The bacillus has only limited power of resistance to destructive physical and chemical agents. It is killed in 10 minutes at 55° C., in 2 minutes at 100° C., or by mercuric chloride solution (1:5000), or by phenol (5:100), or by permanganate of potass (1:100). In warm dry air and sunshine it is sterilized, in thick layers in 2 months (Peuch), in moderate layers in 4 to 15 days (Galtier), and in very thin layers in 3 days (Cadeac and Malet). In moist, cool air and in the shade it is much more resistant. In stables it may remain virulent for three or four months, and thus the disease has often reappeared among the newly introduced horses after a stable has been abandoned for a length of time. The microbe does not grow in infusions of hay, straw or horse manure, and it is doubtful if it can maintain an active saprophytic existence. Its vitality and virulence, however, persists in putrefying materials for 14 to 24 days, and in water from 15 to 20 days. Hence it is largely propagated through drinking troughs and occasionally through ponds, lakes and sluggish streams. Again the virus is likely to be preserved in and transmitted by rotten or even sound woodwork, as of mangers, racks, buckets, shafts and poles, and by harness, halters, blankets, combs, brushes and rubbers. Sometimes direct transmission takes place in snorting or coughing, or by the animals biting or licking each other. As the virus is spattered on surrounding objects, the walls, stable utensils, soiled fodder and feed, and even the attendant’s clothes may be the medium of transmission. Contagion during copulation is not unknown, nor infection of the fœtus in utero from a diseased mother. Carnivora (dog, cat, lion) fed on the diseased carcasses have become infected. Experimentally infection has been conveyed by administering, by the mouth, balls containing the virus (Renault, Coleman, etc.), and again by transfusing the blood from a bad case of glanders into the veins of a sound horse (Viborg, Coleman, Renault, Hering, Chauveau, Nocard). Transmission through the air on dust is counteracted by the speedy destruction of virulence on dust, and horses often stand side by side in adjacent stalls for months without communicating the infection. Such escapes may, however, in some of these cases, be attributed to the immunity secured by a previous exposure and slight attack. That the germs may be exceptionally conveyed through the air appears to have been proved by Viborg and Gerlach, who collected the floating dust in a stable containing infected animals and successfully inoculated with it.
The microbes are especially found in the visible lesions of glanders, in the mucous, cutaneous and subcutaneous swellings and abscesses, in the swollen lymph glands, in the nodules and ulcers of the mucous membranes and skin, in the morbid discharges, from the nose, eyes, pharynx, guttural pouches, larynx, trachea and bronchia, and in the discharge of farcy buds and abscesses. They are not necessarily distributed through all the tissues, and in chronic cases, with strictly local lesions, the infection appears to be often confined to these or nearly so, and the contamination of other animals is slow and uncertain. When, however, the disease is acute and advanced, or generalized, every part must be looked upon as probably infecting. Thus virulence has been shown in the blood, the exhalations of the serous membranes, saliva, the aqueous humor (Cadeac and Malet), the tears, (Viborg), the muscles, and the bones. Galtier says the milk, sperm, bile and intestinal mucous are non-virulent, also the vaccine lymph raised on glandered animals, but much must depend on the grade and stage of the disease and no one would care to run unnecessary risks with these liquids.
Infection Atria. Inoculation on a skin wound or abrasion, is a most effective mode of transmission, but the virus undoubtedly enters in certain cases with the air, food or water, or by accidental lodgment of a speck of the virus on the mucosa of the nose or eye or other natural opening. Through the healthy mucosa the bacillus may enter by penetrating the soft epithelium, or entering the mucous follicles, but it will find the way smoothed for it, if there has been friction, abrasion, desquamation or congestion. The skin in its healthy state is usually resistant, but Babes has conveyed infection by rubbing on the virus mixed with vaseline, and without displacing the epithelium. The channel of entrance was the hair follicles. Injected into the blood, intravenously, or into a serous cavity, the bacillus infects with great certainty and promptitude.
There is ample evidence that primary lesions appear not only in the skin and nasal mucosa, but also in the bronchia, intestines, and other parts. Much time and ink have been wasted in attempts to prove that pulmonary lesions are always secondary, and doubtless many are so, but the cases in which the lesions are confined to the bronchia or parenchyma, and the many parallel cases of direct infection of the lungs by other diseases (tuberculosis, lung plague, contagious pneumonia, influenza, etc.,) furnish conclusive enough evidence that the germ may be inhaled and colonize this part first. Cases of inhalation bronchitis, are equally corroborative, and not only may the grosser solids be aspired, but infection droplets can easily gravitate down when from congestion or inflammation the action of the tracheal and bronchial cilia, is suspended.
FORMS AND LESIONS OF GLANDERS IN SOLIPEDS.
Glanders appears in two primary forms—acute and chronic, and each of these is further divided according as the lesions are exclusively or mainly seated in one part of the body or another. The generic term glanders is habitually used to designate that form in which the lesions are situated in the nose, the nasal sinuses, and the submaxillary lymphatic glands—nasal glanders. When the principle lesions are situated in the lungs and lymph glands of the chest, the case is one of pulmonary glanders. When the skin and subcutaneous lymphatics are most prominently affected it is known as farcy or cutaneous glanders. When the skin and nose are simultaneously affected the name farcy glanders is sometimes applied. But as the bacillus may enter by very varied channels the primary lesions may appear in still other organs. Thus in stallions the first symptom is often a glanderous orchitis. In other horses it may be a glanderous arthritis, and in still others infected by ingestion it may be an abdominal infection.
Symptoms of Nasal Glanders in Solipeds. Acute. After an incubation of three to five days the subject shows prostration, weariness, stiffness, erection of the hair, and even tremor or shivering, inappetence, thirst, hyperthermia, rapid pulse, weeping eyes, the discharge becoming purulent, snuffling breathing, and a discharge from the nose, at first serous, with a remarkable viscidity which tends to glue together the long hairs or even the margins of the nostrils. This discharge may be reddish, greenish, or brownish and may become distinctly purulent and opaque. The alæ nasi are swollen, hot and painful, and the mucosa red, congested, thickened, with a blackish or violet tint especially along the median part of the septum nasi. On these, violet patches appear on the second or third day, pronounced elevations of very varying size indicating the centres of active hyperplasia. They are usually yellowish or grayish, surrounded by a deep violet areola, and may become confluent forming patches. The centre of each undergoes rapid degeneration, forming a rounded ulcer with salient edges, a yellowish base, more or less pointed or streaked with red, and a viscid seropurulent or bloody discharge which may concrete in crusts or scale. The whole septum may become one continuous ulcer with excavations of various depths surrounded by hyperplastic elevations, and involving not only the mucosa, but even the cartilage and leading to perforations.
From an early stage of the attack the submaxillary lymphatic glands and the investing connective tissue become swollen, forming a mass of firm bean- or pea-like nodules, with no excessive heat nor tenderness, and with little disposition to suppurate and discharge. If this has lasted for some time the glands often become more firmly attached to adjacent parts (maxilla, tongue) by the contraction of the exudate.
The swelling of the alæ nasi also often extends to the skin of the face, and firm, rounded cords formed by the swollen lymphatics stretch upward toward the eye, or the submaxillary glands. Upon the turgid lymphatics may appear more or less rounded nodules from the size of peas to hazel nuts, which, unlike the submaxillary glands, tend to soften, burst and discharge a viscid, glairy, sanious liquid.
At the same time the morbid process is liable to show itself in the cutaneous lymphatics of one limb, usually a hind one, in the form of firm cords, with degenerating or ulcerous nodules (farcy buds) and pasty patches. Or the throat or lungs may become involved, with local swellings, violent cough, dyspnœa and fever. The swellings of the cutaneous lymphatics usually follow the course of the veins, in the hind limbs the branches of the saphena, and extend from below upward, and the first nodules may be on the fetlock or hock.