Part 17

CONTAGIOUS PNEUMONIA IN THE HORSE.

Synonyms. Definition. Historic notes. Accessory causes: youth, native susceptibility, inclement weather, exposed stables, nasal and bronchial catarrh, sores as infection atria, lack of stable hygiene, crowding, underfeeding, overwork, excitement, exhaustion, infection from stables, etc., convalescents; doctrine of recrudescence. Bacteriology: streptococcus pneumoniæ contagiosæ equi: pathogenic to mice, rabbits, and Guinea pigs. Cocco-bacillus of Lignieres in early lesions. Lesions: bilateral, multiple foci, congestion, consolidation, purulent, necrotic, infarction, sequestra in purulent sacs, pleuritic effusion; enlarged, congested liver with centres of degeneration and necrosis. Congested spleen, kidneys, lymph glands and gastro-intestinal mucosa. Yellow mucosæ, mahogany colored muscles. Incubation, 3 to 10 days. Symptoms: staring coat, early extreme hyperthermia, accelerated pulse and breathing, cough, icteric mucosæ, anorexia, dulness, defervescence in 3 to 5 days; convalescence in 10 days; or prostration, swollen eyelids, trembling or interrupted labored breathing, cough, nasal flow yellow, multiple centres of percussion flatness, crepitation, râles; urine scanty, yellow or reddish, albuminous, acid, alkalinity as a symptom; throat symptoms, inhalation bronchitis, cardiac phenomena, swelling of legs, stupor, trembling, staggering, vertigo, paresis. Course: duration 2 to 3 weeks, defervescence. Fatal cases, toxin poisoning. Diagnosis: by age, history, tardy infection, prostration usually less than in influenza. Prognosis: gravity depends on violence of attack, susceptibility, hygiene, treatment. Mortality 1 to 20 per cent. Permanent lesions from sequestra, adhesions, cardiac, hepatic, nervous or arthritic disease. Treatment: pure air, sunshine, comfort, hygiene, pure water, rest, cold rectal injections, damp compresses, hot bath, diaphoretics, expectorants, alkaline diuretics, antipyretics, heart stimulants, derivatives, antiseptics, nerve sedatives, tonics. Prevention: early removal, disinfection, quarantine new horses, disinfection of public and sale yards and stables, certificates. Immunization: by a mild attack; serum-therapy.

Synonyms. Ataxic or Adynamic Pneumonia; Stable or Hospital Pneumonia; Pleuro-Pneumonia Contagiosa Equorum; Contagious Pleuro-Pneumonia; Bilious Pneumonia; Edematous Pneumonia; Brustseuche.

Definition. An infectious adynamic type of pneumonia occurring in horses, asses and mules, characterized by marked hyperthermia; by infiltration of lung tissue, often bloody, infarcted or caseated and usually circumscribed; by a deep yellow discoloration of the visible mucosa and other white tissues; and by complicating lesions of the pleura, heart, pericardium, liver, bowels, or kidneys.

Historic Notes. This affection was formerly confounded with equine influenza, and it was only in the second third of the nineteenth century that the differentiation was attempted. S. Prangé describes this as a special epizoötic disease in the French hussars in 1841, Leconturier in Belgium in 1845, Seidamgrotzky in Germany in 1882 (strongly emphasizing the contagion), and Dieckerhoff in Berlin in 1883. The latter showed that horses, recovered and immune from influenza, still contracted brustseuche and perished. This distinction was fully corroborated by Lustig, Cagnat (1884), Brun, Delamotte (1886), Jolly, Benjamin, Leclainche, Trasbot, and others. The presence of a particulate, living, self-multiplying cause (microbe) was recognized as the essential condition of the disease (as we still recognize the necessity for such an organism to explain rabies) though the micro-organism itself was as yet undiscovered.

At the same time many concurrent factors had to be considered as accessory in different cases.

Accessory Causes. Young horses often show a greater susceptibility than older animals, mainly because they retain all the unimpaired susceptibility of the colt, while old horses have already passed through the disease and become immune. On the other hand, in the absence of acquired immunity, the older, worn out and debilitated animals are the most susceptible and tend to have the disease in its worst form. Susceptibility and immunity are therefore more important factors than mere age. Immunity usually lasts for several years, or throughout life, yet in some animals, or under given conditions, it is overcome much earlier. Inclemency of the weather, or special exposure of any kind, as in severe rainstorms, or working with the feet and legs in water, may become the occasion of an attack. Exposure to cold northwest storms (America, Atlantic Slope), or northeast (Europe), standing without blanket in a temperature at zero, confinement in draughts of cold air between doors or windows, without clothing and after severe exercise, weaken the whole system and increase susceptibility. The presence of a nasal or bronchial catarrh, or of another debilitating disease may act in the same way. The weakened tissues seem to invite the entrance of the germ. Palat, Boiteux and Trasbot found that horses with local sores or suppurations fell readier victims than others;—perhaps the germs entered by the traumas; perhaps the tone of the whole system was lowered, so that the resistance was lessened.

Close, foul air, bad ventilation, imperfect sewerage, and overcrowded stables not only contribute strongly to infection but tend to aggravate the cases. Underfeeding and overwork act in the same way and in this connection may be named the excitement and exhaustion attendant on a long journey by rail. This, like the foul, crowded stable, furnishes many more opportunities for infection and reinfection, so that the invasion of the exposed animal system is all but certain. Infection clings to the loading banks, yards, feeding stables, mangers, troughs, buckets, cars, litter, and manure, so that young horses shipped from the west to the Atlantic Coast States, very frequently come down with contagious pneumonia, and contaminate the stables in which they are placed. Peters suggests that the germ is preserved in the soil water, so that after apparent subsidence it may be again brought to the surface in time of rains or freshets, to start a new epizoötic. Convalescent horses may carry the germ for weeks, on the mucosa or in sequestra in the lungs, and contaminate horses with which they come in contact.

It is remarkable that the contagious pneumonia is far less diffusible on the air than influenza, so that it is much more constantly the result of direct contact of a sound, with an infected animal, or with a place or thing that the sick animal has contaminated. It therefore spreads much less rapidly, remains confined to individual stables for a length of time, and in the absence of active interchange of horses tends to die out of its own accord. As the infection is not generally and speedily acquired, so immunity fails to become general, and the infection tends to fix itself permanently in places where many strange horses congregate, (market stables, sale stables, livery stables, etc.), and the constant influx of fresh animals keeps the flame burning by accessions of fresh fuel. In such cases it is manifest that the germ outside the animal body either rests in a dry condition, or lives as a saprophyte in earth or organic matter, and often loses much of its virulence. Under such circumstances animals that would prove readily susceptible to a virulent germ, prove nonreceptive to this resting germ, until under some special devitalizing influence, like exposure, exhaustion or local disease, it finds its opportunity and the weakened system succumbs. Then, acquiring new force through its life in the debilitated system, it starts on a recrudescence, and an epizoötic is mistakenly supposed to have started without a preëxisting microbian cause.

Cadeac even advocates the theory that the same germ possessed of greater or lesser virulence, is always present in ordinary stables and horses, and habitually causes in exposed or debilitated animals an ordinary fibrinous pneumonia with no perceptible tendency to transmission by contagion; that, in other cases when a considerable number of horses have their defensive powers impaired, it gains a wide extension; and, that in some such cases, the germ that has been living as a comparatively harmless saprophyte, suddenly acquires an unwonted potency, and breaking down the barrier of partial immunity, attacks exposed animals on a large scale and irrespective of weather perturbations, or debilitated conditions. He quotes from Trasbot instances that seem to support this hypothesis, which is not at all in disaccord with the habits of bacterial life, yet we require a solid basis in bacteriological experiment to make it unassailable.

Bacteriology. Siedamgrotzky (1882) found in the hæmorrhagic centres in the affected lung and in the pleural exudate micrococci. Dieckerhoff (1882) and Mendelsohn (1883) found in the pleural exudate streptococci. Chain cocci were also found by Peterlein (1884), Perroncito (1885), Delamotte and Chantemesse (1888), and Mosselman and Lienaux (1893).

Schütz (1887) found a diplococcus which he studied very fully and this is corroborated by Lustig’s ovoid bacterium, by Cadeac’s micrococcus and diplococcus. In Dr. V. A. Moore’s cultures at the N. Y. S. Veterinary College cocci were found constantly in pure culture, sometimes as a diplococcus, but under slightly altered conditions the streptococcus form predominated. As the difference between two, and three or more cocci in chain form is merely a question of early or late separation of cocci which multiply in line, the apparent discrepancies in the above observations do not imply any real difference in the microbe.

Inoculated in pure cultures the Schütz diplococcus killed mice in 24 to 48 hours with enhanced virulence of the germ. In the rabbit, subcutem, it usually killed in 24 to 48 hours, but some survived; intravenously or intratrachealy it killed more certainly and speedily and in either case with pleural, pericardial and even peritoneal lesions. In the Guinea-pig, subcutem, it caused extensive effusion, and death in two to six days with chest lesions. In the dog it caused hyperthermia, but no marked lesion and no mortality. In the horse there were no infectious resultant lesions. A pure culture thrown into the lung tissue of an old horse at the N. Y. S. V. College, determined an extended pleuritic adhesion and lung hepatization. The age of this subject was opposed to any marked susceptibility. The apparent immunity of the horse in Schutze’s cases might depend on the insusceptibility of the animals selected during or after an epizoötic, or on the absence of the predisposing causes so strongly insisted on by Cadeac.

Rats, chickens and pigs proved immune.

On peptonized gelatin at 98° F., and less rapidly at ordinary temperature, it grew as white, opaque, colonies which gradually extended and united in many cases. The gelatin was not liquefied. In peptonized bouillon it produces turbidity for one or two days, after which the microbe precipitates leaving the liquid clear. The reaction is unchanged.

It lost virulence rapidly when kept in artificial culture or at a temperature of 122° F., and was killed by a temperature of 150° F. Yet it survived drying at moderate temperatures. Cadeac found that the dried expectoration or blood, diffused in the inspired air produced pneumonia with certainty in solipeds. Schütz and Fiedaler injected pure cultures into the lung, and in other cases into the trachea, thereby inducing pneumonia. Twenty grammes of the culture injected into the trachea raised the temperature 2° or 3°, but this lessened on repetition and after four or five treatments the subject proved immune.

Lignieres (1897) discovered his cocco-bacillus in the exudation in the tissues in the early stages of contagious pneumonia, from which it disappears, giving place to other bacteria, and usually streptococcus, as the disease reaches its maximum. (See Equine Influenza for description). His theory is that the cocco-bacillus, which is slightly smaller than the bacillus of chicken cholera, and appears like a diplococcus when stained, and which may not be found after the first eight days of infectious pneumonia, is the starting point of disease, in this and influenza, making the system very receptive of the streptococcus of strangles and of other bacteria, the identity of which determines the nature of the malady. The diplococcus or streptococcus of Schütz in his opinion is none other than the strangles streptococcus which finding a congenial home in the animal invaded by his cocco-bacillus, pervades the system and determines the pathological phenomena of contagious pneumonia.

There are certain obstacles to the unreserved acceptance of Lignieres’ conclusions, among the chief of which is the absence of evidence that horses, successfully inoculated with his cocco-bacillus in pure cultures, can infect others standing near them with the same rapidity and certainty, as does the casual case of influenza, or even of contagious pneumonia. The same holds true of the supposed identity of the streptococcus and that of strangles. Abscesses containing streptococci, were formed in the seats of inoculation with Schütz’s organism, but there is no evidence that the horses suffering from such abscess affected susceptible horses standing beside them, as do ordinary cases of strangles. The cocco-bacillus may be a concurrent cause of contagious pneumonia, but we need more proof to show that it is the essential cause, even as we need proof of the absolute identity of the streptococcus of strangles and brustseuche.

Lesions. The pneumonia is far more likely to be double than in the fibrinous form, and the area invaded, in its ratio with the high intensity of the fever, is usually less. The consolidations are especially common near the lower borders of the anterior parts of the lungs. There may, however, be a number of centres in each lung, to be accounted for by the inhalation of the germ and the starting of the morbid process at the various points on which it falls. This, like the double character of pneumonia is therefor in keeping with the contagious origin. Each centre of condensation shows a small area, hepatized, purulent or necrotic, with a surrounding zone of dark bluish red congestion. The consolidated areas are less dry and granular than in fibrinous pneumonia, seeming to be largely infiltrated with a still liquid exudate and dark blood, and thus tend to a greater tenacity, and less friability. Black areas of infarction form in the lung, the thrombosis of the arteries, cutting off the free normal circulation and the isolated portion fills up with dark blood globules and forms a sequestrum. In the inflammatory and still living parts the color is lighter with, it may be, some straw colored exudate, and always an active leucocytosis, as in other inflamed parts. When infiltration is located near the root of the lung, it is usually attached to the primary bronchi, or larger bronchia and may extend into the upper portion or almost the entire substance of the lung.

Simple abscess is rare, yet purulent sacs containing the gangrenous masses or sequestra are common.

Pleuritic areas are common over the congested and hepatized foci, yet as these are usually circumscribed in extent, an excessive hydrothorax is exceptional. Yet the pleuritic effusion may at times become abundant. Friedberger and Fröhner say seven gallons or more. It may become purulent or even septic, exhaling an offensive odor. Adhesions and fringes on the pleura are frequent.

The heart and pericardium may be affected, the first showing the pallid, soft, or parboiled appearance of high fever, with at times fatty degeneration or petechiæ, and the latter congestion, exudation, thickening, false membranes and liquid effusion.

The enlargement of the congested liver is a marked feature. It frequently attains the weight of 30 pounds. It may ooze dark blood freely from the cut surface, has usually a yellowish tinge, and shows points of fatty degeneration or even of commencing necrosis. The spleen is like the liver, charged with blood, and shows an increase of pulp and even petechiæ or circumscribed hæmorrhages.

The kidneys are congested, friable and petechiated.

The bronchial lymph glands and less constantly the mediastinal and abdominal ones, are congested, pink to dark red and somewhat enlarged.

The gastric and intestinal mucosa may be congested, thickened, hæmorrhagic or ulcerated.

The white tissues generally tend to an icteric hue, and the muscles assume a mahogany aspect.

Incubation appears to be longer than in equine influenza, varying in different cases from 3 to 10 days.