Part 38

In cutaneous glanders the lesions may begin in the papillary layer by active congestion and infiltration and proliferation of lymphoid cells which cause an eruption of rounded papules like small peas that degenerate and soften and form superficial ulcers. When the derma is mainly involved the inflamed area becomes the seat of larger hard nodules which are at first deeply congested, with capillary thrombi, minute extravasations and rapid cell proliferation; later on section they show numerous caseated centres with a dense fibroid framework and surrounded by an area of active congestion and capillary hæmorrhage; later still the caseation and softening has caused rupture of the investing epithelium and the discharge from the ulcerous cavity of a yellowish, glairy, grumous liquid (open farcy buds). Sometimes the nodule undergoes fibroid induration and fails to ulcerate, becoming the counterpart of the cicatrices in the nose. When the infective inflammation extends to the subcutaneous connective tissue, diffuse engorgements and extensive swellings occur from the general infiltration of the abundant lymph plexuses. Lymphoid cells accumulate in the perivascular sheaths and lymph plexuses, the walls of the lymphatic trunks running out of these swellings become swollen and indurated and at intervals, mostly on the seat of the valves there is the proliferation of small round cells to form farcy buds. In chronic cases the fibroid thickening involves the skin, subcutaneous connective tissue and walls of the lymph vessels binding the whole into one dense resistant mass, more or less studded with corded lymphatics, firm nodules, and ulcerous sores.

The lymphatic glands in the line of circulation from the infected centres are constantly involved. Hypertrophy, congestion, serous infiltration, and rapid cell proliferation are present and a section will usually show caseated or caseopurulent centres confined by the outer dense fibrous envelope. Exceptionally, these necrosed contents will escape through an ulcerous opening, forming a deep cavity which is slow and difficult to heal. In the vicinity of these glands and in the loose intermuscular connective tissue abscesses of the size of an egg or an orange or larger are sometimes met with.

Nodules and ulcers are found on the pharyngeal and intestinal mucosa, similar to those of the larynx.

The spleen, and less frequently the liver, may be the seat of caseating nodules exactly comparable to those of the lungs. Glanders of the kidney is rare.

Nodules have been seen on the ventricular endocardium and one case of nodules of the choroid plexus (Boschetti).

In stallions, glanderous, caseating foci in the testicle and dropsy of the scrotum are common, while mares may have similar formations in the mammary glands or ulcers of the vaginal or uterine mucosa.

Infiltrations of the joints and other synovial cavities are not uncommon and glanderous infiltration of the bones with caries is also found. In chronic cases, fragility of the bone is marked, and the blood contains an excess of leucocytes. These may be traced to disease of the bone marrow, as well as of the spleen and lymphatic system.

GLANDERS IN SWINE.

The healthy, vigorous pig is practically immune. Experimental inoculations have uniformly failed to produce the disease. Exception must be made when inoculation is made into the aqueous humor, in which there is comparatively little resistance by leucocytes. Sacharoff succeeded in giving the disease in a fatal form to a young pig in this way. To weak and debilitated pigs, on the other hand, the disease may be conveyed as shown by Spinola, and Cadeac and Malet. The symptoms were engorgement of the tissues in the seat of inoculation with the formation of glanderous nodules, which undergo molecular degeneration and ulceration; swelling of the lymph vessels extending from the infected point, and of the adjacent lymph glands; the formation of glander nodules in the lungs, liver and spleen, and of nodules and ulcers on the nasal mucosa.

GLANDERS IN SHEEP AND GOAT.

Casual glanders is uncommon in the small ruminants, yet it has been seen in goats that fed on the soiled provender left by glandered horses (Ercolani, Trasbot, Mesnard). Sheep have suffered after inoculation (Renault, Bonley, Gerlach, Bollinger, Croker, Peuch, Galtier) showing nodules and ulcerous swellings in the seat of inoculation, with extension in some cases to the nasal mucosa and lungs, and a fatal result. In other cases the lesions remain localized and the disease progresses to recovery.

GLANDERS OF RODENTS: RABBIT, GUINEA-PIG, MOUSE, RAT.

The Guinea-pig is especially susceptible, and like the rabbit and mouse may contract the disease by eating the soiled fodder of glandered horses. It is usually selected for inoculation for diagnostic purposes, because in the male, the insertion of the virus in the peritoneum determines a rapid swelling of the testicle and cord, with a glistening, violet engorgement and tension of the scrotum, suppurative adenitis and death in three to six days. In other situations the inoculated part swells rapidly and ulcerates, the adjacent lymph glands become swollen and tender, similar lesions form in other parts and notably in the nose which discharges profusely a whitish, sticky fluid, the breathing is hurried, and emaciation is marked. Death occurs in a few days and ulcers, and abscesses are found in the lungs and other internal organs, as well as in the nose. In less susceptible subjects or under smaller doses of the virus the local swelling and ulceration in the seat of inoculation are slight, but there persist engorgements of the adjacent lymph glands, swelling (cording) of the lymph vessels adjacent, and nodules and abscesses, (cutaneous, subcutaneous, intermuscular, intravisceral), arthritis, emaciation, dyspnœa and death in two to four months. In some cases with a very small dose of the poison, there is no local swelling, and no generalization nor subsequent manifestation of the disease.

In the rabbit the lesions are less certain and often less marked. There is sometimes no swelling in the seat of inoculation, in the neighboring lymph glands, nor elsewhere, and the rodent might have been supposed to have escaped, only that successful inoculation of the ass may be made from the tissues inoculated (Galtier). In such a case a certain immunity of the rabbit must be inferred. In less resistant rabbits, or with a larger dose, an ulcerous swelling forms in the seat of inoculation, the adjacent lymph glands become engorged or even purulent, corded lymphatics intervene, and nodules and caseous degenerations appear in the lungs, nose, spleen, liver, and other organs.

The hedgehog, ground squirrel, the field mouse, house mouse, mole have been successfully inoculated.

The frog immersed in water at 30° C., forms a good culture ground for the bacillus which may be found in its blood, in pure cultures, from the second to the fifty-fifth day. These cause no local lesion, nor obvious, constitutional disorder. It seems possible that, in summer, the infection may be propagated by frogs in the drinking water.

GLANDERS IN CARNIVORA.

All carnivora are liable to contract glanders by eating the flesh of glandered horses, asses and mules, and this has been noted especially in menageries. Lions, tigers, bears and wolves, have shown the ulcerous lesions in the nose, and the nodules in the lungs, spleen, liver, kidneys and elsewhere. The carcass of the diseased horse is, however, often devoured without evil result, and even when the carnivora become affected the disease is not always fatal.

In the dog, experimental glanders has been closely studied by many observers. Casual glanders has been contracted by living with the glandered horse; by licking his nasal or other discharges, and by eating his flesh. The disease has also been conveyed from dog to dog by licking each other. In many cases even inoculated glanders produces only a local ulcerous inflammatory lesion with or without hard swelling of the adjacent lymphatics, and engorgement of the lymph glands. After a rather tardy granulation and cicatrisation, the symptoms subside and the animal is restored to health. Yet such benignity does not depend on any lessened virulence of the bacillus, for an inoculation of the discharges on the ass produces acute and fatal glanders.

GLANDERS IN MAN.

Recognized by Lorin 1812. Causes: infection from soliped, man less susceptible; infection from man, clothing, stable bucket, inhalation, etc.; industrial disease; native immunity. Symptoms: incubation; mistaken for carbuncle, small pox, measles, erysipelas, anthrax; anamnesis; anthrax focus has darker center, no caseation, no corded lymphatics; nodules and ulcers in nose, swollen submaxillary glands and lymph vessels, general illness, diarrhœa, vomiting, dyspnœa, mental derangement, stupor, coma, internal deposits, bloody sputa, fœtid breath, hepatic pain, icterus, muscles, bones, bowels, typhoid, pyæmic, osteo-myelitic, or acute tuberculous symptoms. Death in 3 days to 4 weeks. Chronic cases, cutaneous, muscular, osseous, skin nodules in group or chain, glandular swellings. Diagnosis from pyæmia by lack of chills, and the sanious pus; from syphilis by futility of potassium iodide, and history; inoculate ox or white mouse; find bacillus. Lesions: as in horse, more early coagulation necrosis, ulceration, abscess; pus more viscid than in pyæmia, walls of abscess more irregular, lymphoid cell proliferation more abundant and extended (glands, spleen, liver, lung, nose, etc.), history; distinguished from variola, rötheln, and erysipelas by the many miliary or pea-like neoplasms with cellular caseating centres; lymphoid deposits in bone marrow, with friability.

Until the early part of the present century glanders in man was not traced to its origin in the soliped. Lorin in 1812 recorded a case in which the human hand had been accidentally inoculated from handling a horse suffering from farcy. Soon other cases were put on record by Waldinger and Weith, Muscroft, Schilling, Rust, Sedow, and a host of followers. Later Rayer, Tardieu, Virchow, Leisering, Gerlach and Koránye have thrown much light on the subject.

Etiology. Man is manifestly less susceptible than the soliped, considering the great number of exposures relatively to the victims. Yet the infection of man is altogether too common to be lightly passed over. The infection is almost always derived directly or indirectly from the horse, yet a number of cases have been derived from the human being through handling the dishes, towels or handkerchiefs of a patient, dressing his wounds, or performing a necropsy. Other cases like that of Dr. Hoffmann of Vienna, came from handling artificial cultures of the bacillus mallei.

Glanders is preëminently an industrial disease, attacking persons of the following occupations: hostlers 42, farmers and horse owners 19, horse butchers 13, coachmen and drivers 11, veterinarians and veterinary students 10, soldiers 5, surgeons 4, gardeners 3, horse dealers 2, policeman, shepherd, blacksmith, employe at a veterinary school, and washerwoman, 1 each.

The modes of transmission are essentially the same as in the animal. In the great majority of cases there has been the direct contact of the infecting discharges with a wound of the human victim. Handling the diseased horse with injured hands, giving him a bolus and scratching the hand on the teeth, examining the nose, sleeping under a blanket which has been used on a glandered horse, removing the dressings of such an animal or performing a post mortem examination on him are familiar examples. The particles scattered by the diseased animal in snorting, will infect the mucous membrane of the eye or nose, and all the more readily if these are already sore or abraded. Infection of man by ingestion has been discredited mainly because the carcasses of glandered horses have often been eaten with impunity; but this may be largely accounted for by cooking, the bacillus being destroyed by a temperature of 131° F. Carnivora such as dogs, cats, lions, polar bears and prairie dogs have been infected by feeding. Men also have been infected through drinking from the same bucket after a glandered horse. After making full allowance for the inimical action of the gastric juice, we must admit that this has often failed, and there is the added danger of abrasions of the lips, mouth and throat and of the entrance of the microbe into the tonsillar follicles and gland ducts. Still other cases are recorded of men sleeping in stables, but not handling horses, who contracted glanders, presumably, through the dust borne bacillus inhaled. The bacillus, is however, so readily destroyed by thorough desiccation that this mode of transmission is exceptional. Some men are immune to glanders, and suffer only when predisposed through a course of ill health, and yet a large proportion of the cases on record have been in strong hearty men.

Symptoms of Glanders in Man. In man as in the horse, glanders occurs in the acute and chronic forms. In the acute supervening on an external inoculation, incubation is from one to four days. When it enters through other channels it may seem to extend to a week or more.

When a skin abrasion has been inoculated it will show in a few days a soft inflammatory swelling or a firm nodule with a puffy reddish areola, and it may be mistaken for a carbuncle. In not a few cases the small nodule has been mistaken for small pox. In my experience a horsemen on a ranch on which over a hundred horses showed glanders, died of an ulcerous skin affection which was variously supposed to be a malignant small pox and measles, though neither malady was known to exist in the district. Other cases are confounded with gangrenous erysipelas. The absence of these other affections from the locality, and the fact that the patient was employed about glandered horses, should go far to correct such mistakes. The early supervention of ulceration is further diagnostic, and discovery of the bacillus mallei in the products will be conclusive. From anthrax it is easily distinguished by the absence of the dark centre of the sore in the early stages, and of the large sized bacillus anthracis. The caseation or liquefaction of the necrotic centre further distinguishes it from the characteristic anthrax slough, and the thickening and induration of the lymphatic walls are not present in anthrax. Sometimes the inoculated case proves mild and recovers in two or three weeks with healing of the ulcer, but in other cases there is an extension to adjacent tissue and a general infection with the supervention of nasal glanders.

There is a spread of the erysipelatoid inflammation and swelling, and the formation in such newly invaded tissue of nodules and ulcers in successive crops. In acute cases too, the nasal mucosa becomes involved with the formation of the nodules and ulcers that are so pathognomonic in the horse. The discharge is then somewhat sticky and often tinged with blood. In acute cases according to Senn, the nose may be completely destroyed and deep facial ulcers may be formed in a week. The submaxillary glands are enlarged and painful and the facial lymphatic vessels leading from these to the nose may be red, thickened and tender. Suppuration and ulceration of the glands may ensue. Headache, prostration, nausea, inappetence and vomiting with diarrhœa usually supervene. Then follow dyspnœa, wakefulness, troubled dreams, anxiety, nocturnal delirium, stupor and coma. The pulse may rise to 120 and the temperature to 104° F.