Chapter V: Front Matter (5)

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.