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.