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.