Part 140

The following table gives the number of cases occurring in the equine family in two of the principal countries of Europe in the last few years: {911}

Cases of Glanders in-- Great Britain. Germany. 1878 888 2753 1879 1367 1880 2048 1941 1881 1710 1774 1882 1389 1838

As both countries systematically suppress this disease through their veterinary sanitary officials, it cannot be doubted that the figures for America, if obtainable, would be relatively higher.

Glanders prevails especially in horses, asses, mules, and other solipedes, and is communicated by inoculation to all domestic animals except the genus Bovis. In the sheep and goat the receptivity is considerable, and the disease may prove fatal in fifteen days (Gerlach) or it may be delayed for seven weeks (Bollinger). The Carnivora (dogs, cats, lions, polar bears) contract the affection by eating diseased flesh, as do some rodents (prairie-dogs, rabbits, guinea-pigs, mice), and, by administration, solipedes. Swine contract the disease by inoculation (Gerlach, Spinola), though in these and in the dog the constitutional symptoms are usually slight and recovery may follow the local affection.

The susceptibility of man is doubtless less than that of the solipedes, judging from the few cases of glanders compared with the frequent exposures, yet when once established in the system it can hardly be said to be less malignant or fatal.

ETIOLOGY.--The one known cause of glanders is contagion, and the recent experiments of Capitan and Charrin in France and of Schütz and Löfler in Germany, demonstrating that the bacillus of the glanderous deposits is the one essential cause of the disease, effectually dispose of any claim of its spontaneous origin. Glanders can no longer be considered spontaneous, further than that its germ is now proved capable, like that of anthrax, of survival and multiplication out of the animal economy, so that infection may come from other objects than a sick animal; and it may even yet appear that the bacillus, living at times as a harmless saprophyte out of the animal body, may acquire deadly properties under certain conditions of the environment. At the same time, the most extensive acquaintance with glanders and the broadest generalizations from known facts do not warrant the assumption of the extension of the disease by the growth of the bacillus out of the living body, unless it be on the rarest possible occasions, while the soundness of extensive countries (Australia, New Zealand) for a century or more speaks strongly against any frequent development from a harmless saprophyte.

To the same effect speak the experiences of the English army. At the beginning of the century, under the teaching of Coleman, most cases were attributed to lack of stable care, and extensive experiments were made in the treatment of the disease, with the result of a very high mortality from this cause. Now, when contagion is looked on as the main or sole cause, and all suspected horses in the army are promptly destroyed, the disease is only seen in recently-purchased animals or after the inevitable exposures of a campaign. In the French army the doctrine of the {912} non-contagiousness of chronic glanders led to a greater prevalence of this disease than in any other country of Europe. Prior to 1836 it was about 90 per 1000 per annum, whereas now, under the doctrine of contagion and a corresponding practice, glanders kills but 2 per 1000 per annum (Rossignol).

But while the essential cause of glanders is the specific bacillus, an individual susceptibility is no less requisite to an attack. This may be innate or acquired. As we have seen, it varies according to the genus, being greatest in the solipede. But many solipedes show a strong power of resistance. Of 138 horses similarly exposed by cohabitation with glandered horses, but 29 (21 per cent.) suffered. Of 28 inoculated with glanders virus, but 9 (32 per cent.) succumbed (Lamirault, Bagge, Tscherning). The accessory causes which predispose the system to the reception of glanders may be included under one general term--low condition and ill health. Three of these causes, however, deserve especial mention: 1st. Impure and rebreathed air. Prior to 1836 the yearly losses per 1000 of the French army horses were from 180 to 197. At the date named the ventilation of the stables was greatly improved, and the mortality fell to 68 per 1000 per annum, one-half from glanders. Later improvements have reduced the 34 cases to 2. During the Italian War, in 1859, 10,000 of these horses were kept for nine months in open sheds, with but one case of glanders. In the expedition to Quibéron during the Napoleonic wars, a cavalry contingent, believed to be healthy, shipped on new transports, encountered a storm, and had the hatches fastened down, so that several horses were suffocated. Among the survivors, landed at Southampton and placed in stables hitherto unchallenged, many soon developed glanders in its worst form. Similar results followed the English expeditions to Varna in 1854, and that to Abyssinia in 1867. In badly-ventilated mines and stables, especially cellar stables, glanders, once started, is always most virulent.

2d. Cold, damp, draughty stables greatly favor the progress of glanders. Leblanc reports the case of a stud of 240 horses that had had no glanders for eight years, but which lost half their number in three months after removal into a new stable, very lofty, but dark and damp, and subject to cold draughts. It is worthy of notice that they had also been subjected to double work, and were consequently emaciated, but there was not known to be any unusual exposure to contagion. In a Boston street-car stable, where glanders had long prevailed, Thayer cut it short by destroying the infected animals and by improving the ventilation by windows hung at the bottom and opening inward, so that the air entered in an upward direction, and cold draughts on the horses were avoided.

3d. Debility from ill-health, low feeding, or overwork.--The nervous and nutritive debility consequent on chronic disease, overwork, and exhaustion lessens the power of resistance to specific poisons, but in such circumstances there is always the added predisposition of an excess of waste material in the blood, a specially abundant food for the disease-germ. So notorious is this that it used to be held that the specific poison of glanders was generated in connection with the excess of creatine, creatinine, and lactic acid resulting from muscular action. Of the effect of {913} low diet we have a striking example, furnished by Bouley, of a stud of 120 horses, 60 of which were attacked within a year after they had been placed on a food insufficient to repair the body-waste, and from which the disease disappeared after the slaughter of the infected and improvement of the ration. So long as glandered horses were preserved for work, the then nearly ubiquitous germ attacked nearly all that were run down by chronic diseases; hence glanders was looked upon as the natural winding up of exhausting diseases in the horse, as tuberculosis was thought to be in the human subject. Modern discovery shows that without the germ all such debilitating causes are impotent, but it can never disprove the great potency of these in laying the system open to attack, nor the value of vigorous health and sound hygiene in fortifying the system against it.

The channel of infection manifestly varies in different cases. In direct inoculations the morbid process develops first at the point of insertion, and secondly in the nearest lymphatic glands and internal organs. When contracted in the ordinary way, the lesions are usually first seen in the posterior nasal passages, the larynx or the lungs, or in the superficial lymphatics, especially of the hind limbs. This susceptibility of the deeper portions of the air-passages seems to imply that the bacillus, borne on the air, is lodged on different parts of the respiratory mucous membrane, and first sets up the morbid process in the thinnest or most susceptible portion. That it can be thus borne on the air is shown by the experiments of Viborg and Gerlach, who separately collected the particulate elements from the exhalations of glandered horses and successfully inoculated them. That the virus is not usually carried far on the air in a virulent form is attested by the many instances in which horses have stood for months in the same stable with a glandered animal without becoming infected. That infection may also take place through the ingestion of infected matters is undoubted, as glanderous products mixed with food, or even made into balls and enclosed in paper and administered to horses in this form, have produced the disease. The virulence is said to be lost by passing through the digestive canal of man (Decroix), dog, pig, and fowl (Renault), but even to Carnivora the infection may be conveyed in the food.

While the virus is concentrated in the material of the special glanderous deposits and the discharges from these, yet no part of the body can be considered as free from the poison. Viborg, Coleman, Hering, and Chauveau have communicated the disease by transfusion of blood from a glandered horse to a healthy one; hence every vascular organ must be liable to infect. The secretions of the diseased body (tears, saliva, mucus, sweat, urine, and milk) have each been successfully inoculated, and the conveyance of the disease to the foetus in utero and to the female by coition imply that even the generative secretions are virulent. Failures to convey the disease by inoculation with the blood and secretions have often occurred, however, and they must be held as less virulent than the products of the local disease-processes.

The claims that inoculation with pus, ichor, and other irritants have produced glanders must be entirely discredited. The deposits and ulcers in the lungs and elsewhere resulting from such inoculations have been either septicæmia, mistaken for glanders in the earlier days of pathological anatomy; or the septic and other inflammations set up by these {914} inoculations have merely served as fertile spots for the planting and growth of the glanders bacillus accidentally present, and which to a healthy system might have proved harmless.

In 1882, Chauveau had demonstrated the particulate nature of the glander germ by his unsuccessful inoculations with the liquids filtered from dilutions of pus taken from a pulmonary glanderous ulcer. The filtrate and the liquid mixture formed by mixing the pus with five hundred times its own weight of water retained their virulence undiminished. In 1868, Christol and Kiener discovered in glanderous products a bacillus which they figured as made up of a chain of nearly globular elements apparently enclosed in a common sheath. In 1881-82, Bouchard, Capitan, and Charrin cultivated these microphytes in a neutralized extract of meat through five successive cultures, using in each case a milligramme of the previous culture, or less than 1/1000 part of the culture-liquid. Counting that the milligramme of pus would give to each centigramme of the first culture-liquid 1,000,000,000 bacilli, it follows that the second culture would, on the principle of dilution, contain 1,000,000, the third 1000, the fourth 1, while for the fifth it was as 999 to 1 that it would receive nothing unless the germ were multiplied in the culture-liquid. Inoculation of a cat with this fifth culture, started originally from a nasal ulcer of a glandered horse, led to a fatal result in twenty-five days, with suppurating tumor of the left testicle and inguinal glands. The products of the first cat were inoculated on a second, those of the last on a third, those of the third on a guinea-pig, and those of the guinea-pig on an ass, producing in every case specific lesions of glanders, including miliary nodules and abscesses, and death respectively on the following days: 16, 7, 31, and 10.

In September, 1882, and the two succeeding months, a similar course of experiments was conducted by Schütz and Löfler at Berlin. The virulent matter used for starting the culture was procured from a pulmonary deposit and spleen of a glandered horse; the cultivation was continued through eight successive culture-fluids. One horse was successfully inoculated with the product of the eighth culture, and a second with both the fifth and eighth. The first died on the fifty-eighth day, and the second, now very weak, was sacrificed on the fifty-ninth. Both showed the most extensive lesions of glanders alike in the skin, the lymphatic glands, the pituitary and laryngeal mucous membrane, and the lungs. To demonstrate the bacillus they take a thin layer of the infecting liquid on a cover glass, dry it, stain with methyl violet, wash with dilute acetic acid, dehydrated by absolute alcohol, and clear by oil of cedar. Like other pathogenic microphytes this may be preserved for months or years if thoroughly dried, but in the moist condition it is easily destroyed by heat (133° F.; Viborg, Hofacker, Renault), chlorine, and the disinfectant chlorides and sulphites.

SYMPTOMS.--Acute nasal glanders in horses has a period of incubation lasting from three to five days in inoculated cases. Where in infected subjects the incubation appears to have extended over months or a year, there have usually (or always) been deposits in internal organs which passed without recognition until the lesions appeared in the nose. At the outset there is fever, which appears before any local lesions are recognizable, even post-mortem (Chauveau), and soon with languor, {915} and loss of appetite, there is a serous nasal discharge, often from one side only. By the sixth day this has become yellowish, the margin of the nostril is often swollen, and upon the pituitary membrane may be detected elevations of various sizes of a general yellowish tinge, dotted with minute red points and surrounded by a bright-red or purple and slightly elevated areola. These may be simple, pea-like nodules or more or less extensive patches, which in certain cases extend over nearly the whole pituitary membrane. At the same time the submaxillary lymphatic glands on the same side become the seat of a hard nodular painless enlargement, feeling like a conglomerate mass of peas, and often showing a tendency to become more closely adherent to some adjacent part (bone, skin, base of tongue); but they only ulcerate exceptionally. Extensive hot, painful engorgements also often appear on other parts of the body, and if on the limbs or joints cause lameness. Soon the swellings on the mucosa become eroded and are gradually destroyed, forming large unhealthy, chancrous-looking ulcers, tending to become confluent and to eat deeply through the mucosa into the subjacent tissues. These are mostly reddish gray or yellowish gray, with raised ragged red or yellowish-red margins. They bleed readily, and may be black from hemorrhage, or greenish or of some other shade from decomposition. The discharge is always somewhat glutinous and sticky, but it may vary in color from simple white to yellowish, greenish, brownish, or red, according to the destruction of tissue, the septic changes, or the effusion of blood.

By the sixth to the fifteenth day the acme has been reached. The alæ of the nostrils are glued together by the drying discharge, and this, with the general swelling of the nasal passages, renders the breathing snuffling and difficult. The lymphatics on the side of the face are usually inflamed and corded, and the same is true of the cutaneous lymphatics of the hind limbs of some other part of the body (farcy). Death usually ensues from suffocation, preceded by the most painful dyspnoea.

Chronic glanders in horses often sets in insidiously, but frequently also it first shows itself by constitutional disturbance, which gradually subsides as the local lesions are formed. Among frequent premonitory symptoms may be mentioned intermittent or continued lameness, oedema of one or more limbs, infiltration of the testicle, cough, and bleeding from the nose. The general health may appear good, and if in good hygienic condition the digestion and nutrition may be sufficient, the body plump, and the skin shining; but there is usually some dulness of the eye, dryness of the coat, lack of endurance, and a tendency to sweat easily and to run down rapidly under hard work or debilitating conditions. The discharge, at first clear, becomes turbid, grayish, sticky, and purulent, tending to agglutinate the hairs and edges of the alæ nasi, and is expelled by snorting in masses. The nasal mucosa, and especially over the septum, is the seat of the peculiar elevations, ulcers, and firm white, condensed deposits resembling cicatrices, usually low enough down to be seen or felt. The submaxillary lymphatic glands are the seat of the nodular enlargement described in acute glanders, and, as in that affection, there may be pulmonary or skin deposits shown by cough or oedema, with swelling and cording of the cutaneous lymphatics with nodules and ulcers.

These cases often maintain this indolent type for years, spreading the {916} infection widely, but they tend sooner or later to develop the acute type, especially under some debilitating conditions.

When the mucous membrane of the larynx and bronchi is first attacked the nasal lesions may be delayed for a time, but the cough, the variously colored tenacious expectoration, the excessive tenderness of the larynx, and the nodular enlargement of the adjacent lymphatic glands, with the general ill-condition, suggest that which is later confirmed by the specific lesions in nose and skin.

When the affection is confined to the bronchia and pulmonary parenchyma, there are the usual signs of bronchitis, disturbed breathing, with hard, soft, mucous, or dry husky cough, and blowing, mucous or sibilant râle, at points crepitation, and at others some diminution of murmur and resonance. The breath is mawkish or fetid, and expectoration more or less sticky and charged with bacilli; but all these symptoms are at times equivocal, and inoculation alone can attest the true nature of the disease. This should be practised by preference on a donkey or an old horse in poor condition but with general good health. Then the disease shows itself in the acute form in six days. If solipedes are not available, rabbits or guinea-pigs may be used for inoculation.

In acute cutaneous glanders or farcy, premonitory symptoms resemble those of ordinary acute glanders, which indeed is usually present as well, and always supervenes before farcy terminates in death. The local lesions consist in inflammation of the lymphatic vessels, which become like firm cords, the appearance at intervals along these cords of rounded glanderous nodules varying in size from a pea to a hickory-nut, and with a marked tendency to ulceration and the formation of hot, painful oedematous swellings. The swelling of the lymphatics appears by preference in the lower part of a hind limb, and the first nodules may be near the fetlock or tarsus. The ulcers forming about the sixth day have a yellowish-white appearance with red points and raised irregular borders, and the discharge is grumous and viscous, with a yellowish or reddish tinge. The disease extends toward the body, the upper air-passages become involved, and death speedily follows.

Chronic cutaneous glanders, chronic farcy, usually begins by a local swelling, mostly of the fetlock, in the midst of which a careful examination detects a small glanderous nodule. This tardily softens, ulcerates, and discharges the characteristic ichor, the lymphatics leading up from it become thick and rigid (corded), and new nodules appear. Though very indolent, these finally tend to ulcerate, and in time oedematous swellings appear in the vicinity or at distant parts of the body, with nodules at intervals. This will go on for months, or even for years, and recoveries occasionally take place, while in other cases, and especially when the conditions of life are bad, acute glanders supervene.

MORBID ANATOMY.--The lesions consist essentially in a cellular growth in the connective tissue, determined by the presence of the specific poison, and in destructive changes in the elements of such growth--softening, fatty degeneration, ulceration, and discharge. In certain cases of nasal glanders at the earliest stage there is merely an increased proliferation of the mucous corpuscles, which become more granular or purulent. Soon, however, the fibro-vascular layer is involved, the affected part being the seat of dark bluish congestion, and {917} of the proliferation of small rounded lymphoid cells, comparable to those of the early stage of tubercle, and enclosed in more or less dense fibrous areolæ. The common nasal nodule or patch has a soft velvety surface, dirty gray or grayish yellow, and the lymphoid cells are so circumscribed in nests that when soaked in water the cells are washed out and the fibrous reticulum is left hollowed out like a honeycomb. In this fibrous reticulum are many spindle-shaped and a few rounded cells. Its vascularity is easily demonstrated by injection. The centre of each nest is the palest part of the mass, and unless stained by extravasation it contrasts with the reddish areola. These islets of lymphoid cells, at first isolated and each the size of a pin's head, may enlarge and become confluent, forming the larger nodules. With this increase the centre of each becomes turbid, and the cells are found to have become granular and fatty, and to have in part broken up into a granular débris. This characterizes the period of ulceration, and erosions and ulcers follow in ratio with the extent of the neoplasm and the rapidity of its growth. If the growth is tardy, the ulcer, with irregular eroded and everted edges, may remain for some time stationary or even recede, while if rapid, new tubercles form around the margin of the first, and by the disintegration of their elements the ulcer is continuously extended. The lesions are especially common on the septum nasi and turbinated bones. Similar lesions may be found in the nasal sinuses or larynx.

The nodules found in the lungs strongly resemble miliary tubercles, but are usually less numerous. As in the nose, they have a punctiform, central, grayish, turbid portion, encircled by a more translucent ring, surrounded in its turn by a vascular area. They are also composed of the same granular rounded cells, though they may, especially in the chronic forms, have undergone caseous, fibrous, or calcareous degeneration. The acute tubercles are often surrounded by circumscribed pneumonia with considerable exudation. They are distinguished from genuine tubercle by their vascularity and by the absence of giant-cells.

The cutaneous deposits are composed of the same histological products imbedded in the dermis or in the subcutaneous connective tissue, and extending in some cases deeply between the muscles, with no clear line of demarcation from the sound tissue. Not only the chains of nodules (farcy-buds), but the connecting lymphatic trunks, are the seat of the characteristic cellular product, and in chronic cases there is the enlargement of the adjacent lymphatic glands as well. In these there is a special tendency to early disintegration and ulceration.

In the diffuse glanderous swellings (infiltrated glanders, inflammatory glanders) the affected tissues are the seat of an inflammatory process with profuse exudation throughout, while in the interstices of the connective tissue are numerous granular glander-cells. The same tendency to necrobiosis is shown as in the other forms of glanderous neoplasms, and such diffuse swellings become the seats of very extensive, deep, and irregular ulcers, or frequently of fibroid growth and induration, forming the so-called cicatricial deposits. These are hard, firm, and resistant, and histologically consist of a dense fibrous stroma interspersed with the spindle-shaped cells. They are especially common in chronic cases, and such an appearance on the nasal mucous membrane is always suspicious, as this dense fibroid appearance rarely follows a simple traumatic lesion.

{918} Diffuse glanderous infiltrations in the nose may implicate the entire mucosa of one or both nasal chambers, and the ulcers are liable to be greater than from the nodular form of the disease. They are also especially associated with thrombosis of the veins, which occurs to a less extent in the nodular form and conduces to the dark-blue tint of the mucosa.