Mule._ The disease usually remains discrete,
the lesions in the generative organs or other seat of infection being
the marked symptoms, and recovery the rule. Œdema of the end of the
penis, obliteration of the folds around the orifice of the urethra and
eversion of the urethral mucosa are the most constant features, distinct
even in semi-erection. Œdema of the sheath and skin eruption may follow.
Exceptionally a mule proves as susceptible as the horse, and shows the
disease with the same fatal severity.
_Symptoms in Dog._ A bitch, 15 days after vaginal injection of the
infected equine blood, showed severe vaginitis and hyperthermia (100°).
On the 23d day she aborted, followed by muco-purulent discharge, vulvar
œdema, pallor of the mucosæ, anæmia, rapid emaciation, paresis and
occasional convulsions. Blood drawn from the vulva contained the
trypanosoma. She died on the 66th day. The temperature rose to 103°.
Two male dogs that lined the above infected bitch showed after 12 days,
engorgement of the sheath and scrotum, muco-purulent discharge, and
abundance of the trypanosoma in the blood of the affected parts.
Cutaneous lesions on the loins, thighs, sides or forehead, showed
erection of the hair, with infiltration, or shrivelling and
bloodlessness.
Other dogs showed arthritis, corneal opacities and ulcers, hypopion,
cataract, nasal discharges, facial periostitis, dyspnœa and syncope.
_Symptoms in Rabbits._ Rouget found in inoculated rabbits, extensive
gangrene of the skin, involving even the cranial bones, ulcerative
keratitis, hypopion, panophthalmia, following on the earlier genital
troubles of vaginitis, swelling and discharge.
_Treatment._ Some cases recover spontaneously a few may be aborted in
the earliest stage of the disease, but cases that have advanced to any
extent and assumed a grave character are practically hopeless.
An important element in treatment is to do away as far as possible with
the cause of generative excitement since the disease is aggravated and
more rapidly advanced by frequent copulation. Rodloff from a very wide
experience speaks highly of castration of the stallion. Castration of
the mare has not been specially advocated and the absence of marked
lesions in the ovaries, may deter the veterinarian, yet whatever
promises to lessen in any degree the genesic excitement is not to be
despised, and the measure has besides a sanitary value for other
animals.
Early local treatment is the most promising, and especially if it can be
applied to exposed animals during apparent incubation. Injection of the
urethra, sheath, vulva, vagina and uterus with antiseptic lotions, and
apply them to the external sores. Mercuric chloride 1:2000, carbolic
acid 2:100, silver nitrate 1:250, calcium chloride 1:100, or chlorine
water may be taken as examples. When local swellings have supervened it
would be entirely appropriate to incise them freely or even to excise
them and cauterize thoroughly with stronger agents.
Internal treatment by mercuric chloride 1½ to 3 grains, potassium iodide
2 to 5 drs., arsenic 7 to 14 grains, has been widely used but to little
purpose. The same may be said of Rodloff’s treatment by tonics and
carminatives (sal ammoniac, camphor, iron, angelica, gentian, ginger and
valerian.)
_Prevention._ The one thing to be secured is the prevention of
copulation with any animal that has been affected, or exposed to this
disease in the past three years.
1st. Any stallion or mare once affected must be excluded from breeding
for at least three years after apparent recovery.
2d. Every such animal that has been exposed by copulation with a
suspected animal must be excluded from breeding for the same period even
if no active symptoms have been shown.
3d. Every affected or exposed animal, should be quarantined in the hands
of his or her owner and placed on an official register and the sale,
gift or loan of such an animal, or its movement to a new place where it
might propagate the disease should be made a misdemeanor.
4th. In any county or district in which the disease exists all stallions
and mares should be registered and none should be allowed to be used for
breeding purposes without an official certificate showing that each of
the animals mated is free from all suspicion of having been exposed to
this infection.
5th. If any stallion or mare is imported from a country in which dourine
exists it should be accompanied by an official certificate showing that
it has not in the past three years been exposed to the possibility of
infection with dourine.
6th. In the absence of such certificate the imported animal (capable of
breeding) should be kept in strict quarantine for the period of three
years.
7th. A much more radical measure, which may be made to supersede all of
the above, would be to castrate every soliped (stallion or mare) which
has suffered from the disease in the past three years, and every such
animal that has by coition been exposed during that length of time to
even a remote opportunity for contagion. This would embrace all
apparently sound mares that had been served by a stallion which had
shown slight symptoms of the disease, or by a stallion which had not
himself shown such symptoms, but which had served a mare that had shown
such symptoms; or one that had served a mare that had not shown such
symptoms, but that had been previously served by a stallion which had
shown such symptoms, or that previously covered a mare that had shown
such symptoms. In such cases the State might well afford to indemnify
the owner for any reduction in value of the castrated stallion from that
borne by the animal as a prospective breeder, the breeding for which
indemnity is sought being understood to count only from a date of three
years after the sanitary castration. A mare once attacked should be
remorselessly castrated or killed. A perfect recovery in a horse can be
better attested; that of a mare is always uncertain, and most secondary
outbreaks after the apparent extinction of the poison have come from
breeding mares that have apparently recovered, or that after exposure
have shown no appreciable symptoms.
When a State is so lost to all sanitary considerations as to abandon an
affection of this kind to take its course, the owners of stallions and
mares cannot be too careful to avoid the exposure of their valuable
breeders to the risk of infection. Each mare brought for service should
be admitted only when accompanied by a certificate showing all previous
services in the last three years, with the identification of the
stallion, and this irrespective of whether the service has been fruitful
or not. In such certificate the owner of the mare should bind himself to
make good all damage or loss that may accrue from his failure to set
forth in the certificate every such service and every symptom of illness
affecting the generative organs from which the mare has suffered in the
three years antecedent.
The owner of the stallion should give a similar guarantee that the horse
has in the past three years served no mare that was in any way open to
suspicion, and that the animal has not suffered from any affection of
the generative organs which had any of the characteristics of dourine.
No mare should be served which shows swelling, nodules, distortion, or
gaping vulva, a muco-purulent discharge, or too frequent or too
prolonged _heats_.
No stallion in such locality should be allowed to serve which shows
pasty swelling of the sheath, swelling, shrinking or distortion of the
penis, red, angry, tender meatus urinarius, or a muco-purulent
discharge.
Unless in case of Arabian horses the appearance of white spots on the
dark ground of the sheath, penis, vulva, or perineum, should be ground
for debarring from service until an absolutely stainless record covering
a number of years has been shown.
MAL DE CADERAS.
This is a disease caused by _Trypanosoma Equinum_ described by Voges who
studied the affection in the Argentine Republic as it exists in a region
extending from Santa Fe, and Corrientes on the south to Bolivia on the
north. It resembles surra in prevailing in tropical heat, during wet
weather, in its intermittent character, in the presence of the mature
trypanosomata in the blood at the beginning of a paroxysm and their
disappearance toward the end of it, in the supervention of rapid and
extreme emaciation, debility and anæmia, in the destruction of red blood
globules and the passage of the coloring matter by the kidneys, in the
presence of paresis and œdemas, in its expending its energy mainly on
the soliped and in the constancy of the mortality. Death occurs in two
to five months in horses, and six to twelve months in asses and mules.
Swine and water hogs contract the disease casually and it is inoculable
on white and gray rats, mice, rabbits, dogs, goats, sheep, chickens,
turkeys, ducks and monkeys, (Nyctipithecus felinus), and exceptionally
on Guinea pigs. The same measures of prevention would be indicated as in
cases of surra and dourine.
INFECTIOUS PARAPLEGIA OF SOLIPEDS IN MARAJA.
Synonym. Definition: Infectious, anæmic, dropsical paraplegia. Origin:
Decomposition of myriads of horse carcasses in torrid heat; rodents;
swine; horses. Causes: Microbe uncertain; infection in corral and
vicinity; manure; rubbish; flies; hot dry weather. Symptoms:
Decreasing severity; preliminary weakness, dulness, emaciation,
dyspnœa. Paresis: Fifty per cent. paraplegic; marasmus; difficult
defecation or urination; paretic penis; anorexia; ardent thirst with
diuresis; rumbling of bowels. Œdema, epigastrium, abdomen, sheath,
mammæ, head. Cutaneous sloughing, stupor, asthenia, rapid emaciation,
hemiplegia, impaired peristalsis. Blood dark, viscid. Lesions:
Intestinal congestion; petechiæ of serosæ; icterus; enlarged, soft,
congested liver; spleen engorged, softened; kidneys swollen,
congested; petechiæ on bladder; congested lungs, thoracic serosæ,
cerebral meninges. Relation to surra. Mortality excessive or constant.
Treatment hopeless. Prevention: Keep sound from sick and from infected
places and things; kill and bury sick; disinfect harness, trappings,
wagons, utensils, buildings, manure and rubbish heaps; destroy flies
and mosquitoes, vermin (rodents), etc.
_Synonym._ Quebra Bunda: Broken Buttock.
_Definition._ An acute infectious disease of horses characterized by a
condition of fever, with rapid loss of condition, resulting in rapid and
extreme emaciation, local dropsies, cutaneous eruptions and ulcers, a
rapidly advancing anæmia and debility, with lessening control of the
hind quarters and death in almost all instances.
_History of the Disease._ Luis Calendrini da Silva Pacheco says the
malady was unknown on the island until 1830, when, on account of the
great excess of wild horses and their devouring the pastures needed for
the more valuable cattle, great numbers were killed and their hides
marketed. This continued for over a year without any attempt to dispose
of the carcasses. These accordingly lay in heaps in a damp climate,
under the equatorial sun, in a condition of putrefaction, exhaling the
most offensive odors. Stimulated by frequent complaints, the government
ordered that the carcasses should be burned to ashes, but no success was
accomplished, in one case 800 bodies having been merely roasted a little
on the surface. The district around Chaves contained the greatest number
of horses, there the greatest number were killed, and there the disease
broke out. A number, variously estimated at from 25,000 to 60,000 were
driven into the little bay of Juncal and killed by burning the grass,
which, however, did not at all consume the bodies. The disease attacked
first the capivaras (rodents) in the district of Chaves, killing off the
whole race; then the wild and domestic swine suffered, and finally it
ravaged the equine race, and though confined to Chaves for two years it
was extended through sales of horses and raged with such fury that in
five years not a horse was left alive in the island, except a small
remnant of a few hundreds in Chaves, where the infection started.
_Causes._ The microbian cause of the disease has not been definitely
ascertained, so it is idle to speculate whether we have to deal with a
saprophyte which has taken on deadly pathogenic properties, or whether
the infection was carried to the island by winged insects or birds
attracted by the decaying carcasses.
Certain conditions may be named as accessory or favoring causes. The
wild horse often escapes so long as he is on the pasture, but when
lassoed, taken to the corral and broken, he will die in four to six
days. This suggests that the infection is laid up and preserved in the
corrals or stables, the mangers or racks, or possibly in the water
supplies. The contact with even the reins (harness) of other horses is
alleged to be a prominent cause of infection. Another significant point
is that around every hacienda, within a radius of a mile, there are
numbers of carcasses, so that there is every opportunity for the
infection of the wild and susceptible horses caught and brought in. Near
the buildings, too, are accumulations of horse and cattle manure and
rubbish heaps of all kinds, the breeding places of the flies, which are
probably important factors in conveying the infection. Again, the
attacks are more numerous and severe and death earlier in the hot, dry
summer weather, while there is a pause and a lesser intensity in the
cool or rainy season. All domestic animals, save when kept up for
breaking or work, live in the open field day and night and subsist on
the green food (capine, gramineæ), and are thereby exposed to all
climatic changes.
_Symptoms._ At the first appearance of the disease (1830) it proved
fatal in a few hours, but after a year’s prevalence, when the more
susceptible animals had been killed off, the progress of the malady
became slower, death being deferred to the 8th or 15th day, so that the
symptoms could be more definitely followed. From 7 to 14 days before the
more obvious symptoms, there were lifelessness, tardy movement, hurried
breathing, debility, weakness and emaciation without work or other
obvious cause. Exercise caused difficult breathing, dilated nostrils and
great agitation of the flanks.
One of the most constant symptoms was the loss of power of the hind
limbs which would sway and stagger, the femurs turning inward, as if
dislocated, and on uneven ground the animal could not walk without
falling. When down, he could not rise without assistance. In the earlier
experience of the malady (1835) only 8 to 16 per cent. failed to show
these paraplegic symptoms, whereas in recent years 50 per cent. or more
escape them. In these cases the emaciation goes on alone, gradually
encreasing until the patient appears like a living skeleton. Some retain
an appearance of liveliness, yet all stand on three limbs, and change
from one hind limb to the other every six or eight seconds.
The retraction of the abdomen is a marked feature, yet expulsive
contraction is defective, the patient fails to put himself in the
position for urination or defecation, and there is more or less
detention of urine or fæces, the latter being dry, moulded, covered with
mucus and of a reddish yellow color. After a time the urine escapes in
fine jets, so small that in the absence of stretching to urinate, or
raising of the tail, they are easily overlooked. The urine may be
normally clear, or dark colored. The penis hangs out of the sheath
several inches farther than in health.
Appetite is sometimes impaired, or completely lost, but usually the
patient eats and drinks to the last, but without proper digestion or
assimilation. It does not check the advance of marasmus. Thirst often
becomes excessive and in such cases, there is diuresis together with
frequent and excessive rumbling of the bowels. The loins are very
sensitive to pinching.
About sixty to seventy per cent. in different outbreaks show œdema, in
the epigastric region it may be six inches in diameter, or it may extend
from the sternum back so as to include the abdomen, sheath, or mammæ,
and perineum, and even the hind limbs. Considerable serous oozing takes
place from this for four or five days after which it dries up.
In about seven to fourteen per cent. the head became œdematous and
swollen, with an abundant fœtid purulent discharge from the nose and
eyes, and extensive ulceration of the pituita and conjunctiva. Such
cases became completely blind prior to death. In other cases extensive
ulceration of the skin set in with the formation of most repulsive
sores.
The nervous symptoms assumed various forms; in some there was stupor
with head resting on the ground; in others extreme debility and
paraplegia with phenomenally rapid emaciation; in a few hemiplegia, or
even delirium was shown; in all there was a marked paresis of the
digestive organs and especially impairment of peristalsis. The blood
assumed a dark gluey aspect.
The most constant symptoms appear to be dyspnœa under exercise, paresis
of the hind limbs and intestines, genital atony, a wonderfully rapid and
extreme emaciation, œdema, and a tendency to impaired nutrition or
ulcerous degenerations of the pituita, conjunctiva or skin.
_Lesions._ Congestion or inflammation of the intestines was usually
noted, with petechiæ on the peritoneum, especially the omentum, and on
other serosæ. The serosæ, mucosæ and other normally white tissues were
of a yellowish color, more or less deep. The liver was enlarged, much
softened, gorged with black blood, and sometimes of a greenish color.
The spleen was more or less black, and friable sometimes coming to
pieces in handling. The kidneys were always enlarged and gorged with
black blood. The bladder was usually distended and showed petechiæ on
its mucosa. The lungs and bronchia bore evidences of congestion, and the
pericardium had become dull, rough and lusterless. The horses that had
rested their heads on the ground showed meningeal congestion.
Sr. Calendrini claims to have had recoveries in some cases, followed by
relapses, and states that a second relapse is usually fatal. Many
features of the disease reminds one of surra—for example its relation to
hot weather, its relation to buildings and enclosures with their
accumulations of decomposing organic matter and swarms of flies, the
decomposition of the blood, anæmia, icterus of the white tissues,
petechiæ, extreme weakness, muscular atrophy, and marasmus. Calendrini’s
cures followed by relapses suggest the further coincidence of
intermissions. If now the trypanosoma were discovered in the blood it
might be recognized as at least a near ally of surra.
_Mortality._ _Prognosis._ The disease is nearly always fatal. At the
time of its first appearance (1830) Calendrini had 5,000 horses, and in
1835 he mounted his last horse a half-tamed animal lassoed on the Campo.
One Haziendiero invested $25,000 in horses and in 30 days he had lost
$18,000 worth. Others with 35,000 head lost the whole.
_Treatment_ proved one continuous failure. Bleeding, purgatives,
coloquintidas, saltpeter, cream of tartar, lemon, vinegar, nicotine,
buchu, by mouth and rectum, strychnia, camphor, caustics, prolonged
baths in the river, and a great variety of other measures, only seemed
to hasten a fatal result.
_Prevention._ Calendrini finally struck the true note of rational
prophylaxis, in the immediate killing and burial of all affected
animals, and the strict separation of all sound horses from the places
where they had been, together with the thorough disinfection of all
harness, utensils, wagons, etc. For a number of years his district
(Soure) had by this means been kept free from the plague.
This might be profitably extended so as to include the thorough
disinfection of any buildings and yards where the sick had been, the
removal of manure heaps and disinfection of their sites, also of all
rubbish heaps as breeding places of flies, the use of petroleum on all
stagnant water devoid of fishes and frogs as being the sources of
mosquitoes, and the application of suppressive measures which would
include the rodents (capivaras), and swine which have been shown to
propagate the infection.
INFECTIOUS PARAPLEGIA IN SOLIPEDS IN EUROPE.
Definition: Infectious, non-febrile affection of solipeds with lesions
of the genito-urinary mucosa and nerve centres, paresis and paralysis.
History. Causes: Microbes varying; bacteria of colon group; infected
urine, genital mucus, brushes, combs, rubbers, mares especially
exposed; infection local or general. Lesions: Congestion, exudation,
swelling, discharge from vulva, vagina, bladder, ureter, kidneys;
lumbar spinal cord, brain. Symptoms: Mare, swollen open vulva,
congestion and petechiæ, bloody mucus; horse, swollen sheath, pendant
penis, congested papilla, discharge; paresis of hind limbs, falls,
inability to get up, incontinence of urine; paresis of fore limbs, of
thoracic muscles, asphyxia, fever in late stages. Recovery. Diagnosis:
From hæmoglobinuria by absence of dietetic cause, the infectious
progress and genital lesions. Prognosis: One-fourth to one-third die
or fail to recover. Treatment: Antiseptic washes and irrigations of
vagina, urethra, bladder, skin; internally oil of turpentine; slings.
Prevention: Isolation, disinfection, separate attendants, litter,
sponges, etc., fly nets, screens, insect powder, removal and
disinfection of manure and garbage.
_Definition._ A contagious, non-febrile affection of solipeds,
characterised by congestive and hæmorrhagic lesions of the
genito-urinary mucosa, the spinal cord and its meninges, and by
paraplegia or paresis of the hind limbs.
_History._ This was described in 1888 by Comeny, as occurring in a
regiment of French cavalry. Other outbreaks have been observed in 1892
(Rancoule); in 1896 (Blin and Lambert). Earlier outbreaks have doubtless
been confounded with cerebro-spinal meningitis, hæmoglobinuria or simple
paraplegia, the genito-urinary symptoms having been overlooked or viewed
as secondary.
_Causes._ The disease, as hitherto observed, has been invariably
associated with microbian infection of the genito-urinary mucosa, but no
one microörganism has been found to be constantly present. In the 1888
cases, Nocard isolated from the kidneys and lumbar cord a small, motile
bacillus which was not stained by Gram’s method and the inoculation of
which proved fruitless. Zschokke, in 1889, found in the kidneys, lungs,
liver and spleen of both horses and cattle, the victims of a progressive
infectious paralysis, a bacterium coli commune 1.5μ long by 0.7μ broad,
which stained in methylin blue and grew in agar and gelatine, and when
inoculated under the skin of a goat provoked paralysis. It had no effect
on a pig. In keeping with this, Thomassen, in 1893, alleged that the
bacillus coli communis in certain conditions, when colonized in the
solid organs, produced a toxin which caused paresis and paraplegia. Blin
and Lambert, in 1896, found in the urine, in pure cultures, a short
ovoid microbe, motile, non-liquefying and bleached by Gram’s solution.
It grew on gelose and peptonized gelatine as a creamy surface layer
which did not extend into the medium, and assumed a brownish color as it
became older. On potato it formed a superficial bright yellow film. In
bouillon the surface film which formed gradually precipitated to the
bottom of the vessel.
This microörganism was not found in the blood, liver, muscles nor spinal
cord.
Inoculation into the pleural cavity of the horse induced
pleuro-pneumonia.
The contagion appears to be transmitted through the urine and morbid
discharges of the urino-genital canal, falling on the litter and floor
and thus contaminating the tail, and indirectly the generative organs.
The brushes, combs and rubbers used on one horse after another are
similarly incriminated. The mares, having a wider exposure to infection,
appear to suffer most. Comeny saw eighty sick mares to twenty-eight
horses, and the mortality was thirty-four mares to three horses. The
smallness and length of the male urethra and its frequent flushing
throughout its whole length with urine seems to give a greater measure
of immunity to the horse.
In the Blin and Lambert cases the indications pointed to a local
infection and to the presence in the spinal cord of the toxins alone. It
may be assumed that in such cases there was a purely local infection. In
the Zschokke cases on the other hand, with microbian infection of
internal parenchymatous organs the presumption is that the paralysis was
due to a totally different infection, as appears to be further indicated
by the morphology of the microbe. They may have been, however, but the
advanced and generalized stages of a primary local infection.
_Lesions._ These appear to vary with the progressive advance of the
malady. In an ass which was killed as soon as paraplegia appeared and
the necropsy made at once, the lesions were confined to the vulva,
vagina and bladder. In advanced cases the ureters and kidneys are
visibly involved together with the spinal cord, especially in the lumbar
region, and in certain instances the brain.
The vulva is swollen, held habitually open so as to expose the erect
clitoris; the mucosa is irregularly swollen and petechiated, and there
is a glairy or bloody discharge. The swelling usually extends to the
inner side of the thighs, the mammary glands and the adjacent wall of
the abdomen. The vaginal mucosa is congested, swollen so as to bulge
irregularly at intervals and covered with a glairy muco-purulent matter
often mingled with clots of blood. The urethra and bladder are red and
congested, with marked thickening and ecchymosis of the mucosa and an
abundant serous exudate which extends into the muscular and peritoneal
coats as well. Minute extravasations are found in the two outer coats
and petechiæ of the serosa is the rule. In fatal cases the ureters and
kidneys are involved, the renal parenchyma is greatly congested and
softened, the cortical part especially being of a dark red, and the
glomeruli distinctly enlarged. An oily sanguineous liquid can be
squeezed from the cut surface. The lumbar portion of the spinal cord
together with its meninges, is congested and arborescent, and in bad
cases this may extend upward to the head and involve the brain and its
coverings.
There is general congestion of the venous system with black blood,
especially noticeable in the arborescent lines on the inner surface of
the skin and in the serosæ, and the liver and spleen are gorged with
black blood, which, however, reddens on exposure to the air. Muscles and
parenchymatous organs may show a parboiled appearance. In the male the
swelling appears about the sheath and penis, the papilla, the urethral
mucosa and that of the bladder are deeply congested and petechiated, and
the kidneys and medulla may be implicated as in the mare.
_Symptoms._ In the _mare_ the early symptoms are the swelling and gaping
of the vulva, with the muco-purulent or sanguineous discharge and the
presence of redness, congestion and petechiæ of the mucous membrane.
In the _horse_ there is swelling of the sheath and a pendant condition
of the penis, which in its turn may be irregularly reddened and swollen,
and the papilla and orifice of the urethra are deep red and angry.
Most commonly these early local symptoms are overlooked until attention
is drawn by some lack of control of the hind quarters. When moved the
animal sways or staggers behind, knuckles forward at the fetlocks and
drags the toe along the ground. This weakness encreases, and although
for a time the animal can stand steadily, he is liable to fall when we
make him take a step, and when down he will require help to get up. In
advanced stages the animal remains recumbent and cannot be made to stand
even with help, the fore limbs have become implicated in the paralysis,
and in the end the respiratory muscles are involved and the patient dies
asphyxiated. This marks the occurrence of severe lesions in the medulla
oblongata. Incontinence of urine is a frequent symptom. Fever usually
sets in, in advanced cases. Recoveries may take place from the first and
second stages, the control of the muscular system improves, the animal
lies down and rises with greater ease, the drooping penis is retracted
within the sheath, incontinence of urine ceases, micturition becoming
less frequent and more abundant at a time, and finally muscular control
becomes once more perfect. Convalescence may be complete in eight days
if it begins early, while it may require two or three months when the
disease has been more advanced.
Some subjects survive without overcoming the paralysis, so that they
simply _eat their heads off_ if preserved.
_Diagnosis._ From hæmoglobinuria this disease is to be distinguished by
the history which fails to show its supervention on a period of hard
work and high feeding, followed by one or more days of rest and then
sudden exercise; by the swelling ecchymosis and discharge from the vulva
or sheath, and by the occurrence of several cases in animals that have
had an opportunity for a common infection. In case of death the
condition of the kidney, bladder and urethra, and the marked congestion
of the lumbar portion of the cord is significant, the congestion,
petechiæ and extravasations are deeper and the glairy discharge is
present.
_Prognosis._ From one-fourth to a third of the animals attacked either
die or are rendered permanently useless.
_Treatment._ Antiseptic washes and irrigations of the genito-urinary
passages, and the adjacent parts, if employed early enough, would tend
to abort the disease. Even if resorted to later, they would be of some
value in limiting the multiplication of the microbe and the absorption
of its toxins. For this purpose boric or salicylic acid, salicylate of
soda, permanganate of potash, or silver nitrate may be taken as
examples. They should be as thoroughly applied as possible, the bladder
being thoroughly evacuated and injected several times a day. As internal
medication, oil of turpentine and other stimulant antiseptics that are
eliminated by the kidneys might be tried in small doses frequently
repeated. Keep in slings. The patient that cannot stand up is lost.
_Prevention._ This consists in isolation of the healthy, thorough
disinfection of the stalls, gutters, combs, brushes, rubbers, blankets,
and the hands of attendants. Litter used for the sick should be burned
and manure piles secluded and disinfected. Even flies are to be dreaded,
so that darkness in the stable, fly nets, fly screens, and insect powder
and other means of insect destruction will be in order. Sponges and
other means of dressing should not be used indiscriminately on different
animals.
PROTOZOAN CATTLE FEVER. TEXAS FEVER. PALUDISM OF CATTLE.
Symptoms. Definition: protozoan, tick-borne, febrile, affection, of
wild damp lands, and warm seasons, with enlarged spleen and liver and
hæmolysis. Historic Notes; Old World; Australia; tropical and
subtropical America. Causes: contact of cattle from salubrious
districts with the insalubrious or with cattle from such; Piroplasma
bigeminum; a bovine parasite, reducing red globules by ¾ths.;
successive forms of piroplasma; the cattle tick, boöphilus bovis,
bearer of piroplasma; demonstration of the tick agency; toxic saliva
of tick; toxic property in blood; question of identity of
infection-bearing ticks. Lesions: putrefaction rapid, icterus, ticks,
blood oozing in skin, hydræmia, hæmoglobinæmia, few red globules,
small petechiæ, slight serous exudates and effusions: congestion,
petechiation, sloughing, perforation of gastric mucosa, congestion of
intestinal mucosa, in rectum like port wine; liver enlarged,
congested, biliary radicles in acini gorged with bile; spleen
enlarged, engorged; kidneys œdematous, blood-stained; bladder
petechiated; urine opaque or red, in convalescence watery; womb;
fœtus. Incubation three to ten days; delays due to hatching of ticks.
Symptoms: Acute case: anamnesis; hot season; hyperthermia 104° to 109°
F.; hurried breathing and pulse; anorexia; dulness; costiveness;
icterus; prostration; weakness; delirium; urine turbid, red; blood
hydræmic; diarrhœa; emaciation. Duration one to seven days. Fatal
(90%) to exotic cattle; mild in indigenous, or cool season. Mild case;
temperature 103°, anorexia, dulness, costiveness, enuresis,
albuminuria, pallid mucosæ, emaciation, round protozoön in globules,
ticks, oligocythemia. Differential diagnosis, from anthrax. Treatment:
laxative; antiseptic; mucilaginous food; picking off ticks;
anti-ixodic lotion; tick-free pasture or place. Prevention:
destruction of ticks; picking; dipping or smearing with tick killing
preparation, paraffin or extradynamo oil and sulphur, danger with
shipping; dressing of all cattle at intervals during warm season;
cultivation of tick-infected land; exclusion of cattle for one summer
and two winters; soil cattle for three weeks in each of two tick free
pens, to let ticks drop; danger of nonimmunized cattle in infested
area; suggestions for extinction by States. Immunization: Infection of
sucking calf; infecting by a few ticks: by graduated injections of
piroplasma blood; technique; injection of blood from body of tick.
Limited value of artificial tolerance. Marketing of the beef. Federal
restrictions.
_Synonyms._ Splenic fever; Spanish fever; Mexican fever; Southern cattle
fever; Australian tick fever; Tristeza; Red water; Black water; Bovine
periodic fever; Bovine yellow fever; Maladie du bois; Holzkrankheit;
Moor evil; Wood-ill; Ixodic Anæmia; Roumanian hæmoglobinuria.
_Definition._ A specific fever of cattle, enzoötic during the warm
seasons in the low, malarious grounds and wooded or uncultivated
districts of different countries, caused by a protozoön in the blood and
red globules, which is conveyed from animal to animal by ticks, and
leading to engorgement of the spleen and liver, destruction of the red
globules, hæmoglobinuria, and oligocythemia.
_Historic Notes._ This malady has doubtless existed from time immemorial
in different malarial districts of the Old World, where the wood and
moor ill is now coming to be recognized as a protozoan tick-borne
disease. The malady exists in Roumania (Starcovici, Babes, Gavrilescu),
Turkey (Nicolle, Adil-Bey), Sardinia (San Felici, Loi), Southern France
(Lignieres), Italy (Celli, Santori), Algiers, Tunis (Lignieres), Finland
(Krogins, Von Hollens), West Indies, Mexico, Nicaragua, United States of
Columbia, South America as far south as the Argentine Republic, German
East Africa (Koch), Transvaal (Theiler), S. Australia (Pound). In
Australia imported European cattle found the infection waiting for them
in the uncultivated bottoms. In America it doubtless prevailed on the
seaboard and islands of the Gulf of Mexico from the time of the
importation of Spanish cattle, but for the first definite account of it
we are indebted to Dr. James Pease, who records the widespread
destruction of the native herds in Lancaster, Co., Penn., in connection
with the introduction of cattle from the south. None of the southern
cattle died, but wherever they traveled, the native stock perished all
but universally. Other droves from South Carolina were equally
destructive to all cattle along their track. The recorded symptoms of
anorexia, great weakness, often inability to stand, trembling, groaning,
bloody urine, bleeding from the nose, costiveness, congested kidneys,
and decomposed, incoagulable blood serve to identify the disease.
Later, whenever southern cattle were moved north, the disease followed
their trail. Florida cattle left infection along their route until they
reached the border of Virginia, where it usually ceased. When taken from
the Georgia mountains to the lowlands, they died without infecting the
native stock, and, when such native stock of the lowlands were moved to
the hills or the north, they conveyed the fever to the stock among which
they came, though themselves well and improving all the time
(Wilkinson). Similar experiences were had in all the middle states up to
the war of 1861, but, in too many cases, the real source of infection
was overlooked. It was observed that the disease was confined to the
vicinity of the main highways and drove roads running north, and spared
the lands lying somewhat back of these routes. Attention was drawn to
the Texas cattle in 1853 when a herd of 450 which had wintered in Jasper
Co., Mo. moved north passing through Vernon Co. in June, and causing
losses of 50 to 90 per cent. of the native cattle along their course,
and only along that line. Such invasions occurred yearly, and in 1858
$200,000 worth of native cattle perished from this cause in Vernon Co.
alone (A. Badger). During the war (1861–64) the cattle, in Texas
especially, encreased without meeting with an adequate market, and, on
the opening of the trade once more, they were sent north in large
numbers carrying infection with them. When Forts Smith and Gibson had
been occupied by the Union soldiers, the southern cattle poured in along
the military road and the Kansas farmers along this route suffered
severe losses, as well as those to whom the southern cattle were finally
distributed (Bray).
_Causes._ Up to 1889 the true cause of Texas fever was unknown. It was
well established that cattle brought from the lowlands of the southern
states, during the warm season, though themselves in apparently the best
of health, proved deadly to northern cattle with which they came in
contact, to those that followed them in the same pasture during the same
warm season, and even in many cases to the mountain cattle of the south.
In the same way northern cattle, removed to the infected regions in the
south, contracted the fever and almost all perished. This was equally
true of cattle taken from the northern states to Jamaica or other
islands in the Gulf. In the winter season, after the first severe frosts
of autumn and before the last keen frosts of spring, the southern cattle
could be safely introduced into the northern states and on this a modus
vivendi, for a trade in southern cattle in the winter only, was based.
_Microbiology._ _Piroplasma bigeminum_: _Apiosoma bigeminum_. (Apios
pear, geminus twin). In 1888 Starcovici discovered pyriform organisms
(_Babesia bigeminum_) in the red blood globules of Roumanian cattle
suffering from hæmoglobinuria, and Babes, after a study of the
organisms, named them _Hœmatococcus_. The following year Theobald Smith
found them in the Texas fever blood, and recognized them as protozoa
(_Pirosoma bigeminum_). Wadoleck proposed _Apiosoma_, Bonome
_Amœbosporidia_, and Patton, _Piroplasma_. The latter pointed out that
_Pirosoma_ was already in use for another organism. Th. Smith’s
discovery identified Texas fever with the Roumanian hæmoglobinuria, and
stimulated the Bureau of Animal Industry to an extended research which,
in the main, elucidated the true nature of the disease. In a long series
of experiments the observers produced the disease in healthy susceptible
cattle, by injecting them, in the warm season with the blood of sick
animals, and as constantly failed in the experimental inoculation of
similar blood on non-bovine animals such as sheep, rabbits, Guinea pigs
and pigeons. In Australia, Pound had violent fever in two injected sheep
but no pyroplasma, and their blood injected on the ox, had no effect. In
none of these latter were the blood globules invaded by the parasite,
nor were the corpuscles lessened in number. In the affected cattle, the
red cells were reduced from the normal 7,000,000 per cubic mm. to
1,800,000 and even lower in some cases.
The _Piroplasma Bigeminum_ passes through a series of forms in the
blood. Theobald Smith found in the red globule and attached to its
margin a _pale round body_ 0.5μ in diameter, and staining freely in
_alkaline methylene blue_ and other basic anilin dyes and in
_hæmatoxylin_, but not in acid coloring fluids. These he found in the
red globules in acute cases, often in company with the pear-shaped
bodies, and usually in the absence of the piriform bodies in chronic
cases, in non-fatal relapses, in cases occurring in cooler weather,
(late autumn or early winter) and in immune southern cattle. The red
cells containing these rounded organisms were not crenated nor
distorted, though 50 per cent. of them might contain the parasite. He
looked on these as the earlier stage of the organism which later
developed into the _piriform body_, by segmentation of its substance.
The _piriform_ or _spindle-shaped bodies_ were usually found in pairs
connected at their pointed ends by a filament and extending across
nearly the whole breadth of the red globule. _Free microörganisms_,
pear-shaped or round, he failed to find in the blood of the large
vessels, but saw them only in the cardiac capillaries and especially in
the kidneys. In some cases the dim remnant of the disintegrated blood
globule could still be detected around the parasite.
Laveran and Nicolle, examining the blood of Italian cases by fixing and
staining, found the two forms, round or oval, and piriform, and claimed
that the first passed into the second by segmentation.
Lignieres working in Buenos Ayres with the most ample opportunity as
regards fresh material and authority to use it, watched the successive
changes in the living organisms, and reached further conclusions. He
diluted the blood with a 7 per cent. salt solution, or with ox serum or
both, until the globules stood apart in the field. The blood can be kept
under observation for days under a cover glass luted with sterile
paraffin, and the changes clearly traced. Securing the blood from a
subject having a great abundance of infected globules (usually at the
height of the hæmoglobinuria) he found mainly the _piriform parasite_
intraglobular and free, and in the latter an active whirling motion was
kept up by means of the flagellum at its pointed end. As usually
arranged in pairs (gemina), whether inside or outside the globule, they
are connected by the flagellum attached to their pointed ends. Careful
observation enables one to detect in the pyriform mass a small brightly
refrangent point like a nucleus. In this form the piroplasma is 3 to 4μ
in length.
After 4 or 5 hours, and on toward the 8th, the piroplasma has assumed
the _round_ or _oval form_ with a small linear prolongation (flagellum)
and shrunken to 1 to 1½μ in diameter. All the piriform bodies pass into
the rounded so that this last is the second stage of their development
and not the first as was formerly supposed. The round forms are always
present in great numbers in the cortex of the kidney in the second stage
of the disease (toward the subsidence of the hæmoglobinuria). The
refrangent nucleus is no longer to be seen.
After, one, two or more days there appears in the round parasite a
_chromatine mass_, which breaks up into 2, 3, 4 or 5 smaller _chromatic
bodies_, which Lignieres considers as germs. He has seen no division of
the protoplasm, but on the contrary the germs escape, yet remain for a
time attached to the outer surface of the parent organism. They show
rapid jerking movements.
Lignieres claims to have followed all these changes in the blood kept in
a sterilized glass cup at room temperature or in the thermostat, and in
the stomach of the tick, as well as on the warm stage of the microscope.
He claims to have made a further success in cultivating the parasite in
ox-blood serum highly charged with hæmoglobin. It was only occasionally,
and by the use of blood extraordinarily rich in the parasites, that
success was obtained. In one such case he produced five successive
cultures, the product being the rounded forms only and within these the
germs. There were no piriform bodies. These are not formed outside of
the red globules. The third successive culture in this medium grew with
great readiness, producing larger parasites with less disposition to
contract, but the fourth and fifth cultures were encreasingly poor.
Inoculation with these cultures failed to produce the disease. To
explain this the doctrine of passive germs, strong for survival, but
weak pathogenically, is hazarded.
To summarize, the successive stages of the piroplasma are: 1st. The
intraglobular _pear-shaped bodies_, with flagellum often connecting two
bodies. 2nd. The _rounded bodies with refrangent nucleus_—intraglobular
or extraglobular. 3d. The _free round bodies_ with the nucleus divided
into 2 to 5 _chromatin masses_. 4th. The _free chromatin masses_, large,
_active_, _infecting germs_, and small, _passive_, _noninfecting germs_.
The insuccess of inoculations of cattle with the last-named bodies
throws an air of doubt upon them as links in the pathogenic chain.
Definite information on the antecedents, environment, food, etc., of the
cattle unsuccessfully inoculated, including the season, shelter and
meteorological conditions might have brought us a step nearer to the
full life history of the piroplasma.
_The Cattle Tick_: _Boöphilus Bovis_: _Ixodes Bovis_: _I. Dugesii_: _The
Invertebrate Host of the Texas Fever Organism_. As early as 1868 shrewd
observers had noticed that in all outbreaks of Texas fever the affected
animals were covered with ticks, and drew the natural inference that the
disease was due to the bites of these insects. But the prevalence of
ticks in localities where the disease was unknown served to draw
attention away from the important fact that was suggestive of the true
explanation of the disease. The truth, however, constantly obtruded
itself that casual cases were never found in the absence of the tick.
Finally, in 1889, Kilborne conceived the idea of putting the matter to
the test, and with the approval of the Chief of the Bureau of Animal
Industry, set aside special paddocks for this purpose. Five native
cattle were placed, at midsummer, with three South Carolina cattle, from
which all ticks had been carefully picked, and they completely escaped
infection.
After seventy-one days, on September 6th, when the hottest weather had
passed, two were turned into a lot with four South Carolina cattle of
the original herd which had stocked the pasture with ticks. Of the two
one died of Texas fever, September 20th, and the other sickened in the
last week of September, and had a relapse in October, but finally
recovered. Of eleven other native cattle placed in this tick-infested
field up to September 30th, ten sickened and one escaped. One animal
placed in the field October 19th escaped.
Again three North Carolina cattle and three natives were placed in a
field September 14th and 15th. The new generation of ticks was retarded
by the cool season, so that few larvæ appeared on the native stock yet
one of the three sickened.
These results were confirmed by a series of other similar experiments.
In a further experiment, September 13th, thousands of ticks, mostly
mature, from North Carolina, were scattered over a second lot and four
native cattle turned into it next day. Three sickened and one, to
outward appearance, escaped.
These results were corroborated by experiments made in succeeding years.
In addition the disease was produced regularly in native stock by
placing on their skin the six-legged larvæ of boöphilus bovis, which had
been hatched in glass vessels in the laboratory. It was also shown that
the Washington winter destroyed the ticks in infected pastures so that
native cattle could be safely turned on them the following spring or
summer.
To summarize:—
1. The blood of southern cattle containing the piroplasma produced the
disease when injected into a healthy susceptible animal.
2. The animal with piroplasma in its blood, did not convey the disease,
in the absence of ticks, to a susceptible animal kept with it.
3. The animal with piroplasma in its blood and covered with ticks
conveyed the disease to a susceptible animal kept with it.
4. The ticks hatched and raised in glass vessels in the laboratory, when
put on susceptible animals, infected them.
5. Ticks taken from cattle harboring the piroplasma, and put on the skin
of susceptible animals, or on their pastures in the warm season,
infected the exposed stock.
6. The six-legged larvæ developed in the laboratory from the eggs of
mature ticks, taken from cattle having the piroplasma, conveyed the
disease.
7. On bare pastures as far south as Washington the winter frosts
destroyed the ticks so as to render the pastures safe on the following
season.
8. Ticks artificially raised in a warm laboratory, produced the disease
when placed on susceptible cattle in a warmed stable (65° to 80° F.) in
winter.
9. In the Gulf states, in stables which the cattle occupy constantly or
enter twice daily for milking or feeding, the ticks may live through the
entire winter. The same has occurred in the warm swill stables in the
north.
10. When taken into a new locality, it is rarely the mature ovigerous
ticks that bite and infect the native cattle of the place, but the next
generation of larvæ, so that time must be allowed for the laying and
hatching of ova.
11. Ovipositing usually occupies about a week, while hatching varies
with the temperature from two to six weeks.
12. Cases can be adduced in which native cattle followed, on the same
pasture, the tick-bearing infecting cattle, and remained for a week or
more, and yet escaped, the larvæ being as yet unhatched from the ova.
Other native cattle, following these two or three weeks later, perished
almost without exception.
13. This delay in the hatching may be indefinitely prolonged, and thus
in the southern states, the winter may be tided over, without the loss
of vitality in the ova, especially if it is covered by leaves, moss,
wood, or decaying vegetable matter.
14. When dealing with lung plague in Chicago in 1888, I noted the facts
that every cow that entered a city stable through the stock yards during
the dry, hot, midsummer weather died of Texas fever within a month,
while those that passed through the same yards during a particular rainy
week, all escaped. Berkau has shown that, in the absence of the coating
of the glutinous saliva, the eggs do not hatch, and here we may assume
that this covering was washed off by the rains and the eggs perished.
15. It has long been noticed that the ticks are scarcely at all
dangerous to young calves living on milk. This applies not only to
calves born of cows native to infected localities, and therefore
possibly having a congenital immunity, but also to the calves of
northern and susceptible cows, and which were exposed simultaneously
with their dams. It suggests a special defensive power in even the
bovine system when sustained on animal food. In the Bureau of Animal
Industry experiments, calves of four months, already using vegetable
food freely, sickened but still, as a rule, recovered.
16. The Bureau fed three cattle with adult live ticks (2000 to one
animal) but no infection resulted.
17. Four cattle were injected intravenously with the liquid charged by
crushing ticks in a mortar with distilled water. In some cases the
liquid was put through a Pasteur filter, in others only through two
thicknesses of filter paper. No infection ensued.
18. Lignieres injected, subcutem, in different animals the pulp of the
ticks at all stages of life, ground in a mortar with distilled water,
but found in no case tristeza as the result nor any destruction of red
globules.
The apparent paradox involved in the last three items probably finds its
explanation in the statement of Nicolle and Adil-Bey that, in biting,
the tick instils into the wound a venomous saliva which causes local
congestion and infiltration and presumably operates on the blood
globules as well. Curtice describes the two racemose glands situated
under the head shield, the secretions of which are pressed out by the
movements of the mouth ring and appendages. How much of this irritant
and toxic action is inherent in the saliva, and how much due to the
protozoan contained in it, has not been shown. Nicolle, Adil-Bey and,
later, Lignieres showed a similar toxic property in the blood. Three to
five cc. of blood taken from an acute case at the crisis and injected
into the marginal vein of the ear in a rabbit, killed the subject in a
few seconds. A similar amount thrown into the peritoneum of a Guinea pig
destroyed life in a few minutes. It is probable that the dilution of the
venom in the mass of tick pulp and distilled water reduced its toxic
quality to such a low ebb that the red globules were comparatively
unaffected by it and successfully resisted the attacks of the microbe.
The name _Boöphilus bovis_ was given to the bearer of the Piroplasma by
Cooper Curtice who made a special study of the tick, and its
development. For the description see _Parasites, Ixodes_. Among the most
marked and distinctive features of the female are the extreme shortness
and relative breadth of the rostrum, the slender palpi, the eight rows
of spines on the lower surface of the labium, the smooth mandibles with
terminal hooks, the limbs long, slender, in seven segments, and each
furnished with a terminal pad (pulvillus) and one hook (fore limbs) or
two hooks (hind). Curtice has identified the ticks of hæmoglobinuria in
various other countries with the boöphilus. The _Garrapata_ of Mexico
and the West Indies, the Hæmaphysalis rosea of Cuba (Koch), the Ixodes
Annulata of Florida (Say), the Ixodes Dugesii of Italy (Nequin), the
Ixodes Algeriensis and the Ixodes Egypti he found to be identical. There
may be some doubt as to the Rhipicephalus Annulatus Microplus of Buenos
Ayres, but as it agrees with the boöphilus in size, in the thickness of
its rostrum, in the eight rows of hooks on the lower surface of the
labium, in its host and habits, in the fact that it transfers the
piroplasma to cattle, and that it prevails on the same continent in what
were formerly colonies of Spain it is in all probability the same tick.
Curtice holds that it was originally a North African tick, which was
carried by the Spaniards to their American colonies. The Rhipicephalus
Annulatus of Roumania is probably the same, together with the ticks that
convey the Piroplasma in the other countries of Europe. There remain the
Hæmaphysalis of South Africa and the “Scrub-tick” of Australia to be
identified with, or differentiated from the Boöphilus. The life history
of the Queensland “scrub” tick coincides with that of the boöphilus of
America (Pound). As Australia derived her cattle from Britain it is
improbable that the tick was imported from Europe.
_Lesions._ If the course of the disease has been short, followed by an
early death, the carcass may be full and rounded, but if the animal has
been sick for five or six days there is marked loss of condition and
weight—emaciation. As after any other affection occurring during very
hot weather, decomposition sets in early, though not quite so speedily
as in anthrax, in which the subject dies full of rich blood. Something,
too, depends on the condition at death, putrefaction being manifestly
slower in protracted and debilitated cases. The color of the skin, the
mucosæ and normally white tissues varies in the same way. As it has been
largely seen in our northern States (and Australia) in fat cattle, which
contracted the disease in railway cars, cattle markets, or dealers’ or
butchers’ parks, etc., the deep orange hue of the white tissues is one
of the most marked features, and even the muscles have a deep mahogany
yellow hue. In poor milch cows and stock cattle in the South, on the
other hand, the icteric hue is often conspicuous by its absence. Cattle
killed early for experimental purposes may also show less icterus. The
color appears to be influenced largely by the abundance of red globules
in the blood when the animal was attacked, by the rapid destruction of
these globules, and the saturation of the blood and tissues with
hæmoglobin in solution. The presence of ticks on the skin, especially
along the ventral aspect, inside of the thighs, on the scrotum, udder or
perineum, sufficiently explains the number of minute infiltrations into
the derma, the oozing of blood or serum, and the matting of the hairs
into little tufts.
The _pale, watery condition of the blood_ was recognized as one of the
most constant features in 1868, together with the disappearance of the
red globules. The clot is remarkably soft and, at the crisis of the
disease, the serum is of a reddish hue by reason of the hæmoglobin in
solution. When, however, the urine is no longer stained, the hæmoglobin
having been eliminated, the serum assumes its normal pale amber hue. For
the first counting of the red globules in this disease we are indebted
to the Bureau of Animal Industry. The average count in healthy cattle
approximated to 6,000,000 per mm. of blood, and in three days this would
descend to 4,000,000, 3,000,000, 2,000,000 or even 1,183,000. The rates
of decrease was ⅛ to ⅙ of the entire number in one day. In case of
recovery the repair of the red globules was slow, from one to two months
being required to bring them up to the normal standard. Lignieres claims
recoveries after the count had gone as low as 300,000 per mm., and in
fatal cases, a few hours before death, it may be but 31,000 per mm.
In high conditioned animals, with high fever often aggravated by travel,
the muscles may be dark and firm, but in those out of condition and in
the advanced anæmic stages of the disease the muscles are pale, and
there may be subcutaneous œdema below the chest and belly. These last
features are especially noted by Smith and Kilborne.
The _lungs_ are usually normal. Sometimes limited congestions,
punctiform petechiæ, emphysema and small areas of œdema or hepatization
are noticed (Smith and Kilborne).
The _pericardium_ contains a little bloody serum and is marked by
petechiæ.
The _left heart_ is usually empty, but the _right heart_ full of fluid,
or later, of clotted blood, in the latter case without buffy coat. The
endocardium, and especially on the musculi papillares, is marked by
petechiæ, punctuate or in considerable patches. The cardiac capillaries
are full of blood, with numerous piroplasmata.
The _peritoneum_ often contains a little reddish serosity, and a slight
gelatinoid exudation is sometimes found around the kidneys or elsewhere
in the abdomen. Petechiæ are frequent.
The _stomachs_ usually show petechiated spots on the mucous membranes,
and more or less diffuse congestion. Sloughing of the mucosa at such
points is not uncommon, and even perforation of the folds of the third
and fourth stomachs. The Bureau of Animal Industry and Lignieres both
found these stomach lesions very inconsiderable. The smaller pinhead
erosions described by Gamgee were identified by the Bureau of Animal
Industry as bites of the strongylus convolutus. The _small intestines_
are usually moderately congested.
The _cæcum_ and _colon_ show more congestion, becoming at times of a
deep red or almost black hue, and considerable extravasation of blood
may take place. This is especially marked in the rectum, which may be of
a port wine hue, comparable to that seen in rinderpest or hæmorrhoidal
anthrax. The fæces are often dry and massed in balls in cæcum and
rectum, while if diarrhœa has set in, the discharges may be colored with
blood or blood elements. Yet in the cases reported by the Bureau serious
lesions of the intestines were rather the exception, and some subjects
showed scarcely any lesion.
The _liver_ is usually enlarged, averaging three to five pounds heavier
than in a healthy ox of the same weight. In these enlarged and congested
cases it is of a deep yellowish brown color, and often shows yellow
spots on the darker ground. Microscopically each acinus has a bright
yellow centre from which yellow radiating canals diverge to join the
peripheral gall duct. In the superficial or portal portion of the
acinus, the hepatic cells are granular from fatty change, yet the
nucleus is usually still recognizable. Toward the central zone it may
have disappeared. The further this has advanced, the softer, the more
easily pitted and the more friable the liver. The congestion of these
radical gall ducts with the dense colored bile, displays the structure
of the acini in a clear and beautiful way, which no injection can
accomplish. When the affected tissue is teased out and placed under the
microscope the inspissated contents of the bile canaliculi may be seen
as yellow cylindroid casts sometimes bifurcated to represent the union
of the two canals. If stained in Ehrlich’s acid hæmatoxylin, the
necrotic elements refuse to take the stain so that the contrast between
the dead and the living tissues is enhanced. Fatty degeneration is
common in the liver of healthy beef cattle so that this is less
significant than the congestion of the acini, and the phenomenal
distension of the radical gall ducts with inspissated bile.
The _gall bladder_ is usually full (½ pint to 1 quart or more), and its
mucous membrane congested and sometimes petechiated. The _bile_ is thick
and viscid, like tar, it may be yellowish green, darkening on exposure
and contains hæmatoidin crystals and abundance of flocculi showing
bright yellow or orange by transmitted light and reddish brown by
reflected light.
The _spleen_ is always enlarged, often enormously so. From an average
weight of 1.5 lb. to 1.7 lb. for a 1000 lbs. ox, it will rise to 2, 7 or
even 10 lbs. One measured 27 inches long by 7½ inches wide and in the
centre 3 inches thick (Rauch). Even in apparent health the Gulf coast
cattle have spleens averaging about 2½ lbs.
The spleen is gorged with blood which appears purple as seen through the
stretched and attenuated capsule, and darker petechial spots are found
at intervals. When cut into, the pulp alone appears dark, brownish red,
grumous, and showing under the microscope many red blood cells, larger
cells granular and undergoing fatty degeneration, yellow flocculi,
crystals of hæmatoidin, and granules of black pigment. It is the excess
rather than the nature of these agents that is significant. The pulp may
be pressed or washed out, bringing the trabeculæ and Malphigian bodies
into view.
The _kidneys_ are most seriously affected in acute and rapidly fatal
cases. There may be œdema, with blood staining and even extravasation on
their lower surface and in the adipose tissue. The gland may be enlarged
and the cortical substance congested of a dark brownish red or black.
Its capillaries are gorged with red globules in which the piroplasmata
are very numerous. The medullary portion is much paler, and with fatty
granules in the epithelium, and oil globules in the tubules. The renal
pelvis is more or less petechiated and marked by extravasations.
The _bladder_ is marked by petechiæ and usually contains some quarts of
urine more or less deeply stained with hæmoglobin. The depth of color is
in exact ratio with the extent and rapidity of the destruction of red
globules, and of the elimination of their coloring matter. When the
destruction is proceeding rapidly the urine may be as dark as port wine;
when their disintegration has lessened it may be pale though the
temperature is still high (105° F.) In slight and tardy cases there is
reason to believe that the redness of the urine may be omitted
altogether as is the icteric discoloration of the mucosæ, and hence
cases seen in animals indigenous to the protozoan fever districts, have
been described as a distinct disease. In these mild cases and advanced
stages there is usually a certain amount of albuminuria remaining. In
the early stages the urine is strongly alkaline, effervesces with acids,
and has a high specific gravity (1030–1040); later when abstinence and
suspended digestion and assimilation causes the patient to subsist on
its own tissues the reaction may become distinctly acid and the specific
gravity reduced (1010–1020). It no longer effervesces. During
convalescence while there is a great deficiency of red globules and
other blood solids, the urine tends to become pale and watery, of a low
specific gravity, and lacking in even its normal pigments.
The _womb_ will at times show petechiæ and in pregnant cows the fœtus
will show sero-sanguineous effusions or even extravasations in the chest
or abdomen, and hæmoglobinuria (Lignieres).
_Incubation._ Outbreaks occurring in the North, in herds into which
southern infected cattle have been brought, were at first held to
indicate an incubation of thirty or forty days (or even sometimes
sixty-five), but this is now explained by the time required for the
laying and hatching of the eggs of the mature ticks and the evolution of
infecting young larval or seed ticks. The actual incubation, as shown by
the subcutaneous or intravenous injection of the blood of an infected
ox, extends from three to ten days. The hyperthermia is usually shown on
the third day, and the more manifest outward symptoms on the sixth.
Extreme heat of the weather, a special susceptibility of the animal
infected, and especially a large dose of the blood and protozoa will
hasten somewhat the onset, but three to six days may be set down as the
rule after the ticks have introduced the parasite into their victim.
Cattle taken from the northern states and placed on southern pastures,
or passing over trails already well stocked with the ticks, are infected
at once and sicken in from three to ten days. Cattle in their northern
home placed on a previously uninfested field with southern cattle just
arrived, do not suffer for thirty, forty, sixty, and in exceptional
cases, even ninety days. The paradox is explained by the time wanted for
the laying of the eggs and the hatching of the tick larvæ. The female
tick does not lay eggs until she is fully mature, and if the ticks on a
southern ox are still immature there is a variable period of delay until
the eggs are mature enough to be deposited. Then the ovigerous tick
drops off her host and spends one week in laying her eggs. In warm
weather these eggs take three to four weeks to hatch, so that usually
five weeks elapse before the young (seed ticks) can climb upon the ox
and infect him. Add three to six days more for the actual incubation and
we account for about six weeks of delay in the appearance of the disease
in northern cattle. If we consider further that a wet season occurring
after the eggs have been laid and before they are hatched tends to
divest them of their protective covering and to expose them to
destruction, and that, in any case, a cold season will delay the
hatching until the recurrence of warm weather, and that the absence of
bovine victims will doom the new-born larva to an arrest of development,
so that a further indefinite delay may be entailed, we have abundant
explanation of the frequently delayed evolution of symptoms. Yet in
general terms the apparent prolongation of incubation is due to
fortuitous circumstances which delay the infection, and not to any
actual extension of the incubation itself.
_Symptoms of Acute Type._ Cattle infected outside the area of habitual
prevalence and stock from noninfected districts, conveyed into the
infected ones in hot weather, usually contract the disease in its acute
and fatal form. The period of the year is often significant, a number of
animals being attacked at once in the hot dry period of late summer or
autumn—July to September in North America, February to May in Argentina.
The first symptom is a rise of temperature, and this may last two or
even three days before other morbid phenomena are noticed. It may rise
to 104° F. in the first day and later to 107°, 108° or 109°. The more
acute the case and the hotter the weather the greater the rise. The
highest records are obtained late in the day, the lowest in the morning.
The temperature often rises for two to four days, and then suddenly
drops with the occurrence of collapse and imminent death. While the
thermometer is of the highest value in taking the temperature, yet the
extraordinary hyperthermia is easily detected by grasping the root of
the horn or ear, or by feeling the nose, feet, anus or lips of the
vulva.
After 2 or 3 days the respirations become accelerated to 60 to 100 per
minute, and the pulse to 90 to 100 or more. There is complete loss of
appetite and rumination after the development of these symptoms, the
mouth is hot and it may be dry, the muzzle dry, the head pendent, the
eyes dull or semiclosed and congested (usually icteric), the bowels
confined, to be relaxed again as the fever subsides. A disposition to
stand or lie down in water has been frequently noted. Nervous symptoms
are usually present. The extreme dulness, languor, and apathy, the
drooping head and ears, the unsteadiness of the support the animal
staggering or propping himself up by spreading all four limbs, and the
tendency to assume and retain a recumbent position, are marked phenomena
in our domesticated northern cattle. The paresis may absolutely
incapacitate the animal from getting up. In our wilder range cattle it
may show itself in active delirium and Lignieres notes the same of the
Pampas cattle in Argentina. The animal lying dull and apathetic
(triste), on being approached may raise his head, open his eyes and
glare threateningly at the intruder. Sometimes when trembling violently,
and swaying ready to fall, he will marshal all his remaining energy to
plunge at a man on foot or mounted. Some have become blind and
unconsciously walked against obstacles, others have been noticed to run
in wide circles.
The milk secretion is suppressed, any little that can be drawn in the
advanced stages having a thick, creamy appearance. Abortion is common in
the pregnant cow.
The condition of the urine has, however, always drawn especial attention
and the names _red-water_ and _hœmoglobinuria_ have accordingly been
largely applied to the disease. When, in infected areas, the milder
types of the disease have failed to show _red-water_ (Jamaica), the
identity of the affection with Texas fever has even been denied. Shortly
after the rise of temperature, the urine becomes turbid, and this
gradually encreases to a more or less deep red. It assumes its darkest
hue when the destruction of red globules is most active and during
convalescence it disappears. The suppression of urinary secretion may
account in some cases for the absence of this symptom even at the crisis
of the fever, yet, as a rule, it is present at such time, and, even
though it may have escaped notice during life, the _red-water_ is found
in the bladder at the necropsy. It may be of all grades, from the merest
tinge of redness to a reddish brown, coffee-grounds, or blackish aspect.
The coloration is not due to red globules, but to the hæmoglobin which
has escaped from the disintegrating globules, and been eliminated by the
kidneys. It is always associated with albumen, and, in the advanced
stages and during convalescence, when the elimination of hæmoglobin has
ceased, that of albumen continues in small amount for weeks.
The thin, watery appearance of the blood when the disease has reached
its height, is constant and even more characteristic than the
_red-water_. A single drop drawn from the skin will show to the naked
eye the pale, thin, transparent appearance, but examination under the
microscope will confirm this. It remains, too, for a length of time,
being recognizable for a month in cases of recovery. In connection with
the watery blood, the mucosæ and the muzzle (if naturally white) assume
a pallid aspect. This is best marked in the absence of icterus, yet even
with the yellow discoloration, the absence of ramifying red vessels is
very characteristic.
The bowels are at first constipated and the fæces passed in small, hard
balls. Later they may assume a reddish brown or chocolate color, and a
covering of mucus and fine blood clots. Diarrhœa supervenes in some
cases. In passing the fæces, the everted mucosa usually shows a dark red
color.
_Course and Duration._ Acute cases, above all if traveled or otherwise
excited, may terminate in death in 24 to 48 hours. More commonly death
will take place in 4 to 7 days. Some patients survive longer, but owing
to the extraordinary loss of blood globules and the lesions of important
solid tissues they are unable to rally, become steadily weaker and
perish in from two weeks to three months. Such animals are pale and
bloodless, weak on their limbs, careless of food, and encreasingly
emaciated. The pulse is weak and irritable and the eyes sunken. The
temperature becomes normal or nearly so, soon after the suspension of
the hæmoglobinuria. In cases of recovery there remains for a month or
more an unnatural pallor, with marked loss of condition and weakness
which are only gradually overcome. Convalescent animals are liable to
die of indigestion when overfed.
The _mortality_ averages not less than 90 per cent. in susceptible
mature cattle from a healthy district in the hot season. Later, from
October onward, the tendency is to a milder type of disease and a
greater ratio of recoveries.
_Symptoms of the Mild Type._ This is seen mainly in cattle indigenous to
the Texas fever district, in sucking calves, and in mature cattle from
healthy districts but attacked during the cool or winter season. It can
be produced at will by placing a limited number of ticks (5 to 20) on
the skin of susceptible cattle, especially in the cool season. Again, it
occurs as a relapse in cattle that have survived an attack earlier in
the season.
Though there are all gradations from the violent type, yet we may set
down as mild all cases in which the temperature does not rise above 105°
F., running frequently about 103° F. There is loss of appetite, dulness,
languor, costiveness, scanty urine, albuminous but not hæmoglobinuric,
pallor of the mucosæ, and marked loss of condition. Examination of the
blood shows the presence of the parasite in the red globules but usually
in the coccus or round form only, and the destruction and disappearance
of the globules is much less marked so that, though the blood is anæmic
and watery, it is not nearly so much so as in the violent and fatal
cases. Without the examination of the blood it may be impossible to
distinguish these cases from other febrile affections, yet occurring as
they do in the infected district in a number of animals at once, in the
cooler season, and showing albuminuria, and marked anæmic symptoms, they
should lead to suspicion and a search for the boöphilus on the skin, and
the oligocythemia and the protozoa in the blood.
_Differential Diagnosis from Anthrax._ As anthrax is the one disease
with which Texas fever is most likely to be confounded, it may be
profitable to collect in tabular form their differential features:
=Protozoan Cattle Fever.= =Anthrax.=
A disease of given districts, Prevails in rich, swampy
wooded, swampy, uncultivated, impermeable soils: not
and places where cattle from permanently implanted on open
these districts are taken. well drained lands.
Always shows Boöphilus, minute or Has no essential connection with
mature, on the skin of the the Boöphilus: latter usually
patient. absent.
Extends in warm season, as the Practically never conveyed by the
Boöphilus from an infected Boöphilus.
district is introduced.
Can be carried by the Boöphilus
apart from cattle.
Infection destroyed by winter Infection not destroyed by winter
frost above 35° of N. latitude. frosts.
Attacks bovine animals only. Attacks mammals, generally,
especially herbivora.
Lapse of 5 to 6 weeks after Outbreak may occur at once after
introduction, for tick introduction of infection.
development, precedes outbreak.
Confined mainly to summer season. Occurs at any season: most
prevalent in summer.
Sucking calves nearly immune. Sucking calves susceptible.
Mucosæ become increasingly pale; Mucosæ dusky brownish red, not
icteric in violent attacks. pallid, nor icteric.
Urine red or blackish in acute Urine exceptionally red: blood
cases at height of the disease. globules, in some cases.
Hæmoglobin. Albumen.
Blood becomes increasingly thin Blood becomes thick, tarry,
and watery: Oligocythemia. incoagulable; not watery nor
oligocythemic.
Blood reddens more or less in air: Blood reddens little, or not at
then becomes darker. all on exposure.
Spleen greatly enlarged, purplish, Spleen greatly enlarged; pulp very
often firm: pulp reddens dark does not redden in air.
slightly in air.
Liver enlarged, congested, often Liver enlarged, congested, dark
yellow, with fatty and necrotic red or violet.
areas: remarkable yellow
injection of radical bile ducts.
Bile abundant, thick, tarry. Bile fluid.
Kidneys pale, or congested, black. Kidneys congested.
Lymph glands slightly enlarged, Lymph glands enlarged; often
petechiated or (rarely) hæmorrhagic, black; peripheral
hæmorrhagic. œdema.
Pallor in violent cases, in Tissues generally reddish,
plethoric, icterus of tissues, bloodvessels dark, prominent.
especially of white ones.
Muscles in acute cases mahogany Muscles pale, grayish, unless they
colored. are seat of congestion or
extravasation.
Blood and its red globules show Blood shows bacillus anthracis,
the pyroplasma in different but no pyroplasma.
forms.
_Treatment._ Up to the present medical treatment has been essentially
unsatisfactory. Lignieres gave quinia sulphate in large doses by the
mouth, and in doses of 2½ drams subcutem daily, before and during
infection without any visible effect on the progress of the disease.
Methylene blue to (¾ to 1¼ dr.), salicylate of soda (7½ drs. daily),
arsenious acid (1¼ dr. daily), cacodylate of soda (7½ grs. subcutem)
were also tried with no good result. The Metropolitan Board of Health,
New York, claimed a succession of recoveries under the use of carbolic
acid in the drinking water and sprinkled on the ground so that the
animals inhaled it. The cases were, however, the survivors after the
first and more acute cases had perished, and the results no doubt
depended largely on the mildness of the attacks. The same agent in other
hands has not been equally successful. A large number of other agents
have been used in vain.
Among the most important measures are a laxative food, like flax seed
gruel, a careful picking of all ticks from the surface, the washing of
the skin with a 5 per cent solution of creolin, and the removal of the
animals to a tick-free pasture, lot, or building. This at once arrests
the introduction into the blood of fresh and continuous accessions of
the pyroplasma and, if begun early enough, will determine a mild and
non-fatal case.
_Prevention._ The prevention of the protozoan cattle fever is based on
the life history of the parasite, and may be directed (1st) to the
_destruction of the Boöphilus Bovis_; or (2nd) to _encreasing the
resisting power of the exposed animal, to the Piroplasma Bigeminum. 1st.
Destruction of the Ticks. (a) On the cattle._ The _picking of ticks from
the skin_ is effective if the object is to make the animal safe for a
few days only as the boöphilus habitually clings to the skin of the one
ox from the stage of seed tick to that of ovigerous female, ready to
drop off and lay its eggs. An animal going direct to slaughter may
therefore be sent through an uninfested district, even in the hot season
with a fair amount of safety, after the careful gleaning of the ticks.
The greatest care, however, must be taken to manipulate thoroughly all
parts of the skin and above all, the ventral aspect, the inner sides of
the limbs, the scrotum, udder and perineum. The animals must be shipped
at once after such gleaning of ticks with no further opportunity of
taking on a new supply, the cars and other conveyances must be cleaned
and treated with acaricides and the litter burned as soon as they are
vacated, and the cattle must be passed over no loading banks, chutes nor
yards that may by any possibility be used for other cattle unless these
are going into slaughter house.
The picking will safely remove all the larger larvæ, and the mature
ticks which are ready to lay their eggs, but it cannot be implicitly
trusted to remove also the all but invisible embryos or seed ticks, and
if the host is preserved these grow up and mature, while if they are
accidentally dropped or brushed from the surface, they climb upon the
first available ox and mature on that. By passing from ox to ox they may
be kept alive for a time in the pens adjoining the slaughter house, but
fortunately they do not travel over a few feet and if no cattle escape
from such pens there is small risk of their preservation.
_Dipping_ or _smearing_ to destroy the seed ticks on the skin becomes an
essential adjunct to, or substitute for, picking. The Bureau of Animal
Industry has experimented largely on dips with most important and
valuable results, even if they have proved only in a measure successful
and desirable. Aqueous dips they early discarded. Poisonous agents like
corrosive sublimate and arsenic are liable to poison through absorption
and licking, with the added drawback that neither these nor calcium
sulphide are at all effective in destroying the ticks. Proprietary sheep
dips were abandoned on similar grounds. Baths of cotton seed oil were
introduced by Francis, but proved not quite effective even when phenic
acid, benzine, gasoline, or different mineral oils were added. _Paraffin
oil_ gave the best results, and later a staple sold as _extra dynamo
oil_, which in combination with _sulphur_ (1:100) proved most
destructive to the ticks, was adopted. But in the hot season, when such
dipping is required, any one of these baths produced _heating_, and
illness in the cattle, and together with the exertion and excitement
served to rouse into dangerous activity the germs already present in the
blood. Ophthalmia, too, was a very frequent result. If the cattle could
be kept on their native pastures the dipping might be permissible, but
this was to lose the object aimed at—the wholesomeness of these cattle
on uninfected ranges. When shipped north in the hot weather the losses
were so great as to be prohibitory.
If, however, it could be reserved for use on the southern pastures, to
prevent the maturing of the ticks and the laying of eggs for a future
generation, it might be employed to rid the infested pastures of the
boöphilus, and consequently of infection. The question, then, is reduced
to the comparative advantage of the destruction of the ticks, on the one
hand, and the cost of frequent dipping throughout the warm season, on
the other. The following season there ought to be no ticks left.
Cooper Curtice advocates kerosene 1 gallon in combination with an equal
amount of lard, 1 lb. sulphur, and 2 lbs. pine tar. Melt the lard, add
the sulphur and tar, bring to the boiling point, cool, add the kerosene
with stirring. Rub daily with a brush on the whole skin but especially
inside the arms and thighs. On tick-infested pastures it must be
continued through the season, and if thoroughly done will leave the
fields tick-free the following year. Like oil dipping it would
manifestly be incompatible with immediate shipment on a long railway
journey, but Curtice vouches for its efficacy as a means of eliminating
ticks from southern pastures. The main question is the expense. What
would be perfectly adapted to small herds of very domesticated cattle in
North Carolina would be a herculean and expensive task in the large
herds of Texas. Curtice mentions cotton seed oil, fish oil and even a
small proportion of linseed oil as good substitutes for the lard.
_Destruction of Ticks on Pastures._ Fields, farms and larger areas can
be freed from the boöphilus by the thorough application to the cattle
pastured on them of one of the above-described methods, provided that no
strange cattle are admitted on the land. The ticks are sluggish and,
unless carried on the bodies of animals, do not crawl many feet from
where they drop. If cattle are kept in the next lot, they should not be
allowed to come in contact with the treated or protected stock, but a
double fence with an interval of five or six feet, will prove a
sufficient barrier to the advances of the tick, apart from its bovine
host.
_Cultivation_ of a tick-infested soil for one year or more, with
complete exclusion of cattle from November or December until March or
April of the second year thereafter, will exterminate the ticks. During
the intervening summer there may be plenty of young live ticks on this
land, but, in the absence of the bovine host, and blood, these cannot
reach maturity, lay their eggs and thus leave new generations. In the
course of the second winter therefore they are exterminated. In
restocking such land, it is all important to see that the cattle placed
upon it do not introduce any ticks on their bodies. Equally essential is
it, to see that cattle are excluded from the cultivated land in winter
as well as in summer. During warm days ovigerous female ticks, dropped
from the skins of such cattle, may produce eggs and larvæ to start a new
crop in the coming summer. But as has happened to the wood ticks of the
North, so in the South, cultivation of the soil and the exclusion of
cattle for a length of time, will exterminate the race of ixodes.
_Exclusion of cattle for two winters and the intervening summer_ will
eradicate the ticks even in the absence of cultivated crops. To reach
full maturity and propagate its kind, the tick must have bovine blood.
If therefore the ticks of a whole season (spring, summer and autumn) are
denied bovine victims, and thus cut short in their development, no crop
is left for the succeeding spring. If then a cattle pasture is divided
in two parts by a double fence with an intervening space of 5 or 6 feet,
and if the cattle are confined to one of these parts for a whole year
and are transferred to the second half in January after dipping or
smearing with ixodicide oil they may be kept entirely free from ticks
thereafter. That half of the pasture which is abandoned in the second
year, will be tick-free and salubrious in the third year.
Another resort, advised by Curtice when a large tick-free pasture is
available, is to place the infected cattle in a pen, and _soil_ them for
three weeks, no longer. Then transfer them to another clean pen and
_soil_ them there for three weeks more. Then examine closely, and if
entirely free from ticks they can be put in the large clean pasture.
Should they still carry a few ticks they should be placed in a third
clean pen for two weeks more, when they will be tick-free and may be
turned into the large pasture without the formality of examination. This
is substantially based on the period of parasitism of the tick on the
skin of the ox, and its development from the newly hatched larva (seed
tick), to the ovigerous female. This period is from three to four weeks.
The greater number of the ticks are therefore dropped off as mature
ticks to lay their eggs in the first pen, while the remainder are
similarly left in the second pen. As the stock leaves the two pens in
succession long before the deposited eggs have had time to hatch out,
they can take on no more ticks and emerge from the second pen clear and
safe. The same pens cannot be used repeatedly, as the eggs develop into
seed ticks in 15 days in hot weather, and at once attack cattle.
A stockowner who, independently of his fellows, adopts one of the above
expedients in an infested district, is however confronted by the risk of
the infection of his herd, by the accidental or careless contact of his
cattle with outside ones, and especially with the places where they have
been. A broken fence and the entrance of tick infested cattle, or the
escape of his tick-free cattle into infested lands, will be the death
warrant of all that have not been previously exposed to the disease.
Another consideration is that this rigid seclusion of the protected herd
must be continued indefinitely so long as ticks are maintained anywhere
in the district. The protected animals cannot be driven over a highway
without exposing them to almost certain death. Even if a group of
adjacent stockowners agree to purify their respective farms, they cannot
debar their less careful neighbors from using the highways for
tick-infected stock, nor from turning such out on adjoining fields. The
veriest scrubs, admitted to the highways, woods and unfenced grounds,
keep up the general diffusion of the fever germ and its tick bearer and
undo the best directed efforts of any combination of owners of high
class and valuable stock.
Well directed legislation, excluding cattle for one or two years, from
all woods and unenclosed lands, and enforcing some one of the available
methods for the clearing of fenced and stocked lands (cultivation,
pasturage by cattle on alternate years, frequent dipping or smearing,
passing the stock through a succession of pens), could be made to put an
end for all time to the obnoxious tick. If even some other than bovine
animals should be discovered to harbor the boöphilus and pyroplasma it
could be included in the prohibition and the work made complete. The
results would far more than compensate for any necessary outlay.
Illinois, with 55,414 square miles of area has over 3,000,000 cattle.
The coast states from Virginia to Texas, with Arkansas, Indian Territory
and Oklahoma, amount to 767,215 square miles, and in the same ratio
should sustain 43,340,040 head. A stock of 25,000,000 at $20 per head
would amount to a capital of $500,000,000. Immune from the pyroplasma
these cattle would draw freely on the best blood of the north and under
the milder skies would compete with the northern cattle on more than
equal terms. Living in the open air, they would in the main escape
tuberculosis and the other stable-propagated diseases of the north, and
their dairy and beef products would enter the market free from
suspicion, and command a readier sale, if not a higher price. The stock
themselves could be moved to northern markets at all seasons without
restriction, and escape the serious losses that now come from a sudden
transfer, while pyroplasma-infected and susceptible, to the violent
excitement of travel, and the frost-bound destination. Their owners
could watch the markets and sell in the best, in place of being
compelled, as at present, to hurry them in during November and December,
and to sell often at a ruinous sacrifice. With the extinction of the
boöphilus the present unrestricted pasturage and all other privileges
now enjoyed would return, freighted with a value never borne before, and
the few Southern cattle and cattle products need fear no competition in
the markets of the world, and could no longer be justly subjected to any
restriction.
There would remain the constant danger of the introduction of the
boöphilus anew from Mexico, the West Indian Islands and the Central and
South American States, where in the absence of frosts the boöphilus
cannot be extirpated in the same way, and here accordingly all
importation must be forbidden. Cattle from Southern Florida and from
islands on our Southern Coast may demand a similar exclusion. There is
too much at stake to permit any laxity, and no infected area should be
allowed to send out its cattle until it has been abundantly well proved
that such district or State is absolutely tick-free.
2d. _Immunization: Encreasing the Resistance to the Piroplasma
Bigeminum._ That cattle can be fortified to resist the attacks of the
piroplasma is shown in the immunity possessed by the indigenous herds
generally, in the regions infested with this parasite and the boöphilus.
To begin with, there may be a survival of the fittest, the more
susceptible strains of blood having been long ago cut off. But the
immune southern cattle if kept for years outside of the infested area
and then returned to it, suffer a mortality about as great as that of
northern cattle in the same circumstances. Their earlier immunity,
therefore, is not merely a racial difference, but must be due in
greatest part to an acquired resistance, and further, this resistance is
not permanent but must be renewed at short intervals. The immunity may
be in part acquired in the womb of the infested dam, in the last months
of gestation, but it is chiefly post-natal through the attacks of the
ticks.
_a. Infection of sucking calf._ The indigenous cattle acquire immunity
mainly through the attacks of the boöphilus, in the first month or two
when they are still on an exclusively milk diet, that renders the
piroplasma practically harmless. Following a parallel method, calves,
living on milk alone, can be taken into the infected regions and exposed
to the attacks of the ticks with safety, and with the result of
protection for the future. Escaping the first invasion, they continue to
harbor as many ticks summer after summer, as will reinforce yearly their
acquired power of resistance, so that they continue measurably safe
though spending the life in the area of the infection.
Francis and Connoway applied this to Jersey calves of two to six weeks
old applying to each 25 to 50 ticks. It led to slight hyperthermia, some
dulness and inappetence, but on recovery they all gained flesh and
condition. Two died from exposure but necropsy showed no sign of Texas
fever. The following summer all were infested with 200 to 500 ticks
apiece but not one sickened in consequence. These were Jersey calves
(the least susceptible breed) and the experiments were made in cool
weather in autumn. The limitation of the practice to the cool fall or
winter months renders the operation much more safe.
_b. Infecting Older Animals by a limited number of Ticks._ Yearling
Jerseys, Holsteins and Shorthorn were subjected to 25 to 50 ticks in
July, they showed only slight rise of temperature, and later resisted
the free exposure to tick infestation. It must be recognized that these
were still young animals, with presumably greater resisting power than
the mature, but on the other hand they were of the susceptible northern
herds, they were first infested in the hottest season, and the acquired
resistance appears to have been perfect throughout the succeeding
summer. The added precaution of subjecting them, in late autumn or
winter only, to the ticks raised in a warm room or thermostat, would add
greatly to the safety of the operation. After recovery from the effects
of the first crop of ticks, a second crop of 50 to 100 should be placed
on the skin so that the system may be thoroughly habituated to them and
the measure of resistance correspondingly strengthened.
This measure may be advantageously applied to valuable cattle that are
to be moved into the infecting territory, but it has serious drawbacks.
The relative strength of the poison introduced by the ticks to the
susceptibility of the animals on which they are placed, can never be
perfectly gauged, and a certain small but appreciable number of deaths
result from this first infesting. This has been observed in North and
South America, Australia, Roumania and Turkey. Again, the plan entails
the necessity for clean, non infected premises (lots or buildings) for
each fresh lot of cattle, as the places previously used are left in a
tick-infested condition, and are likely to furnish a dangerous excess of
ticks to any susceptible animal. The buildings could, of course, be
disinfected and purified, but this entails considerable expense.
_c. Infection by Graduated Injections of Blood Containing the
Pyroplasma._ Up to the present this is the most promising method of
securing resistance to the pyroplasma. It is advised to take the blood
from an immunized northern animal or from one indigenous to the infected
district. Such an animal is not, however, strictly speaking _immunized_.
It has acquired a _tolerance_ so that it is no longer in much danger of
succumbing to the pyroplasma, but it does not exclude the pyroplasma
from its system. The _micro-parasite_ is still found in the blood,
though mainly in the coccus-like form in the interior of the red
globules. The animal to be fortified against the disease is therefore
inoculated with the germ of the disease itself, though it may be, at the
time, in a somewhat inactive form. If, however, the inoculated animal is
specially susceptible, or if the dose is excessive, the disease is
produced in deadly form. The virulence is less in the case of blood
drawn from a northern animal just recovered from the disease, than from
an animal indigenous to the infected district, and which harbors the
pyroplasma, it may be in spore form (Lignieres), without showing obvious
disease. The former source of the blood is therefore the more desirable,
while the latter is the more easily obtained. The precaution, however,
should be adopted of reducing the dose when taken from an indigenous
animal. Another important precaution is to select the winter or cooler
season for the operation rather than the summer.
The animal which is to furnish the blood may be fixed in stocks, or held
with a bull ring, or it may be cast so that it can be kept still. The
hair is clipped or shaved from over the jugular vein in the upper third
of the neck and the surface is washed with soap and water and with a
five per cent. aqueous solution of carbolic acid. A thick cord inch (¼
inch) is tied tightly around the back part of the neck so as to compress
and raise the jugulars. With a sharp pointed bistuory sterilized by
boiling, a small incision is made through the skin, directly over the
centre of the jugular and a cannula and trochar ⅒th inch in diameter and
sterilized by boiling, is passed obliquely upward through the coats of
the vein and the trochar withdrawn. The blood flows through the cannula
and is received in a sterilized (scalded) glass beaker. The blood is
stirred slowly with a sterilized glass rod until all the fibrine has
coagulated when the latter is lifted out and the remaining liquid blood
is ready for use. The blood is injected with a hypodermic syringe which,
with its nozzle, has been thoroughly sterilized by boiling. The point
selected for injection is usually back of the scapula on the middle of
the chest. The skin is clipped or shaved, washed with soap, soaked in a
five per cent. carbolic acid solution, then pinched up, perforated with
the point of the bistuory, and with the nozzle of the syringe passed
through this wound the blood is injected into the subcutaneous
connective tissue. The slight wound may then be covered with tar or
collodion or merely left undressed. The mass of blood in the connective
tissue may be diffused through its meshes by rubbing so as to favor
absorption.
The dose of defibrinated blood employed is 5cc. if from an _immunized_
northern ox, or 3cc. or even 2½ cc. if from an indigenous animal. The
animal operated on should be in good health and condition, well fed, and
kept if possible in the shade, in a cool stable, or under trees.
In some respects it is preferable to operate on the animals before they
are moved from the north or other noninfected territory, but as there is
danger of infection in preserving and carrying the blood, the treatment
is more conveniently deferred until the animal reaches the infected
region where the blood can be had fresh. In such cases the animals
should be shipped in carefully disinfected cars, and before leaving they
should be liberally oiled or larded so that the ticks will not climb
upon them, in being led to their stable. They must be kept stabled until
the febrile effects of the injection have entirely passed, usually a
month or more.
_d. Injection of Blood from Bodies of the Ticks._ In view of the
difficulty of shipping infected blood without danger of contamination or
sepsis, and the occasional accidents that happen to animals injected
with such blood outside of the infected area, attempts have been made
with dried blood, or that charged with antiseptics (calcium oxalate), or
that had been frozen, but in every instance the virulence of the
pyroplasma was destroyed. Dalrymple and Dodson availed of the blood
drawn by mature ticks, which, in their blood-gorged condition, were
shipped to the points where the injections were to be made. The mature
ticks charged with blood were taken from infected indigenous cattle, and
at once shipped. On their arrival they were washed externally with a
mercuric chloride solution (1:1000) to destroy any adherent saprophytic
or other bacteria, mashed in a sterilized mortar, with a few cubic
centimeters of boiled water and the fluid portion drawn off and injected
subcutem, into the animal to be protected. From 3 to 12 mature female
ticks were used for each animal. The results were the same, only milder
than when the blood of the indigenous animal was used direct, and the
subsequent tolerance of the pyroplasma proved satisfactory.
It is difficult to explain the moderate effect of the considerable mass
of blood injected in such cases, as compared with the deadly effect of
the small amount that could come from the insertion of the rostra of
even 50 or 100 ticks. But perhaps the venomous saliva instilled in
concentrated form into the bites, protects the pyroplasma in the very
limited area, until it gains sufficiently in numbers and force to hold
its own even in the circulating blood.
_Limited Value of Artificially Induced Tolerance._ It must be added that
all these measures for securing a partial immunity in the individual
animal, and which enable us to safely introduce previously susceptible
cattle into an infected district, virtually imply the continuance of the
infection and infection bearer (boöphilus) for all time. They give no
promise of the extinction of the bovine infection at even a remote
future time, nor the abolition of the taxes for prevention, which must
oppress the southern cattle owner so long as the disease continues. They
are most valuable measures truly, but mere temporizing ones at the best,
and they could just as well give place to the more sanitary, economical
and statesmanlike measures for its radical extinction.
_Marketing of the Beef._ The piroplasma is not communicable to man, so
that the carcasses of well conditioned cattle, which bear the infection
need not be rejected as human food. It is only in severe and advanced
cases in which anæmia, emaciation and pallid innutritious muscles are
marked features, that the flesh is objectionable, and then only as being
somewhat lacking in nutriment and digestibility,—not because of
poisonous qualities. Danger of infection to cattle might be apprehended,
but, if used outside the infected area, the second condition of the
disease—the boöphilus—is lacking, while within the existing area of
prevalence of the fever, the propagation from the carcass to the animal
is infinitely less likely than from one live animal to its fellow.
_Federal Restrictions on Cattle within Infected Areas._ The orders of
the Secretary of Agriculture prohibit the removal of cattle from the
following states and territory into any states that extend northward of
the line indicated: California, Oklahoma, Indian Territory, Arkansas,
Tennessee, Virginia and the states south of these to the Gulf of Mexico.
Exceptions are made in the case of fat cattle, sent out of an infected
area, for immediate slaughter at the point of destination; conveyed in
cars or boats placarded as containing Southern cattle and receiving no
other; fed and watered enroute in yards that admit no local or other
cattle and which can be reached without passing over any highway or
unfenced open ground; and unshipped at their destination directly into
yards reserved for Southern cattle only and within the same enclosure as
the slaughter house. If reshipped the cars used must be subjected to the
same restrictions. The cars, boats, chutes, alleyways, pens and troughs
are to be disinfected by thorough cleaning; by saturation of all wood
work, etc., with a mixture of 1½ ℔s. lime, ¼ ℔. phenic acid and 1 gallon
of water, or ¼ ℔. chloride of lime in a gallon of water, or a jet of
steam under a pressure of 30 ℔s. to the square inch. The manure and
litter must be mixed with quicklime, or saturated with a 5 per cent.
solution of carbolic acid, or secluded in a well fenced enclosure from
February 1st to November 15th of each year. This is made the duty of the
stock yard companies.
Cattle may be freely moved north from the infected area at any time from
November 1st to December 31st, if inspected by an officer of the U. S.
Dept. of Agriculture and found free from infection.
Provision is also made for sending infected cattle northward at any
season, if they have been first dipped and pronounced free from the
disease by an inspector of the department.
Cattle from Mexico are admitted under analogous rules.
PROTOZOAN ICTERO HÆMATURIA IN SHEEP. PALUDISM OF SHEEP. CARCEAG.
This is described by Babes and Starcovici as prevailing among sheep in
the delta of the Danube, and held by them to be identical with the
Roumanian Hæmoglobinuria of cattle (compt. rend. de l’Acad. des
Sciences, 1892). Its essential cause is a piroplasma affecting the red
blood globules, and very analogous to that of the protozoön of Texas
fever, but its especial election for the sheep shows a specific
difference, inasmuch as the Texas cattle fever does not attack sheep.
Not only the parasite, but the symptoms and lesions as well, furnish a
close counterpart to those of the cattle infection. It remains to be
seen whether the pathogenic difference is due to a distinction in the
piroplasma or to the absence from the Southern States of America of the
particular tick or other insect which attacks the Danubian sheep.
Bonome (1895, Virchow’s Archives) describes the same disease as
prevailing in Italy, describing the parasite and lesions at great
length.
Finally my colleague Dr. W. L. Williams, and later Dr. Knowles, have
identified the disease in the upper part of Deer Lodge Valley and the
lower part of Silver Bow Valley in Montana, prevailing among sheep only,
extending year by year, and proving disastrous to the sheep husbandry.
Sheep were introduced into these valleys as early as 1875, but it was
only in 1891 that the flock masters recognized the existence of this
disease. By 1895 it prevailed over an area of 300 square miles. It made
its advent in 1891 in four or five large flocks (2,000 to 10,000 head
each) on land which they had occupied for nine years, and so
disastrously that several sheep ranchers, after an experience of a year
or two, sold out to the butcher and abandoned the sheep industry.
All or nearly all cases seen in 1896 were in parturient ewes, (4 to 6
days after parturition), the constitutional condition attending on
lambing proving a most potent factor in causation.
The protozoön repeated the characters of that found in the sick sheep in
Italy and the Danubian delta, and the conditions of the blood and the
structural lesions supported the idea of identity.
Altitude seems to have little or no effect as a causative factor, as the
disease is domiciled alike on the low alluvium of the Danube and the
Deer Lodge Valley of Montana over 5,000 feet above the ocean. In both
regions there is the common condition of inundation or its equivalent
irrigation, for the Montana range is dry and arid, interspersed with
alkaline bogs inimical to vegetation, but prolific and fruitful under
irrigation. The Montana disease has been attributed to mineral poisons
carried on the winds from the extensive copper smelters in Butte and
Anaconda, but the smelters had been in existence for eight or ten years
before this disease was observed, and from its appearance the infection
has gradually extended, attacking sheep only, and sparing other domestic
animals, which would have suffered as well from a mere mineral poison on
the vegetation. The doctrine of a mineral poison is equally contradicted
by the habitual prevalence of the disease in spring and autumn, while it
is dormant in winter and summer. In winter the flocks eat hay cut from
the richer valley lands and meadows, while in summer they are pastured
on the foothills and mountains, and drink from the mountain springs
surrounded by alkaline bogs. The autumn outbreak occurs long after the
mountain grasses have dried up, when the flocks are thrown back on the
supplies obtained from the alkaline bogs and the valley pastures. In
late winter and early spring the growth naturally starts first in the
same boggy and valley areas, and both facts suggest a microbian
infection—protozoan or bacteridian. If an intermediate host or
bearer—insect or other invertebrate—is to be assumed it implies two
generations of these, a spring and an autumn one, in the same season, or
otherwise a restriction of such invertebrate to the low valley pastures
and the alkaline bogs on the higher levels, and that they disappear from
the drier, arid areas in summer. It cannot be an obligate parasite like
a louse or melophagus which would be constantly present, nor a musquito
absent in early spring. But up to the present no invertebrate host or
intermediate bearer has been identified. Cases were at first reported in
the Angora goat, but this animal is now known to be immune.
_Microbiology._ The parasite is formed in the red globules and blood
serum of the affected sheep and closely resembles the microbe of Texas
fever. In the blood globules the parasite is seen in different forms,
round, oval, oblong or curved and from one tenth to one sixth the
diameter of the red globule. A single red globule may show from one to
four of the microörganisms. They may at times show indications of
division, and at others, automatic amœboid movements, from one portion
of the blood globule to another, or from the periphery toward the
centre. The affected blood globules are usually enlarged, having lost
their biconcave outline, and become biconvex or spherical, with
irregular crenated surface, and a dull, lustreless appearance instead of
a clear red or yellow aspect. The protozoön stains readily in anilin red
or methylene blue.
_Lesions._ The condition of the carcass was good or even high, in sheep
attacked when in good flesh, and in which the affection ran a rapid and
fatal course. In sheep attacked while in low condition on the other
hand, the case tended to be milder and more prolonged, and the body was
emaciated and anæmic. Dropsical swellings were common on the ears and
sides of the head and neck.
The skin, connective tissue, fat, and other normally white tissues were
usually of a yellow color, varying from sulphur to lemon color. The
muscles were pale and soft with a yellowish tinge.
The blood was pale, thin and watery, especially in protracted cases,
formed a loose coagulum, or remained fluid with a grayish red color.
There was marked leucocytosis (1:4 or 5).
The stomach and intestines were more or less icteric, and contained
little ingesta.
The liver was congested, softened, shrunken in protracted cases, colored
of a deep yellow especially in the interior, and with gorged biliary
radicles so that the acini stood out very prominently. The gall bladder
was usually well filled with a thick, flocculent bile, yellowish green,
blackish green or chocolate color.
The spleen appeared shrunken, somewhat spherical, 2 to 3 ozs., firm, and
with a dark, reddish brown pulp.
The kidneys were greatly enlarged, weighing 12 to 16 ozs., dark red or
bluish black, friable, and on section exuding freely a bloody or
chocolate-colored liquid. The capsule was easily detached. The bladder
contained a bloody or chocolate-colored urine, but was sometimes empty.
The heart cavities were empty or contained small diffluent blood clots.
Petechiæ were common on pericardium and endocardium.
Yellowish or yellowish green gelatinoid effusion was often present, not
only on the head and neck, but also on the inner side of the thighs, and
in one or other of the serous cavities.
_Symptoms._ The first indications noticed are dulness, listlessness, a
dragging behind the flock, ceasing to graze, arched back, and stiff or
unsteady movements. There is moderate fever, yellowness of the visible
mucosæ and skin, and rosy, bloody, or reddish brown urine.
Puffy dropsical swellings are noticed, especially on the ears, sides of
the face, on the neck or thighs, and the patient lies down most of the
time.
The patient usually dies in a state of collapse which has lasted for
several hours, yet in certain cases it is preceded by a convulsive
agony.
It is certain that the affection may appear in a mild form, as sheep
slaughtered in apparent health are found to show the general icterus,
the congested liver, and the leucocytosis with crenation of the red
globules which characterize the disease. The icteric carcasses are said
to be recognized and condemned at Kansas City and Omaha.
The _duration_ of the affection is from 1 to 5 days, though it may last
longer, and severe attacks usually end in death.
The _prevention_ of this disease can, as yet, be based only on the same
principles that guide us in the case of Texas fever. Search should be
made for an invertebrate host of the protozoön, by the extinction of
which infection may be stopped. The spring outbreak could be opposed by
feeding hay on safe ground until the higher pastures furnish sufficient
vegetation. To counteract the autumn attack, the sheep might be fenced
out from the alkaline bogs, and the forage supplied in the form of hay
or soiling crops. If it should appear that any wild animals harbor or
transmit the parasite, a campaign of extermination upon them would be in
order. If, as seems to have been the case in the early nineties, the
movement of sheep from the infected flocks and pastures tends to cause
the disease, this should be legally interdicted. Finally, the complete
extermination of the sheep on infected areas could be practiced, and
their place supplied by the immune Angora goat.
PALUDISM IN DOGS. MALIGNANT PROTOZOAN JAUNDICE.
Distribution: Senegal, Lyons, E. Africa, Paris, Pas de Calais, Cape
Colony. Microbiology: piroplasma: differentiation from that of Texas
fever: pathogenesis: tick-borne. Symptoms: incubation 3 to 5 days;
dulness, prostration, apathy, drowsiness, anorexia, thirst,
hyperthermia, icterus, hæmoglobinuria, offensive odor, emaciation,
protozoön in globules, loss of globules. Death in collapse. Lesions:
body shrunken, emaciated, fœtid; dark tissues, mahogany yellow,
petechiæ, enlarged congested liver and spleen; muco-enteritis; bloody
urine. Treatment unsatisfactory. Prevention: keep from tick infested
land; clear and cultivate land; smear dog with insecticide ointment
when hunting.
In certain malarial districts dogs suffer severely and even fatally from
a febrile affection in which violent shivering is followed by great
hyperthermia and yellowish or brownish red discoloration of the visible
mucosæ. It was frequently attributed to malaria, and even sought to be
identified with intermittent fever in man. Marchoux in 1899 studied this
disease on the malarious seaboard of Senegal, and recognized the
existence of hæmoglobinuria and the presence in the red globules of a
hæmatozoön. Leblanc, about the same date, found a protozoön in the blood
of dogs at Lyons, suffering from “red water,” and Koch later found a
double piroplasma in the red globules of suffering dogs in East Africa,
both considering the disease analogous to Texas fever in cattle. Nocard
and Almy in 1901, at Charenton, Paris, met with a similar affection in a
dog which had just returned from a fox hunt, and was covered with ticks.
Its urine was brownish red, like coffee-grounds, and highly charged with
albumen and hæmoglobin. Many of the red globules were affected and
contained minute, spherical refrangent bodies which, when stained with
carbolized thionine, appeared like those of Texas fever. There were but
2,800,000 red globules in a cubic millimetre of blood.
The injection of 5 grammes of the blood into the jugular of an aged
bitch caused in the 3d day hyperthermia (105° F.) and an extensive
invasion of the red globules which still counted 6,100,000 per mm. On
the 4th day the animal was thoroughly prostrated, refused to eat, had
hæmoglobinuria, and many individual red globules enclosed from 4 to 8
hæmatozoa each. On the 5th day the count of the red globules was but
4,400,000 per mm. By the 6th day the urine was nearly normal, and
appetite returned, but the red globules counted but 3,500,000 per mm.
Menveux went to Pas de Calais with an Irish setter to hunt rabbits. The
dog came in every night covered with ticks. In 5 days he sickened, with
extreme prostration, diarrhœa and red urine and died on the 25th day.
Wm. Robertson describes the disease in Cape Colony. The piroplasma was
first identified at Grahamstown by Purves and successfully inoculated by
Spreul. By intravenous inoculation symptoms appeared on the fourth day
and death followed about the sixth, while by subcutaneous inoculation
the course was slower and the animal died about the eleventh day.
Robertson inoculating from animal to animal carried it through a
succession of thirteen dogs all of which perished. He found the blood to
be infecting on the third day after inoculation subcutem, and the
globules invaded on the fourth. They were especially numerous in blood
taken from the spleen.
_Microbiology._ The protozoön resembles that of Texas fever, but is
larger, longer, less pyriform, and more like an oat seed, staining
slightly in the centre which shows one clear spot, and more deeply at
two or three places in the margin. It stains well with carbol thionine
blue or methylene blue, but not readily with hæmatoxylin. The dog’s
blood, containing abundance of parasites, failed to infect horse, sheep,
ox, cat, fowl, Guinea pig, rabbit, rat or mouse (Robertson).
Robertson found the ticks on every affected dog which had contracted the
disease by simple exposure and which came under his observation.
Specimens sent to Neumann were identified as Hæmaphysalis Leachi. Mature
ticks from an infected dog were preserved and their eggs hatched in an
incubator. The resultant six-legged larvæ, placed on susceptible puppies
a month old proved harmless and no protozoa appeared in their blood.
This was repeated when the same generation of ticks had reached the
stage of nympha, and it was after two months from the hatching that the
ticks, now mature, when placed on the same puppies conveyed the disease.
On the thirteenth day the temperature reached 105° F., and the red
globules swarmed with parasites, many single globules containing no
fewer than eight. They were of various shapes, spherical, pyriform or
cloveshaped many tapering finely toward the ends like an oat. The
puppies died respectively 14 and 18 days after infection.
Experiments made on other dogs with the larval and mature ticks, fully
confirmed the conclusion that the immature insect was harmless. A 14
days old puppy infected by mature ticks died on the 11th day so that the
immunity of the other puppies cannot be due to a milk diet, as in the
case of calves and Texas fever. Intravenous inoculation with the
infected blood invariably conveyed the disease.
_Symptoms._ On the third day after inoculation the dog is dull,
prostrate, apathetic and drowsy, refuses food and shows thirst.
Temperature may reach 103° to 106° F. On the fourth day the mucosæ
assume a yellowish tinge, and by the fifth this has encreased to a deep
chrome yellow, which involves any white portions of the skin as well.
Hæmoglobinuria is now well developed, the liquid being often as dark as
claret, and the patient may lie perfectly prostrate, giving off an
offensive odor from the skin, lungs, and especially from the mouth. The
tongue is furred, the teeth dirty, and the gums may be congested or even
ulcerated. Emaciation advances rapidly. The temperature may oscillate
from day to day or it may rise steadily to a climax, and then descend
suddenly when collapse occurs. In all cases the protozoön is found in
the red globules, or free in the blood. In the worst cases the red
globules may be so reduced in number that they can scarcely be found.
Death comes usually by collapse. In some instances the hæmoglobinuria
may be absent yet the disease advances to a fatal result.
_Lesions._ The carcass is usually shrunken and emaciated and exhales a
fœtid odor. The mucosæ, white skin, and all naturally white structures
(fat, connective tissue, fascia, tendons, ligaments, brain, spinal cord,
etc.), are stained of a deep yellow. The muscles, liver and other darker
tissues are of a mahogany yellow; petechiæ appear on the heart and
serosæ; the liver is greatly enlarged and friable (10 lbs.) the spleen
is swollen, gorged with blood and a soft, black, bloody pulp; the
stomach and small intestines are empty, yellow and sometimes congested.
The large intestines show muco-enteritis throughout with an abundant
rusty red exudate. The kidneys are yellowish with cortex somewhat pale.
The bladder also yellow contains dark colored urine. The red blood
globules are greatly diminished in number, many are crenated, broken up
and distorted and they contain the piroplasma in large numbers.
No system of _treatment_ has proved successful. Essays would naturally
be made with quinia and other antiperiodics.
_Prevention_ would naturally be sought in keeping dogs off from the
uncultivated land and brush during the tick season (summer, autumn), in
clearing and cultivating the tick infested pastures, in drainage, or in
smearing the coat of the dog with the oil of tar liniment or other
insecticide when he goes hunting.
PALUDISM IN HORSES.
Alleged identity with ague. Geographical distribution. Points of
difference from ague. Causes: low, damp, undrained, inundated
localities, hot seasons; inoculation, congenital. Symptoms: restless,
drowsy, stiff, shivering, hyperthermia, tremors, cough, frothy, rusty
expectoration, excited breathing and pulse, anorexia; puffy,
petechiated eyelids; epiphora; dyspnœa: albuminous, yellow or red
urine with casts: hæmoglobinæmia: colics, constipation, fœtid
diarrhœa. Death in a few hours to 6 days, or months. Lesions:
reduction in blood globules, crenation, watery blood: petechiæ:
enlarged, blood-gorged liver and spleen; congested, swollen, softened,
kidneys; congested lungs with extravasations: in chronic—anæmia,
dropsies, lung hepatization and suppuration. Prevention: keep
susceptible horses from low, infected lands from June to November and
from their water: protect from insect enemies. Treatment: quinia
sulphate or bromide, hot baths, etc.
Cadeac and others describe an intermittent or remittent febrile
affection of the horse, as identical with ague, and due, they allege, to
the presence in the blood of the _plasmodium malariæ_ of Laveran.
_Geographical Distribution._ It has been observed on the low marshy
grounds of Sicily, the Danube bottom lands, Algiers, Tonkin, Madagascar,
Soudan, Senegal and Cochin China (Dupuy, Lenoir, Pierre, Colin). Dr.
Gelston informs me that in the American cavalry in the Philippines
extensive losses are sustained from this disease.
_Microbiology._ The causation of the disease is attributed to the
_plasmodium malariæ_, which is carried by the Anopheles and inoculated
in the skin of man, in malarious regions at night, but we are confronted
with the difficulty, that accepting the alleged identity, the disease in
the horse should be coextensive with that occurring in man. Yet we have
in the New World many areas characterized by the all but universal
prevalence of intermittent fever in man, and at the same time by its
entire absence in the case of the equine races. It may further be
considered that protozoa, found in the red globules of birds, were at
one time considered identical with those of malarious fever, but have
been demonstrated to be entirely different so far as pathogenesis is
concerned. There is every presumption that the protozoa of the red
globules found in the horse in this disease are also distinct
pathogenically.
Laveran has sought in vain for his plasmodium in the blood of the
affected horses, while Pierre found in the blood globules of the Soudan
victims refrangent, crescent shaped bodies, thickened and staining
deeply in the centre, which in his opinion represented the growing
hæmatozoa of Laveran. Gelston found the rounded and crescent shaped
forms abundant in the red globules. The disease in the horse is said to
be conveyed by direct contact, which would again distinguish it from
intermittent fever of man. If the protozoön is the cause, and not a mere
sequel or attendant on the disease of the horse, the indications are
that it is peculiar to the equine race and distinct from the germ of
human malaria.
_Causes._ Like malarial diseases in man, it is confined to low, damp,
undrained or inundated localities, and shows in the hot seasons when the
surface dries out. The elevated plains and tablelands which are
habitually dry or well drained are exempt. Cadeac alleges that infection
is usually inhaled in the floating dust. The mortality of Algerian
horses taken to the Soudan is 90 per cent., while but 25 to 35 per cent.
of the native horses in the Soudan or in Senegal suffer. This difference
is manifestly the result of the survival of a comparatively immune
strain of blood, or of immunity resulting from a previous invasion.
Subcutaneous inoculation on a soliped failed, while transfusion of blood
from the affected horse to a sound mule produced the disease. It is also
claimed that it is transmitted from the affected mare to the fœtus in
utero, which showed characteristic visceral lesions after birth.
_Symptoms._ Premonitory symptoms of restlessness, drowsiness, or
stiffness, are followed by violent shivering, elevation of temperature
(104° or 106° F.), muscular tremors, rapid breathing, hacking cough with
expectoration of frothy mucus, tumultuous heart beats, and small
irritable pulse. There is complete anorexia, an opaque, infiltrated,
petechiated, mahogany colored, conjunctiva, epiphora, and sometimes
blood extravasations into the vitreous. The lungs may become intensely
congested, with rapid, panting breathing, dyspnœa, a frothy, rusty
expectoration, and extended head and limbs. This may prove fatal in a
few hours. Otherwise there may be remissions of the fever and dyspnœa at
somewhat irregular intervals. Sooner or later are observed urinary
changes, the liquid becomes albuminous, yellow, or red, or it shows
distinct casts. These indicate the destruction of the red globules and
the escape of hæmoglobin. In other cases there are slight colics and
constipation alternating with a greenish yellow fœtid diarrhœa. The
early nervous prostration and drowsiness may merge into vertigo, or
paralysis. Vertigo is a very prominent feature in the Philippine cases
(Gelston). The skin which, at first, may often be pricked without
response, sometimes becomes tender, itchy and congested, with erection
of the hairs and the formation of pustules, or small abscesses like
hazelnuts.
_Course. Duration._ In very acute cases death may take place in a few
hours. More commonly illness lasts from three to six days. In certain
instances it becomes chronic and may last two or even three months, the
early congestion of the mucosæ giving place to pallor and anæmia with
advancing emaciation, dropsies and finally marasmus and death.
_Lesions._ These are mainly in the blood, red globules being distorted,
crenated, massed in clusters and greatly diminished in numbers so that
the liquid appears thin and watery. The mucosæ, internal organs and
serosæ are petechiated and the serous cavities contain a yellowish
serum. A yellowish tint pervades the white tissues generally. The liver
is congested, virtually gorged with blood, enlarged and yellow or
yellowish brown. The spleen is greatly enlarged, blood gorged, and shows
irregular, rounded swellings indicating the seats of extravasation of
blood. In some instances rupture has taken place. The kidneys are
congested, enlarged, softened and of a brownish red or black color, with
circumscribed extravasations especially in the cortical area. The lungs
are violently congested, with many areas of blood extravasation, and
they do not collapse when the chest is opened. The heart is petechiated,
with a parboiled aspect and shows areas of commencing necrosis or fatty
degeneration.
In the chronic form the watery condition of the blood is remarkable, the
serous cavities (peritoneum, pleuræ, pericardium, arachnoid) contain
considerable effusion, dropsical conditions of the limbs and dependent
parts of the body are common, the lungs show hepatization and minute
centres of suppuration, and other viscera may show fibroid degeneration.
_Prevention._ It is advisable to keep susceptible horses from the low
marshy infected lands from June to November and to avoid especially
water that is drawn from such lands. It is not needful to take the stock
to any very marked elevation provided the land is dry and free from wet
or swampy areas. The native horses or those that have been long in the
marshy district and have thus secured a partial immunity may profitably
replace the more recently imported and susceptible horses during the
dangerous summer months.
The habit of the paludal protozoa of securing their transfer from one of
the higher animals to another through the intermediation of insects in
which they undergo developmental changes essential to their survival,
would further suggest the adoption of especial precautions against such
invertebrate enemies in the affected district.
_Treatment._ Pierre employed quinia sulphate or bromide 45 grs. in
distilled water 1 oz., intravenously, Gelston, creolin, subcutem. Hot
baths, 95° to 100° F. are claimed to lower the temperature and
contribute to the arrest of an attack. Other complications are treated
according to indications.
SURRA: ROT.
Synonyms. Definition: Acute protozoan remittent fever, of rainy season
or after, with destruction of red globules, anæmia, emaciation,
dropsy, icterus and cutaneous or mucous eruption or discharge.
Distribution: India, Burma, Cochin China, Persia, Phillipines, etc.
Trypanosoma Evansi: a fusiform flagellate infusorian with undulating
membrane, attacking the red globules: agency of flies as carriers,
infection of dogs; of crows; feeding, licking; rats; open sores;
stables; yards; pastures; pickets; stagnant water; manure or rubbish
heaps; abattoirs. Lesions: anæmia; trypanosoma swarms during relapses;
leucocytosis; œdemas; effusions; blood extravasations; splenic
enlargement; emaciation; gastric and intestinal congestions; gastric
ulcers; kidneys petechiated, swollen; brain effusion. Incubation, 2 to
8 days. Symptoms: local swelling, 2 to 4 inches by 4th day; decreases
to 14th day; the general symptoms; hyperthermia 102° to 104° F., night
highest; dulness; sluggishness; inappetence; icterus; cutaneous
eruption; remission in 1 or 2 days; exacerbation after 3 to 10 days;
catarrhs; petechiæ; stocked legs; pectoral swelling; encreasing anæmia
and emaciation; ulcers on mucosa or skin; generative excitement; fœtid
diarrhœa; urine profuse, bilious, albuminous or with casts; thirst;
intestinal rumbling; debility; marasmus; hair erect; skin dry, rigid.
Duration variable. Diagnosis: based on above, confirmed by finding
blood parasites, constantly fatal in horses. Surra in camel, ox,
buffalo, rabbits, rats, mice, dogs, cats, apes. Treatment:
unpromising; mercurials, iodides, chromates, arsenates,
terebinthinate, phenic acid, santonin. Dry, clean, airy stable, dry
grain, tonics. Prevention: keep horse and mule from infecting
locality; use oxen rather: stables, pickets, etc., apart from marshes,
pools, manure and rubbish heaps; disinfectants, insecticides, seclude
all surra-affected animals: smudges. Sanitary police.
_Synonyms._ Sar, Zahrbad, Gumzahrbad, Kushkzaharbad, Sokra, Sokhra, Tap,
Tapdik (Punjab): Phitgya, Purana (Meerut): Berbag (Bombay): Tarai,
Tebersa, Wabai-ki-bokhar, Pernicious Anæmia, Trypanosomosis, Relapsing
Fever, etc.
_Definition._ An acute, relapsing, protozoan fever of equines, camels
and elephants, inoculable on other animals, occurring during or after
the rainy season, and characterized by hyperthermia which is liable to
be intermittent, remittent or relapsing, anasarcous swellings, petechiæ
of the mucosæ, icterus, cutaneous eruption, nasal, ophthalmic, vaginal
and other mucous discharges, rapidly advancing anæmia, emaciation and
debility, and above all, by the presence in the blood, at intervals from
one to six days, of swarms of protozoa, analogous to those found in
dourine or nagana.
_Geographical Distribution._ Surra has long been known to the English
veterinarians in India, occurring during or just after the rainy season,
and especially on the low flooded lands, along canals, rivers, lakes,
etc., and later in Burma, Cochin China, the Persian Gulf, Persia.
Lingard claims its existence in East Africa, North and South America,
Australia and Southern Europe, but he has evidently confounded it with
nagana and other affections. The discovery of the disease by Dr. Slee in
1901, among American, Australian and Chinese ponies in the Philippines
is suggestive of a very wide diffusion of the infection in Southern Asia
and adjacent islands, with which an American work on veterinary medicine
must deal.
_Cause. Parasite. Trypanosoma Evansi._ The essential cause of the
disease, Trypanosoma Evansi, discovered by Dr. Griffith Evans,
Inspecting Veterinary Surgeon, British Army, in 1880, is a flagellate
infusorian, pointed at one end, near which is a dark centrosome, and
from this a flagellum running along the free border of the broad
undulating membrane to the extreme opposite end of the parasite and
extended beyond this as a waving lash. The length of the Trypanosoma
Evansi is 20 to 50μ, (10 to 14μ, Smith and Kinyoun, Manila), its breadth
1 to 1.5μ. By reason of its large size and active motion it is easily
detected in a film of fresh blood under ⅙th inch objective, and no less
easily when dried and stained on a cover glass. It must be borne in mind
that the mature parasite appears in the blood at intervals in swarms, so
that examination at one time of day, or on a particular day, may fail to
detect it, while examinations made earlier or later are successful. The
general structure and successive stages of growth of the parasite appear
to be the same as described for the Trypanosoma Equiperdum of Dourine,
to which accordingly the reader may turn for description. The
distinction from that parasite is to be found mainly in the
pathogenesis. In this respect it should be noted that the parasites are
strongly attracted by the red globules, upon which they fasten
themselves by the blunt ends, shaking the cell in the most vigorous
manner and even breaking pieces off and carrying them away. They are
most strongly attracted by the concave part of the disc, and when there
are rouleaux they will bore between the globules and even push them
apart (Evans).
The appearance of the disease at the conclusion of the rainy season when
the waters dry up and become foul, has led to the idea that the parasite
lives in waters, but as this is also the time of the great swarming and
activity of flies, and as the trypanosoma is found in the bodies of
tabanidæ and hippoboscidæ that have bitten affected animals (Lingard),
and as horses crowded together so that the fly with piercing apparatus
still wet can pass from horse to horse (Evans), the opinion has grown
that it is a compulsory parasite which is transmitted through the bites
of insects. In 1880, Griffith Evans found that the native Hindoos
attributed the disease to the bites of a very large brown fly which was
active in July (probably a tabanus), in 1897, Pease identified the
incriminated fly as the tabanus tropicus. Finally, Rodgers, in 1901,
took flies that had been on surra horses, kept them 4 days or longer and
found that their bites failed to produce surra; whereas those that were
allowed to go directly from the sick to the healthy animal produced the
disease in the latter. The direct experimental inoculation from horse to
horse infallibly conveys the disease so that the flies are not needed to
pass the parasite through an intermediate stage of its existence, but
merely to carry it. It follows that no particular fly is the bearer but
any insect may carry the infection from a bite or sore to inoculate it
on a sore or by a bite on a fresh animal. Different observers have
noticed the tendency to the infection of dogs and other animals that fed
from rubbish heaps, or upon the carcasses of animals dead of surra,
suggesting at once the intervention of the swarms of flies that
congregate at such places. This is probably another example of the
shrewd insight of the common mind, as in the case of the tick-borne
Texas fever.
Lingard finds another bearer in the crow which sits on the backs of
affected horses, pecking at the wounds, and passes at once to other
healthy horses to peck their sores.
Experiments in feeding the infested blood to sound animals, have
apparently succeeded, and the observation that dogs and cats suffer from
eating the carcasses is in favor of this view. Horses that lick the
infested sores, or the blood drawn by the flies may readily infect
themselves, and especially if the mouth bears scratches caused by
fibrous food, leech bites, or sores from bits, or if the pharynx or
stomach has been wounded by bots or spiroptera.
The water and food are blamed by the natives in some quarters, but
Pease’s observations on the Bombay tramway horses, which all perished
though kept on boiled water and carefully picked fodder from sound
regions, would suggest that this if a channel of infection at all, is
not the main one.
The bowel excretions of rats harboring trypanosoma, when mixed
experimentally with the food of the horse, have been charged with
causing surra, but there are objections to the acceptance of this as a
common cause. The alleged period of incubation in the horse in such
cases was 40 days in place of the usual 7 or 8 days, when inoculated
from a horse first affected in this experiment on a second the usual
incubation of 7 or 8 days was shown, and though the horse fed on rat’s
dung in the infected region of Bombay contracted the disease, the
experiment failed when the same dung was fed in a high dry region
unaffected by surra. The natural inference is that Bombay experimental
horses contracted the affection in the usual way, probably through
insects.
In the rainy season the Indian rats swarm with the Trypanosoma Lewisi,
an entirely different species, and though they can be successfully
inoculated with the T. Evansi of Surra, the T. Equiperdum of Dourine,
the T. Brucii of Nagana, and it is alleged the T. Equinum of Mal de
Caderas, yet these are not their common parasite. The presumption is
that the rat affected with Trypanosoma Evansi could transmit the disease
to the horse through one of the many possible insect channels or
otherwise.
Neither condition, sex nor age appears to affect receptivity. Open sores
especially open the way for infection.
The position of stables, yards, pastures or picket grounds near stagnant
water, manure or rubbish heaps, abattoirs or other places that breed or
attract flies, is a much more important consideration. Foul stables, or
those having light from both sides are more exposed to flies.
_Pathology and Lesions._ The pathology of the disease consists in the
rapid destruction of the red blood globules by the trypanosomata. It is
a form of rapidly advancing pernicious anæmia due to the great and
active voracity of the trypanosoma. The swarming of the trypanosoma in
the blood at the period of the relapse and the absence of the mature
form in the intervals is remarkable. The trembling movement in the blood
at the period of swarming results from their prodigiously active
movements. The red globules may assume various forms, crenate,
echinated, (Ranking), and more or less broken up or disintegrated, their
numbers steadily decrease, leaving the blood thin and watery with rusty
serum and yellow (icteric) staining of the white tissues, even the
bones. Encrease of white globules, actual or relative, has been a marked
feature (always present in typical cases, Burke).
Petechiæ are especially common on the conjunctiva, vaginal mucosa,
endocardium, and less marked in the nose, mouth, and serosæ.
Œdemas are common, yellowish, gelatinoid exudate at the base of the
heart, subcutem, between the muscles of the limbs or elsewhere, and as
effusions into the pleuræ, pericardium or peritoneum.
Distinct blood extravasations have been noted beneath the endocardium.
The spleen is often enlarged, excessively so if death occurred during a
paroxysm. The lymph glands are swollen and appear dropsical.
The whole body is emaciated and shrunken, the visible (unpetechiated)
mucosæ are pale and bloodless, often yellow, yet rigor mortis is well
marked.
Gastric ulcers are common (Steel, Burke, G. W. Evans) apparently
preceded in many cases by capillary embolism, congestion and
degeneration. Intestinal congestions are frequent (Steel, Burke), but
ulcers are rare (Geo. H. Evans).
The liver may be normal (Griffith Evans), or especially during a
paroxysm (Lingard) congested, inflamed and enlarged. The pancreas is
usually normal.
The kidneys are petechiated, congested, œdematous, or the seat of blood
extravasations.
Instances have been noted of cerebral and meningeal œdema (Steel,
Lingard), encrease of fluid in the arachnoid or lateral ventricles, or
in the spinal cord, with gelatinoid exudation in the lumbar portion
(Lingard). Like other tissues, in advanced stages the nerve centres are
usually anæmic (Geo. H. Evans).
_Incubation._ As made out by inoculation cases this extends from two to
eight days, according to the dose—five to seven days being the most
common. Infection by inoculation subcutem in mules showed a hyperthermia
on the fifth day; or by ingestion (feeding the virus) on the sixth day
(Steel). Longer (alleged) incubation depends mainly on the first slight
paroxysms having been overlooked, or set down for the frequent bilious
and icteric condition which is common in mules and horses in India
(Steel), or to a later infection by insects or otherwise.
_Symptoms._ In experimental cases a small raised swelling in the seat of
the inoculation, appears in 24 hours, encreasing to 2 to 4 inches in
diameter, and 1 to 1½ inch high by the 4th day, and loosely connected
with the parts beneath. From the 4th to the 14th day it decreases in
size and softens and general symptoms set in.
In casual cases these general symptoms are the first to be observed.
There is a transient fever 102° to 104°, highest toward night and
without preliminary chill, hot mouth and skin, dulness, sluggishness,
inappetence, yellowness of the mucosæ, petechiæ on conjunctiva or vulva,
and sometimes nodules like those of urticaria on the skin. After a day
or two these symptoms subside, the temperature is 101° F., or below, the
mucosæ clear and pale, and spirit and appetite nearly normal. These
slight first paroxysms are rarely seen by the veterinarian, having been
looked upon as one of the oft-recurring bilious attacks of a hot
climate. The remission lasts for 3 to 10 days when the second paroxysm
sets in, like the first but often more marked: temperature 102° to 104°,
eyes especially the membrana nictitans petechiated, epiphora, slight
catarrh from nose or vulva, it may be stocking of the legs, or pitting
swelling under the breast bone, or abdomen, or in the sheath. Like the
first, the second paroxysm subsides, and after another interval a third
sets in, to be followed in like manner by a fourth, a fifth and so on,
if the patient survives. With each the symptoms become more pronounced,
the mucosæ are left more pale and bloodless, debility and weakness are
greater, emaciation is more marked, œdema of the limbs or body more
extensive, hyperthermia may reach 105° or more, the pulse is weaker and
the heart more liable to palpitation, and the respirations may reach 50
or 60 per minute. Yet in sparely built animals dropsy may be entirely
absent (Steel). Steel often found superficial, circumscribed ulcers on
the tongue, inner sides of the lips, nose, eye, or vulva, beginning as
epithelial degeneration, followed by superficial erosion and early
healing. Sometimes, similar erosions appeared on the skin. Generative
excitement may be present, the mare appears to be in heat, while the
horse has erections, which are supposed to depend directly on the
implication of the generative centre in the lumbar myelon. The
submaxillary glands sometimes swell and even suppurate and discharge a
gluey pus (Griffith Evans). The bowels are usually costive at first, the
fæces may be glazed, but in advanced stages they become soft, pultaceous
and fœtid. The urine at first normal in amount, becomes later abundant
or even profuse (Griffith Evans, Ranking, Nariman and Vaz, Lingard). It
is at first yellow and turbid, later of a dingy green or greenish
yellow. Sometimes it diminishes as the disease advances. It may contain
bile, albumen, or even casts (G. H. Evans), though the latter appear to
be exceptional. The reaction varies, sugar is absent, and the parasite
has not been found in it. Appetite though interfered with during the
paroxysms, remains fair or even voracious in the intervals and the
animals may eat to the last (Burke). Thirst usually encreases with the
advance of the disease, in keeping with the free urinary secretion.
Rumbling and gurgling of the bowels are common and even tympany at times
(Lingard).
In the advanced stages the picture is one of great anæmia, marasmus and
general debility. When moved the animal will stumble over the slightest
obstacle, even the litter, recovering himself with effort and
difficulty. If he should fall he is liable to remain down indefinitely,
the side next the ground becoming drenched with sweat though there is no
general perspiration. The hair becomes encreasingly dry, withered and
erect, the skin dry, powdery, rigid and more and more firmly adherent to
the bones and muscles, losing all its natural pliancy and mellowness,
and becoming like that of a dead animal. It is bloodless, and sloughs
readily over the prominent bones, where compressed or bruised in lying,
owing to the lack of nutritive and reparatory action. The visible mucosæ
are absolutely bloodless. The muscles as a whole are wasted to an
extreme degree, but this atrophy is most marked in the back and loins,
along the longissimus dorsi and in the quarter in the gluteal muscles.
The patient may remain recumbent, from sheer weakness, for a length of
time at the last, or he may get up after a long recumbency and stand to
the end.
Death may occur early with general anasarca and extreme hyperthermia
(110° F.). In the great majority it appears to result largely from
perforation of the stomach, clots in the heart, or general debility and
heart failure.
_Diagnosis._ With symptoms such as are above described the discovery of
the trypanosoma in the blood completes the diagnosis. Trypanosoma is
found in dourine, nagana and other affections so that the discovery of
it alone would not be conclusive as to the existence of surra. Nor can
the discovery of the parasite always be made at the first or second
attempt. The swarm of mature trypanosomata is found with the advent of a
paroxysm, and as the veterinarian is often called during the decline of
the attack the parasites have already retired and elude his
investigation. It becomes needful to take the temperature and examine
the blood daily sometimes for eight or ten days, and when with a sudden
rise of temperature he finds also a swarming of the mature
trypanosomata, the diagnosis is perfect. A drop of blood placed on a
cover glass, pressed down upon the slide, and placed under the
microscope, will show the parasite with eel-like movements among the
blood globules. There may be very few during the first or second
paroxysm, but they become numerous and very obvious as the disease gains
its height. Evans recommends to use defibrinated blood.
They may be dried rapidly on a cover glass, fixed in absolute alcohol
one or two minutes, then stained ten minutes in a mixture of the two
following liquids united just before using:
A.—ONE PART OF THE
MIXTURE.
Methylene blue 1 Grams.
Borax 2.5 „
Distilled water 100 „
B.—FOUR PARTS OF THE
MIXTURE.
Eosin .1 Grams.
Water 100 „
The plasma of the trypanosoma appears blue, the flagellum red and the
chromatin of a different shade of red. It may be permanently mounted in
balsam.
_Mortality._ The disease is constantly fatal in horses, though the
animal may survive for months.
SURRA IN CAMELS.
Haggar describes this as having remissions or intermissions as in the
horse, the trypanosoma disappearing during the intervals to reappear
with the hyperthermia. The temperature may rise to 106° F. and the
animal wastes away to a veritable skeleton. A remarkable feature of the
disease is the formation of immense abscesses containing a thick,
cream-colored pus on the sides of the chest in the vicinity of the pad,
and in the sheath and scrotum or udder near to the stifle pad. The
mortality is nearly as great as in the horse or mule, yet the camel
drivers say that a small percentage recover.
SURRA IN BOVINES.
The domestic ox, the sacred cow of India (Lingard) and the water buffalo
(caribao) of the Philippines contract Surra. It is interesting to notice
that in these animals the disease is relatively mild and recoveries are
frequent.
In the Indian buffalo it causes dulness; advancing emaciation; slight
temperature variations; muco-purulent inflammations of the conjunctiva,
cornea, and pituita; and occasionally eruptions under the breast or
belly.
Among _lesions_ were atrophy, softening of lymph glands, enlarged liver
and spleen (slight), petechiæ and blood extravasations on the
pericardium, epicardium and other serosæ, and on the intestinal mucosa
which sheds its epithelium in patches.
Stall enzoötics in cattle do not seem to affect horses casually. The
disease is easily conveyed to rabbits, house rats and mice, dogs, cats
and apes. Goats and ducks appeared to be immune (Penning).
TREATMENT OF SURRA.
In well established cases in the horse, ass or mule no treatment has
succeeded in saving the patient. Almost every germicide has been called
into requisition but without good effect. Among these may be named:
mercuric chloride subcutem, iodine and potassium iodide intratracheally,
iodoform subcutem and intravenously, oleum terebinthinæ subcutem and
intravenously, potassæ bichromas by veins and stomach, cinchona
alkaloids and arsenic, phenic acid and iodine, quinine, hydrargyri
biniodidum, santonin, potash. The claims of different agents, notably
arsenic and phenic acid, have been supported by the manifest improvement
of condition under their use and the disappearance of the trypanosoma,
but both these conditions may often appear during intermissions, without
medication. The usual outcome is that the animal dies and the only claim
that can be made is a slight extension of life. This is favored by dry,
clean, airy stables, change of water, rich grain and succulent food
(oats, rice, linseed, barley, gram sorghum, bran, middlings, salt,
etc.), with iron, arsenic, and other tonics, yet the best that can be
said for them is that they have deferred somewhat the inevitable death.
_Prevention of Surra._ The first consideration is to avoid placing
equines and especially horses and mules, or camels in the infecting
localities in the rainy season and just after it. Oxen and buffaloes can
be used in such places with greater impunity. If they must be used in
such localities, place the stables or pickets in dry locations well
apart from marshes, and stagnant water. Keep the stables dark during the
surra season, open to light on one side only and with screens in the
windows. Make a deep pit for the manure, keep it well darkened and
screened and turn every particle of manure into this several times a day
so that the stable shall be perfectly clean. All rubbish heaps should be
similarly dealt with. The flies breed in the manure and decaying organic
matter. After each sweeping of the stable sprinkle the manure in the pit
with some disinfectant, phenic acid, tar water, copperas, etc. Smear the
skins of the animals with tar water, coal tar water, naphthalin, daily
if necessary to prevent the attacks of the flies. Other suggestions in
this line can be found under _parasites_.
An important consideration would be to seclude every animal attacked
with surra. The flies can only carry and inoculate the poison when there
is some source from which they can obtain it. Until we shall learn how
many animals, tame and wild, casually contract the Trypanosoma Evansi we
cannot speak of how effective this may be made, but it is at least a
substantial advance in the line of restriction, since the infected horse
or mule in the vicinity of healthy ones is a constant peril, and as
given insects attack by preference, given favorite genera, the horse
flies, coming from the diseased animal are much more likely than other
flies to attack the sound horses. In a surra season it would be a wise
economy to destroy the infected equine at once, as according to all past
experience, sentence of death has already been passed upon him, and his
preservation even for a hour is hopeless for him, but full of the
gravest danger for others. The carcass and all pertaining to it, blood
especially, should be promptly and deeply buried and the place
thoroughly disinfected.
In the same way smudges made by burning green grass or other vegetation,
tar, leather or other material producing empyreumatic products offensive
to the fly may be employed.
_Sanitary Police._ The Department of Agriculture forbids the landing in
the United States or its dependencies of any animal from the
Phillipines. If the infection should by any accident be imported no cost
should be considered too high to secure a prompt and thorough extinction
of it.
NAGANA. TSETSE FLY DISEASE.
Trypanosoma Brucii: attacks horse, ass, mule, cattle, buffalo,
antelope, camel, hyena, dogs, etc. Elephants and zebra, pigeon and hen
immune. Tsétsé fly. Inoculation only certain channel; virulence in
dead body 24 hours; in vitro 3 to 4 days, or when dried or heated
(122° F.) Symptoms: hyperthermia; anæmia; leucocytosis; buffy coat;
œdemas; catarrhs; wasting; debility. Lesions: as in surra; trypanosoma
in blood at intervals, bone marrow, lymph glands, spleen. Immunizing
unsuccessful. Prevention as in surra.
This is an infective disease caused by the _Trypanosoma Brucii_, which
has been supposed to be identical with _Trypanosoma Evansi_ but differs
in its morphology and in its infectiveness toward a greater variety of
animals. It is 25 to 30μ long by 1.5 to 2.5μ broad, less pointed at its
posterior (nonflagellate) end, broader undulating membrane, more deeply
staining protoplasm, and more sluggish movements. It invades the blood
of horses, asses, mules, cattle, buffaloes, antelopes, camels, hyenas,
and dogs, and can be inoculated on cats, rats, mice, rabbits, hedgehog,
boshbok, zebra hybrids, Guinea pigs, goats, sheep, weasel, and monkey
(Macacus rhesus). Elephants are immune though they suffer from T.
Evansi, and the zebra is immune though a soliped.
The _tsetse fly_ (glossina morsitans) is credited with being the main
agent in transmitting the parasite to mammals, (see _Diptera_).
Kauthack, Durham and Blandford found that Guinea pigs were more
resistant than rabbits, surviving the inoculation for a longer time.
Bruce also found the native South African sheep and goats more
refractory than others, yet their hæmatozoön was as deadly to other
animals as that of horse or dog. Pigeons and South African hens proved
refractory. Manifestly in Africa the present races of some animals are
the products of the survival of the fittest.
_Inoculation._ The disease has been produced experimentally by
inoculation only. Feeding experiments on rabbits, cats and Guinea pigs,
the sucking by puppies of an infected dam for 14 days, coitus, and even
the careful dropping of infected blood under the eyelid failed to convey
it. Lousy rats with sores on face, one cat doubtless scratched by a
bone, and one rabbit supposed to be infected by sexual congress (Rouget)
offer exceptions, which in the light of the general results must be
looked on as probable inoculations through wounds.
Successful inoculations were made with blood, lymph gland, spleen, bone
marrow, aqueous humor, serum, œdema fluid, and testicular juice. The
effectiveness of inoculation did not vary materially with the different
fluids used, with the amount, nor with the point selected for its
insertion, subcutaneous, intravenous, intraperitoneal, or on a mere
scratch.
Virulence is lost in the dead body in 24 hours or less; when the
infected blood is kept aseptically _in vitro_, in 3 or 4 days at most;
or when completely dried. Heating to 122° F. for 30 minutes sterilized,
while at 114.8° F. for half an hour the trypanosoma became nonmotile,
but not quite non-virulent.
_Symptoms._ _Hyperthermia_ is marked about the time of the appearance of
the infusoria in the blood. (Horse 106.7°; dog 104°; rabbit 105.8°), and
in the horse there was a paroxysm with each new swarm of the parasite.
In one ass intermissions were not observed. In rabbits there was no
constant ratio between the temperature and hæmatozoa, hyperthermia was
constant or nearly so. The horse had marked hyperthermia up to death,
dogs and cats showed a marked descent even to subnormal, before death.
_Anæmia_ is a marked feature the red globules being greatly reduced, and
they show a tendency to clump in masses instead of forming rouleaux. The
serum added to healthy blood has the same effect on that. _Leucocytosis_
is not constant nor excessive (15,000 to 34,000 per c.m. at the
highest). In clotting the blood may form a buffy coat.
_Œdema_ is common in horse, rabbit, cat and dog especially about the
head, legs, belly and genital organs. Rabbits often show swellings,
excoriations and sores of the labia, prepuce and penis favoring
inoculation by this channel.
_Conjunctivitis_ is common in cats, dogs, rats, rabbits, often in
connection with facial œdema, and corneal opacities and ulcers, and
turbidity of the aqueous humor may follow.
_Nasal catarrh_ often interferes materially with breathing.
_Muscular wasting_ and _debility_ are prominent phenomena, especially in
horse, dog, cat and rabbit, the loss of weight reaching 20 or 30 per
cent.
_Lesions._ These are like those of surra. Enlargement of the lymph
glands, spleen and liver, firmness, friability and dark color of the
spleen; effusions, petechiæ, and even hæmorrhages of the serosæ, lungs
and stomach, and great atrophy of the muscles and adipose tissue are
prominent features. The liver is always fatty in rabbits. In the shafts
of the long bones, the fat is replaced by red marrow. The bone marrow is
sometimes red, at others pale.
The _trypanosomata_ in the blood vary greatly. In infected rats and mice
they appear 3 or 4 days after inoculation, are almost constantly present
thereafter, and as a rule, encrease steadily up to 2,000,000 or
3,000,000 per c.m. In dogs they appear in 4 to 6 days, in cats in 5, in
Guinea pigs in 5 to 7, and in horses in 7 days. In rabbits there were
found 60,000 per c.m., in dogs 100,000 to 300,000, and in Guinea pigs
200,000 to 500,000. In one Guinea pig they did not appear until 6 weeks
after inoculation and then rapidly encreased to a fatal termination.
More commonly a few can be found about a week after inoculation, and
then they disappear for a variable period. They have been found in the
bone marrow when they could not be recognized in the blood. Again, after
subcutaneous flank inoculation in the rat, they were found in the
corresponding inguinal glands 1 to 3 days before they could be detected
in the blood. After death they are found most abundantly in the bone
marrow and spleen, but they have not been found in the intestinal
contents nor urine except in the case of hæmorrhages or local sores.
_No soluble toxin_ appears to be formed, and _no immunization_ is
effected by the serum. Blood serum kept several days until the infusoria
had died and then passed through a Berkefeld filter had no apparent
effect on the animal economy even in large doses. Blood heated to 122°
F. was equally harmless. The same is true of extracts of organs and of
bile from infected animals.
Attempts to secure _immunity_ by injecting the blood serum of affected
animals, after it had been sterilized by heat, filtration, or standing
one week _in vitro_ proved of absolutely no effect. The blood of the
fœtus almost at full term proved valueless, and the young born of
infected mothers proved fully susceptible when inoculated. The serum of
the Guinea-pig, which is naturally somewhat resistant, proved no
protection to other animals. Bile mixed with infecting blood _in vitro_,
kills the trypanosoma, but such blood has no protective effect on
animals. Sewer rats and white rats inoculated and re-inoculated with the
common rat trypanosoma (T. Lewisi) until immune from that organism, show
a full susceptibility to the trypanosoma of nagana.
_Flesh feeding_ and _vegetable feeding_ have made no difference in the
susceptibility in the case of rats. Feeding with the hæmatozoa has
produced no immunity.
It is evident that prevention must follow the same lines as in Surra,
due consideration being had of the greater number of genera susceptible.
LUNG PLAGUE OF CATTLE.
Synonyms. Definition: infectious, cattle fever, with long incubation,
insidious onset, excessive pulmonary exudation, infarctions and
sequestra. History: ancient, modern; England, Norway, Sweden, Denmark,
United States,—its extinction in 1887 to 1892—Massachusetts, New
Jersey, S. Africa, Australia, Tasmania, New Zealand. Causes: contagion
only. Bacteriology: Nocard’s organism cultivated in collodion capsules
_in vivo_, as actively motile refrangent points, morphology uncertain.
Modes of transmission, exhalations from sick inhaled by susceptible,
ingestion of infected food, pastures, watering troughs, ponds,
commingling of herds, attendants, dealers, stables, manure,
unrestricted commerce, convalescent cattle, breed, hot seasons.
Lesions: profuse exudation in lymph networks of lungs, marbling,
parenchymatous cell proliferation, compression and gangrene of
lobulets, thrombi, sequestra, infarction, fibroid sac, or
stalactite-like fibroid peribronchial formations, hepatization,
pleural effusions and false membranes, pericardial, bronchial, lymph
glands congested. Incubation: 6 to 30 days, protracted cases, bearing
on quarantine. Symptoms: conditions affecting gravity, breed,
excitement, heat, chill, susceptibility, usually insidious, infrequent
cough, roused by cold water, dusty food, exertion, etc., hurried
breathing when driven, slight auscultation râles, hyperthermia (103°
to 108° F.), dulness, anorexia, suppression of milk, stiffness, no
pandiculation, troubled breathing, auscultation, and percussion signs
of extensive consolidation, tenderness of chest walls, in bad cases
stands obstinately, head extended, mouth open, tongue protruded,
grunts with expiration, heavy breath, nostrils dilated, nasal and
buccal discharge, rapid emaciation, fœtid diarrhœa, erect hair, pale,
scurfy, adherent skin, varied chest râles, abortion. Mild in winter,
severe in summer. Loss of one-third or one-half weight in one week.
Chronic cases, fibroid and necrotic changes, sequestra. Diagnosis:
Anamnesis, inoculation: from _tuberculosis_ by high fever, rapid,
extensive infiltration, early succession of new cases, failure to
react under tuberculin, absence of tubercles; from _bronchitis_ and
_pulmonary strongylosis_, by the succession of cases in place of many
at once, the extensive exudation, the evident cause (exposure or
infected place), and by the lesions; from _fibrinous pneumonia_, by
absence of climatic cause, the more extensive consolidation, more
troubled breathing, and coexistence of old and recent lesions; from
_infectious pneumonia_ by the greater area consolidated, more exalted
hyperthermia, more marked dyspnœa, the absence of white points of
alveolar cell proliferation, and by the old and recent lesions; from
_septicæmia_ hæmorrhagica, by its occurrence at all seasons, on all
soils, by the absence of sanguineous swellings at other parts, by the
absence of cocco-bacillus from the exudate, and by its
non-inoculability on sheep, horses, pigs and rodents; from _needle in
pericardium_, by its epizoötic prevalence, fever, and the absence of
preliminary gastric and later cardiac, morbid phenomena; from
_emphysema_ by the fever, absence of drumlike tympany, and presence of
consolidation; from _aspergillosis of the lung_ by the fever, more
rapid progress and extended consolidation, by the harmlessness to
birds, by the absence of aspergillus from expectoration and lung; from
_insolation_ by the absence of the causes of heat stroke, of the
implication at once of a number of exposed animals, of the excessive
hyperthermia, the brain symptoms and sudden deaths. Treatment: a poor
economy, to be punished when extinction is attempted. Prevention:
importation under three months quarantine, surveillance of three
months more in case of single animals; applied to lung plague
countries and those adjoining; disinfect cars and boats that have been
used in lung plague country; exclude hay and fodder from lung plague
country; also litter, bags, head ropes, horns, hoofs, hides, hair. To
extirpate: stop all ingress of possibly infected cattle, stop movement
of cattle, prohibit common or unfenced pasturage, kill without
indemnity in case of violation, record all cattle, make necropsy of
all dead, kill and pay for all infected herds, disinfect all infected
premises and things, use horses in removing and plowing under manure.
Unaided owner may: breed all his stock, in buying bull quarantine him,
allow no intercourse between his herd and others, get new cattle from
herds only that have had no illness nor losses for a year, and no
exposure, and bring by thoroughly safe route, in disinfected cars or
boats, then quarantine, under special attendants. Immunization; by a
first attack, inoculation in tail, intravenous, of sterilized exudate.
Conditions permitting and forbidding immunization.
_Synonyms._ Bovine Pleuro-Pneumonia, Contagious Pleuro-Pneumonia,
Peripneumonie (Fr.), Lungenseuche Vieseuche (Ger.), Pneumosarcia,
Peripneumonia Exudativa, Epizoötic Pleuro-Pneumonia, Pulmonary Murrain,
Slijmlongziekte (Dutch), Pulmonea dei Bovina (Ital.), Phush phush
pirdaho, Pheepree (Bengalee).
_Definition._ An infectious febrile disease, occurring casually in
cattle only, so far as known, and characterized by a prolonged
incubation (10 to 90 days), a tardy insidious onset, inflammation of the
bronchia, lungs and pleuræ, a profuse exudation into the interlobular
connective tissue and chest, a very extensive area of consolidation,
pulmonary infarction, and sequestra.
_History._ It is difficult or impossible to identify this disease among
the various animal plagues in ancient times. Yet when lesions are given
it may be admitted in different cases. Aristotle, writing 350 years
before Christ says “the cattle that live in herds are subject to a
malady which causes the breathing to become hot and frequent. The ears
droop and they cannot eat. They die rapidly and the lungs are found
spoiled.” Here the facts that cattle alone suffered, that large herds
suffered most, that the lungs were the seat of very marked lesions, and
that fever and mortality were both marked, point forcibly toward lung
plague. Valentini’s description of a fatal lung disease in cattle also
stands out prominently in the obscure records. The first full and
definite report is that given by Bourgelat of its prevalence in
Franche-Compté in 1769. Later the records are frequent and from all over
Europe, indicating its general prevalence before as well as after
Bourgelat.
Much more important are its definite extensions into new countries after
a long interval of immunity as showing that with trustworthy records
such invasions can always be satisfactorily accounted for by the
introduction of cattle or their fresh products from a previously
infected area. Into Holland it was imported from Germany in 1835 by
Vanderbosch a Guelderland distiller and spread over the whole country.
Attempts were made in Friesland, and at first successfully, to stamp it
out by slaughter and disinfection, but the demands of the trade toward
England grew so enormously that it was being constantly introduced anew
and the measure was abandoned. The British Consul at the Hague, in 1839
sent some Dutch cows to a friend in County Cork, Ireland, which led to
the general infection of that island and indirectly of Great Britain. In
1842, under the Free Trade Act, England became at once deluged with lung
plague cattle from Holland, Belgium and France on the one side, and
Ireland on the other. Soon the whole island had been infected except
exclusively breeding districts (Welsh and Scottish Highlands, etc.) into
which no cattle were ever introduced from outside.
In 1847 an importation of English cattle into Sweden conveyed the
disease, where it prevailed for some time and even infected Denmark
through shipments of cattle, but was finally extirpated by the pole axe
and disinfectants.
In 1860, Norway imported infected Ayrshire cattle for the Royal
Agricultural College at Aas, but the imported and exposed stock were
promptly destroyed and the previous immunity of the country has been
maintained up to the present.
Denmark was infected in 1848 by importation from Sweden, and on
different other occasions from Germany and England, but by prompt and
rigid suppressive measures, stamped out the disease on each occasion.
This was true also of Schleswig so long as it remained a part of
Denmark, but the infection entered in the commisariat parks of the
German army in 1864, and the principality remaining in German hands, the
lung plague became permanently established.
Mecklenburg-Schwerin and Oldenburg also maintained vigorous suppressive
measures and for long kept clear of the infection.
Into Brooklyn, lung plague was introduced in 1843 through the purchase
of an English ship cow by a dairyman (Peter Dunn). From this centre the
infection spread until it prevailed in Connecticut, New York, New
Jersey, Rhode Island, Pennsylvania, Maryland, Virginia, District of
Columbia, Ohio, Indiana and Illinois.
In 1879, measures were taken in New York and New Jersey to extirpate the
disease but failed to receive the requisite continued support and were
practically abandoned. It was only in 1887 when the infection had
reached Chicago, the largest cattle market in the world, that the
National and State Governments were aroused to the gravity of the
danger, and, the Federal Government supplying the funds and the Illinois
Government the authority, the beginning of a real attempt at extinction
was seriously undertaken. The author acted as chief of the national
veterinary force in Illinois in 1887, and takes great pleasure in
recording that at the end of three months from the date of his arrival,
the last acute case of the disease had been disposed of and the
frightful danger that had threatened the nation through the Chicago
stock yards had been removed. The supervision was maintained for a year
later, and some old sequestra were later found in the lungs of cattle
slaughtered, but no acute nor dangerous cases of the disease. This was
followed by vigorous suppressive work in other infected states and by
September, 1892, the quarantine was raised and the nation pronounced
free from lung plague. The last cases were met with in New Jersey, early
in 1892. In this last anti-lung-plague crusade the National Government
inspected 1,605,721 cattle in 166,951 herds, made 356,404 necropsies,
purchased 21,961 head of cattle, and disinfected 4,128 premises. 7,438
cattle were found affected at the necropsy.
Another line of infection was started by 4 Dutch cows, landed at Boston
in 1859, and before the end of the year the infection had extended into
20 different townships in Mass. In 1860, a State Commission was created,
with Dr. E. F. Thayer as veterinary commissioner, and in the next few
years they destroyed 1,164 cattle, and stamped out the plague at a total
cost of $77,511.07.
An importation of infected cattle into New Jersey was made in 1847, by
Mr. Richardson, who on discovering the nature of the disease, made an
end of that particular contagious centre, by slaughtering his whole herd
at a cost of $10,000.
South Africa was infected in 1854 by the landing of a Dutch bull at Cape
Town. As there were no railroads and all inland carriage was conducted
by ox-wagons, it soon spread over the colonies and extended thence into
the native states, and has continued to the present time.
Australia was infected in 1859 through an English cow landed at
Melbourne. When the disease was identified, the whole herd was
slaughtered and paid for, and the farm quarantined. But the quarantine
was broken by a teamster turning his work oxen into the pastures under
cover of night, and the infection escaped and has prevailed over
Australia to the present day.
Later the disease extended in a similar manner, to Tasmania and New
Zealand.
_Causes._ The one essential cause of lung plague is contagion from a
preëxisting case. Before the days of bacteriology, this had been
demonstrated as conclusively as any truth can be. All extensions into a
new country or district could be traced to direct importation from a
preëxisting area of infection. Until such importation such lands have
been immune from time immemorial; at once after, the infection has
spread from the imported animals as a centre; if the stock is divided up
and scattered, several primary centres are formed from each of which the
plague makes extension. Again, isolated islands (Channel Islands) and
purely breeding districts (Scottish Highlands) into the herds of which
no store cattle from outside are admitted, remain immune through
centuries, no matter how prevalent lung plague may be in the countries
immediately around. The immemorial immunity of the Western Continent, up
to the date of the arrival of the now famous Dunn cow, the continued
immunity of Canada and Mexico after the infection of the Eastern United
States, and the immunity of the United States since the last infected
cattle were destroyed in 1892, are equally conclusive in this respect.
_Bacteriology._ The history of lung plague forcibly illustrates how
harmless microbes of large size, that may be easily discovered, and
which existing in the environment, readily find their way into diseased
and susceptible parts (in this case into the bronchia), may be held to
be the pathogenic cause. Willems and Van Kempen, in 1852, found microbes
in the exudate. Lustig in 1885 found four separate microbes in the
lesions, 1st, a short, thick, liquefying bacillus to which he attributed
the disease; and 2d, 3d, and 4th, three forms of micrococcus. Poels and
Nolen, in 1886, demonstrated bacilli of variable size (0.9μ), solitary,
in pairs and chains, cultivable in different media, and inoculable by
injecting such cultures into the lungs, but the resulting lesions were
not marked by the full lung plague exudate. Arloing, in 1887, separated
from the exudate the _bacillus liquefaciens bovis_, a very short,
slender bacillus, often in pairs with flagella, motile, staining easily
in anilin but not in Gram’s solution, quickly liquefying gelatine as a
culture medium and assuming a form that might be taken for micrococci,
quickly obscuring peptonized bouillon, and growing on potato. The
exudate placed in a thermostat at 95° F. encreases in potency. The
bouillon cultures injected under the skin or into the lung, produced
characteristic lesions of lung plague.
In the light of the later experiments of Nocard and Roux in 1897–8, it
would appear that Arloing’s bouillon cultures were probably complex,
containing not only the _bacillus liquefaciens bovis_, but also, the
infinitesimal microbe which is the true cause of the lung plague. In
seeding culture media with the exudate taken with all possible
precaution against contamination, from the interlobular pulmonary
connective tissue, they and others constantly failed to obtain results.
Better success attended their efforts with Martin’s culture bouillon for
producing diphtheritic toxin. Five pigs’ stomachs are minced, pounded to
pulp, mixed as follows: stomach 200 grs., pure muriatic acid 10 grs.,
water 50° C., 1000 grs., left in a thermostat at 50° C. for 12 hours,
(to 24), then heated to 100°C. to destroy the action of the pepsin, then
lowered to 80° C., alkalized, filtered from flocculi that formed, heated
to 120° C., and filtered. This is then mixed with peptonized meat juice
prepared as follows: fresh beef or veal, minced and pulped, 500 grs.,
and water, 1 litre, are kept for 20 hours at 35° C., the liquid
expressed, 5 grs. common salt added, mixed in equal proportions with the
peptonized liquid from the pig’s stomach, heated to 70° C. to coagulate
albuminoids, filtered, alkalized and sterilized. To this mixture is
added ¹⁄₂₅th part of blood serum (sterile) from the rabbit or cow.
This bouillon was inoculated with the pulmonary interlobular exudate,
enclosed in collodion capsules, having very thin walls, and inserted
aseptically into the abdomen of the rabbit. In 15 days the rabbit was
sacrificed, and the capsules enucleated from their envelopes of exudate
and cells. The contents showed the slightest possible shade of opacity,
but they contained neither cells nor any other definite organism. Under
a magnifying power of 2000 diameters the liquid contents were found to
be full of brilliantly refrangent points, actively mobile, but so minute
that their form could not be made out even when staining was resorted
to. The contents of these capsules when inoculated on cattle produced
the unequivocal phenomena of lung plague infection in a period of from 8
to 15 days. Other collodion culture cases inoculated from this produced
the same cultures in the peritoneum of the rabbit. Collodion cases
charged with the uninoculated peptonized bouillon, and placed in the
rabbit’s peritoneum remained absolutely clear, with no refrangency nor
motility under high powers and with no infectivity when inoculated. The
rabbits used for the infective cultures often became emaciated to the
last degree and even died, but their tissues proved in no respect
infecting to culture media nor when inoculated. The attempt to cultivate
the germs in collodion cases in Guinea pigs completely failed.
This ingenious form of culture devised by Metchnikoff for experiments on
the more delicate organisms, has been used by Nocard to accustom the
tubercle bacillus of mammals to grow in the bird and opens up great
possibilities for future investigators. The collodion, being impermeable
to leucocytes and bacteria, allows these to grow almost together, only
on the opposite sides of the collodion wall, restrains phagocytosis, and
protects the microbe against the destruction which would otherwise
overtake it.
_Modes of transmission._ The exhalations from the sick convey the
infection to susceptible healthy cattle. Yet even this was denied by one
veterinary teacher in Great Britain in the latter half of the 19th
century. The transmission of the disease by mediate contagion was denied
by those in authority in Great Britain up to the end of the century and
this delusion contributed largely to the loss of many millions by the
nation. Experiments made at Brown Institution were held to sustain this,
but not an atom of evidence was furnished to show that the exposed
animals were susceptible ones. Diseased lungs kept for a year at 21° F.
proved infecting when inoculated (Laguerriere).
_Contagion through the air_ in the same stable was admitted even by the
English sceptics. It may be carried in this way for forty yards, or if
dried on dust or light materials to a great distance.
_Infection through food_ soiled by breath or nasal defluxion is a common
cause. In our great swill stables during the prevalence of the plague,
it was notorious that the disease advanced rapidly along the line of a
feeding trough to the sixty or more animals using it, and that the
rapidity of the advance was determined largely by the fact that the
first animal was at the higher end of the trough. If at the lower end
there was no upward current to carry infection to the others. _Open
pastures_ where the sick have fed and _watering troughs_ or _ponds_ are
common sources of infection. The permanence of infection in and around
large cities is largely due to the common pasturage by different herds
in succession on the same unfenced lots waiting to be purchased for
building. For this reason the plague always extended in summer when the
cattle frequented these lots, and diminished in winter when they were
strictly confined to stables and yards.
_Mingling of different herds_ on _great unfenced areas_ has been the
main cause of the maintenance of the infection from time immemorial in
the hills and forests of central Europe and on the boundless Steppes of
Europe and Asia. This alone is chargeable with the permanence of the
affection, in spite of all efforts for its extinction, in South Africa,
Australia, Tasmania and New Zealand.
_Contagion carried by attendants_, _cattle dealers_ and even _dogs_, is
generally recognized, I have elsewhere quoted the case, in E. Lothian,
Scotland, in which the son of the steward, who was cattleman on an
infected farm, was the means of infecting first, his father’s cow, and
later the whole of the stock on the place; also the case at Quincy,
Mass., in which a farmer coming straight from the slaughter of sick
cattle, infected his own herd; also the case of Mr. Jewell, of Long
Island, who carried the infection from the herds visited, to his own
family cow in a thoroughly secluded stable.
_Infection through infected and emptied stables_, was a common
experience in dealing with the lung plague in America. Cows kept alone
and only introduced after the predecessor had died habitually contracted
the disease, though brought, through the most carefully guarded
stockyards, from healthy districts. Stables have continued infecting for
a year after having been vacated, (Friedberger and Fröhner).
_Infection through manure_ spread on ground to which susceptible cattle
had access was an occasional occurrence.
An _active, unrestricted commerce_ is however the most prolific means of
infection in cultivated countries. Slow as the disease progresses, and
long as the animal diffuses infection, it soon attacks and kills or
immunizes all the susceptible animals in the single herd, and if no
other susceptible animal is bought or born into the herd, the germ in
due time loses its pathogenic potency and infection is at an end. In
this way many centres of infection started in herds on well fenced farms
have worn themselves out. But the case was far otherwise in the city
dairies and swill stables. The trade demanded that the stalls emptied by
deaths should be filled up to consume the swill, or supply the milk
route and thus fresh susceptible cattle were constantly exposed in the
infected stable. The dairy cows were supplied by dealers who charged
exorbitant prices for them and held a chattel mortgage for the amount.
They had come through the infected dealer’s stable, and if they did not
come up to the milk yield promised, they were either passed on to
another dairy or returned to the dealer’s stable carrying back a new
load of infection. The wagons used to carry the cows through the city
were constantly infected and infecting. The swill stables became the
final destination of the surviving cows that had gone dry and thus
infection constantly gravitated into them.
In Europe where the great cattle and meat trade with England and the
constant demand for cattle to consume the marc of the beet sugar and
other factories, cause a continuous draught upon the infected districts
the great western centres of enterprise and commerce have found it
impossible to exterminate the plague.
In the country districts in England outbreaks were almost exclusively
confined to the times when fresh cattle were purchased at one of the
great fairs. Hence the late autumn, the period of laying in feeding
cattle, witnessed the greatest extensions.
In Ireland, as shown by Ferguson, the whole cattle trade seemed to be
arranged as if for the speedy and universal diffusion of infection.
Calves, bought by jobbers from all sources, were bunched together with
every opportunity for intercommunication and infection. As soon as they
were a little further matured, they were assorted in lots and sent to a
fair, where they were sold, and found their way to great common
pastures, and this process was repeated again and again until they had
reached full maturity. On the way to and from each market they were
quartered over night in a public yard which had just been vacated by
other animals, often diseased, traversed the same roads, and drank and
fed from the same troughs which diseased ones had just used.
The _introduction of apparently recovered cattle_ is generally credited
with the infection of a fresh herd and Friedberger and Fröhner quote
with approval Walley’s assertion that a recovered animal with a
sequestrum in the lung can infect a herd into which it is taken. I have
failed to produce even local exudate, subcutem or in the lung, from
sequestra which were much more recent, but the animals operated on were
rendered immune and inspired me to carry out a system of immunization by
the use of the sterilized fresh exudate. The actual date of the
expiration of virulence in the necrotic lung tissue has never been
demonstrated and probably varies in different cases.
The _receptivity_ of different breeds has been discussed and the
Holsteins and Shorthorns have been thought to show the greatest
susceptibility. These are among the cattle that are most prized, bought
and sold, and exposed to infection. The Shorthorn especially has a great
development of the circulatory system, including the connective tissue
with its great lymph sacs and channels, and the microbe we are dealing
with shows a marked preference for the lymph system, in which it finds
its appropriate field of development. Susceptibility is greatly
encreased by a _warm climate_ or _hot season_, under which large herds
may die without a single exception, the disease running a fatal course
in two or three days. In cooler climates 20 per cent. will often escape
at first (French Commission Experiments, 1849).
_Lesions._ If death has taken place early, the lesions are usually
essentially pulmonary, though they may implicate the pleuræ and
mediastinum. In many cases the lung alone is involved, yet even then the
predilection of the microbe for the lymph network of the interlobular
tissue is strongly manifested in the serous infiltration of that, rather
than of the lung structure proper. This determines the much talked of
marbled lung, the pulmonary lobules standing out at first as a more or
less deep red brown or black, while the marbling is caused by the
yellowish or grayish infiltrated tissue surrounding each pulmonary
lobulette which appear set in, as in mosaic on the surface of a section.
Sometimes a blood extravasation discolors the interlobular exudate as
well, yet it retains its soft liquid appearance which sufficiently
distinguishes it from the firmer lung tissue. These yellowish
interlobular markings vary much in thickness, but in acute cases this
may be up to half an inch or even more. In the lesions of longer
standing the interlobular exudate has usually coagulated, or even
undergone fibroid organization, so that it compresses and condenses the
lobules which it surrounds.
The pulmonary lobules may show the earliest changes of the alveolar and
lobular capillaries, with formation of an exudate, and an active
proliferation of small round cells in and around the alveoli. Later the
exudate coagulates, forming the familiar red hepatization, and this in
its turn may pass into the gray, or it may liquefy and undergo
absorption and resolution. Other changes are not uncommon. The excess of
interlobular exudate will compress the pulmonary lobules so as to reduce
their size and expel the blood from their structure, giving them a pale
color, or this compression becomes still greater, completely arresting
the circulation and inducing lobular gangrene. Thrombi in the afferent
and efferent vessels contribute to the necrotic change, and sequestra of
varying size, from that of a nut to that of an infant’s head or larger,
are formed. The earliest stage of this necrosis is usually infarction of
the lung, a definite area of which becomes saturated with dark blood
cells so that in contrast with the rest of even the hepatized lung, it
is almost as characteristic as the marbling. The further progress of
this necrosis is varied. Most commonly the exudate surrounding the
necrotic mass becomes organized into white fibrous tissue and forms an
investing sac in the interior of which is the dead lung tissue, showing
for a time distinctly, the bronchia, blood vessels, lobulettes, and
interlobular tissue. This gradually becomes detached and floating in a
liquid debris, slowly undergoes solution, and is absorbed, the sac
meanwhile closing in on the cavity. A large sequestrum may be a year or
sixteen months in undergoing complete solution. In other cases the
pulmonary lobulettes undergo an individual softening while the
interlobular tissue becomes organized and when cut across, the lung
presents a distinct honeycombed appearance. In still other cases a
considerable area of both lobulettes and interlobular tissue is necrosed
and liquefied, while the exudate, around the bronchial tubes, that
supplied it, becomes organized, and on the necropsy the latter are found
to constitute a thick branching mass of a very characteristic
appearance.
The newly affected lobulettes have a watery or gelatinoid or dropsical
appearance and if freely incised give out a large amount of serum and
flatten down in doing so. When hepatized the cut surface is granular,
and microscopic examination shows the terminal bronchia and alveoli
filled with a fibrinous exudate containing great quantities of red blood
globules and leucocytes. The distension of the lung is enormous, so that
when the entire organ is infiltrated it may weigh from 50 to 100 pounds.
In recent cases the lung may be extensively affected without affecting
the _pleuræ_; in other cases both are early involved. In advanced cases
the pleuræ are always implicated. First there is the subpleural
infiltration over the affected part of the lung; later the pleural
surface has reddened arborescent patches, with a slight solid exudate,
and a yellowish (sometimes blood-stained) serum collects in the bottom
of the cavity; later still the affected portion of the lung is covered
more or less thickly with false membranes, while others cover the organ
or the parietal pleura below this level, and hang in shreds or bind the
lung to the ribs. In old standing and recovered cases these may be
largely represented by dense, white fibrous investments covering the
lung or the rib, or establishing permanent adhesions. The amount of
pleural effusion may be about two gallons in bad cases, and like the
invasion is either unilateral or bilateral. The _pericardium_ is usually
more or less involved in pleuritic cases.
The _larger bronchia_ sometimes contain false membranes.
The _bronchial_, _prepectoral_ and _mediastinal lymph_ glands are often
enlarged, congested and infiltrated with an abundant exudate.
Similar infiltration of the lymph glands of the pharynx, mesenteries.
sublumbar region and groin are described, together with hypertrophy and
congestion of the intestinal follicles, and congestion of the muscles
and intermuscular tissue, of the articular and tendinous synovial sacs,
and even of the meninges of the brain and cord. I know of no facts to
show that these conditions result from anything else than the toxins and
the general constitutional disorder. The indications are that the
microbes are speedily destroyed in the circulating blood, and
intravenous injections and caudal inoculations alike fail to cause the
characteristic lesions in the lung, their favorite point of casual
election.
_Incubation._ This usually lasts from 6 to 30 days, being greatly
abridged by hot weather and often prolonged in the cold. Delamotte
claims to have seen it extend to 5 months, and in one case a calf turned
out on Montauk Point, L,. I., from an infected place was noticed ill on
the 104th day. Australia, South Africa and Norway were each infected by
cattle that had been three months out of their native infected land. I
have seen cattle pass three or four months after purchase in an
unthrifty condition, yet without cough or other recognized diagnostic
symptom and then come down with lung plague. Such doubtless explain the
alleged protracted incubations, the system has been invaded, ill health
ensues, but the lungs are only slightly affected for a length of time.
In other cases one animal in a herd has had a mild attack, which escaped
notice, and it was only later that the disease was recognized in a
second victim, infected from this first.
The bearing of this on imported animals is evident. An animal imported
alone should be kept under surveillance for a month or two after
quarantine, while in any considerable herd the disease would certainly
manifest itself during the prescribed three months detention.
_Symptoms._ These vary greatly with the animal and its environment.
Other things being equal it may develop more suddenly and violently in
the obese Shorthorn, Angus, Hereford, Ayrshire or Dutch, and less so in
the spare Brittany or Jersey. In very hot weather the attack is very
sudden and severe. A chill from exposure, an attack of bronchitis or
pneumonia, the excitement attendant on parturition, on travelling by
rail or driving may precipitate and aggravate the seizure. Under some
such conditions there may be sudden and extreme hyperthermia, rapid
pulse, oppressed breathing, percussion and auscultation evidence of
extensive pulmonary consolidation and death in two or three days, while
the body is still plump and fat.
Individual susceptibility appears to have influence, the same stable
presenting simultaneously cases of acute and fatal type and others that
are slow, and insidiously progressive. In newly invaded countries and in
bovine families that have not been exposed to the infection for many
generations the tendency is to a higher proportion of severe and fatal
cases, while in herds native to districts that have been continuously or
frequently exposed, mild cases tend to predominate. The more susceptible
strains of blood have been killed out, and the surviving strains show a
greater power of resistance.
Apart from the predisposing environment the tendency of lung plague is
to set in slowly, insidiously, and for a time almost without outward
symptom. For a week, fortnight, month or more there may be a slight
cough heard only at rare intervals and neither painful nor specially
troublesome. Though sometimes hard, it is more commonly small, weak,
short and husky, noticed only when the animal rises, drinks cold water,
goes out to the cold air, or eats dusty or fibrous fodder, and is
usually attended by arching of the back, extension of the head, opening
of the mouth and protrusion of the tongue. For weeks there may be no
indication of constitutional disorder, appetite, rumination, milking,
and other functions appearing to be normal. Driving the animal may
unduly accelerate the breathing, and a careful auscultation may detect
an unusually loud blowing sound behind the middle of the shoulder, a
mucous râle, or a wheeze. In some cases the disease never advances
farther, the trouble subsides and the subject is thereafter immune.
Cases of this kind occurring as the first in a herd, explain some
instances of what are claimed to be specially prolonged incubations.
In the great majority of cases further symptoms appear, hyperthermia
sets in, varying in different animals from 103° to 108° F., the animal
becomes dull, depressed, loses in appetite, rumination and milking,
omits pandiculation on rising, shows stiffness of the hind limbs,
sometimes knuckles forward at the fetlocks, wanders apart from the herd,
is found lying apart, shows extra thirst, bloats slightly, and shows
some constipation. Pulse and breathing are accelerated, auscultation
signs are more marked, and on percussion, areas of flatness may indicate
lobular consolidation, usually more extended than in ordinary pneumonia
with the same grade of constitutional disturbance. The muzzle becomes
hot and dry, the roots of the ears and horns hot, and the hair stands
erect along the dorsal aspect or in patches over the body. Pinching of
the dorsal spines, sternum or intercostal spaces, may cause marked
wincing and a deep groan. The eye is dull, lacking in prominence and
clearness, and the lids are often partially closed. At this stage
improvement sometimes ensues and after inappetence and suppression of
milk for one or two days, the patient may take to feeding and milking as
before, and apparently recover, though with a large pulmonary
sequestrum.
In the continuous and violent cases all the symptoms are aggravated.
Fever may run to its extreme height, there is complete anorexia and
suspension of rumination, pulse and breathing are rapid, the victim no
longer lies down but stands with feet apart, arms and elbows turned out,
head extended nearly on a line with the neck, mouth open, tip of the
tongue projecting, and each expiration accompanied by a moan, so loud
that it may be heard at a distance (often 50 yards). The breath is
heavy, feverish, mawkish. The flanks heave violently, the nostrils are
widely dilated and discharge muco-purulent, often bloody liquid, strings
of fœtid saliva drivel from the open mouth, there may be tympany or even
colic, the eyes are sunken, and the conjunctiva and nasal and buccal
mucosæ are of a dull brownish and yellowish red. Emaciation advances at
a rapid rate, and the constipation may be superseded by a profuse, fœtid
diarrhœa which wears out the animal. The skin is dry, scurfy, withered,
pale, and clings firmly to the bones, and the interior of the vulva may
show the pallor of anæmia. The spine, sternum and intercostals are more
than ever tender, and pressure on the tender areas may detect a lack of
movement of the lung which is felt on the healthy parts.
On percussion very extensive areas of consolidation are revealed by the
dulness and flatness. If pleuritic effusion exists the resulting
flatness is extreme below and up to a given horizontal level, the line
of which may, however, be elevated at points by consolidation of the
lung at such parts. Auscultation may reveal almost any of the abnormal
sounds of pneumonia or pleurisy. Absence of respiratory murmur over
large areas, with blowing, heart or abdominal sounds in unwonted
situations (where the murmur is absent), and abnormally loud murmur
where the lungs are still pervious; crepitation around the margins of
the consolidated portions; the creaking sound of stretched false
membranes, scarcely distinguishable from crepitation; mucous râles;
wheezing sounds of various pitches; exceptionally splashing sounds, and
if the animal has just risen, the metallic tinkling sound. In other
cases the pleural friction sound is prominent.
Abortions are common in pregnant animals.
_Course._ This varies greatly. In our northern states in winter, many
would seem to recover after a few days illness; in summer, many died in
a few days with excessive exudate, dyspnœa, and prostration. Others died
early from tympany of the rumen. In others still, profuse, fœtid,
colliquative scouring led to an early death. In extreme cases there
would be a loss of one-third or one-half the weight in a single week. In
the less rapidly fatal cases all the symptoms became aggravated, the
emaciation progressed, and a liquid pultaceous condition of the bowels
continued for two, three, four, or even six weeks, the animal finally
dying in a state of marasmus. In such cases the shrunken, pallid skin
and mucosæ bespoke an extreme degree of anæmia.
Recoveries may take place from comparatively advanced stages, but they
are liable to be slow and imperfect, the animal remaining unthrifty for
a length of time. In some of the more favorable cases, when the recovery
is less interrupted or retarded, fattening may take place rapidly, so
that it would appear as if the loss of a portion of lung, and the
lessened consumption of hydrocarbonaceous matter contributed to the
deposition of fat.
In some cases the active morbid processes subside, but are not quite
arrested and the malady assumes a chronic form, the exudates become
organized, causing a sclerotic or fibroid condition of the lung and
especially of the interlobular tissue, which compresses and carnifies
the lung tissue, or leads to necrotic changes and the formation of
sequestra, or again to liquefaction and the formation of vomicæ. Here
the proliferation of the germ may go on, though little new tissue is
invaded, and the animal may remain infecting for a long period. The
patient remains thin, and weak, is easily blown under exercise, has a
small, accelerated pulse, little power of digestion or assimilation,
shows frequent tympanies, and may have profuse diuresis or diarrhœa. The
cough is frequent, often paroxysmal, easily roused, loose, mucous,
painful and may be attended by muco-purulent discharge. Such animals are
liable to die in the end in marasmus.
In some cases the malady is complicated by other infections, leading to
the formation of abscesses in the lungs, pleuræ, chest walls, bronchial
glands, joints or elsewhere, or tuberculous deposits may complicate the
lung plague, and there may be an early death or a long drawn out
decline.
_Diagnosis._ So many different affections resemble lung plague closely
during life, that a certain means of diagnosis is a great desideratum.
Yet many points help one to reach a reasonably certain diagnosis:
1. Does lung plague exist in the country? If not the presumption is very
strongly against it.
2. Have the suspected animals been recently imported from a lung plague
infected country? or have they been in contact with animals recently
imported from such a country?
3. Have they been fed on provender imported from such a country?
4. Have they been attended by a man recently from such a country and
whose clothes have not been sterilized?
5. Have they been carried on any imperfectly disinfected car or ship
which has carried the cattle of such country?
6. Has the affection attacked a considerable proportion of the herd at
the same time? A rare thing with lung plague.
7. Has the attack come on slowly and insidiously? Very characteristic of
lung plague.
8. Has hyperthermia been marked? Indicative of lung plague.
9. Have a succession of cases occurred at intervals of several days or
weeks, irrespective of weather? Suggestive of lung plague.
10. Have the indications of consolidated lung been early and over
extensive undivided areas? Like lung plague.
11. Have cases been milder in cold dry weather and more violent in hot
and moist? Such is lung plague.
12. Does the same subject present lung lesions of very different
ages;—infiltration with tough, elastic lung; red hepatization; gray
hepatization; black infarction; sequestra, etc.? Bespeaks lung plague.
13. Do the infiltration and red hepatization show a marbling with very
extensive filling and turgidity of the interlobular and subpleural
connective tissue, and abundant effusion into the chest? This is the
nature of lung plague.
14. Does the lung exudate when inoculated in the tail of a susceptible
bovine animal (one that has never had the disease), produce local
inflammation and exudation and procure immunity? This characterizes lung
plague. Does it fail to cause inoculation swelling, in an animal that
had lung plague. Lung plague is still more indicated.
15. If the disease has lasted long enough in a place to determine, has
it affected any other than bovine animals, and does inoculation of the
lung exudate into any other genus of animal cause the disease? Other
genera are immune from lung plague.
_Tuberculosis_ is distinguished by the habitual absence of the high
temperature, the numerous circumscribed areas of flatness with wheezing
or other abnormal lung sounds, in the midst of a general field giving
the normal respiratory murmur, by the enlargement or induration of
superficial lymph glands, by the response to the tuberculin test, and by
the lung tubercles and diseased lymph glands,—congested, indurated,
caseated, calcified—found at the necropsy. Inoculation of other genera
causes tuberculosis.
_Simple bronchitis_ is usually connected with climatic change or
exposure, tends to affect a number at once, gives the blowing and mucous
râles, without indications of extended lung consolidation or pleural
effusion, and after death does not furnish lesions of all ages, recent
and remote.
_Verminous bronchitis_, attacks the young only or mainly, and never
seriously injures the mature, involves all or nearly all the young in
the herd, shows less hyperthermia, and less extensive consolidation,
more wheezing in the lungs, and a free expectoration in which the worms
(embryos or adults) may be found by careful search.
_Simple fibrinous pneumonia_ is likely to arise from climatic conditions
or from exposure, attacks several at once and none later, has less
abrupt rise of temperature, less tenderness of the chest walls, less
dyspnœa, less obstinate standing, and after death, less interlobular
exudate and marbling, and no presentation of old and recent lesions in
the same lung.
In the _infectious pneumonia_ occasionally seen in western cattle, the
distinction must be made mainly by the less elevated temperature, less
dyspnœa, the lack of the early signs of extensive consolidation of the
affected lung, and after death, absence of the extensive interlobular
infiltration, and in the predominance of the whitish points or mottling
indicating the broncho-pneumonia and the cell proliferation in the
terminal bronchia and alveoli.
The pulmonary form of _hæmorrhagic septicæmia_ (Wildeseuche) is
distinguished by its enzoötic character, in connection with wet lands,
its occurrence in the summer season, its association with other forms of
localization, in the abdomen, muscular system, etc., its dependence on a
cocco-bacillus, easily found in the exudate, and its inoculability on
the smaller ruminants, horses, pigs and rodents.
The _perforation of lungs and heart by a sharp pointed foreign body_
from the reticulum, occurs sporadically in one animal which has usually
been kept indoors; it shows as a rule less fever, may be preceded by
tympany or other gastric trouble, shows a line of consolidation from the
reticulum forward, is earlier or later complicated by morbid heart
sounds or rhythm, and commonly shows a pitting swelling beneath and
beside the sternum.
_Pulmonary emphysema_ is sporadic only, usually devoid of sudden
hyperthermia, or constitutional disorder, has a dry paroxysmal cough,
wheezing sounds on auscultation, and a drumlike sound on percussion. If
associated with bronchitis or pneumonia and attendant fever, the case is
more equivocal.
_Aspergillosis of the Lung_ usually advances more slowly, in the
comparative absence of sudden hyperthermia, shows more limited areas of
consolidation, less dyspnœa, and usually affects smaller animals (birds)
as well. At the necropsy the presence of aspergillus in bronchia and
lung tissue is conclusive.
The _acute pulmonary congestion_ of heat stroke is sufficiently
identified by the conditions under which it occurs, its sudden and rapid
progress, the implication of the brain, and its occurrence in other
animals similarly exposed.
Such conditions as _atelectasis_, _pulmonary actinomycosis_,
_distomatosis_, or _echinococcus_, the _congestion of mercurialism_,
etc., should be readily recognized by the attendant conditions, analysis
or necropsy.
Attempts have been made to diagnose lung plague by securing a reaction,
local or general, as the result of injection of the sterilized lung
exudate or cultures, but they have proved eminently unreliable. The
susceptibility of the serum to change under manipulation, the existence
of hyperthermia before the injection, and the disposition to local
infiltration under the lung plague poison are apparently insuperable
obstacles.
_Treatment._ No treatment has been devised that would warrant the
preservation of the infected animals when the alternative of prevention
is available. The question is an economic one, and with a disease that
is so insidious, with such a long incubation, with so many occult and
chronic cases liable to escape observation and recognition, and with
such a constant and prolonged exhalation from the lungs of the virulent
material and the certainty almost of the diffusion and preservation of
the latter, no more suicidal policy could be adopted than the
preservation and treatment of the sick.
If allowed at all, treatment should be conducted in an isolated
locality, well secluded from visitors and wandering animals including
birds, and under the most intelligent antisepsis. It should proceed on
general principles according to the individual manifestations of the
disease, and might include serum therapy from immunized animals.
_Prevention._ For a country like the United States, now happily free
from the lung plague infection, the important object is its permanent
exclusion. For this the federal quarantine for three months now in force
ought to be effective. The only question would be in the case of small
importations of one or two animals, which might introduce infection
under an apparently prolonged incubation, or with a chronic type of the
disease. Small importations of one or two, might be dismissed at the end
of three months quarantine under a _ticket of leave_ system, under which
they and the herd into which they are taken can be kept track of for
three months more. In the larger imported herds the possibility of the
escape of infection under a three months quarantine is so infinitesimal
that it may be practically ignored.
Similar precautions must be taken against the importation of cattle from
a country reputed to be free from the lung plague, but which imports
cattle from an infected country without imposing the three months’
quarantine.
The use, for transportation of cattle from one part of an immune country
into another, of cars or boats which have been used for transporting
cattle in an infected country can only be permitted after the vehicles
in question have been thoroughly cleansed and disinfected and attested
so by the official experts.
The landing in an uninfected country of hay, fodder, or cattle-food of
any kind, or of litter, grain bags, head ropes, manure, or other article
coming from an infected country must be prohibited until such article
shall have been thoroughly disinfected.
Horns, hoofs, hides, hair and other products introduced into the country
must be disinfected. The treatment adopted to exclude anthrax would be
amply sufficient for lung plague.
_Measures to Extirpate the Infection._ Stop all accessions of possibly
infected cattle from outside. Proclaim the infected area, prohibiting
all entrance and egress of cattle, and all movement of cattle from herd
to herd within the area, except under special license, based on the
soundness of each herd for six months antecedent. Prohibit absolutely
the pasturage of cattle on public highways and unfenced or
insufficiently fenced places. Send to instant slaughter cattle found in
such places in violation of this rule. Make an accurate census, with
individual description of each bovine animal in the infected district,
and make a necropsy of each such animal dying at the hands of the
butcher or casually. Hold the owner guilty of a misdemeanor with heavy
penalty, for every bovine animal that goes amissing in the infected
district without official post mortem examination. When an infected
animal is found in a herd have the whole herd, marked, appraised
slaughtered under official supervision and with necropsy of each animal.
If any herd has been losing animals, or had sick animals within a year,
buy and kill the whole herd. Indemnify the owners to the amount of at
least two thirds or three fourths of the sound market value for all
except the advanced and acute cases of the disease, and such animals as
have been moved into the State less than three months before. These
latter may be sacrificed without indemnity. Disinfect thoroughly all
infected premises and things at public expense. Close the fields against
all outside cattle for three months. Burn all hay, straw, litter, and
grain in the infected buildings or see that they be fed to horses, sheep
or pigs apart from where cattle are kept. Burn or disinfect all manure
or have it drawn out and plowed under by horses, and the wagons and
implements used in doing so thoroughly disinfected. Allow restocking of
the disinfected premises from sound districts only, and keep up the
strictest supervision and control of the herds for from three to six
months.
_For private Control in the absence of Government Action._ The
stockowner in a secluded locality, not bordering on a highway or railway
can as a rule secure the immunity of his herd by such measures as the
following. Breed all the stock on the farm. If a change of blood is
required buy the bull young and keep him strictly by himself for at
least four months, allowing him to mingle with other cattle only after
he has been thoroughly attested. Allow no animals to go outside for
service or any other purpose and afterward return to the herd. Allow
none to enter from without for any such purpose. If from any cause
cattle must be bought, secure them from healthy herds and transport them
in thoroughly disinfected cars, boats and by healthy roads, and never
through an infected district. Place them in special premises at least
one hundred paces from all other cattle, and under special attendants
for three months.
_Immunizing through a First Attack._ When lung plague was at its worst
in Great Britain, Mr. Harvey a dairyman on a large scale in Glasgow
practiced the method of buying heifer calves and exposing them in his
infected stables until they contracted the disease. He had a loss of 20
per cent. and the surviving 80 per cent. were then turned out on his
farm and raised and when they came in milk, were sent into Glasgow as
new milch cows immunized from the plague. He thus reduced his losses to
the minimum of one fifth of the inexpensive calves, and warded off the
heavy losses previously sustained in the valuable milch cows and
preserved the still more valuable trade in the milk of healthy animals.
The method was a mere temporary makeshift, depending for its success on
the permanent maintenance of the lung plague, but so long as there were
no well considered government measures for its extinction its permanence
was assured in any case, and Mr. Harvey was working no injury to any
one, while he was substituting a profitable occupation for a losing one,
and supplying his customers with milk from sound cows in place of those
that were continually coming down with the plague. Under official
measures for the plague-extinction his attempt would have been most
reprehensible, but in the absence of such measures it was highly
meritorious.
_Inoculation in the Tip of the Tail._ This is an advance and in some
respects an improvement on the Harvey system, as the infection and
lesions are localized in the tail, and the mortality is reduced to 2 per
cent. In practice a recently attacked animal is selected, and a portion
of the lung which is strongly infiltrated but not yet hepatized. This is
laid upon a clean scalded plate and incised with a clean scalded knife
when an abundance of a clear yellow serum drains out. This is drawn up
into a sterilized hypodermic syringe, and the tails having been washed
and sterilized, the nozzle is inserted under the skin of each in
succession and a drop or two of the liquid discharged subcutem. If
despatch is important the washing may be dispensed with and the nozzle
wiped and dipped in strong carbolic acid between each two successive
insertions.
Various modifications of this procedure have been made. To avoid the
inevitable entrance of ærial germs, flamed pipettes have been inserted
into a puncture in the turgid lung, made with a flamed knife, the point
is then broken and the serum is drawn up to fill the vacuum caused by
the heat employed in sterilization. The point is then sealed by melting
the glass in the flame of an alcohol lamp, or by melted wax.
Nocard washed the surface of the infiltrated or hepatized lung with
boiled water, then with a sterilized knife cut out a deep segment so as
to leave a conical cavity and covered this with an awning to keep off
dust. The space soon fills with the draining exudate in a very pure
condition.
Pasteur inoculated a calf in the dewlap or behind the elbow, where an
enormous engorgement forms, involving the whole ventral aspect, and
supplying an almost unlimited amount of serum, which may be collected
with such precautions against contamination as are indicated above. The
product is thus secured at a comparatively cheap rate, and the risk of
its diffusion on the air in breathing is lessened enormously.
Another method is to employ the serum from the swellings in the
inoculated tails and carry it on indefinitely from tail to tail.
Arloing in his turn employed the cultures in vitro of his
pneumo-bacillus, but with the modern evidence that this is not the
infective germ, such cultures can not always be implicitly relied on.
In place of the hypodermic syringe, Australians have used a simple
thread soaked in the exudate and drawn through beneath the skin. Others
have used a small lancet with a groove hollowed out in the middle of the
flat surface of the blade on one side, and which carries in the required
drop of the serum.
To preserve the exudate for some time against decomposition, it has been
kept on ice, or mixed with chloral hydrate or phenic acid (½ its
volume), and glycerine (½ its volume) for two or three months.
_Injection into the veins_ practiced by Burdon-Sanderson has the
advantage of producing no local lesion whatever and yet securing a fair
measure of immunity. It is, however, a much more delicate operation as
it entails a possible though remote possibility of producing capillary
thrombi, and some danger of infection of the wound in the vein. To avoid
this latter, the jugular vein is raised as for phlebotomy, and a short
needle is passed into it. A longer and more delicate needle is now
passed through this, and the injection of a few drops of the exudate is
made through the latter. The small needle is then carefully withdrawn to
be followed a few seconds later by the large.
_Injection of the Sterilized Exudate Subcutem._ In 1881 having found
that liquids obtained from old sequestra, produced no local lesions when
inoculated subcutem, but secured immunity for the subjects, I inoculated
ten susceptible cattle with the fresh pulmonary exudate which had just
been heated for 30 minutes to 180° F. No local inflammation nor exudate
occurred in any of them, but subsequent inoculations with fresh
unsterilized lung plague exudate were resisted in the same way. Six of
these immunized cattle were subsequently placed in two infected stables
and herds, (Mr. Butts, Brooklyn, N. Y., and Mr. Christopher Slade, White
Hall, Baltimore Co., Md.) and retained there for three months without
showing the slightest indication of disease. Later I applied the measure
on a number of herds with thoroughly satisfactory results. About ten
years later a similar resort was had by Arloing and Rossignol with
corresponding success.
Two advantages come from this method: 1st, there is no local infection
and no marked swelling so that the injection can be made on the side of
the neck where the skin is thin, and clean, and the connective tissue
abundant, and where there is less risk of extraneous infection than in
the too often dirty or filth soaked tail; 2d, as no living germ is
introduced there is no possibility of propagating the disease to other
neighboring susceptible animals. Two per cent. of loss, of animals
inoculated by the Willem’s method is counted on, but with the sterilized
virus there is not even a remote probability of loss. Infection cannot
occur from the animal injected with the sterilized virus, so that it can
be safely applied among cattle that have not been exposed to infection,
but which are likely to be in the future, and these injected cattle can
be left to mingle with others that have not been injected without a
shadow of danger to either.
_Conditions permitting and forbidding Immunization._ Immunization is
permissible or commendable in all cases in which lung plague is already
widely spread in a land destitute of fences and in which cattle roam at
large, and herd mingles freely with herd. Here the extension of the
disease is inevitable and continuous and effective measures for
extinction are impossible. It is permissible where the plague is widely
spread among cultivated and fenced farms, but where no authoritative
measures are in force for its extinction. In such case, with the
Willem’s system the inoculated herd should be kept thoroughly secluded
in premises or well fenced pastures, apart from any highway, and not
adjoining any other cattle pasture.
When on the other hand official measures are in force for the extinction
of lung plague, every form of immunization based on the production of
the pathogenic germ in the living body of the bovine, or even in vitro,
is to be unqualifiedly condemned. The risk of the escape of the
infection through subtle, unsuspected channels is too great to allow of
its reproduction in any form. By restriction of cattle movement,
slaughter and disinfection, extinction of lung plague is easy and
certain, but, whatever may be true of an individual herd, no country has
ever permanently extinguished lung plague infection, when the virus was
systematically multiplied for uses in inoculation.
CATTLE PLAGUE.
Synonyms. Definition: infectious fever of polygastrics, with sudden
onset, violent progress, high mortality, congestions of mucosæ,
petechiæ, concretions on buccal and vulvar mucosæ and on skin,
erosions of gastro-intestinal mucosæ, and pulmonary interlobular
emphysema. Historic notes: ancient—China, Hindoostan, Steppes; in
middle ages—Europe, Britain; recent—Europe, England (1714 and 1740),
Scotland (1770), Central Europe (1796–1816), Southern Europe (1827),
Germany (1830–1), Egypt (1841), Britain (1865), France (1870–1), S.
Africa (1881), Abyssinia (1890), Japan (1892), The Phillipines
(1898–9). Animals susceptible: ruminants, peccary, (swine?).
Bacteriology: minute corpuscles in cell nucleus (Semmer, etc.), which
are held back by Berkefeld and Chamberland filter. Accessory causes:
such as favor preservation, multiplication and diffusion of germ.
Susceptibility varies with previous exposure of the race. Immunity
after one attack. All liquids and secretions of the sick are virulent;
also manure, hay, straw, dust, stables, troughs, cars, boats, loading
banks, yards, milk, flesh, fat, sausage cases, hairs, horn, hoofs,
wool, bristles, hides, bones, halters, harness, shafts, poles, goads,
boots, clothes, feet (animals), wheels, runners, vermin, wild animals.
Virulence lost in drying. Manure preserves for weeks. Lost at zero,
and at 131° F. Lesions: congestion, petechiæ, hæmorrhages and erosions
on fourth stomach, small intestine, rectum, vagina and mouth,
emaciation, sunken eyes, diarrhœa, wart-like epidermic elevations,
concretions on mouth; conical papillæ dark, like port wine; petechiæ
and extravasations in subderma and submucosa; swollen intestinal
glands; spleen normal; liver, pale, soft; kidneys swollen, congested,
petechiated, softened; lungs with spots of congestion and
extravasation and emphysema: petechiæ on heart and pericardium: blood
has excess of fibrine and leucocytes, black. Incubation 2 to 9 days.
Symptoms; hyperthermia (104° to 108° F.), white epithelial concretions
on gums, followed by abrasions, congestion of visible mucosæ,
weariness, debility, thirst, constipation followed by diarrhœa, tender
loins, drooping head and ears, weeping eyes, grinding teeth, rapid
pulse, expiration with arrest and click, suppression of milk, relaxed
sphincters. May become aggressive or soporific. Diagnosis: by rapid
and deadly progress, and manifest infection; from _malignant catarrh_
by the active spread, numbers attacked, concretions on mouth, and
known exposure; from _thrush_ by the high fever, contagion to old as
well as young, and severe abdominal symptoms; from _aphthous fever_ by
the high temperature, the absence of distinct vesicles on mouth, teats
and feet, by the comparative immunity of swine, and by its high
mortality; from _dysentery_, by the early hyperthermia, the
concretions in the mouth, by rapid general extension irrespective of
filth and crowding, and by the implication of stomachs and small
intestines, rather than the large; from _gastro-enteritis_, due to
chemical irritants, by the lack of such manifest cause, and its rapid
progress from herd to herd; from _anthrax_, by its rapid spread beyond
an anthrax locality, the buccal and skin concretions and
desquamations, by the insusceptibility of horse, dog, and rodent, by
the absence of splenic enlargement or incoagulable blood. In sheep:
mortality in Steppes, 30 to 50 per cent.; in new countries 90 to 95
per cent. Treatment: to be condemned where its permanence is not
accepted. Serum-therapy: blood serum of immunized animal subcutem.
Prevention by immunization: mixture of virus and bile; inject with
highly immunized and defibrinated blood, and expose to the sick, only
admissible where extinction is despaired of. Exclusion: exclude all
ruminants and their products which come from suspected lands, or admit
on certificate and quarantine, or for slaughter only. Extinctions:
Trace and kill all ruminants that come in proximity to every infected
animal, or to any place or thing where it has been, disinfect
thoroughly the carcasses, products, places and things, register all
ruminants around a wide area of possible infection, make necropsy in
every case of death, appraise and sacrifice any herd showing the
infection. Each seaboard state should provide for instant action by
the Federal Government. Question of extinction in the Philippines.
_Synonyms._ Pestis Bovina, Rinderpest, Magenseuche, Viehpest,
Viehseuche, Pockenseuche (German). Pest Bovine, Typhus Contagieuse,
Typhus du gros Betail (French). Tifo Bovino (Italian). Dzuma (Polish).
Tchouma Reina (Russian). Low peng (belly sickness, China). Pushima
(Hind., Burma.).
_Definition._ A contagious fever of polygastric mammals (bovine, ovine,
caprine, cervine, exceptionally porcine), characterized by sudden
invasion, rapid advance, hyperthermia, great constitutional disorder,
congestion and blood extravasations of the mucosæ generally, but
especially of the gastric and intestinal, epithelial and epidermic
hypertrophy in the form of white concretions or warty-like masses on the
mouth, (vulva), and skin, followed by erosions, by pulmonary,
interlobular emphysema, by a catching, arrested inspiration, followed by
an expiratory moan, and by an early and very high mortality.
_Historic Notes._ As the most rapidly developing and deadly of the
cattle plagues, this attracted the greatest attention of people in
earlier times, and thus its invasions and ravages can be more
satisfactorily identified, than those of the tardier and somewhat less
deadly lung plague which usually followed in its wake.
Sanctus Severus and Vegetius Renatus indicate its advent into Western
Asia on the borders of the Caspian and Black Seas, coincident with the
irruption of the Mongols in the first Christian century. It still
prevails in China and adjoining countries, including Hindoostan, and
since that date the Steppes near the Black and Caspian Seas have been
looked on as the perennial home of the plague. Before 376, A. D., the
chronicles of epizoötics in Europe suggest anthrax affections which
prevailed widely in man and beast, and since that time the special
plagues of cattle come into prominence. At this date the Huns began a
great onward movement from the region of the Caspian and Black seas into
Dacia (Hungary), Northern Italy, Germany and Gaul, and this was the
occasion for a general diffusion of Rinderpest over these countries.
After this date cattle plague spread widely on the occasion of any great
European war in which the eastern nations were involved or which was so
general or continued as to draw upon Eastern Europe for the supply of
the commisariat parks. One great epizoötic culminated in 810 after the
wars of Charlemagne; one occurred in 820 in connection with invasion of
Hungary by the Franco-German army; one in 1223 to 1225 laid waste
Central Europe and is said to have reached Great Britain; in 1233–4 it
again gained a wide extension following the invasion by hosts of Mongols
from Siberia; great extensions are recorded in Italy in 1616 and 1625
during the 30 years’ war; in 1709 Charles XII wintered with his army in
the Ukraine and his return was followed by the most disastrous mortality
ever seen in Europe and which lasted from 1710 to 1717. This reached
England in 1714 and was there stamped out by killing and burning the
sick, disinfecting the buildings and closing up the infected pastures.
Paulet claims that Europe lost 1,500,000 head of cattle in the first
three years of this invasion. It continued more or less prevalent in the
eastern countries of Europe, and, following the course of war, entered
Italy in 1735, and extended westward. Again in 1740 in connection with
the war of the Austrian Succession it extended westward invading the
Western Countries from France to Denmark inclusive, and once more
extended into England, where it prevailed until 1756 and caused an
unprecedented destruction. It was finally stamped out as on the previous
invasion. During this invasion Europe lost 3,000,000 head of cattle
(Delafond). In 1770 another invasion of Great Britain occurred through
the landing of infected Dutch hay at Portsoy, N. B., but this was
quickly suppressed by the destruction of every bovine animal in the
infected herds, and the thorough disinfection of premises, supplemented
by a daily scrutiny of all cattle within a radius of 18 miles. In the
second half of the 18th century cattle plague prevailed more or less
generally in all Continental Europe, except Norway, Sweden and the
Spanish peninsula, into which no cattle were imported, and carried off
200,000,000 head of cattle (Freidberger and Fröhner). In 1796 to 1816
the cattle plague followed the marches and countermarches of the various
armies in connection with the French revolution and the Napoleonic wars,
causing unheard of losses throughout Europe. In 1827 it spread widely in
connection with the war of independence in Greece, and again in 1830–1 a
wide extension occurred in connection with the Polish revolution. In
1844 Russia lost 1,000,000 head of cattle. In 1841 a shipment of
Roumanian and Anatolian cattle to Alexandria, Egypt, carried the plague
and in two years upwards of 350,000 head of Egyptian cattle perished,
only a few being left. From this date the great development of
manufactures in the Western European nations, and especially in Great
Britain, the consequent increasing demand for beef, and the inauguration
of rapid transit from Eastern Europe by steamer and rail, introduced an
era of the extension of the cattle plague by commerce rather than war,
and Röll gives the losses in Austria alone in 1847 to 1864 at 500,000
head. In 1865 a cargo of cattle from Revel on the Baltic, landed the
infection at Hull, whence it speedily extended over the entire country,
and prevailed for 18 months, but was stamped out by vigorous measures of
destruction and disinfection. In all 279,023 head were reported attacked
of which 233,629 died or were killed and 40,165 recovered. In 1865 the
plague was once more imported into Egypt, this time from the Danubian
Principalities. A wide extension took place in the parks of the French
and German armies in the war of 1870–1, as many as 43 departments in
France having suffered. In 1872 it was imported from Russia into Great
Britain but was speedily extirpated, and again in 1877 from Germany when
it spread somewhat more widely but was easily suppressed. In 1881 it was
introduced into S. Africa in Asiatic cattle during the war in the
Transvaal and coming after the long continued prevalence of lung plague
it threatened the cattle interests with ruin. In 1890 it reached
Abyssinia by cattle sent for the supply of the Italian Army. In 1892
Japan suffered through importation from the main land. The latest
extension of cattle plague was in 1898–9 into the Phillipines in the
shipments of Asiatic cattle sent for the supply of the American army,
and there as elsewhere in unfenced countries it is proving the cause of
disastrous losses.
_Animals Susceptible._ In spite of its name—cattle plague,
Rinderpest—this affection is not like lung plague peculiar to bovine
animals. Yet bovine animals are by far the most susceptible, by them it
is mainly propagated, and upon them comes the greatest mortality.
Infection, however, extends to all other ruminants,—sheep, goats, deer,
elk, antelopes, gazelles, aurochs, yaks, camels, dromedaries, buffaloes,
etc. Swine which show a pouch on the left sac of the stomach show a
certain susceptibility, it killed the peccaries in the Jardin des
Plants, Paris, and Viseur in France and Pluning in Sumatra, claim to
have seen cases in the domestic pig. The horse, dog, rabbit, bird, and
man are immune.
_Bacteriology._ In a disease with such destructive changes in blood and
tissues, bacteria are found, almost of necessity, in the seats of the
lesions and even in the blood. No constant microörganism has, however,
been isolated, cultivated in artificial cultures, and successfully
inoculated on other and susceptible animals. Saweljeff isolated
sporulating motile bacilli which break up into micrococci and
streptococci, with the cultures of these on agar he produced what he
believed to be cattle plague. Metchnikoff found a short bacillus with
rounded ends, forming cocci and leptothrix-like threads, non-liquefying,
and producing cattle plague in calves. Sacharow found a bacillus 0.25μ
to 1.5μ long and Tokishige a very small short bacillus the cultures of
which produced rinderpest in cattle. It would seem as if here as in the
case of lung plague, the experimenters had retained the real but
invisible pathogenic agent in what they took for pure cultures. Semmer
attributes the disease to fine corpuscles which have so far eluded
current methods of staining and cultivation, and that they exist in the
number of from one to six in the enlarged cell nucleus. Nicolle and Adel
Bey sustain this position, having found that the unseen virulent germ
passed through the more open and thinner Berkefeld filter, but failed to
traverse the denser Berkefeld and Chamberland porcelain filters even
when favored by a somewhat higher temperature. As this filtration
usually removes the germ and renders the liquid noninfecting they hold
that the real germ is almost certainly intraleucocytic. When in
exceptional cases a few pass through the filter it is held to be only
such as were free in the liquid, and these are usually so small in
number, that inoculation with the filtrate does not kill, nor always
produce appreciable symptoms, but only immunity.
_Accessory Causes._ The essential cause being the germ, accessory causes
are of necessity such as contribute to the preservation of that microbe
and its introduction into the systems of susceptible animals.
_Susceptibility_ has a powerful influence even in races habitually
subject to rinderpest. The highest susceptibility inheres in cattle, and
yet the surviving cattle of the Steppe race, which has been exposed to
the infection for centuries, mostly recover from the plague, while fresh
cattle imported into the Steppes perish almost without exception. Sheep
and goats contract the disease but it is more severe and deadly in the
latter than in the former animal. Both, however, can carry the infection
back to the bovine animal, as can also the whole group of ruminants. The
Guinea pig contracts the affection by inoculation and may thus become an
indirect means of conveying infection from ox to ox.
_Immunity_ follows a first attack. Calves born of cows that passed
through cattle plague during the last months of gestation are usually
immune.
_Exposure to infection_ arises in various ways. All of the secretions of
the diseased animal are apparently infecting, and the virus possesses
great vitality, so that the channels of infection are almost endless. It
is carried in the manure, washed on in streams, and drains, dried up on
hay, straw, feathers and other light objects, or in dust, and blown
about by the winds, left in stables, in feeding and watering troughs, in
railroad cars, steamboats, ferry boats, loading banks and yards, it is
carried in the fresh milk, flesh, fat, sausage cases, hairs, hoofs,
horns, wool and bristles, in hides and bones, in halters and harness, on
wagon shafts and poles, on goads, on boots and clothes of men, and the
feet of dogs, birds and other animals, on the wheels of vehicles, the
runners of sleighs, and by vermin and wild animals. The various infected
products, however, soon lose their virulence after drying. Galtier
assures us on the basis of the experiments of a Russian Commission, and
the experience of France, Belgium, England and other countries that
dried or salted hides can be introduced with perfect safety, and that
rendered suet, and dried skins, horns, bones and hairs are equally
harmless. On stalls, mangers and racks on the other hand, in an obscure
and still atmosphere, virulence may be preserved for three months
(Müller, Dieckerhoff). Again in litter and manure in the open air, and
even in yards and pastures it may retain its vitality for weeks
(Chauveau). The infection is destroyed by a temperature of zero, or 131°
F. (Semmer).
Whatever determines a movement of animals from an infected locality,
determines the extension of the plague, hence war, and commerce, the
food demands of a large and encreasing manufacturing population, the
inauguration of new routes of rapid transit by steam over land or sea
all contribute in their various ways to the extension of rinderpest.
_Lesions._ The most significant feature of the morbid lesions is their
concentration on the fourth stomach, small intestine, rectum, oral
cavity and vagina. The respiratory apparatus, eyes, skin, muscles, and
nervous system suffer to a lesser extent. If the case has gone on to a
fatal result there is usually marked emaciation, the natural openings
(mouth, nose, eyes, anus) are soiled with morbid discharges
(muco-purulent, feculent) the thighs smeared with offensive liquid
fæces, and the skin may be yellowish red, or dark, with a general scurfy
condition and distinct eruptions, especially of rounded wart-like
epidermic concretions on teats and udder. The eyes are deeply sunken,
the conjunctiva of a yellowish red, and the lips and muzzle dry, swollen
and it may be eroded.
The buccal mucosa is swollen, fœtid, with marked epithelial desquamation
and more or less deep and extended erosions on the upper and lower lips,
gums, dental pad of the upper jaw, cheeks, hard palate, and root of the
tongue. There may still be some of the characteristic, white, epithelial
concretions, or the epithelium may hang in loose semi-detached shreds,
or there may be extensive areas of abrasion, in transverse cracks or
broad patches, and finally extensive petechiæ. The conical papillæ on
the cheeks and dorsum of the tongue are especially liable to dark red
petechial discolorations.
The subderma and submucosa are also suffused with these congestions and
petechiæ, and like the epidermic layer show a marked increase of all
elements and of the cell nuclei.
The congestions, petechiæ, desquamations, erosions, are found on the
fauces, pharynx, gullet, nasal mucosa, trachea, and bronchia, to a
greater or less extent in different cases. There may be even limited
areas of superficial necrosis and even the formation of false membranes.
In the diseased epidermis and epithelium, in the necrotic plaques and
false membranes there are spores and mycelia of fungi and bacterial
growths.
In the rumen, reticulum and manifolds, the mucosa and submucosa usually
show limited areas of thickening and punctiform or arborescent
congestion with softening and even detachment of the epithelium.
The abomasum is profoundly involved, especially in the vicinity of the
pylorus. The folds are of a deep blood red or purple, or blackish, port
wine hue, or they may be in part brownish red, or when necrotic, slate
colored or mottled. The peptic glands are swollen, elevated and dilated,
and patches and spots of softened and loosened epithelium are easily
detached leaving a deep red surface with, it may be redder oozing
points. Ulcerous sores may show on the summits of the folds. The
contents are a viscous, fœtid grayish yellow, or reddish liquid, without
solid ingesta.
The small intestines show similar lesions, deep, dark red congestions,
most intense on the summits of the folds, softened, loosened, ragged
patches of epithelium, erosions, ulcers, circumscribed sloughs, casts of
the gut formed by desquamating epithelium, and congested, enlarged, and
prominent aguimated and solitary glands are more or less in evidence.
The contents are liquid and yellowish, grayish or reddish and fœtid.
Microscopically the distension of the glands, (of duodenum, Lieberkuhn
and Peyer), the proliferation and softening of the epithelium, the
enlargement of the nuclei of these and of the cells of the submucosa,
and the profusion of microörganisms are marked features.
In the cæcum and colon the lesions are usually less prominent, though
swelling, softening and desquamation of the epithelium often exists, and
points and patches of congestion, ecchymosis, and necrosis are not
uncommon, particularly in the cæcum, and may extend to the muscular
layer.
The terminal portion of the rectum is especially liable to marked
congestion and blood extravasation, with more or less desquamation and
erosion. The summits of the mucous folds are often of a dark red (port
wine) hue, and as this is everted and exposed in defecation or later by
the relaxation of the sphincter it becomes a marked lesion even in life.
The spleen is normal in strong contrast with anthrax in which similar
gross lesions are often found on the mucosæ and especially the rectum.
The liver is usually rather pale and soft, as in other cases of high
fever and centres of necrosis may be present. The gall bladder contains
a variable amount of thin bile. The pancreas is nearly or quite normal.
The lymph glands generally and especially those of the mesentery and
abomasum are congested, enlarged and softened.
The kidneys are congested, often petechiated, swollen and softened, with
centres of necrosis. The bladder, vagina and uterus show mucous
congestion, and thickening uniformly or in spots with muco-purulent
secretion.
The lungs show spots of hyperæmia, extravasation and at times
hepatization, but a very characteristic lesion is the interlobular
emphysema already referred to as connected with the abdominal pain and
the sudden arrest of inspiration. This gives a gross appearance of
marbling as in lung plague, only in this case the inflated interlobular
tissue is dark colored instead of white as in lung plague, and it
collapses at once when incised.
The encephalon, medulla and nerves present more or less hyperæmia and
even exudation.
The heart is usually pale except in the spots infiltrated by blood, but
it may be mottled with petechiæ and particularly on the endocardium. The
pericardial fluid is often red. The blood is at first little altered,
but later undergoes marked changes, notably an increase of fibrine (50
per cent.) and a decrease of water (as in Asiatic cholera). There is
marked leucocytosis, and distortion of the red globules. Before death it
becomes black and incoagulable.
The whole capillary system tends to be relaxed and over-distended
(congested).
_Incubation._ As seen in England the incubation was from four to five
days. Four to nine days are claimed by Galtier as the extremes, yet he
quotes incubations apparently as short as 12, 24, 36 and 48 hours
respectively. A source of fallacy rests in the prevalence of cattle
plague in the district and the possibility of infection through
unsuspected channels, before the recognized exposure. Something must
also be allowed for the greater susceptibility and the larger dose of
the poison which would tend to shorten the incubation. Thus the western
improved breeds, which suffer a mortality of 80 to 95 per cent. (Refik
Bey), and the winter season, when the virus is concentrated in small ill
ventilated houses, both tend to shorten the incubation. At the Albert
Veterinary College in 1865, Gerlach went direct from the infected stable
to the sound one, and in 48 hours several of the cattle in the latter
had a manifest rise of temperature. Roloff observed the elevation of
temperature in 36 hours after exposure, and Ranpach and Ravitsch as
early as 11 hours after the inoculation.
_Symptoms._ The earliest symptom is abrupt hyperthermia, (104° to 108°
F.). This is virtually pathognomonic in a herd or locality in which the
disease exists, or in suspected animals presumably coming from an
infected region. The temperature usually rises to its height on the
third or fourth day, and falls materially when other symptoms are
developed. In some instances death supervenes during the high
temperature, but in the majority the temperature goes below the normal
before death.
Often on the second day, or the third, white epithelial eruptions or
concretions appear on the inner sides of the lips, closely resembling
the eruption of muguet (thrush) and often showing also on the dental pad
of the upper jaw and along the gums of the lower. In connection with the
high temperature, which is absent in _thrush_, this symptom is virtually
pathognomic. These concretions are more or less abundant in different
cases, sometimes so slight as to be easily overlooked, and in other
cases encreasing up to the sixth day, and covering not only the lips,
dental pad and gums, but extending back over the hard palate, pharynx
and gullet. The concretion is as soft as cream cheese, easily detached
and leaves a bright red abrasion (not ulcerated) when removed.
By the fourth day there are dry or staring coat, sometimes rigors,
sometimes small, accelerated pulse (60 to 120 per minute), some loss of
appetite and impairment of rumination, dry muzzle, a general flush of
the mucosæ (mouth, vagina, rectum), and deep blood red discoloration of
many of the buccal papillæ. There is weariness or debility, the animal
remaining down much of the time, also marked thirst, constipation, the
fæces covered with mucus or blood, rapidly advancing emaciation, and
marked tenderness of the skin, especially of the loins. The head and
ears are drooped, saliva drivels, the mouth has a fœtid odor, the eyes
weep, and there may be grinding of the teeth. The skin may be hot and
the white and delicate parts (udder, teats) suffused by a deep blush.
The milk is decreased at first and finally completely dried up.
As the malady advances the belly becomes tender, the constipation is
succeeded by diarrhœa with much attendant rumbling, the fæces are at
first watery, greenish and acid, and later highly offensive, yellowish
brown or gray, and alkaline. These become encreasingly profuse, fœtid
and liquid, assuming perhaps a pea soup or rice water consistency before
death. The sphincter, at first firm and quickly responsive, finally
undergoes permanent relaxation, with constant exposure of the dark red
mucosa.
When the disease is fully established the respirations often become
highly characteristic. There is not the sudden catching and shortening
of the inspiration as in pleurisy, but a sudden closure of the glottis
with an audible clicking sound in the course of the expiration, and,
after a perceptible interval of holding of the breath, the expiration is
resumed with or without an accompanying moan. This phenomenon is so
characteristic as to be largely diagnostic. Whether it is due to
abdominal pain roused by the sudden forward movement of the diaphragm,
or to nervous disorder alone, it is a valuable symptom always to be
looked for. It further explains the interlobular emphysema usually met
with in the lungs in this disease.
In the more violent cases death supervenes from the sixth to the ninth
day, but in the indigenous breeds of Eastern Europe and Asia, which
represent a _survival of the fittest_, the great majority suffer mild
attacks and recover, and even in newly invaded countries, when the
invasion has spent itself and the less susceptible are largely attacked,
a fair proportion survive for a longer period and even recover.
In these milder, protracted, or surviving cases the skin symptoms are
likely to come out prominently. Chief among these and very constant at
the height of the disease is an abundant unctuous exudation which dries
on, forming a crust, comparable to what is seen on the skin in the
fevers of swine. At different points, notably on the teats, udder, inner
sides of the thighs, and arms, and on the neck, lips and face generally,
are epidermic concretions having a warty-like appearance, and
respectively seated on a very slightly swollen and congested point of
the dermis. The deeper layers of these epidermic concretions often
soften, so that they have been mistaken for vesicles and pustules, and
hence the error by which cattle plague was held to be but a malignant
form of cowpox. But these concretions are histologically distinct from
vesicles; there is no liquid exudate on the papillary layer raising the
epidermis in the form of a little sac, but merely an excessive
production of the cuticular cells with abnormally large nuclei, as
happens generally to cells in active proliferation, and an admixture
with those of spores and mycelium of fungi which have no special
significance.
Papules, vesicles and pustules may form on the diseased skin and are
described by different authors, but they are not characteristic of the
disease as are the epidermic proliferations.
In some rare cases nervous symptoms appear, the animal moves unsteadily
without proper sense of balance, it may toss its head and horns as if
attacking an enemy or it may sink into a somnolent or comatose
condition. Wasting advances rapidly, abortion occurs in pregnant
females, the weakness becomes extreme, the animal remains constantly
down, unable to rise, rests his head on the ground, breathes heavily and
stertorously and perishes with or without convulsions.
_Diagnosis in Cattle._ Individual symptoms of cattle plague may be found
in other diseases, but the aggregate symptoms, in a rapidly spreading
and fatal affection, and connected with a previous prevalence of the
disease in the country or district, or distinct evidence of the
introduction of infection should in every case obviate error. The chief
diagnostic symptoms are: a sudden, very marked rise of temperature; a
congestion or blush of the visible mucosæ generally (mouth, nose, vulva,
eyes); the formation of white curd-like epithelial concretions on the
inside of the lips, dental pad, or gums of the incisors; the formation
of red spots or petechiæ on the mucosæ; later the desquamation of the
softened epithelium with the formation of erosions or even ulcers; the
wart-like rounded epidermic eruptions on the skin; the great abdominal
tenderness with tucking up of the abdomen, and sudden arrest of the
expiration with a sharp clicking sound and moan; the fœtid, watery
diarrhœa and exposure of the dark red, congested and hæmorrhagic rectal
mucosa; the discharge from nose, mouth and eyes; the characteristic
fever odor; and the rapid progress of the disease from animal to animal,
and to a fatal issue. The rapidly advancing contagion and its fatality
in cattle, sheep and goats, together with the immunity of horses, dogs,
birds and human beings are important elements in diagnosis.
_Malignant Catarrh of Cattle_ is distinguished by the absence of active
contagion, one or two only in a herd being attacked; by the absence of
the curd-like concretions on lips, dental pad, and gums; by the
involving of the matrix of the frontal horns; by the great congestion,
swelling and discharge from the eyes; and by the impossibility or
improbability of the cattle plague contagion in the particular locality.
In localities where cattle plague actually prevails, it may sometimes be
impossible to distinguish at first, and then every precaution should be
taken to prevent diffusion of infection in case it should be cattle
plague.
_Thrush_ of the mouth, though causing an eruption of the same kind,
occurs in sucklings only, is unattended by fever, marked congestion, or
severe abdominal symptoms.
_Foot and Mouth Disease_, though equally contagious, and spreading with
the same rapidity, is easily distinguished by the very slight
hyperthermia, the vesicular character of the mouth and mammary eruption
(the cuticle being raised by an abundant clear straw-colored liquid
exudate); by the absence, in nearly all cases, of severe abdominal
disorder; by the all but constant vesiculation of the interdigital
space, and by its mild and non-fatal issue. Swine contract it as readily
as cattle and sheep, and horses, dogs, birds and men by inoculation.
_Dysentery_ is marked by the absence of the early, abrupt hyperthermia,
though the temperature may rise gradually to a high point; also of the
curd-like concretions on the buccal mucosa; by the earlier onset of the
fœtid diarrhœa, and by the indisposition to contagious diffusion apart
from the confined, foul, crowded buildings. The lesions are mainly on
the large intestines while in cattle plague they are on the small
intestines, fourth stomach, mouth, throat and skin.
_Gastro-enteritis and Stomatitis_ from corrosive agents and irritant
bacteria, can be traced to a definite local cause, do not extend beyond
the herd or animal poisoned, and usually occur where the possibility of
cattle plague can be excluded. There is usually an entire absence of the
white epithelial concretions, of the blush of the mucosæ generally, and
of the wart-like epidermic proliferation.
_Anthrax_ of the alimentary tract and rectum is distinguished by the
fact that it is largely an enzoötic disease, not spreading widely by
simple contact; that it is easily transmissible to horse, dog and man;
that it lacks the buccal epithelial concretions and characteristic
desquamations and the warty-like skin products; that it shows marked
enlargement and engorgement of the spleen; and that the blood and local
lesions contain the large sized, square ended anthrax bacillus.
_Diagnosis in Sheep and Goats._ This is based on the same phenomena as
in cattle; the sudden and exalted hyperthermia, blush or petechiæ of the
visible mucosæ, concretions on the lips, gums and skin, epiphora,
salivation, prostration, emaciation and diarrhœa. These last symptoms
are, however, less marked than in cattle and the mortality and
infectiousness are materially reduced. Pneumonic complications are much
more common in sheep.
_Mortality._ Among native cattle in the Steppes the mortality is 30 to
50 per cent. whereas elsewhere it is 90 to 95 per cent. Among sheep in
Austria it reached 60 to 66 per cent. Among camels in Asia and Africa
the fatality proved as high as among cattle. The Italian buffalo usually
recovered after seven days illness.
_Treatment._ The therapeutic treatment of cattle affected with cattle
plague has been eminently unsatisfactory and is so certain to become a
means of extension of the disease that it is legally prohibited in all
countries, in which the plague has not been allowed to become generally
diffused. Where it has become general in an unfenced country in which
accordingly its permanence is virtually ensured, it may be employed.
_Serum-therapy_ is advocated by Refik Bey. An animal is hyper-immunized
by repeated inoculations. His blood is then withdrawn and the serum
obtained from it is injected in a dose of 25cc., subcutem, at a
temperature of 104° F. The temperature is taken from the 3d to the 5th
day and if it does not at this time rise above normal the treatment is
ended. If still above normal a second dose of 25cc. is given. It is
claimed that the serum is harmless and may be safely given in a single
dose of 50cc. in case it is impossible to keep watch of the animal for
five days.
_Prevention by Immunization._ Semmer attempted this by inoculating
cattle with virus which had been weakened by heat or by passing it
through the body of a Guinea pig. The results were, however, far from
perfect and even in Russia the method failed of any wide acceptance.
Koch and Edington in South Africa practised extensive inoculations with
a mixture of the virus in bile. Still better results are claimed by
Danyoz, Bordet and Theiler in the Transvaal. These treated the animals
by injecting 25cc. to 50cc. of highly immunized blood, defibrinated, and
while the subjects were thus rendered temporarily insusceptible, they
were exposed to infection by contact with diseased animals.
As with serum-therapy, measures of this kind are only permissible in a
country in which cattle plague is already generally diffused, and where
there are no fences to limit the continued diffusion of the infection.
The preservation of the cattle artificially infected until highly
immunized, and again of the sick cattle requisite to give the disease to
the cattle operated on, and finally of these last through the mild
attacks that are to render them immune, affords an endless number of
loopholes for the escape of contagion which would forbid the adoption of
the method whenever the extinction of the disease is possible. When on
the other hand a disease is already spread universally in a country
destitute of fenced enclosures, in which herd mingles with herd in the
most perfect freedom, and where accordingly extinction is impossible,
the method is admissible and even commendable as a means of reducing the
otherwise ruinous mortality.
_Exclusion and Extinction of Cattle Plague._ For countries adjoining
lands infected with cattle plague such general measures as the following
are imperative: Prohibition of all imports of cattle, sheep and other
ruminants, camels and swine from such infected countries, also of the
fresh hides and other products of such animals, and of litter, fodder
and other things that may have been stored in the buildings with
infected cattle or otherwise soiled by them. Prohibition of imports of
all cattle or other ruminants from adjacent countries (which may be
plague-free), but which animals have been carried in undisinfected cars
or boats that had been in previous use for such species of animals drawn
from infected countries, or that had been passed through infected
countries, yards, buildings, loading banks, chutes, piers, gangways, or
other places, or furnished with fodder, halters or appliances from such
infected localities. In Eastern Europe the practice is to patrol the
frontiers day and night to prevent the smuggling of cattle through from
the infected country. Infected animals or herds, that it is sought to
pass, are turned back or slaughtered. Sheep from countries that had been
previously infected are often admitted on affidavit of the official
veterinarian in the country from which they come, that during the three
months before they left, there had been no contagious disease of cattle
nor sheep in the locality, and on the further condition that they shall
be slaughtered at the point of entry, or, if brought by rail, at the
nearest slaughter house approached by such railroad after entry. In
France, sheep, sent from Russia by sea, in French bottoms, certified as
above by the Russian authorities, and accompanied on the voyage by a
French veterinarian and certified sound by him, are allowed to circulate
freely after three days detention at the port of arrival without
evidence of disease.
In the United States the 90 days quarantine of cattle (dated from the
time of shipping at the foreign port), and the 15 days for sheep and
other ruminants under strict veterinary supervision is safe as regards
the importation of cattle plague in live animals. The greatest danger
will doubtless come from intercourse with the Phillipines, which were
infected with the cattle plague during the recent war. The greatest
possible precautions as regards the carriage of cattle on transports or
other ships, will be necessary. Not only should no Phillipine cattle be
imported, but no vessel, that has carried Phillipine cattle or sheep,
should be allowed to take on board home cattle nor other ruminants until
it has been thoroughly disinfected.
Cattle or sheep should be rejected when imported on ships which, on the
same voyage or a recent one, carried fresh hides or other fresh products
of animals, derived from a country in which rinderpest exists.
Hides that are thoroughly dried and salted, those that have been freely
exposed for one week to the sun and air, and such as have been treated
by active antiseptics, (caustic quicklime, mercuric chloride, lime
chloride, formalin, phenic acid, etc.), need be held under no such
restriction. The same applies to thoroughly dried, sunned and aired
hair, wool, hoofs, horns, bones and sinews. Rendered tallow is equally
safe.
_Extinction of Cattle Plague in a Country._ This should never be called
for on the American Continent. The introduction of such a deadly
disease, with such a short period of incubation, and such severe
symptoms and rapid course, would argue a most reprehensible
carelessness, which it is to be hoped will never be shown by the Federal
Bureau of Animal Industry. Yet under the stress of a great European war
this plague invariably overleaps the barriers successfully maintained in
time of peace, and the same has happened to the two great
English-speaking powers in connection with the wars in South Africa and
the Phillipines respectively and therefore it cannot be said that
importation is impossible under any possible circumstances.
In case of a recent importation the infection would be easily
controlled. Trace at once to its destination every bovine animal and
other ruminant that arrived on the infected vessel, and all that came in
contact with them since, or with the gangways, wharfs, streets,
highways, yards, houses, fields, cars, loading banks and other places
and things that might have been contaminated; stop all cattle and sheep
traffic or movement for a large area around each centre of possible
infection caused by such cattle; remorselessly kill every head of such
animals carried by such vessel, or that came in direct contact with
them; bury, burn, boil or dissolve in mineral acids, every animal thus
exposed; thoroughly disinfect the importing ship, and every house, place
or thing the imported stock came in contact with, together with all the
dejections and debris, and even the surface of the graves; make a census
of all cattle within the different quarantined areas, and hold the
owners or custodians responsible, under a heavy penalty, to report every
death and every case of illness; whenever the cattle plague is found in
a place dispose of the entire herd as has already been done with the
infected imported stock, and in a very few weeks the plague can be
completely extirpated. The violence of the individual attack, and the
very short period of latency, makes the work incomparably easier than
the extinction of lung plague. There is never a long period of
uncertainty (incubation), there is virtually never a slight or occult
case of the disease, there is no equivocal chronic form of the
affection. The attack is made boldly and above board, and can be met
successfully if met promptly and energetically. The danger in such cases
lies, less in the nature of the disease, than in the army of foolish,
even if well meaning, meddlers, who denounce the temporary interference
of trade, the payment of indemnities to the cattle owners, the
interference with private property, the destruction of valuable
thoroughbred herds, the interruption of the dairyman’s business, the
cost of disinfection, and a thousand other things, and who too often
succeed in hampering and delaying action, until the infection has
reached and spread over great unfenced territories thereby getting
beyond control, or, short of this, has so established itself as to
necessitate the outlay of a hundred thousand for every hundred that
would have been demanded at first, and a long continued restriction of
trade in place of the very transient interruption required by early,
sharp, decisive action.
One of the most important prerequisites is that every state, but
especially those on the seaboard and with ports of entry, should enact
such laws as would make it possible for the Executive to act at a
moment’s notice and to call in the help of the Federal Government to
make an early and effective application of the only successful remedy.
Most things can wait for the call, assembling and action of a
legislature; the infection of cattle plague can not. Such laws are not
superfluous. If never called for they still show a wise provision
against a terrible, though remote, possibility; if really called for and
they are not found ready, the great cattle industry and even the
agriculture of the continent may be largely sacrificed by the neglect.
As guardian of the interests of The Philippines the United States is
to-day called upon to consider the question of exterminating the disease
which our interference brought upon the islands. On the unfenced lands
of these islands we have to face on a smaller scale the problem of
stamping out the plague which has baffled the wisdom of Europe and Asia.
The individual islands may perhaps be taken independently, the cattle
collected in small herds under fence, and by the sacrifice of a few the
remainder of any herd that shows infection may be immunized, and the
premises where they are confined disinfected until finally no more cases
occur. But whatever method is adopted the seclusion of all within well
fenced areas is the most important consideration. No nation has ever
succeeded in extirpating this nor any other important infection in
animals when they are allowed to run at large and mingle freely, herd
with herd, on unfenced land.
PICTOU CATTLE DISEASE. HEPATIC CIRRHOSIS.
This is a fatal affection of cattle met with in the counties of Pictou
and Antigonish, Nova Scotia, which seems to make a slow extension from
farm to farm, but does not spread widely after the manner of a disease
propagated by contagion alone, apart from other concurrent causes.
_Alleged Causes._ E. F. Thayer (1880) tells us that the inhabitants
traced its origin to the arrival from Scotland, about 1853, of a ship in
earth ballast, containing the seeds of the common ragweed of Europe
(Ambrosia Artemisiæfolia), alleging that the trouble extended with the
extension of this weed. This plant has a strong odor (it is known in
Pictou as “Stinking Willie”), and, like other plants shedding an
abundance of odoriferous pollen, has been charged with arousing “hay
fever,” but though very common in Europe it has never been charged with
producing anything like the Pictou cattle disease. The coincidence of
the plant and the disease is manifestly a mere accident. Professor
Lawson, of Halifax, investigated the flora of the district but was
unable to find any poisonous plant to which the mortality could be
attributed. D. McEachran tells us that many farms are covered with the
ragweed, so that it is abundant in the hay, yet they are absolutely free
from the disease.
The idea of a mineral poison must be dismissed in the same way. Pictou
lies on the Silurian formation with abundant coal fields, and the
chemical analyses made for McEachran were entirely fruitless of results.
Wyatt Johnston investigated the question of communicability by contagion
from animal to animal, but he found that neither contact, nor
inoculation produced positive results. Nothing positive has come of
investigations into the possible microbiology of the disease. In blood
from the jugular vein of a cow suffering from the disease, Thayer and
McEachran found bacteria, under an object glass magnifying 600
diameters. Wyatt Johnston, “in a series of pretty exhaustive
bacteriological examinations, in which all the tissues, including the
blood, the spleen, the kidneys, lungs, and the fluids from the lymph
glands” were employed, failed to find any constant or characteristic
organism.
Attacks are very rare in winter, the disease usually appearing in the
warm summer months, from June to August, and after the animals have been
some time at pasture. This might lead to the suspicion of bacteria or
other microbe on the growing vegetation; or of some insect enemy which,
maturing at that season, transfers the poison from animal or other
source to animal; or of some poison, vegetable or mineral, which acts
injuriously on the liver, and which can only be had in the pasture.
This, however, is mere hypothesis.
Liver affections are common in hot, damp seasons, but Pictou and
Antigonish do not differ in climate from other counties in Nova Scotia,
and much less do the infecting farms from those adjacent.
McEachran compares the disease to what occurs in the human being during
famines, from the ingestion of innutritious and unsuitable agents
especially deficient in albuminoids. The Pictou farmers, being nearly
all fishermen, neglect the farms during the summer season, so that hay
is only cut after the seeds have been shed, and when little nutritive
matter is left in the stalks. Almost all the cases he saw were on such
neglected farms. Wyatt Johnston, however, found it equally prevalent in
overfed animals, so that hepatic disorder from either extreme seems to
conduce to it. Again, if caused by lack of nutrition in the hay, winter,
rather than summer, ought to be the season of attack and prevalence.
Starvation and excess may both favor the attack, but the gradual
extension from farm to farm, is strongly suggestive of the presence of a
specific cause—probably a living organism.
The limitation of the disease to certain farms and even fields, and the
cirrhotic condition of the liver remind one of the Schweinsberg disease
of horses, and the lupinosis of sheep, in which the poison is evidently
the product of cryptogamic or bacterial growth. With the damp, foggy
climate of Nova Scotia, it would not be surprising if it should be
ultimately shown that the source of the trouble is in a cryptogam which
has as yet only invaded a given limited area. The winter immunity would
be explainable on this basis. So also would be the statement of Wyatt
Johnston that “When it attacks a new farm it affects chiefly animals
that have been on the farm for two or three years. By the end of the
second year it kills or attacks 10 per cent., and by the end of the
third season it has practically involved all the old cattle which have
been allowed to remain on the farm.” The hepatic disorder being a
progressive one and probably due to the toxic products of fermentations
carried on outside the animal body, a few only would show the morbid
results at first, while later, with advancing structural changes in the
liver, and an increase of the toxins that cause it, the number of sick
animals would steadily increase.
_Symptoms._ The animal is at first dull and sluggish, with drooping
head, lusterless eyes, staring coat, normal respiration and temperature,
pulse often about 60 per minute, relaxed bowels and marked diminution of
the milk secretion. The milk acquires a bitter taste and unpleasant
odor. The pulse is usually full and soft, and the eyeballs may bulge
visibly out of the sockets. The diarrhœa tends to encrease, the stools
becoming liquid and black, yet in exceptional cases the bowels are
confined for the first four or five days, or even permanently, appearing
to be completely paretic. By the end of a week the abdomen becomes full
and pendent with hollow flanks (pot bellied), or even rounded and tense,
while manipulation and percussion show an abundant exudation into the
peritoneal cavity. The pulse encreases in frequency (80) but the
temperature is not elevated unless there is concurrent sepsis
(Johnston). Thayer quotes an advanced case with a temperature of 105° F.
He also notes obstinate standing, trembling of the muscles of the hind
limbs, and complete suppression of appetite and milk secretion.
The disease is essentially chronic, often lasting a number of months.
Many cases are doubtless slightly affected before external symptoms are
manifested.
_Lesions._ If the disease has resulted in death there is usually marked
emaciation, yet the abdomen is distended by accumulation of a clear
yellowish fluid. From six to nine or more gallons may be present. The
fat of the omentum, mesentery and sublumbar region has disappeared and
the connective tissue is distended by a clear, amber-colored, watery
fluid. The liver is the seat of marked changes. In the early stages it
is congested and the gall ducts and bladder are filled to repletion with
a thick, dark colored bile, which is further present in abundance in the
intestines. In these early stages Johnston found cloudy swelling and
opacity of the hepatic cells; somewhat later they had undergone distinct
fatty degeneration. In the advanced stages, however, in animals that had
been ill for two or three months, there was distinct fibrous
degeneration, and compression and disappearance of the normal liver
cells, in other words, a condition of marked cirrhosis, the result
doubtless of the early congestion.
Johnston further notes the distension of the submucosa of the fourth
stomach at intervals by a clear, viscid, liquid exudate, so that rounded
swellings appear on the surface, and in some instances, after a month’s
illness, distinct ulcers are shown upon the mucosa.
The lungs, pleuræ, pericardium and nervous system, are usually normal,
unless in case of septic complication when petechiæ and circumscribed
blood extravasations may be seen.
_Prevention._ The Canadian government has gone to great expense in
buying and slaughtering the diseased cattle with no very evident good
result. McEachran suggested the feeding of oil cake and other albuminoid
and oleaginous food to counteract the alleged malnutrition, but
Johnston’s cases in over fed animals show that something more is
demanded. Another suggestion has been made to the effect that cattle
should be exterminated in the affected counties to remove the material
necessary for the maintenance of the poison. But, if the poison is
produced by a cryptogam growing on the vegetation, as seems not
improbable, it would be likely to extend all the same in the absence of
cattle. In such a case the true course is to study the nature of the
organism, and the phanerogam on which it grows, when it might become
possible either to exterminate the flowering plant which acts as a host
for the offending organism, or to spray it with an effective fungicide
and thus reach the object in another way.
INFECTIVE GASTRO-ENTERITIS AND PNEUMONIA IN THE NEW BORN; WHITE SCOUR.
In treating of this disease in Vol. II, page 141–2, the work of Jensen,
Perroncito and Nikolski is quoted, with the remark that “_it is
premature to specify any particular microbe as the sole cause of the
affection_.” Since the publication of that volume, Nocard, investigating
in Ireland a very prevalent and fatal affection of new born calves,
which proved fatal by “white scour” a few days after birth, or by
pneumonia one or two weeks later, identified as the pathogenic agent a
small, nonmotile, ovoid bacterium, taking the polar aniline stain,
bleaching in Gram’s solution, failing to liquefy gelatine, or to form
indol or to grow on potato. In other words it shows the general
characters of the colon group of bacteria, causative of hæmorrhagic
septicæmia, and classed as _pasteurellas_ by Trevisan and Lignieres.
This is not found in blood and lesions in all subjects, but is usually
present in pure culture in the most acute, fatal cases. Its occasional
absence later in the disease is explained, according to Lignieres, by
the power possessed by these germs of robbing the healthy tissues of
their power of resistance and laying them open to the attacks of other
microörganisms which are usually present in abundance, but are harmless
to the healthy tissues in the absence of the Pasteurella. As the disease
advances, therefore, the primary pathogenic agent (the Pasteurella) is
crowded out by the active growth of other bacteria, which accordingly
are found in complex cultures and in great variety. In his first
observations on the victims of the _white scour_, Nocard found only
these complex cultures, of which no one variety, isolated in pure
cultures _in vitro_, and inoculated, proved capable of causing the
disease. Later he found the Pasteurella (cocco-bacillus) in impure
cultures from the diseased femoro-tibial joint of one of the subjects of
the affection, and the pure cultures obtained from this were virulently
infective.
A few drops injected into the peritoneum of a Guinea pig, or veins of a
rabbit, killed in six to eighteen hours with the lesions of hæmorrhagic
septicæmia which characterize the most acute cases of _white scour_. The
blood and viscera swarmed with the microbe.
A calf one day old had 3cc. of the culture injected into the jugular,
the temperature rose in six hours, and in twenty hours the subject lay
with sunken eye, retracted abdomen, a temperature of 95° F., and having
the bed saturated with a yellowish, fœtid, fæcal liquid. Death took
place 30.5 hours after the injection and all the lesions of acute _white
scour_ were met with.
A second calf four weeks old, which had already suffered from _white
scour_ and recovered, had an injection into the jugular of 10cc. of the
same culture. In six hours he suffered a slight rise of temperature, was
dull and breathed short, but in twenty hours he was completely
recovered, full of life and appetite.
In other casual and experimental cases, Nocard found that when death
occurred within one or two days the symptoms and lesions were mainly
those of hæmorrhagic septicæmia and _white scour_, whereas if the calf
survived several days, the impaired resistance of the tissues invited
the invasion of a variety of other germs from the intestines, and
infective inflammation of the lungs, joints and other organs were
brought about by such secondary invasions.
An important question is as to the direct source of the primary
(Pasteurella) infection. The concentration of the acute cases on the
alimentary canal would strongly suggest infection through the food which
in this case means the milk. But careful bacteriological examination of
the milk of the dam of a calf that had just died of _white scour_, and
of other milk secured with careful precautions from cows in an infected
stable, showed that both were clear of the germ. Inoculations and
culture experiments were equally fruitless.
This does not exclude the probability of the contamination of the milk,
obtained under ordinary conditions, with the germ contained in the
floating barn dust, or that which was adherent to the teat and udder.
Another suggestion is that the infection is derived from the infected
womb prior to birth, but as Nocard justly says, if this were so,
abortions would be much more prevalent, as the rapidly fatal issue of
the disease would determine the prompt death of the fœtus and its
expulsion. The coincidence of abortion and _white scour_ in a herd is
not uncommon, and in such cases intrauterine infection of the fœtus is
not improbable, but in the great majority of cases no such coincidence
exists.
We are thus thrown back on infection through the raw surface of the
ruptured umbilical cord, as the rule in such cases. It may be that this
has come from the vagina or vulva, but in the great majority of cases it
is manifestly derived from the infecting bowel dejections and the dust
caused by their desiccation. The extraordinarily rapid progress and
fatal result of the acute disease, and the early abundance of the germ
in the blood and liver, suggest that the microbe traverses the umbilical
vein to the liver, and finding a congenial home in the blood is quickly
distributed through the entire body.
_Prevention_ must be based on the destruction and exclusion of the
microbe.
A thorough disinfection of the stable with mercuric chloride has not
given us uniformly satisfactory results, even when the building has been
kept apparently almost immaculately clean. This argues a renewed
infection through the fæces of the cows, yet it is the rule that the
removal of the cow to a new or unused stable a few days before calving
will usually secure the immunity of the calf. This method is however
open to the objection that the removal to such calving stable of a
succession of cows coming from infected premises soon introduces the
infection and renders it as dangerous as the place they have left. To
carry out such a plan therefore a number of new stables or sheds must be
provided to be used in succession, as they become one by one
contaminated.
Nocard confines his instructions to the antisepsis of parturition and of
the offspring:
“Cows ready to calve should be provided with dry and clean bedding until
after the birth of the calf.”
“As soon as labor sets in, the vulva, anus and perineum should be
cleaned with a tepid solution of lysol in rain water: 20 grammes of
lysol to each litre of water. The vagina should also be cleansed by
injecting with a large syringe a great quantity of the same solution
tepid.”
“As far as possible the calf should be received on a clean cloth or on a
thick fresh bedding, not soiled by urine or fæces.”
“The cord should be tied immediately after birth, with a ligature kept
in a lysol solution, and the cord amputated below the ligature.”
“The stump of the cord and the umbilicus should be washed with the
following solution:
Rain water 1 litre.
Iodine crystals 2 grammes.
Potassium iodide 2 grammes.”
“The disinfection of the umbilicus and cord should be completed by
coating them with
Methylic alcohol 1 litre.
Iodine crystals 2 grammes.”
“When the alcohol has evaporated the cord and umbilicus should be
covered with a thick layer of iodine collodion (1 per cent.) applied
with a brush. When the collodion has dried the calf may be left to the
care of the dam.”
This treatment may be changed by substituting other antiseptics, and by
prompt separation of the calf from the infected stable and dam. It is
also important to disinfect thoroughly and often the cow stable and
calf-pen, to remove instantly any calf that may show signs of scouring
or general disorder and to purify its pen and leave it unoccupied for
some time.
It should be added that the period of danger is in the first few days
after birth, and while the umbilicus is still unhealed. If scouring
should come on later it is much more amenable to treatment. A seclusion
of the calf for one week is usually sufficient to secure its escape.
NOTE ON BACTERIOLOGY AND TREATMENT OF HÆMOGLOBINÆMIA IN THE HORSE.
As supplementary to the article on hæmoglobinæmia (vol. II., page 437)
the later bacteriological investigations of Lignieres must be noted. A
superb Percheron, after two days of idleness, went to work at 10 P. M.,
was attacked at 1 A. M. and died at 3 P. M. Inoculations from blood,
spleen, liver, kidney, bone marrow, myelon and subarachnoid fluid from
the loins to the bulb proved sterile, excepting that made from the
subarachnoid liquid on a level with the bulb, which yielded a rich
culture of a streptococcus that appeared to the eye as small granules.
It proved ærobic and anærobic, stained well with Gram’s (I) solution,
coagulated milk, acidified the culture, formed small, round, grayish
white colonies on peptonized gelatine, without liquefying, failed to
propagate on potatoes, but grew well in serum and bouillon.
Two or three drops proved fatal to mice, producing, when thrown into the
peritoneum a highly acute parenchymatous nephritis with bloody urine.
Very few microbes were found in the kidney. There was loss of control of
the hind limbs and extreme nervous irritability.
Intravenous injection of 300cc. of the culture in a powerful stallion
produced hyperthermia, 102° F. on the second day, 104° on the third,
105° on the fourth, on the sixth day he became paraplegic and died on
the seventh.
A second horse, which received 150cc., was sick for several days, but
without paraplegia, then appeared to recover, but three weeks after he
became paraplegic with albuminous urine and died next day.
In neither of the horses was the urine sanguineous.
Carnivora, swine, ruminants and birds proved insusceptible. The guinea
pig succumbed to intraperitoneal inoculation, and the rabbit to
intravenous.
It is to be noted that hæmoglobinuria was lacking in both experimental
equine cases, and though this may be so in mild casual cases, the same
is not true of violent and fatal ones. It is, therefore, evident that
further research is necessary in this direction.
Accepting the conclusions reached by Lignieres, we are still debarred
from entering the affection in the list of animal plagues proper, to be
met by official restrictions. The streptococcus may be an essential
condition in each case of the disease, or it may be one of several
microbes that may act in the causation, yet the microbe in ordinary
doses as accidentally introduced, does not prove pathogenic excepting in
the presence of concurrent conditions of high feeding and condition,
work, interrupted by one or more days of absolute idleness, and the
resumption of exercise. The presence of the microbe is not enough to
cause the disease in the horse in continuous work, nor in that which is
kept in the stable all the time, nor even in the horse that has worked
steadily and then stood idle for a day, until he again goes to work. One
animal or a few only out of a stable, are attacked, and there is no such
active extension from animal to animal in the vicinity that
characterizes the plagues proper.
The _prevention_ of the disease, therefore, must be sought along the
lines previously laid down and well understood, in the avoidance of
sudden plethora, of transient idleness during a period of high condition
and steady work, and of gradual restoration to work after such period of
rest. Similarly the _treatment_ by rest, depletion, diluents, evacuants,
and nerve sedatives is still in order. A new importance, however,
attaches to the use of nerve sedatives and antiseptics, as calculated to
prove a check on the disorder of the nervous structure and functions and
on the active proliferation of the microbe.
The presence of the streptococcus may also contribute, along with the
permanent changes in the nerve structure, in predisposing to relapses or
second attacks, which are so common unless the animal which has once
suffered is subjected to very special care.
As a fruit of the research by Lignieres, W. A. McClanahan, Redding, Ia.,
essayed internal antisepsis by ½ oz. doses of potassium iodide. In three
severe cases relief was obtained in 15 to 20 minutes and an early and
complete convalescence followed. In the hands of J. H. Kelly of New
Haven, Conn., and T. S. Childs of Saratoga, N. Y., it seemed to prove
equally successful, the first meeting with almost invariable success,
and the latter reporting a series of 10 successive cases, several of
them severe, which all recovered in from 1 to 5 days. The only untoward
result was an open knee joint in one subject, the result of bruises
sustained before Dr. Childs arrived. His treatment was ½ oz. of the
iodide at once, and 1 to 2 drs. every hour or second hour, according to
the size of the animal and the severity of the case.
In other hands this medication has been less successful, which may well
be explained by the violence of the attacks, and the lack of absorption
from the inactive stomach. Unless it passed on to the duodenum, it would
be utterly useless, and hence the exhibition by the rectum or subcutem
might be tried. The parallelism of the treatment of the two diseases of
the plethoric and possibly infected subject,—parturient paresis and
hæmoglobinæmia,—is striking, and it does not seem that the iodide
treatment should be abandoned because of a few unsuccessful cases.
Whether the iodide acts mainly as a microbicide, a chemical antidote to
toxins, an eliminant, or a nerve sedative, or in two or more of these
modes, is unknown, but it would be rational to expect good results along
one or more of these lines. Iodide treatment should supplement, not
supersede, the methods formerly in use.
INFECTIVE ULCERATION OF ANUS AND VULVA IN CATTLE.
This curious affection is recorded as having prevailed in the winter of
1897–8 in different localities in Iowa, Missouri, Kansas and Nebraska.
In 1900 and 1901 it was again reported in different parts of Iowa.
_Causation._ No bacteriology of the disease has been given, and its
appearance in isolated herds which had no known communication with other
herds, and even in the young cattle on a farm to the exclusion of the
older ones, seems to suggest an enzoötic origin, perhaps in food or
water, or in some toxin determined by a fermentation of organic matter
out of the body.
On the Rodkey farm at Blue Rapids, Marshall county, Kan., eight heifers
from ten to fourteen months old, suffered, while the seventeen steers of
the same age and the milch cows escaped. (Steddom). Near Shelby, Ia., a
bull, from a healthy herd, broke into an affected herd and served cows
there, and was afterward returned to his own herd and served cows there,
but did not communicate the disease. (S. T. Miller). No case is recorded
to show that any bull serving affected cows or heifers contracted ulcer
or other disease of sheath or penis.
In one herd near Shelby, Ia., nineteen head of cows and heifers
suffered, while the four steers in the herd escaped. In another herd of
twenty-six head, in the same district, the four cows and eight of the
twenty-two steers suffered. It is not, therefore, confined to the
females. (S. T. Miller).
In all cases the disease appeared in the cooler months, from October to
April inclusive, and while the cattle were secluded in muddy yards.
In different cases they occupied the yards in common with swine which
were charged with wounding the vulva, until the general character of the
outbreak forbade this conclusion. At Blue Rapids it was sixty-two days
after they had been yarded with the hogs before the disease was
observed.
In this case the lot was small, poorly drained and very muddy most of
the time. Calves and hogs drank from the same troughs until the disease
appeared. The water supplied to the calves and hogs was from a well
sixteen feet deep. The cows, which escaped, were supplied with water
from the Blue River.
Cows, heifers and steers were fed on a ration of shelled corn 6 parts,
rye 1 part, oats 1 part, and had an abundance of fodder, consisting of
prairie hay and millet in equal parts. They were in good condition, some
of them fat, and nearly all dehorned. A second herd had shelled corn,
kafir corn and cane, with water from a shallow well, and all (cows and
heifers) suffered.
As showing the localized nature of the cause, C. Muller adduces the case
near Ottumwa, Ia., in which a herd of 30 calves were attacked, and sold
out, the owner filling the same yard a few days later with 30 more
bought in the surrounding country, and which he put on the same rations.
In about 10 days the disease appeared in the second lot.
On the Rice farm, Blue Rapids, were 60 yearling heifers, bought in
Kansas City, and two home cows. In the first week after arrival 5
heifers suffered, in the second week 20, in the third week 40, and in
the fourth week all the 60. The two cows mingling with them were only
slightly affected.
In the Rodkey farm, Blue Rapids, cases, all of the young cattle (which
alone suffered) had been raised on the farm and had not been exposed to
outside cattle.
_Symptoms._ “The ulcer, in almost every case, started as a mere
abrasion, the size of a pinhead, usually on the inner surface of the
labia, near the border of the inferior commissure, gradually eating its
way through until it appeared as a much larger denuded surface on the
outside” (C. Miller). S. T. Miller says: “The first noticeable symptom
was serous exudate, rapidly forming into a brown scab, under which was
very fœtid pus, with extensive inflammation. The affection usually
occurred on the lower portion of the lips of the vulva, in heifers and
cows, and in steers around the anus or root of the tail. The scabs which
formed seemed to spread very rapidly, destroying more and more of the
underlying tissue and forming a thicker and thicker scab. The scab, if
pulled off, would expose a raw surface which would bleed very readily.
In a short time a new scab would be formed.”
Steddom says: “The vulvar lips thickened and continued to discharge for
four or five days. In the meantime certain pustules appeared, 0.1 to 2.5
centimeters in diameter. About the fifth day these ruptured and
discharged yellowish pus.” The mucous membranes of the vulva and vagina
were dry and slightly congested. The ulcers were covered with brown
leathery scabs, which adhered tenaciously and when detached left an
angry, red, purulent, granular, elevated and pitted surface. In some of
the more severe cases, one or both lips of the vulva had sloughed off,
and the sore had extended 10 to 15 centimeters on the skin of the
escutcheon. The pus from this sore did not corrode the adjacent skin.
The more severe cases showed loss of appetite, constipation, hurried
breathing, tucking up of the abdomen, with general dulness and
dejection, and great tenderness of the affected skin with stiff,
straddling gait.
_Pathology._ This is very obscure. The primary cause of the sores is not
evident, though their occurrence on the anus and vulva only, and
especially on the latter would suggest an elective affinity of the
poison (microbian or chemical) for these structures and their products.
If we assume a pathogenic microbe in the fæces, the question arises as
to the cause of the habitual immunity of the steer, and of the margin of
the anus in the majority of the affected heifers. The susceptibility of
heifers rather than cows may imply a previous exposure and acquired
immunity on the part of the mature animal.
Again if we suspect the existence of a necrobiotic agent of organic
origin (like ergotin, secalin, sphacelin) we must assume a superadded
microbian infection, implanted in the primary sore and rapidly extending
it. The prompt recovery under antiseptic treatment shows that no mere
chemical poison maintains the destructive process, for it is manifestly
the microbicide which puts a prompt limit to the disease, and under such
treatment no sphacelating agent in the blood or tissues keeps up the
advance of the ulceration or prevents healing.
_Treatment._ The ulcers healed rapidly under cleanliness and antiseptic
applications. The tail, anus, and vulva were washed with tepid water,
and then dressed with a solution of creolin (5:100), or carbolic acid
(3:100), or mercuric chloride (1:500 or 1000). The ulcers were touched
with a pencil of silver nitrate. S. T. Miller followed the sublimate
lotion by the subjoined ointment: iodoform 20 grains, eucalyptol 40
minims, phenic acid 20 minims, petrolatum enough to make 2 oz. C. Miller
in addition to the carbolic acid lotion applied the common white lotion
(zinc sulphate 1 oz., lead acetate 1 oz., water 1 qt.) and used silver
nitrate on the ulcers. Four dressings on four successive days were given
and in the milder cases healing was completed in 10 or 12 days.
NOTE ON GOOSE SEPTICÆMIA.
As these pages are going through the press, Cooper Curtice’s bulletin on
_Goose Septicæmia_ comes to hand.
This affection in 1900 caused a loss of 3,200 geese in July and August
to Mr. Cornell, a Rhode Island owner. Mr. Snell lost 500.
_Bacteriology._ The blood and tissues swarmed with a minute bacillus
having the general morphological staining and biological characters of
that of chicken cholera and rabbit septicæmia. It differed from these in
the failure to infect chickens, whether inoculated or fed to them. It
proved deadly to geese, ducks, pigeons, rabbits, mice, and more slowly
to Guinea pigs. Geese were infected by inoculation or feeding of the
germs, ducks from inoculation only.
_Symptoms._ The geese were often found dead, and even in those noticed
ill, death supervened so early that no very diagnostic symptoms were
made out. The affected geese moved tardily and unsteadily, and failed to
keep with the remainder of the flock. Some burrowed the head in the dirt
and twisted it around, indicating, it was supposed, spasms of the
throat. Some were seized with the death agony in a few minutes; in
others the illness lasted for hours, and from experimental cases it was
concluded that the period from infection to death, in the majority of
cases, did not exceed thirty-six hours. Some were believed to merge into
a chronic condition, but the owner thought that none recovered. No
diarrhœa is noted.
_Lesions._ The head was the seat of marked venous and capillary
congestion, suggesting asphyxia. The bill and throat contained a large
quantity of tenacious mucus, which was especially viscid in the nose.
Extravasated blood in abundance was present in the gastro-intestinal
mucosa and contents, much of it more or less digested. At some points
there was abundant mucous exudate; at others the folds were only marked
by punctiform petechiæ, or by bloody patches formed by their
coalescence. The cæca were usually normal.
The liver showed numerous punctiform extravasations and yellow patches
of necrosis extending more or less deeply into the hepatic tissue. Other
congestions were seen in individual cases, implicating, in one instance,
the heart and pericardium, and in another the lungs. Petechiæ were
frequent on the pericardium and other mucosæ. The blood was usually
black, tarry, and with little disposition to brighten on exposure to the
air.
_Diagnosis._ It is recognized as an infection of domestic water fowl by
its attacking the larger proportion of that class of animals exposed to
it. It is supposed that those which escape do so because of immunity due
to a previous attack, or by reason of the absence of any wound of the
mouth, throat or stomach by which the germ might enter. It is
distinguished from _fowl_ (_chicken_) _cholera_ by the immunity of the
chicken in this case. It is differentiated from Klein’s _diarrhœal
enteritis_ of fowls, by the fact that neither pigeon nor rabbit is
immune. From the _duck cholera_ of Cornil and Loupet, it is diagnosed by
the immunity of the chicken only, while the rodents and pigeon suffer.
The germ is manifestly one of the family of bacilli of the colon group,
found in the different septicæmias, but sufficiently distinctive from
these other forms, in its pathogenesis, to demand a separate place in
connection with sanitary work.
_Treatment_ is hopeless from our present point of view.
_Prevention_ is the rational resort. In the case of those raising geese
from the egg, it is imperative to abandon, for the season at least, any
pastures that may have become contaminated. It would be better still to
subject such pastures to cultivated crops for one or two years. The pens
should be thoroughly disinfected or abandoned and burned. Mr. Cornell
used his infected pens for ducks without evil result. The drainage from
infected pastures or pens must be guarded against, no geese nor ducks
being allowed on land through which, or on which it passes, and no water
receiving such drainage being employed for geese. In the case of feeders
or handlers of geese who buy the birds in large numbers from many
sources, a subsidiary quarantine should be constantly maintained, by
enclosing the birds in as small groups as possible in separate pens, so
that infection in one pen will not endanger the whole flock. When
infection is shown in a pen, the diseased birds should be at once
destroyed and burned, the pen thoroughly disinfected, and the other
birds returned, or better, divided up into still smaller lots, so that
infection showing in one of these will not endanger the great number
taken from the original infected pen. The utmost care should be taken to
maintain the most perfect cleanliness in the pens of exposed and
suspected geese, and to sprinkle the floors and manure liberally with an
antiseptic, such as a solution of sulphuric acid in water (2:100), or of
phenic acid (3:100), or of a combination of the two. This will do much
to prevent the hatching of flies to act as infection-bearers, and if
these can be further excluded by screens the condition will be still
more satisfactory. Vermin of all kinds should be excluded and whenever
possible, separate feeders and attendants should be furnished for the
suspected geese, and those that have not been exposed.
NOTE ON HÆMORRHAGIC SEPTICÆMIA IN CHICKENS AND TURKEYS.
Lucet describes a septicæmia of chickens and turkeys accompanied by
dysenteric discharges. The microbe resembles the bacillus gallinarum of
Klein (see Vol. II, p. 254), even in the immunity of pigeons and rabbits
when injected subcutem. Rabbits, however, suffer when injected
intravenously. The probability is that this bacillus is identical with
that of Klein. Yet in this whole class of microbes of the colon group,
variations, apparently superinduced by environment, appear to result at
times in a deadly pathogenesis for different genera, and epizoötics
differing from each other.
DISEASES, INFECTIVE OR TOXIC, TREATED IN EARLIER VOLUMES.
=Catarrh; Malignant of Cattle.= Vol. I, p. 105.
— =Chronic, Infective, Summer.= Vol. I, p. 104.
=Anæmia; Pernicious.= Vol. I, p. 375.
=Diphtheria in Calves.= Vol. II, p. 24.
=Ulcerative Stomatitis of Swine.= Vol. II, p. 29.
=Mycotic Stomatitis; Thrush in Sucklings.= Vol. II, p. 36.
=Microbian Tonsilitis in Pigs.= Vol. II, p. 46.
=Diphtheria of Pigeons and Chickens.= Vol. II, p. 67.
=Dysentery of Cattle.= Vol. II, p. 240.
=Infective Catarrhal Enteritis of Birds.= Vol II, p. 254.
=Coccidian Enteritis in Cattle.= Vol. 2, p. 258.
„ „ =Dog.= Vol. II, p. 261.
„ „ =Rabbit.= Vol. II, p. 262.
„ „ =Birds.= Vol. II, p. 263.
=Cerebro-Spinal Meningitis.= Vol. III, p. 118.
=Tubercle and other Infective Diseases of the Vertebræ.= Vol. III, p.
172.
=Parturition Fever= (=Paresis=). Vol. III, p. 299.
=Infectious Conjunctivitis in Herbivora.= Vol. III, p. 368.
=Recurrent Ophthalmia.= Vol. III, p. 404.
=Contagious Pustular Dermatitis in the Horse.= Vol. III, p. 505.
=Rachitis.= Vol. III, p. 565.
=Rarefying Osteitis.= Vol. III, p. 579.
=Rheumatism.= Vol. III, p. 528.
INDEX.
Abortion and ergot, 371.
Abortion, contagious, 370.
Abscesses, secondary, their seats, 5.
Acute hæmorrhagic toxæmia, 141.
Adynamic catarrhal fever of the horse, 112.
Adynamic pneumonia, 95.
Agglutination test in diagnosis, 457.
Amœba Meleagridis, 388.
Anæmia in dourine, 524.
Anæmia, pernicious, 585.
Anasarca, 141.
Anasarcous toxæmia, 141.
Anthrax, 195.
Anthrax and protozoan cattle fever, 560.
Anthrax, apoplectic, 202, 206.
Anthrax, bacillus, 200.
Anthrax bacillus, vitality, 201.
Anthrax, causes, 197.
Anthrax, definition, 196.
Anthrax, differential diagnosis, 209.
Anthrax, disinfection, 213.
Anthrax, drainage of land, 220.
Anthrax, emphysematous, 181.
Anthrax, external, 203, 206.
Anthrax, forms of, 202.
Anthrax, fulminant, 202, 206.
Anthrax, geographical distribution, 196.
Anthrax, History, 196.
Anthrax, immunity after first attack, 198.
Anthrax, immunization from, 214.
Anthrax, immunization, modes of, 216.
Anthrax, imports restricted, 220.
Anthrax in birds, 208.
Anthrax, incubation, 205.
Anthrax in dogs, 208.
Anthrax, infection atria, 202.
Anthrax in horse, 207.
Anthrax in man, 221.
Anthrax in man, causes, 221.
Anthrax in man, forms, 222.
Anthrax in man, intestinal, 224.
Anthrax in man, lesions, 223.
Anthrax in man, prevention, 226.
Anthrax in man, pulmonary, 226.
Anthrax in man, treatment, 227.
Anthrax in sheep and goats, 207.
Anthrax in swine, 207.
Anthrax, interdiction of sales, 214.
Anthrax, internal, 203.
Anthrax, isolation, 213.
Anthrax, lesions, 203.
Anthrax, mortality, 211.
Anthrax, movement of herds, 213.
Anthrax œdema, 223, 225.
Anthrax, pathogenesis, 198.
Anthrax, prevention, 11.
Anthrax, prevention in animals, 212.
Anthrax, prognosis, 211.
Anthrax symptoms, 205.
Anthrax, synonyms, 196.
Anthrax toxins, 204.
Anthrax, treatment, 221.
Aphtha epizoötica, 316.
Aphthous fever, 316.
Apiosoma bigeminum, 545.
Apoplectiform septicæmia immunization, 397.
Apoplectiform septicæmia in chickens, 393.
Apoplectiform septicæmia, lesions, 394.
Apoplectiform septicæmia, pathogenesis, 396.
Apoplectiform septicæmia, symptoms, 394.
Argentina, Lombriz in, 65.
Arteritis and pyæmia, 4.
Aseptic fever, 8.
Asthenia in chickens, 392.
Asthenia in chickens, bacterium, 392.
Asthenia in chickens, pathogenesis, 392.
Asthenia in chickens, treatment, 393.
Australian tick fever, 543.
Avian and human bacillus of tubercle, Nocard’s experiment, 413.
Azoturia, bacteriology of, 649.
Azoturia in the horse, 649.
Babesia bigeminum, 545.
Bacilli in distemper, 168.
Bacillus anthracis, 200.
Bacillus anthracis emphysematosa, 183.
Bacillus Chauvæi, 183.
Bacillus choleræ suis, 24, 26.
Bacillus gastromycosis ovis, 510.
Bacillus liquefaciens bovis, 603.
Bacillus mallei, 233.
Bacillus of emphysematous anthrax compared with that of anthrax, 184.
Bacillus of emphysematous anthrax, vitality, 185.
Bacillus of malignant œdema, 11, 12.
Bacillus of Nicolaier, 293.
Bacillus of rouget, 20.
Bacillus of septicæmia hæmorrhagica in cattle, 56.
Bacillus of septicæmia hæmorrhagica in cattle, vitality of, 57.
Bacillus of septicæmia hæmorrhagica in sheep, 65, 70.
Bacillus of swine plague, 47.
Bacillus pestis suis, 47.
Bacillus tetani, 293.
Bacillus tetani, as a saprophyte, 294.
Bacillus tetani, toxins of, 295.
Bacillus tuberculosis, 410.
Bacillus tuberculosis, action of disinfectants on, 415.
Bacillus tuberculosis, biology, 411.
Bacillus tuberculosis, evolutionary forms, 412, 413.
Bacillus tuberculosis in diagnosis, 457.
Bacillus tuberculosis in man and cattle, 466.
Bacillus tuberculosis in man and ox, common features, 470.
Bacillus tuberculosis in salted meat, 414.
Bacillus tuberculosis, morphology, 410.
Bacillus tuberculosis of man rendered pathogenic to bird, 469.
Bacillus tuberculosis of man variable in potency, 468.
Bacillus tuberculosis, staining, 411.
Bacillus tuberculosis, vitality, 413.
Bacterium choleræ gallinaceæ, 159.
Bacterium coli commune, 27.
Bacterium of chicken asthenia, 392.
Bacteriology of septicæmia hæmorrhagica in cattle, 55.
Barbone, 55.
Bench show distemper, 181.
Bilious pneumonia, 95.
Blackhead in turkeys, 388.
Blackleg, 181.
Black quarter, 182, 55.
Black water, 543.
Blautong, 516.
Blitz catarrh, 113.
Blood clots, infective, 4.
Blood, relation to pyæmia of microbes and toxins in, 5.
Blue sickness, 23.
Blue tongue in horse, 516.
Bones, tubercle of, 436.
Boöphilus bovis, 548.
Boöphilus bovis as the cause of Texas fever, 548.
Boöphilus, dressing for, 564.
Boöphilus, its destruction on pastures, 564.
Bovine periodic fever, 543.
Bovine pleuro-pneumonia, 599.
Bovine yellow fever, 543.
Bradsot, 508.
Brain, tubercle of, 436.
Braxy, 508.
Braxy, causes, 509.
Braxy, definition, 508.
Braxy, geographical distribution, 508.
Braxy, its bacteriology, 510.
Braxy, lesions, 511.
Braxy, pathogenesis, 510.
Braxy, prevention, 512.
Braxy, symptoms, 511.
Braxy, treatment, 513.
Breeding paralysis, 519.
Brine poisoning of pigs, 39.
Broken buttock, 533.
Bronchitis, infectious stable, 111.
Brustseuche, 95.
Buffalo disease, 55.
Caderas, mal de, 532.
Calcified tubercle, 431.
Canine distemper, 165.
Canine madness, 260.
Carbuncular fever, 23.
Carceag, 573.
Caseated tubercle, 430.
Catarrhal fever, adynamic, 112.
Catarrh, infectious bronchial, in dog, 181.
Cattle lung plague, 598.
Cattle plague, 623.
Cattle plague, accessory causes, 628.
Cattle plague, bacteriology, 627.
Cattle plague, channels of infection, 628.
Cattle plague, definition, 624.
Cattle plague, gastro-intestinal lesions, 630.
Cattle plague, historic notes, 625.
Cattle plague, immunity, 628.
Cattle plague, lesions, 629.
Cattle plague, pathogenesis, 627.
Cattle plague, susceptibility to, 628.
Cattle, pulmonary tuberculosis in, 431.
Cattle tick, 548.
Cattle, ulcerative infection of the limbs in, 74.
Chancrous epizoötic, 519.
Charbon, 196.
Charbon blanc, 141.
Charbon symptomatique, 182.
Chauveau’s experiments on tuberculosis, 409.
Chicken cholera, 158.
Chicken cholera, accessory causes, 160.
Chicken cholera, bacteriology, 159.
Chicken cholera, diagnosis, 163.
Chicken cholera, distribution, 158.
Chicken cholera, history, 158.
Chicken cholera, immunization from, 164.
Chicken cholera, incubation, 161.
Chicken cholera, lesions, 162.
Chicken cholera, losses from, 159.
Chicken cholera, pathogenesis, 161.
Chicken cholera, prevention, 164.
Chicken cholera, prognosis, 163.
Chicken cholera, symptoms, 161.
Chicken cholera, treatment, 165.
Chicken pasteurellosis, 158.
Chicken typhoid, 158.
Cholera suis, 22.
Cimurro, 166.
Cirrhosis of the liver in cattle, enzoötic, 641.
Clavelee, 347.
Cocco-bacilli in distemper, 169.
Cocco-bacillus of contagious pneumonia of the horse, 99.
Cocotte, 113.
Consumption, 399.
Contagious abortion, 369.
Contagious abortion, accessory causes, 370.
Contagious abortion, acquired immunity, 380.
Contagious abortion bacillus of colon group, 377.
Contagious abortion, bacteriology, 376.
Contagious abortion, Bang’s bacillus, 377.
Contagious abortion, casual infections, 374.
Contagious abortion, definition, 370.
Contagious abortion, exclusion, 385.
Contagious abortion, experimental infections, 375.
Contagious abortion, extinction, 386.
Contagious abortion, immune infecting, 382.
Contagious abortion in mares, 384.
Contagious abortion, lesions, 383.
Contagious abortion, micrococcus, 376.
Contagious abortion, pathogenesis, 370.
Contagious abortion, pathology, 376.
Contagions abortion, prevention, 384.
Contagious abortion, symptoms, 383.
Contagious abortion, synonyms, 370, 372.
Contagious abortion, treatment, 384.
Contagious abortion, varieties, 377.
Contagious pleuro-pneumonia, 599.
Contagious pneumonia and influenza, 133–4.
Contagious pneumonia causes, 96.
Contagious pneumonia, convalescents infecting, 97.
Contagious pneumonia, definition, 95.
Contagious pneumonia, history, 96.
Contagious pneumonia in horse, 97.
Contagious pneumonia in horses, 95.
Contagious pneumonia in the horse, bacteriology of, 98.
Contagious pneumonia in the horse, course, 104.
Contagious pneumonia in the horse, diagnosis, 105.
Contagious pneumonia in the horse, immunization against, 110.
Contagious pneumonia in the horse, incubation, 101.
Contagious pneumonia in the horse, lesions, 100.
Contagious pneumonia in the horse, prevention, 106.
Contagious pneumonia in the horse, prognosis, 105.
Contagious pneumonia in the horse, quarantine for, 109.
Contagious pneumonia in the horse, serum therapy of, 111.
Contagious pneumonia in the horse, symptoms, 101.
Contagious pneumonia in the horse, treatment, 106.
Contagious pneumonia less diffusible than influenza, 97.
Cornstalk disease, 55.
Coronet, gangrene of, 76.
Coryza contagiosa equorum, 78.
Coryza gangrenosa, 141.
Cowpox, 340.
Cowpox, causes, 340.
Cowpox, course, 346.
Cowpox, diagnosis, 345.
Cowpox, prognosis, 346.
Cowpox, symptoms, 344.
Cowpox, treatment, 346.
Curtice’s smear for boöphilus, 564.
Cynolyssa, 260.
De Schweinitz, serum therapy in swine plague, 52.
De Schweinitz, serum treatment in hog cholera, 45.
Destruction of red globules, 553.
Diagnosis of septicæmia hæmorrhagica in cattle, 61.
Diagnosis of swine plague, 50.
Diastashemia, 141.
Dikkopziekte, 513.
Diphtheria in pig, 23.
Diplococcus pneumoniæ Contagiosæ Equi, 98.
Disinfection in hog cholera, 42.
Distemper, forms of, 170.
Distemper in dogs and cats, 165.
Distemper in dogs, causes, 167.
Distemper in dogs, cutaneous symptoms, 173.
Distemper in dogs, definition, 166.
Distemper in dogs, digestive symptoms. 173.
Distemper in dogs, eye symptoms, 172.
Distemper in dogs, history, 166.
Distemper in dogs, immunization, 176.
Distemper in dogs, incubation, 171.
Distemper in dogs, lesions, 174.
Distemper in dogs, microbiology of, 168.
Distemper in dogs, nervous symptoms, 174.
Distemper in dogs, pathogenesis, 166.
Distemper in dogs, prevention, 175.
Distemper in dogs, respiratory symptoms, 171.
Distemper in dogs, symptoms, 171.
Distemper in dogs, synonyms, 166.
Distemper in dogs, treatment, 177.
Distemper in young horses, 78.
Distemper, mortality, 170.
Distemper of bench show, 181.
Distemper, prognosis, 171.
Distemper, virulent products in, 170.
Dog ill, 166.
Dog pox, 361.
Dogs, paludism in, 577.
Dourine, 519.
Dourine, abdominal lesions.
Dourine, causes, 520.
Dourine, changes in blood, 524.
Dourine, definition, 519.
Dourine, diagnosis, 528.
Dourine, extinction of, 531.
Dourine, history, 520.
Dourine, history in America, 520.
Dourine in geldings, 520.
Dourine, its primary home, 520.
Dourine, lesions in dog, 525.
Dourine, lesions in horse, 523.
Dourine, lesions in mare, 525.
Dourine, microbiology, 521.
Dourine, nervous lesions, 523.
Dourine, pathogenesis, 519.
Dourine, prevention, 530.
Dourine, prognosis, 528.
Dourine, symptoms, 525.
Dourine, symptoms in ass and mule, 529.
Dourine, symptoms in dog, 529.
Dourine, symptoms in horse, 525.
Dourine, symptoms in mare, 527.
Dourine, symptoms in rabbits, 530.
Dourine, treatment, 530.
Dropsies in malignant œdema, 13.
Dropsy of connective tissue, 141.
Druse, 78.
Dunpaardziekte, 513.
Eczema epizoötica, 316.
Edematous pneumonia, 95.
Embolism and pyæmia, 4, 6.
Emphysematous anthrax, 181.
Emphysematous anthrax, accessory causes, 185.
Emphysematous anthrax, causes, 183.
Emphysematous anthrax, definition, 182.
Emphysematous anthrax, diagnosis, 187.
Emphysematous anthrax, distribution, 182.
Emphysematous anthrax, immunization, 191.
Emphysematous anthrax, incubation, 186.
Emphysematous anthrax, lesions, 187.
Emphysematous anthrax, pathogenesis, 182.
Emphysematous anthrax, prevention, 189.
Emphysematous anthrax, symptoms, 186.
Emphysematous anthrax, synonyms, 182.
Emphysematous anthrax, treatment, 188.
Emprosthotonos, 299.
Entero-hepatitis, amœba of, 388.
Entero-hepatitis, diagnosis, 390.
Entero-hepatitis, lesions, 389.
Entero-hepatitis, prevention, 391.
Entero-hepatitis, symptoms, 389.
Entero-hepatitis, treatment, 391.
Enzoötic abortion, 370.
Epizoötic, 113
Epizoötic abortion, 370.
Epizoötic catarrh, 113.
Epizoötic cellulitis, 113, 129, 140.
Epizoötic paraplegia, 519.
Epizoötic pleuro-pneumonia, 599.
Equine influenza, 112.
Equine syphilis, 519.
Equinia, 231.
Ergot and abortion, 371.
Erysipelas in swine, 23.
Eye, tubercle of, 436.
Farcy, 231.
Farcy in cattle, 257.
Fermentation fever, 8.
Fibroid tubercle, 431.
Fibrosis in tubercle, 431.
Foot and mouth disease, 316.
Foot and mouth disease, bacteriology, 318.
Foot and mouth disease, causes, 317.
Foot and mouth disease, definition, 316.
Foot and mouth disease, diagnosis 321.
Foot and month disease, geographical distribution, 317.
Foot and mouth disease, history, 317.
Foot and mouth disease, infection of man, 321.
Foot and mouth disease in man, prevention, 323.
Foot and mouth disease, mortality, 320.
Foot and mouth disease, pathogenesis, 316.
Foot and mouth disease, prevention, 324.
Foot and mouth disease, prognosis, 320.
Foot and mouth disease, symptoms, 319.
Foot and mouth disease, symptoms in man, 323.
Foot and mouth disease, treatment, 325.
Foot and mouth disease, treatment in man, 324.
Foot and mouth disease, virulent products, 318.
Fowl cholera, 158.
Gangrene in malignant œdema, 13.
Gangrene of coronet in horse, 76.
Garrapata, 551.
Gastro-conjunctivitis, 113.
Gastro-enteric epizoötic, 113.
Gastro-enteritis, infective, in new born, 645.
Gastro-enteritis of new born, bacteriology, 645.
Gastro-enteritis of new born, prevention, 647.
Gastro-mycosis ovis, 508.
Genital catarrh, infectious in rabbits, 367.
Genital tuberculosis, symptoms, 449.
Genito-urinary tubercle, 435.
Gerlach’s experiments on tuberculosis, 409.
Glanders, 230.
Glanders, acute, symptoms of, 236.
Glanders, causes, 232.
Glanders, chronic, symptoms of, 238.
Glanders, cutaneous, symptoms, 239.
Glanders, definition, 231.
Glanders, diagnosis, 239.
Glanders, forms of, 236.
Glanders, geographical distribution, 231.
Glanders in carnivora, 245.
Glanders, infection atria, 235.
Glanders in frog, 245.
Glanders in man, 246.
Glanders in man, causes, 246.
Glanders in man, lesions, 250.
Glanders in man, symptoms, 248.
Glanders in man, treatment, 256.
Glanders in rodents, 244.
Glanders in sheep and goat, 244.
Glanders in swine, 243.
Glanders, latent or occult, 239.
Glanders, lesions of, 241.
Glanders, pathogenesis, 232.
Glanders, prevention, 251.
Glanders, synonyms, 231.
Glanders, treatment, 254.
Gloss-anthrax, 55, 203, 206.
Glossina morsitans, 595.
Goatpox, 360.
“Going light”, 392.
Goose septicæmia, 654.
Gourme, 77.
Grapes, 399.
“Grease”, 237.
Great white plague, 399.
Hæmaphysalis Leachi, 579.
Hæmaphysalis rosea, 552.
Hæmatoblasts and blood globules in pyæmia, 4.
Hæmoglobinæmia, bacteriology of, 649.
Hæmoglobinæmia in the horse, 649.
Hæmoglobinæmia in the horse, antiseptic treatment, 650.
Hæmoglobinæmia, iodine treatment, 650.
Hæmolysis in influenza, 130.
Hæmorrhagic septicæmia in chickens, 656.
Hæmorrhoidal anthrax, 203, 207.
Heart, tubercle of, 433.
Hepatic cirrhosis of cattle, 641.
Hog cholera, 15, 22.
Hog cholera, accessory causes, 28.
Hog cholera, accessory causes, removal of, 37.
Hog cholera and faulty feeding, 30.
Hog cholera and interstate sanitary work, 44.
Hog cholera and state rights, 44.
Hog cholera bacillus, 24.
Hog cholera bacillus and allied organisms, table of, 26–28.
Hog cholera, definition, 22.
Hog cholera, diagnosis of, 35.
Hog cholera, disinfection, 43.
Hog cholera, disseminated by commerce, 41.
Hog cholera, extinction in herds, 44.
Hog cholera, fulminant, 33.
Hog cholera, gastro-intestinal lesions of, 33.
Hog cholera germ, carried by animals, 40.
Hog cholera germ, carried by flies, 40.
Hog cholera germ, exclusion of, 40.
Hog cholera, history, 23.
Hog cholera, immunization, 42.
Hog cholera, incubation, 33.
Hog cholera losses in U. S., 24.
Hog cholera, market restrictions, 43.
Hog cholera, poisoning mistaken for, 30, 31.
Hog cholera, precautions for owner, 42.
Hog cholera, prevention, 37.
Hog cholera restrictions in England, 43.
Hog cholera, serum treatment, 45.
Hog cholera, spread through markets and butcher shops, 31.
Hog cholera, Swine plague and Rouget, table of differential symptoms,
38.
Hog cholera, symptoms, 33.
Hog cholera, symptoms of acute form, 33.
Hog cholera, symptoms of subacute form, 35.
Hog cholera, synonyms, 23.
Hog cholera, therapeutic treatment, 45.
Hog cholera, Widal test in, 36.
Holzkrankheit, 543.
Horse, gangrene of coronet in, 76.
Horse pox, 337.
Horse pox, symptoms, 338.
Horse pox, treatment, 340.
Horse sickness, 513.
Horse sickness, definition, 514.
Horse sickness, forms of, 516.
Horse sickness, from damp, green fodder, 514.
Horse sickness, geographical distribution, 514.
Horse sickness, immunity, 515, 518.
Horse sickness, lesions, 517.
Horse sickness, pathogenesis, 514.
Horse sickness, penicillium of, 515.
Horse sickness, prevention, 518.
Horse sickness, symptoms, 516.
Hydrophobia, 259.
Hydrophobia, diagnosis, 282.
Hydrophobia, symptoms, 280.
Ictero hæmaturia in sheep, 573.
Immunization against apoplectiform septicæmia, 397.
Immunization against hog cholera, 42.
Immunization against sheeppox, 357.
Immunization against strangles, 92.
Immunization against Texas fever, 567.
Immunization, from anthrax, 214.
Immunization from canine distemper, 177.
Immunization from chicken cholera, 164.
Immunization from septicæmia hæmorrhagica of cattle, 62.
Immunization from swine plague, 51.
Immunization in rabies, 285.
Infarction in pyæmia, 6.
Infections, purulent and septic, 1.
Infectious abortion, 370.
Infectious bronchial catarrh in dogs, 181.
Infectious entero-hepatitis in turkeys, 388.
Infectious genital catarrh in rabbits, 367.
Infectious stable bronchitis, 111.
Infectious stomatitis in lambs and kids, 367.
Infectious stomatitis in lambs, causes, 368.
Infectious stomatitis, lesions, 368.
Infectious stomatitis, mortality, 369.
Infectious stomatitis, pathogenesis, 368.
Infectious stomatitis, prevention, 369.
Infectious stomatitis, streptococcus of, 368.
Infectious stomatitis, symptoms, 368.
Infectious stomatitis, treatment, 369.
Infective blood clots, 4.
Infective myelo-meningitis, 500.
Infective ulceration of anus and vulva in cattle, 651.
Inflammatory œdema, 153.
Influenza, accessory causes, 122.
Influenza, as compared with croupous pneumonia, 133.
Influenza, bacteriology, 120.
Influenza, catarrhal symptoms, 125.
Influenza, cocci and cocco-bacilli, 120.
Influenza, complications in, 129.
Influenza, contagion, 116.
Influenza, diagnosis of, 132.
Influenza, diagnostic symptoms, 124.
Influenza, digestive disorder, 127.
Influenza, equine, 112.
Influenza, exudations, 129.
Influenza, gastro-intestinal lesions in, 130, 131.
Influenza, hæmolysis in, 130.
Influenza, history, 114.
Influenza, immunity, 123
Influenza, incubation, 123.
Influenza, inoculations, 120.
Influenza, lesions, 129.
Influenza, leucocytosis in, 130.
Influenza, mortality, 134.
Influenza, nervous symptoms, 128.
Influenza of 1872–3, 115.
Influenza ophthalmic symptoms, 128.
Influenza phenomena as compared with contagious pneumonia, 133.
Influenza, prevention, 139.
Influenza, prognosis, 134.
Influenza, pulmonary lesions in, 131.
Influenza, quarantine for, 139.
Influenza, rheumatoid symptoms, 129.
Influenza, symptoms, 124.
Influenza, thoracic symptoms, 126.
Influenza, treatment, 135.
Inoculation in diagnosis, 457.
Intestinal anthrax in man, 224.
Ixodic anæmia, 543.
Ixodic toxæmia, 500.
Ixodis Algeriensis, 552.
Ixodis annulata, 552.
Ixodis bovis, 548.
Ixodis Dugesii, 548.
Klebs’ experiments on tuberculosis, 409.
La Grippe, 113.
Lambs and kids, infectious stomatitis in, 367.
Laminitis in influenza, 129.
Lesions in hæmorrhagica septicæmia in sheep, 67.
Lesions in septicæmia hæmorrhagica in cattle, 59.
Lesions of swine plague, 49.
Leucocytosis in influenza, 130.
Leucophlegmasia, 141.
Liver, tubercle of, 434.
Lockjaw, 292.
Lombriz, 63.
Louping-ill, 500.
Lungenseuche, 599.
Lung plague, 56.
Lung plague, abortions in, 613.
Lung plague, absent from lands breeding all their cattle, 600.
Lung plague, acute symptoms, 612.
Lung plague and aspergillus, 616.
Lung plague, and bronchitis, 615.
Lung plague and emphysema, 616.
Lung plague, and fibrinous pneumonia, 616.
Lung plague and foreign body in the heart, 616.
Lung plague and hæmorrhagic septicæmia, 616.
Lung plague and infectious pneumonia, 616.
Lung plague and Oldenburg, 601.
Lung plague and pulmonary congestion, 617.
Lung plague, and tuberculosis, 615.
Lung plague and verminous bronchitis, 616.
Lung plague, auscultation in, 613.
Lung plague, bacteriology, 603.
Lung plague, bronchial exudates, 610.
Lung plague, causes, 602.
Lung plague, chronic form, 614.
Lung plague, complex infection, 614.
Lung plague, contagion through the air, 605.
Lung plague, course, 613.
Lung plague definition, 599.
Lung plague, diagnosis, 614.
Lung plague, duration of infection in sequestra, 607.
Lung plague, exclusion of infected things, 618.
Lung plague, extension into new countries, 600.
Lung plague, extensions in autumn, 607.
Lung plague, granular, hepatised lung, 609.
Lung plague, history, 599.
Lung plague, honey combed lung, 609.
Lung plague, immunity of secluded islands, mountains, etc., 602.
Lung plague, immunizing by a first attack, 619.
Lung plague in Atlantic States, 601.
Lung plague in Australia, 602.
Lung plague in Brooklyn, 601.
Lung plague in cattle, 598.
Lung plague, incubation, 610.
Lung plague in Denmark, 600.
Lung plague, individual receptivity, 611.
Lung plague in England, 600.
Lung plague, infarction of lung, 608.
Lung plague, infection by mingling of herds, 605.
Lung plague, infection through active trade, 606.
Lung plague, infection through attendants, 605.
Lung plague, infection through convalescent, 607.
Lung plague, infection through food, 605.
Lung plague, infection through manure, 606.
Lung plague, infection through pastures, 605.
Lung plague, infection through stables, 606.
Lung plague, infection through unfenced places, 605.
Lung plague, infection through watering troughs, 605.
Lung plague, infiltrated lung, 609.
Lung plague in Holland, 600.
Lung plague in Ireland, 600.
Lung plague, injection of sterilized serum subcutem, 621.
Lung plague in Massachusetts, 601.
Lung plague in Mississippi Valley, 601.
Lung plague in New Jersey, 602.
Lung plague in Norway, 600.
Lung plague, inoculation in tail, 620.
Lung plague, inoculation methods, 620.
Lung plague in Schleswig, 601.
Lung plague, insidious onset, 611.
Lung plague in South Africa, 602.
Lung plague in Sweden, 600.
Lung plague in Tasmania and New Zealand, 602.
Lung plague, intravenous inoculation, 621.
Lung plague, laryngeal lesions, 610.
Lung plague, lesions, 608.
Lung plague, limits of admissible immunization, 622.
Lung plague, marbled lung, 608.
Lung plague, measures to extirpate, 618.
Lung plague microbe, Nocard’s culture of, 604.
Lung plague, micrococci and bacilli in, 603.
Lung plague, modes of transmission, 604.
Lung plague, only by infection, 600.
Lung plague, percussion in, 613.
Lung plague, pericardial exudates, 610.
Lung plague, pleural exudates, 609.
Lung plague, prevention, 618.
Lung plague, private control of, 619.
Lung plague, proclivity of breeds, 611.
Lung plague, quarantine for, 618.
Lung plague, recoveries, 613.
Lung plague, refrangent corpuscles in, 603.
Lung plague, sequestra, 608.
Lung plague, stalactite-like bronchia, 609.
Lung plague, suppression in America, 601.
Lung plague, symptoms, 611.
Lung plague, synonyms, 599.
Lung plague, thoracic glands in, 610.
Lung plague, transient cases, 611.
Lung plague, treatment, 617.
Lung plague, varying receptivity, 607.
Lymphangitis epizoötica, 257.
Lymphangitis farcinoides, 257.
Lymphangitis saccharomycotica, 257.
Lymphangitis saccharomycotica, distribution, 257.
Lymphangitis saccharomycotica, pathogenesis, 257.
Lymphangitis saccharomycotica, symptoms, 258.
Lymphangitis saccharomycotica, treatment, 258.
Lymphangitis ulcerosa, 257.
Lymph glands, tubercle of, 437.
Lyssa, 260.
Lytta, 260.
Magenseuche, 624.
Maladie de bois, 543.
Maladie de jeune age, 166.
Maladie des chiens, 166.
Maladie du coit, 519.
Mal de Caderas, 532.
Mal de tete de contagion, 141.
Malignant carbuncle, 196.
Malignant œdema, 11.
Malignant œdema, abscess from small dose, 14.
Malignant œdema, cause, 11.
Malignant œdema, diagnosis, 14.
Malignant œdema, immunization, 14.
Malignant œdema, infection channels, 12.
Malignant œdema, invasion by the intestine, 13.
Malignant œdema, lesions, 13.
Malignant œdema, pathogenesis, 12.
Malignant œdema, prevention, 14.
Malignant œdema, symptoms, 13.
Malignant œdema, treatment, 14.
Malignant œdema with proteus vulgaris or micrococcus, 13.
Malignant protozoan jaundice in dogs, 577.
Malignant pustule, 196.
Malignant vesicle, 223, 224.
Malleinization, 254.
Mallein test, 240.
Malleus, 231.
Malleus gangrenosa, 141.
Mammary tubercle, 435.
Mammary tuberculosis, symptoms, 449.
Measles in swine, 23.
Mexican fever, 543.
Microbes, modified by environment, 467.
Micrococci in distemper, 169.
Micrococcus prodigiosus in malignant œdema, 13.
Milk sickness, 325.
Milk sickness, contagion, 327.
Milk sickness, geographical distribution, 326.
Milk sickness, incubation, 329.
Milk sickness in man, 331.
Milk sickness, lesions, 331.
Milk sickness, prevention, 332.
Milk sickness, symptoms, 329.
Milk sickness, treatment, 332.
Miltzbrand, 196.
Moor ill, 543.
Morbus maculosus, 141.
Muscles, tubercle of, 436.
Nagana, 594.
Nagana, alike on flesh and vegetable food, 597.
Nagana, anæmia in, 596.
Nagana, animals susceptible, 595.
Nagana, attempts at immunization, 597.
Nagana, elephants and zebras immune, 595.
Nagana, eye lesions, 596.
Nagana, inoculation, 595.
Nagana, lesions, 596.
Nagana, muscular wasting and debility, 596.
Nagana, not prevented by surra, 597.
Nagana, œdema in, 596.
Nagana, pigeons and hens immune, 595.
Nagana, prevention, 597.
Nagana, symptoms of, 596.
Nagana, toxins, 597.
Nagana, virulent products, 595.
Nagana, vitality of virus, 595.
Nervous fever, 113.
Nocard’s culture of lung plague microbe, 604.
Œdema mycosis, 513.
Œdema mycosis, causes, 514.
Œdema mycosis, pathogenesis, 514.
Omphalitis, 5.
Opisthotonos, 299.
Orthrotonos, 299.
Osteomyelitis, 5.
Ovination, 357.
Ovination, technique, 358.
Oxygen, used by horse, ox and pig, 39.
Paludism in cattle, 542.
Paludism in dogs, 577.
Paludism in dogs, anæmia in, 577.
Paludism in dogs, geographical distribution, 577.
Paludism in dogs, hæmolysis in, 577.
Paludism in dogs, lesions, 580.
Paludism in dogs, microbiology, 578.
Paludism in dogs, prevention, 580.
Paludism in dogs, symptoms, 579.
Paludism in dogs, treatment, 580.
Paludism in horses, 580.
Paludism in horses, anæmia in, 583.
Paludism in horse, causes, 582.
Paludism in horses, duration, 583.
Paludism in horses, geographical distribution, 581.
Paludism in horses, hæmolysis, 582.
Paludism in horses, icterus in, 583.
Paludism in horses, immunization, 582.
Paludism in horses, lesions, 583.
Paludism in horses, microbiology, 581.
Paludism in fresh horses, mortality, 582.
Paludism in horses, prevention, 583.
Paludism in horses, remissions, 582.
Paludism in horses, symptoms, 582.
Paludism in horses, treatment, 584.
Paludism in horses, vertigo in, 582.
Paludism in sheep, 573.
Paludism in sheep, duration, 576.
Paludism in sheep, geographical distribution, 573.
Paludism in sheep, lesions, 575.
Paludism in sheep, microbiology, 575.
Paludism in sheep, prevention, 576.
Paludism in sheep, symptoms, 576.
Pancreas, tubercle of, 435.
Paralysis of breeding solipeds, 519.
Paraplegia, infections, of solipeds in Europe, 538.
Paraplegia, infectious of solipeds in Maraja, 533.
Paraplegia of Maraja, causes, 534.
Paraplegia of Maraja, history, 534.
Paraplegia of Maraja, lesions, 536.
Paraplegia of Maraja, mortality, 537.
Paraplegia of Maraja, prevention, 537.
Paraplegia of Maraja, symptoms, 535.
Paraplegia of Maraja, treatment, 537.
Paraplegia of solipeds in Europe, causes, 538.
Paraplegia of solipeds in Europe, diagnosis, 541.
Paraplegia of solipeds in Europe, history, 538.
Paraplegia of solipeds in Europe, lesions, 540.
Paraplegia of solipeds in Europe, prevention, 542.
Paraplegia of solipeds in Europe, prognosis, 541.
Paraplegia of solipeds in Europe, symptoms, 540.
Paraplegia of solipeds in Europe, treatment, 542.
Pasteurellosis ovina, 63.
Pathogenesis of septicæmia hæmorrhagica in cattle, 56.
Peltrot, 347.
Penicillium of horse sickness, 515.
Peripneumonia exudativa, 599.
Peripneumonie, 599.
Pernicious anæmia in horse, 585.
Perroncito, serum treatment in hog cholera, 45.
Pest bovine, 624.
Pestis bovina, 624.
Petechial fever, 141.
Petechial fever, antistreptococcic serum in, 153.
Petechial fever, a sequel to other diseases, 142.
Petechial fever, causes, 142.
Petechial fever, course and duration, 148.
Petechial fever, definition, 141.
Petechial fever, diagnosis, 148.
Petechial fever in cattle, 153.
Petechial fever in cattle, causes, 154.
Petechial fever in cattle, diagnosis, 156.
Petechial fever in cattle, lesions, 154.
Petechial fever in cattle, prevention, 156.
Petechial fever in cattle, symptoms, 155.
Petechial fever in cattle, treatment, 156.
Petechial fever, intratracheal treatment, 152.
Petechial fever, intravenous treatment, 153.
Petechial fever, lesions, 143.
Petechial fever, mortality, 149.
Petechial fever, prognosis, 149.
Petechial fever, symptoms, 145.
Petechial fever, synonyms, 141.
Petechial fever, treatment, 150.
Peters, serum treatment in hog cholera, 45.
Pharyngeal anthrax, 203, 206.
Phillipines, paludism in horses in, 582.
Phlebitis and pyæmia, 4.
Phthisis in cattle, 431.
Picotte, 347.
Pictou cattle disease, 641.
Pictou cattle disease, alleged causes, 641.
Pictou cattle disease, lesions, 641.
Pictou cattle disease, prevention, 644.
Pictou cattle disease, symptoms, 643.
Pigs poisoned by brine, 39.
Pigs poisoned by soaps, 39.
Pig typhoid, 23.
Pining, 399.
Pink eye, 113, 140.
Piroplasma bigeminum, life history, 546.
Pirosoma bigeminum, 545.
Pleuro-pneumonia contagiosa equorum, 95.
Pleurosthotonos, 299.
Pneumo-enteritis in cattle, 55.
Pneumo-enteritis, infectious in sheep, 63, 70.
Pneumo-enteritis in the horse, 112.
Pneumo-enteritis in pig, 23.
Pneumonia contagious, 95.
Pneumonia in new born, infective, 645.
Pneumonia sporadic, 55.
Pneumosarcia, 599.
Pockenseuche, 624.
Poisoning mistaken for hog cholera, 30, 31.
Potchetchoui, 76.
Powdered soaps poison pigs, 39.
Pox, 333.
Prevention of septicæmia hæmorrhagica in cattle, 62.
Prevention of septicæmia hæmorrhagica in sheep, 68, 73.
Prevention of swine plague, 50.
Prognosis of strangles, 90.
Proteus vulgaris in malignant œdema, 13.
Protoplasma bigeminum, 545.
Protozoan cattle fever, 542.
Protozoan cattle fever, anæmia in, 553.
Protozoan cattle fever and anthrax, 560.
Protozoan cattle fever, bile in, 555.
Protozoan cattle fever, causes, 545.
Protozoan cattle fever, course, 559.
Protozoan cattle fever, diagnosis, 560.
Protozoan cattle fever, hæmolysis, 553.
Protozoan cattle fever, history, 543.
Protozoan cattle fever, immunization, 567.
Protozoan cattle fever, incubation, 556.
Protozoan cattle fever, kidney lesions, 555.
Protozoan cattle fever, lesions, 552.
Protozoan cattle fever, liver lesions, 554.
Protozoan cattle fever, microbiology, 545.
Protozoan cattle fever, mortality, 560.
Protozoan cattle fever, spleen lesions, 555.
Protozoan cattle fever, symptoms, 557, 560.
Protozoan ictero hæmaturia in sheep, 573.
Pulmonary murrain, 599.
Pulmonary tubercle in cattle, 431.
Purples, 23.
Purpura hæmorrhagica, 141.
Purulent infections, 1.
Pyæmia, 1.
Pyæmia and septicæmia, distinction, 2.
Pyæmia, causes, 2.
Pyæmia, delay of access, 5.
Pyæmia, lesions of, 6.
Pyæmia, mortality, 7.
Pyæmia, prevention, 7.
Pyæmia, symptoms, 6.
Pyæmia, treatment, 8.
Pyæmic blood, effect of different doses, 3.
Pyroplasma in cattle, 545.
Pyroplasma in dogs, 577.
Pyroplasma in sheep, 573, 575.
Quarter ill, 182.
Quebra bunda, 533.
Quebra bunda definition, 533.
Rabbits, infectious genital catarrh in, 367.
Rabidus canis, 260.
Rabies, 259.
Rabies, cases in ratio with bites, 265.
Rabies, causes, 261.
Rabies, countries immune, 261.
Rabies, definition, 260.
Rabies, diagnosis, 273.
Rabies, diagnosis in man, 282.
Rabies, eradication from a country, 285.
Rabies, furious symptoms, 269.
Rabies, geographical distribution, 261.
Rabies in camel and deer, 278.
Rabies, incubation, 266.
Rabies, lesions, 283.
Rabies, lethargic symptoms, 272.
Rabies, microbe of, 263.
Rabies, morbific agent, 263.
Rabies, orrotherapy in, 284, 289.
Rabies, paralytic symptoms, 271.
Rabies, pathogenesis, 261.
Rabies, premonitory symptoms, 267.
Rabies, prevention, 285.
Rabies, symptoms in birds, 279.
Rabies, symptoms in cats, 275.
Rabies, symptoms in cattle, 276.
Rabies, symptoms in dogs, 267.
Rabies, symptoms in Guinea pig, 279.
Rabies, symptoms in man, 280.
Rabies, symptoms in rabbits, 279.
Rabies, symptoms in sheep and goat, 277.
Rabies, symptoms in solipeds, 275.
Rabies, symptoms in swine, 278.
Rabies, symptoms in wild carnivora, 280.
Rabies, synonyms, 260.
Rabies, the Pasteur treatment, 285.
Rabies, therapeutic treatment, 284.
Rabies, treatment of bites, 286.
Rabies, treatment with sterilized matter from infected brain, 290.
Rabies, viability of microbe, 264.
Rabies, virulent matters, 262.
Rauschbrand, 182.
Rauschbrand bacillus, 183.
Red fever of swine, 17.
Red globules, destruction of, 553.
Red soldier, 23.
Red water, 543.
Red water absent in mild cases of Texas fever, 558.
Relapsing fever in horse, 585.
Resorption fever, 8.
Rheumatic catarrh, 113.
Rhino-adenitis, infections, 77.
Rhipicephalus annulatus microplus, 552.
Rinderpest, 624.
Rinderseuche, 55.
Rot, 584.
Rothlauf, 15, 17.
Rouget, 15, 17.
Rouget, bacillus of, 20.
Rouget, causes, 17.
Rouget, course, 18.
Rouget, definition, 17.
Rouget, immunization, 21.
Rouget, morbid anatomy, 19.
Rouget, mortality, 19.
Rouget, pathogenesis, 21.
Rouget, swine plague and hog cholera, table of differential symptoms,
38.
Rouget, symptoms, 18.
Roumanian hæmoglobinuria, 543.
Sanitary police for strangles, 91.
Sapræmic fever, 9.
Scalma, 111.
Scarlatina in swine, 23.
Schweinepest, 23.
Schweineseuche, 15, 47.
Scrofula, 399.
Scrub-tick of Australia, 552.
Septicæmia, 1, 8.
Septicæmia from toxins, 9.
Septicæmia hæmorrhagica, definition, 55.
Septicæmia hæmorrhagica, history, 55.
Septicæmia hæmorrhagica in cattle, 55.
Septicæmia hæmorrhagica in cattle, abdominal form, 59.
Septicæmia hæmorrhagica in cattle, accessory causes of, 57.
Septicæmia hæmorrhagica in cattle, bacteriology, 56.
Septicæmia hæmorrhagica in cattle, chronic, 59.
Septicæmic hæmorrhagica in cattle, external form, 58.
Septicæmia hæmorrhagica in cattle, immunization, 62.
Septicæmia hæmorrhagica in cattle, in winter and spring, 57.
Septicæmia hæmorrhagica in cattle, lesions of, 59.
Septicæmia hæmorrhagica in cattle, mortality, 62.
Septicæmia hæmorrhagica in cattle, on wet soils, 57.
Septicæmia hæmorrhagica in cattle, pathogenesis of, 56.
Septicæmia hæmorrhagica in cattle, prevention, 62.
Septicæmia hæmorrhagica in cattle, symptoms, 58.
Septicæmia hæmorrhagica in cattle, thoracic form, 58.
Septicæmia hæmorrhagica in horse, 113.
Septicæmia hæmorrhagica in sheep, 63.
Septicæmia hæmorrhagica in sheep, acute, 66, 71.
Septicæmia hæmorrhagica in sheep, bacteriology, 65, 70.
Septicæmia hæmorrhagica in sheep, causes, 64.
Septicæmia hæmorrhagica in sheep, chronic, 67, 72.
Septicæmia hæmorrhagica in sheep, definition, 63.
Septicæmia hæmorrhagica in sheep, diagnosis, 66.
Septicæmia hæmorrhagica in sheep, distribution, 63.
Septicæmia hæmorrhagica in sheep, lesions, 67, 72.
Septicæmia hæmorrhagica in sheep, mortality, 68.
Septicæmia hæmorrhagica in sheep, prevention, 68, 73.
Septicæmia hæmorrhagica in sheep, symptoms, 65.
Septicæmia hæmorrhagica in sheep, synonyms, 63.
Septicæmia hæmorrhagica suis, 47.
Septicæmia hæmorrhagica, synonyms, 55.
Septicæmia hæmorrhagica, treatment, 62.
Septicæmia in chickens and turkeys, 656.
Septicæmia in geese, 654.
Septicæmia in geese, bacteriology, 654.
Septicæmia in geese, diagnosis, 655.
Septicæmia in geese, lesions, 655.
Septicæmia in geese, pathogenesis, 654.
Septicæmia in geese, prevention, 656.
Septicæmia in geese, symptoms, 654.
Septicæmia in geese, treatment, 656.
Septicæmia, lesions, 9.
Septicæmia, mortality, 10.
Septicæmia, prevention, 10.
Septicæmias, 2.
Septicæmia, symptoms, 9.
Septicæmia, treatment, 10.
Septic infections, 1, 8.
Septic intoxication, 8.
Septico-pyæmia, 8.
Serum therapy in hog cholera, 45.
Serum therapy in swine plague, 52.
Sheep, paludism in, 573.
Sheeppox, 347.
Sheeppox, accessory causes, 349.
Sheeppox, causes, 347.
Sheeppox, definition, 347.
Sheeppox, forms, 347.
Sheeppox, geographical distribution, 347.
Sheeppox, incubation, 350.
Sheeppox in goat, 360.
Sheeppox, mortality, 354.
Sheeppox, pathogenesis, 347.
Sheeppox, prevention, 355.
Sheeppox, preventive inoculation, 357.
Sheeppox, prognosis, 354.
Sheeppox, symptoms, 350.
Sheeppox, treatment, 354.
Sheep, ulcerative infection of the limbs in, 74.
Skin, tubercle of, 436.
South African horse sickness, 513.
Southern cattle fever, 543.
Spanish fever, 543.
Spleen, tubercle of, 435.
Splenic apoplexy, 196.
Splenic fever, 196, 545.
Stable pneumonia, 95.
Staupe, 166.
Stomatitis, infectious, in lambs and kids, 367.
Stomatitis, ulcerous, in lambs and kids, 367.
Strangles, 77.
Strangles, abdominal, 87.
Strangles, accessory causes, 80.
Strangles, bacteriology, 78.
Strangles, cutaneous, 88.
Strangles, definition, 78.
Strangles, diagnosis, 89.
Strangles, forms of, 84.
Strangles, fulminant, 89.
Strangles, general symptoms, 84.
Strangles, history, 78.
Strangles, immunization, 92.
Strangles, incubation, 84.
Strangles, infecting products, 80.
Strangles, mild, symptoms, 85.
Strangles, nervous lesions, 89.
Strangles, pathogenesis, 99.
Strangles, pathology, 82.
Strangles, pharyngeal, 86.
Strangles, prevention, 90.
Strangles, pulmonary, 87.
Strangles of genital organs, 89.
Strangles, sanitary police, 91.
Strangles, synonyms, 78.
Strangles, tracheotomy in, 94.
Strangles, treatment, 92.
Streptococcus coryzæ contagiosæ equi, 78.
Streptococcus equi, 78.
Streptococcus equi, its relation to strangles and contagious pneumonia,
79.
Streptococcus infection of limbs in cattle and sheep, 74.
Streptococcus of apoplectiform septicæmia, 394, 395.
Streptococcus of infectious stomatitis, 268.
Streptococcus pneumoniæ contagiosæ equi, 98.
Streptococcus rhino-adenitis, 78.
Surra, 584.
Surra, accessory causes, 586.
Surra, anæmia in, 590.
Surra, avoidance of infected localities, 593.
Surra, carried by crows, 587.
Surra, carried by insects, 586.
Surra, cattle don’t infect horses casually, 593.
Surra, cattle infect rodents, carnivora and apes, 593.
Surra, cause, 585.
Surra, definition, 585.
Surra, destruction of the sick, 594.
Surra, diagnosis, 591.
Surra, disinfectants on manure, 593.
Surra, disinfectants on skin, 593.
Surra, disinfectants on stables, 593.
Surra, disposal of manure and garbage, 593.
Surra, exclusion of flies, 593.
Surra, geographical distribution, 585.
Surra, goats and ducks immune, 593.
Surra, in camels, 592.
Surra, in cattle, 592.
Surra in cattle in India, 592.
Surra in cattle in Phillipines, 592.
Surra, incubation, 589.
Surra, lesions, 588.
Surra, mortality, 592.
Surra, parasite, 585.
Surra, pathology, 588.
Surra, prevention of, 593.
Surra, remissions in, 589.
Surra, sanitary police, 594.
Surra, smudges, 594.
Surra, sterilization of carcasses, 594.
Surra, symptoms of, 589.
Surra, synonyms, 584.
Surra, treatment of, 593.
Surra, trypanosoma, 585.
Swine, complex fevers of, 52.
Swine, erysipelas, 15, 17.
Swine, erysipelas bacillus and allied organisms table, 27.
Swine, erysipelas, immunization, 21.
Swine, erysipelas, lesions, 19.
Swine, erysipelas, symptoms, 18.
Swine, fever, 15, 23.
Swine, fever bacillus and allied organisms table, 26, 28.
Swine fevers, effects of varying doses, 16.
Swine, infectious fevers of, 15.
Swine, plague, 47.
Swine, plague, accessory causes, 48.
Swine, plague, bacillus and allied organisms table, 26, 28.
Swine, plague and hog cholera, duality, 53.
Swine, plague, bacteriology, 47.
Swine, plague, deadly to wild birds and rodents, 49.
Swine, plague, diagnosis, 50.
Swine plague, hog cholera, and Rouget, table of differential symptoms,
38.
Swine plague, immunization, 51.
Swine plague, lesions, 49.
Swine plague, Marseilles, 54.
Swine plague, McFadyean’s, 53.
Swine plague, pathogenesis, 48.
Swine plague, prevention, 50.
Swine plague, serum therapy, 52.
Swine plague, symptoms, 50.
Swine plague, treatment, 52.
Swine pox, 360.
Symptomatic anthrax, 182.
Symptoms of septicæmia hæmorrhagica, cattle, 58.
Symptoms of swine plague, 50.
Tabes, 399.
Tappeiner’s experiments on tuberculosis, 409.
Tetanus, 291.
Tetanus, accessory causes, 298.
Tetanus, antidotal treatment, 309.
Tetanus, antitoxin treatment, 309.
Tetanus bacillus, 293.
Tetanus, brain emulsion for, 312.
Tetanus causes, 293.
Tetanus, course, duration, 312.
Tetanus, definition, 292.
Tetanus, diagnosis, 304.
Tetanus, form of death from, 304.
Tetanus, general symptoms, 298.
Tetanus immunization, 315.
Tetanus, intra cranial injections for, 312.
Tetanus, lesions, 304.
Tetanus, mortality, 303.
Tetanus, orrotherapy, 310.
Tetanus, pathogenesis, 292.
Tetanus, pathology, 293.
Tetanus, prevention, 313.
Tetanus, symptoms in birds, 302.
Tetanus, symptoms in cattle, 301.
Tetanus, symptoms in dogs, 302.
Tetanus, symptoms in horse, 300.
Tetanus, symptoms in sheep and goat, 302.
Tetanus, symptoms in swine, 302.
Tetanus, synonyms, 291.
Tetanus, treatment, 306.
Texas fever, 542.
Texas fever and anthrax, diagnosis, 560.
Texas fever and anthrax, table of distinctions, 561.
Texas fever, course and duration, 559.
Texas fever, cultivating infested pastures, 564.
Texas fever, definition, 543.
Texas fever, federal restrictions, 572.
Texas fever, immunization against, 567.
Texas fever, immunization by blood, 570.
Texas fever, immunization by blood from ticks, 571.
Texas fever, immunization of limited value, 571.
Texas fever, infecting by small number of ticks, 568.
Texas fever, infection by blood of immunized, 569.
Texas fever, infection of sucking calf, 568.
Texas fever, legislation for its extinction, 566.
Texas fever, marketing the beef, 572.
Texas fever, mortality in severe form, 560.
Texas fever pastures, purifying by exclusion of cattle, 564.
Texas fever, prevention, 562.
Texas fever, prevention by dipping or smearing, 563.
Texas fever, prevention by picking off ticks, 562.
Texas fever, purifying infected pastures, 564.
Texas fever, red water absent in mild cases, 558.
Texas fever, susceptibility of cattle on purified pastures, 565.
Texas fever, symptoms of mild form, 560.
Texas fever, treatment, 561.
Texas fever, value of its extinction, 566.
Texas fever, watery blood in, 559.
Therapeutics in hog cholera, 45.
“The trembles,” 325.
Thrombosis and pyæmia, 4.
Ticks, destruction of, in pastures, 564.
Ticks, dressing for, 564.
Ticks in paludism in dogs, 579.
Toxins as cause of septicæmia, 9.
Treatment of septicæmia hæmorrhagica in cattle, 62.
Treatment of strangles, 92.
Treatment of swine plague, 52.
Trembling in sheep, 500.
Trembling in sheep, accessory causes, 504.
Trembling in sheep, bacilli, cocci and penicillium, 503.
Trembling in sheep, bacteriology, 503.
Trembling in sheep, causes, 501.
Trembling in sheep, definition, 500.
Trembling in sheep, diagnosis, 505.
Trembling in sheep, geographical distribution, 500.
Trembling in sheep, lesions, 506.
Trembling in sheep, pathogenesis, 500.
Trembling in sheep, prevention, 506.
Trembling in sheep, sheepticks, 501.
Trembling in sheep, symptoms, 504.
Trembling in sheep, treatment, 507.
Trismus, 292, 299.
Tristeza, 543.
Trypanosoma Brucii, 595, 596.
Trypanosoma equiperdum, 521.
Trypanosoma Evansi, 585.
Trypanosoma in blood during paroxysm of surra, 591.
Trypanosomosis, 585.
Trypanosoma, staining of, 591.
Tsétsé fly, 595.
Tsétsé fly disease, 594.
Tubercle bacillus, 410.
Tubercle bacillus, diminished pathogenesis when from cold blooded host,
482.
Tubercle, calcification, 431.
Tubercle, cardiac and pericardial, 433.
Tubercle, caseation, 430.
Tubercle, fibroid degeneration, 431.
Tubercle, genito-urinary, 435.
Tubercle in lymph glands, 433.
Tubercle, local, 498.
Tubercle of brain and spinal cord, 436.
Tubercle of bones, 436.
Tubercle of bronchial and mediastinal glands, 433.
Tubercle of eye, 436.
Tubercle of lymph glands, 437.
Tubercle of mammæ, 435.
Tubercles of mouth and throat, 434.
Tubercle of muscles, 436.
Tubercle of pancreas, 435.
Tubercle of skin, 436.
Tubercle of spleen, 435.
Tubercle, relative frequency in different parts, 437, 438.
Tubercle, structure of, 429.
Tuberculin, action on parturient cows, 464.
Tuberculin, dose of, 461.
Tuberculin, reaction under, 463.
Tuberculin test, 458.
Tuberculin test, antipyretics during, 426.
Tuberculin test, effect on sound animals, 464.
Tuberculin test, its reliability, 465.
Tuberculin test, later effect on the tuberculous, 464.
Tuberculin test, precautions, 459.
Tuberculin tests, false certificates of, 426.
Tuberculin test, technique, 461.
Tuberculosis, 398.
Tuberculosis, accessory causes, 415.
Tuberculosis and absence of indemnity, 424.
Tuberculosis and increased trade, 421.
Tuberculosis and private testing of herds, 426.
Tuberculosis and sale of tuberculous, 424.
Tuberculosis and sales of sound stock, 424.
Tuberculosis and unrestricted trade, 423.
Tuberculosis, bacilli of bird, horse and rabbit, 413.
Tuberculosis, breeding healthy stock from infected parents, 489.
Tuberculosis, butter, cheese and whey, 497.
Tuberculosis by feeding, 409.
Tuberculosis by inhalation, 409.
Tuberculosis, cerebral, symptoms, 450.
Tuberculosis, culling out the unthrifty and sick, 491.
Tuberculosis, Danish method in Pennsylvania, 492.
Tuberculosis, Danish method of restriction, 491.
Tuberculosis, decrease of in England, 481.
Tuberculosis, definition, 399.
Tuberculosis, diagnosis of, 456.
Tuberculosis, direct infection from man to ox, 474.
Tuberculosis, encrease in infants in England, 481.
Tuberculosis, expense of extinction in cattle, 486.
Tuberculosis, experiments of Adami and Ravenel, 482.
Tuberculosis from common feeding trough, 428.
Tuberculosis from dusty infected stables, 428.
Tuberculosis from feeding hogs after diseased cattle, 428.
Tuberculosis from feeding offal to hogs, 427.
Tuberculosis from infected milk, 427.
Tuberculosis, gastro-intestinal, peritoneal and mesenteric, 434.
Tuberculosis, generalization of, 499.
Tuberculosis, generally applicable measures, 494.
Tuberculosis, genital in the bull, symptoms, 449.
Tuberculosis, geographical distribution, 402.
Tuberculosis, Gerlach’s experiment, 409.
Tuberculosis, glandular symptoms, 450.
Tuberculosis held virulent in early times, 403.
Tuberculosis, hereditary vulnerability, 415.
Tuberculosis, hygiene of meat, 498.
Tuberculosis, hygiene of milk and meat, 495.
Tuberculosis, hygiene of oleomargarine, 497.
Tuberculosis in apes and menagerie animals, lesions, 441.
Tuberculosis in apes and monkeys, 401.
Tuberculosis in birds, 399.
Tuberculosis in birds, symptoms, 456.
Tuberculosis in cattle, 400.
Tuberculosis in chickens, lesions, 441.
Tuberculosis in dog and cat, lesions, 440.
Tuberculosis in dogs and cats, 401.
Tuberculosis in dogs and cats, symptoms, 455.
Tuberculosis, infection from ox to man, 476.
Tuberculosis in fishes, 399.
Tuberculosis in Hebrews and Christians, 481.
Tuberculosis in horse, ass and mule, 400.
Tuberculosis in horse, lesions, 439.
Tuberculosis in horse, symptoms, 453.
Tuberculosis in indoor subjects, 402.
Tuberculosis in man, 402.
Tuberculosis in man with sound cattle, 472.
Tuberculosis in park and menagerie animals, 402.
Tuberculosis in parrot, lesions, 441.
Tuberculosis in pheasants, lesions, 441.
Tuberculosis in reptiles, 399.
Tuberculosis in rodents, 400.
Tuberculosis in sheep and goat, 400.
Tuberculosis in sheep and goat, lesions, 439.
Tuberculosis in sheep and goat, symptoms, 455.
Tuberculosis in swine, 401.
Tuberculosis in swine, lesions, 439.
Tuberculosis in swine, symptoms, 452.
Tuberculosis, its extinction in cattle, 486.
Tuberculosis, lesions, 429.
Tuberculosis, limited susceptibility of ox to germ from man, 482.
Tuberculosis, mammary symptoms, 449.
Tuberculosis of bones and joints, symptoms, 451.
Tuberculosis of liver, 434.
Tuberculosis of lungs in cattle, 431.
Tuberculosis of lungs, symptoms, 445.
Tuberculosis of man and ox coextensive, 470.
Tuberculosis of skin, symptoms, 450.
Tuberculosis of the abdomen, symptoms, 448.
Tuberculosis of the eye, symptoms, 451.
Tuberculosis of the heart, symptoms, 451.
Tuberculosis, pathogenesis, 399.
Tuberculosis, pharyngeal, symptoms, 450.
Tuberculosis, practicability of its extinction in cattle, 487.
Tuberculosis, primary and secondary infection, 442.
Tuberculosis, raising healthy calves from diseased dams on the range,
490.
Tuberculosis, sanitary police measures, 495.
Tuberculosis, sifting process in N. Y. markets, retention of the
tuberculous, 493.
Tuberculosis, symptoms in cattle, 445.
Tuberculosis, testing imported stock, 493.
Tuberculosis through insects, 429.
Tuberculosis through vermin, 428.
Tuberculosis, treatment, 483.
Tuberculosis, uterine, symptoms, 449.
Tuberculosis, varying pathogenesis, its value in sanitary police, 483.
Tuberculosis, Villemin’s inoculations, 408.
Tuberculosis, virulence, 403.
Tuberculosis, with bad ventilation, 416.
Tuberculosis with conformation, 418.
Tuberculosis with damp stables, 417.
Tuberculosis with debilitating diseases, 420.
Tuberculosis with early breeding, 419.
Tuberculosis with heavy milking, 418.
Tuberculosis with inbreeding, 419.
Tuberculosis with insufficient nourishment, 418.
Tuberculosis with old age, 420.
Typhoid fever bacillus, 27.
Typhoid fever in the horse, 113.
Typhoid in pig, 23.
Typhose, 113.
Typhus, 141.
Typhus contagieuse, 624.
Typhus des chenils, 166.
Typhus du gros betail, 624.
Typhus in pig, 23.
Ulceration of anus and vulva in cattle, 651.
Ulcerative infection of the limbs in cattle, 74.
Variola, 333.
Variola caninæ, 361.
Variola caprina, 360.
Variola equina, 337.
Variola, history, 334.
Variola, nomenclature, 334.
Variola ovina, 347.
Variola, pathogenesis, 336.
Variola suilla, 360.
Variola vaccinæ, 340.
Variole des chiens, 166.
Variolisation, 357.
Venereal disease of solipeds, 519.
Vesicular exanthema, causes, 362, 365.
Vesicular exanthema, diagnosis, 364.
Vesicular exanthema of horse, 362.
Vesicular exanthema, prevention, 364, 367.
Vesicular exanthema, symptoms, 363, 366.
Vesicular exanthema treatment, 364, 367.
Viehpest, 624.
Villemin’s inoculations of tubercle, 408.
Vulva, infective ulceration of, causes, 651.
Vulva, infective ulceration of, in cattle, 651.
Vulva, infective ulceration of, pathology, 653.
Vulva, infective ulceration of, symptoms, 652.
Vulva, infective ulceration of, treatment, 654.
White scour, 645.
White scour, microbiology, 646.
Widal test in hog cholera, 36.
Wildseuche, 55.
Wood-ill, 543.
Woolsorter’s disease, 196, 226.
Yellow water, 153.
------------------------------------------------------------------------
TRANSCRIBER’S NOTES
Page Changed from Changed to
106 A safer and hardly less A safer and hardly less
affective method is to apply effective method is to apply
around the around the
123 immune ones, which for a time immune ones, which for a time
resist, throw off the desease resist, throw off the disease
with with
182 percussion resonance, finally percussion resonance, finally
cold, insensible, withered. On cold, insensible, and withered.
incision black On incision black
185 to 139° F., and it is sterilized to 139° F., and it is sterilized
at a temperature of 212° for at a temperature of 212° F. for
twenty twenty
266 In the _dog_ incubation rages In the _dog_ incubation ranges
from 15 to 60 days, and perhaps from 15 to 60 days, and perhaps
4 4
603 heated to 100° to destroy the heated to 100° C. to destroy the
action of the pepsin, then action of the pepsin, then
● Typos fixed; non-standard spelling and dialect retained.
● Used numbers for footnotes.
● Enclosed italics font in _underscores_.
● Enclosed bold or blackletter font in =equals=.
● Subscripts are shown using an underscore (_) with curly braces { },
as in H_{2}O.
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