Synonyms. Definition: Acute, infectious, microbian disease, often localized in lymph glands and plexuses of nose and air passages, etc.; with hyperplasia, degeneration, necrosis, liquefaction. Affects solipeds, and, by inoculation, man and all domestic animals save cattle, chickens and (usually) swine. Geographical distribution and historic notes: known in Ancient Greece; now where solipeds live and fresh subjects are exposed; Central Europe; great horse trade and movement; war, Franco-German, Napoleonic, Afghanistan, American Civil War, Boer War. Unknown in Australia. Susceptibility: solipeds, Guinea-pig, rabbit, goat, cat, dog, pigeon, sheep, and swine in low condition. Cattle, chickens, white and house mice, linnets, chaffinches, and frog immune. Microbe lives in frog in water at 86° F. Cause: Bacillus mallei. Accessory causes: trade in solipeds, mingling of sound and sick, crowding, common feeding and drinking troughs or buckets and racks, debility, low condition, starvation, overwork, damp, dark, draughty stables, carriage in transports or cars. Insular quarantined lands—Australia, Tasmania, and New Zealand exempt. Bacteriology: Bacillus Mallei; 2 to 5μ by 0.5 to 1.4μ, nonmotile, ærobic grows in ordinary culture media, stains tardily but is easily bleached. Spores uncertain, easily killed by disinfectants, preserved in stables, does not grow in infusion of hay, straw or horse manure, lives 15 to 20 days in water; infection by coitus, and through placenta, by ingestion, by blood transfusion, through dust; microbe in all lesions and discharges, (unless sometimes in milk, sperm, etc.). Infection-atria: skin wound, mucosa, hair follicles, lungs. Forms: Acute, chronic, nasal, pulmonary, cutaneous (farcy), orchitic, arthritic, abdominal, occult. Symptoms: nasal; incubation, 3 to 5 days, languor, weariness, stiffness, horripilation, tremors, inappetence, thirst, hyperthermia, epiphora, snuffling, nasal discharge, serous, viscid, agglutinating, purulent, swollen alæ, violet mucosa, elevated spots and patches with central ulceration, may become confluent, and involve submucous tissues; submaxillary lymph glands swollen, nodular, not tender, non-suppurating, swollen (corded) facial lymphatics, from nose, eye or lymph glands; swellings, cutaneous and lymphatic in skin of limb or body, ulcers (farcy buds), deposits in throat or lungs; chronic cases; slow, indolent, persistent, nasal discharge—unilateral (or bilateral), viscid or not, nodules on mucosa with whitish centres or points; red areolæ, later ulceration, puckered white cicatricial lesions, submaxillary swelling, nodular, large or small, insensible; cutaneous cases; arthritis with lymphangitis, skin engorgement, corded lymphatics with ulcerating nodules, sanious discharge, intermuscular abscesses. Occult cases: lesions in internal organ;—cough, leucorrhœa, enlarged testicle, low condition, weakness, lack of endurance. Diagnosis: inoculation of male Guinea-pig in flank or peritoneum,—ulcer and orchitis, cat, dog, old soliped; mallein test,—swelling, involving lymphatics, fever, 1.5° to 2.5 F. and upward above normal, at 10th to 18th hour, lasting two days. Lesions: cell proliferation in nests in fibrous stroma, pea upward, central degeneration, fatty debris, ulcer or abscess, hyperplasia of lymph vessels, on nasal mucosa like sand-grains, peas, patches, centre grayish or yellowish, blood extravasation, necrotic degeneration, ulcer with ragged edges; fibroid degeneration—cicatricial lesion; lesions in guttural pouch or tube, larynx, trachea, bronchia; lungs—peribronchial, lobular or interlobular inflammation, cell proliferation in foci, degeneration—nodules—and caseation; skin,—cell proliferation, degeneration, rupture, fibroid hyperplasia of lymphatics, exudates in connective tissue; dependent lymph glands congested, hypertrophied, cell proliferation, caseation; lesions in pharynx, spleen, kidney, heart, brain, testicle, scrotum, mammæ, vagina, uterus, joints, bones; bone fragility. Glanders in swine, sheep, goat, rodent, dog, cat.
Synonyms. Malleus, Equinia, Farcy.
Definition. An acute infectious disease caused by the bacillus mallei, which tends to localize itself in the lymphatic glands and plexuses, especially of the nose and upper air passages but also in other parts of the body, where it produces a progressive hyperplasia, with a strong tendency to degeneration, necrosis, and liquefaction. It occurs casually in horses, asses, mules and other solipeds, and is communicable to man and all domestic animals except the bovine races, chickens, and, under ordinary circumstances, swine.
Geographical Distribution. Glanders (Malis) appears to have prevailed in asses in Greece as noted by Aristotle. Its contagious prevalence in horses is recorded by Absyrtus in the time of Constantine, and again by Vegetius Renatus in 381 A.D. At the present time its existence is almost coextensive with the equine family, but its prevalence is in a direct ratio with the facilities for the infection of fresh subjects. In the central countries of Europe where the equine population is greatest and where there is the most extensive trade and movement among horses it secures the greatest relative number of victims. War with its constant opportunities for infection, in crowded cavalry and artillery stables and the successive changing of place, tends greatly to enhance its ravages. Thus in the German army it rose from 966 to 2058 per 100,000 per annum in the year of the Franco-German war; in Spain it was practically unknown until the Napoleonic war in the Peninsula, but after this it proved a veritable scourge; in Hindostan it was hardly known until the Sepoy rebellion yet its ravages greatly hampered the army movement in Afghanistan in 1879; and in the United States it became very prevalent in the armies during the Civil War of 1861–4, and was widely scattered over the whole country on the sale of the army horses and mules. Since that time, as before, it has been most prevalent in the car stables of the great cities, though it has also gained a wide extension in many great horsebreeding establishments in the Rocky Mountain region, where however it proves much less destructive than in the East.
It is unknown in Australia, whence it is excluded by a rigid system of quarantine.
Susceptibility of Different Animals. Horses, asses and mules are the most susceptible, and it is only exceptionally that the disease is contracted casually outside the class of solipeds. The Guinea pig and rabbit are susceptible to glanders in the order named and the former is especially available for experimental diagnostic inoculations. The goat, cat and dog sometimes contract the disease from living in stables with glandered horses, but infection is much more certain when they are inoculated. The pigeon is also susceptible. In the dog the disease is rarely fatal, but the ulcerations tend to heal in 14 days and recovery ensues. In sheep and goats too, many cases recover though in other cases an internal infection takes place followed by death. Swine are comparatively insusceptible, but they may be successfully inoculated when in ill health and low condition. (Spinola, Cadeac and Malet). Cattle and chickens have uniformly proved refractory even on inoculation. White and house mice and rats, have proved immune, also linnets and chaffinches and the frog at ordinary temperature. If however the frog is placed in water at 30° C., he may be successfully inoculated and, though it does not prove fatal, the bacillus may be found in the blood and tissues after a lapse of 50 days.
Etiology. As already stated this disease is due to the presence of a microörganism, the bacillus mallei. Many secondary causes, however, contribute to its propagation. The activity of movement and commingling of horses has been already noticed. Crowding in close yards where the animals bite each other, snort out the virulent discharges on each other and eat and drink from the same troughs, leads to a rapid extension. Even on the western ranges where the disease tends to be mild, Billings observed a deadly extension when yarded during winter storms. Debility from chronic ill health, starvation, overwork and damp, dark, draughty stables, is so conducive to the disease that it was at one time considered as the sole cause. Close confinement in impure air is at once a cause of increased susceptibility and a means of concentration and transmission of the poison. Hence confinement, between decks, of military and other horses, carried by sea, is a source of wide extensions. On the other hand insular places from which strange horses are excluded or into which they are admitted under careful inspection and quarantine have succeeded in preserving immunity. Australia, Tasmania and New Zealand are examples.
Bacillus Mallei. Christot and Kiener claimed to have found a bacillus in the lesions of glanders in 1868. In 1881 bacilli were found by Bouchard in a glander abscess in man, and these were cultivated in vitro and inoculated in a number of animals, by Capitan and Charrin in 1882. Independently in the same year (1882) Löffler and Schütz discovered the bacillus, cultivated it in vitro, and successfully inoculated it on animals. The microbe is rod-shaped, 2 to 5μ long, by 0.5 to 1.4μ thick, the same length as the bacillus tuberculosis but thicker. It is nonmotile, ærobic (facultative anærobic) and grows readily in a variety of culture media at a temperature of 37° C. On neutral bouillon of the flesh of horse, ox, calf or chicken with or without peptone, it grows readily, producing cloudiness in one or two days. In peptonized gelatine it forms a whitish flocculent mass. On glycerine agar with milk it forms in 48 hours a milk white layer, changing to yellowish brown. On potato it forms long slender filaments, in yellow, viscous, glistening colonies, changing to fawn and darker. It grows best at 35° to 39° C. and growth ceases below 25° C., and above 42° C. It stains tardily in aniline colors, and not at all by Gram’s or Weigert’s, but will readily take Kuhne’s stain prepared as follows: take of phenic acid in solution (5:100) 50cc., absolute alcohol 10cc., and 1 to 2 grammes methylin blue. The stain is very easily bleached by acid, differing in this from the bacillus tuberculosis. For decolorizing Löffler recommends 10cc. distilled water, 2 drops of strong sulphuric acid, and 1 drop of a 5 per cent. solution of oxalic acid. Sections should be left in this not longer than 5 seconds. The bacillus often appears granular, and unequally stained in its different parts. It may be difficult of discovery in old standing lesions of horses, but comes out clearly in recent lesions of experimental cases in Guinea pigs and donkeys.
Baumgarten claims sporulation but this is uncertain.
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.
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.
Symptoms of Chronic Nasal Glanders in Solipeds. The chronic form of the disease follows an indolent course, and local symptoms are often so slight or equivocal that the true nature of the malady is unsuspected. If the patient is well fed and cared for and not overworked, the malady may run a course of three, five or seven years, and the victim may pass through many hands leaving infection in every stable it occupies. Diagnostic symptoms, more or less clear, may be obtained from the discharge; the lesions of the mucosa and the submaxillary glands.
The nasal discharge may be bilateral, but if confined to one nostril is strongly suggestive of glanders. It may be profuse or scanty, continuous or intermittent, of a yellowish, purulent tint, or greenish, or grayish and with a special tendency to viscidity. In some indolent cases the nostrils may be clean but if there is any matting of the long hairs, or adhesion of the alæ nasi, the case is specially suspicious. If it is sanious, flocculent, or bloody it is all the more characteristic, and suggests the supervention of an acute attack.
The lesions of the pituitary membrane are varied. Hyperæmia of a purple or violet color is common, especially along the septum, and the mucosa is liable to be somewhat tumid or œdematous. Nodules the size of a pin’s head, a pea or larger appear inside the inner ala, or on the septum or turbinated bones, and at first red from extravasation and, as it were vesicular, become grayish, whitish or yellow with points of red and surrounded by a deeply congested areola. Larger nodules forming in the submucosa approach the surface and stand out the size of the tip of the finger and with the same general character as the smaller. Sooner or later these degenerate and form ulcers which bear a resemblance to those of acute glanders but are less angry, and when small and solitary may be taken for simple erosions. In other cases they become thickened and indurated with sharply defined projecting margins, and a yellowish base with points or lines of red. The presence of red, black, green, or brown crusts may also be noted.
Another lesion frequently observed in indolent cases is a cicatricial white spot or patch in which the hyperplasia has become partially developed into tissue and shows no tendency to ulcerate. The mucosa may even be drawn or puckered around the cicatrix, making the illusion all the more complete.
The submaxillary swelling is even less sensitive than in acute glanders and produces the same sensation as of an aggregation of small, hard, pea-like, masses with no tendency to ulcerate.
Symptoms of Cutaneous Glanders (Farcy) in Solipeds. Acute cutaneous glanders has been already referred to under nasal glanders. The chronic type is often less characteristic, yet may be detected by careful observation of the symptoms. The main symptom may be the swelling of a joint with more or less engorgement of the limb from attendant lymphangitis. There can usually be detected around the margins of such swellings firm, tender cords representing the larger lymphatic vessels and often branching in their course. In the absence of the engorgement, or when it is slight, these cords may be the main evidence of the disorder, and in the hind limb usually follow the course of the flexor tendons on the inner side of the digit, metacarpus and thigh. At intervals along the line of the cords appear nodular masses (farcy buds) varying in size from a pea to a hen’s egg, and showing a great disposition to soften and discharge a glairy, sanious or more or less bloody liquid. The inner sides of the fetlock and tarsus are favorite seats of these nodules but they may form at any point. On the trunk also the corded lymphatics and nodules follow the lines of the veins and lymphatics, and here there may be the complication of large intermuscular abscesses often in connection with the groups of lymphatic glands.
Latent or occult glanders is often met with, the indolent, specific lesions being confined to some internal organs, like the larynx, lungs or womb, or to the testicles, the nasal diagnostic symptoms being absent. A chronic cough, with a slight purulent discharge from the nose, a chronic leucorrhœa, a swollen testicle, or simply a persistent low condition or weakness without apparent cause, may be the only indications, and special means of diagnosis are demanded.
Special Means of Diagnosis. In occult cases, the disease may be identified by inoculation, or by the mallein test.
Inoculation is best performed on a very susceptible animal. If the suspected discharge from the nose, vagina, open sore or preferably from a freshly incised nodule is inoculated subcutem in the flank of a male Guinea pig, or better in the peritoneum, there develops a local ulcerous sore and on the second or third day a violent orchitis in which pure cultures of the bacillus can be obtained. The caseous and purulent centres are found not only in the testicle but along the line of the spermatic cord, affecting the tunica vaginalis and connective tissue. Death usually follows in four to fifteen days. The cat and dog can also be utilized, inoculation being made on the forehead. Old wornout, but otherwise healthy asses, and even horses make very available subjects, inoculation in the nose speedily developing acute glanders. In the absence of a good subject the suspected animal is sometimes availed of, scarifications being made in the nose and the morbid product rubbed in freely. The rapid development of ulcerous wounds is characteristic. If, however, the case is chronic, and if a fair measure of immunity has been acquired this test may prove misleading.
Test by Mallein. Mallein is the sterilized and concentrated toxic product obtained from a pure culture of bacillus mallei in a peptonized glycerine bouillon. When injected hypodermically in a small physiological dose this has no effect on a sound horse, but in one affected with glanders it develops in several hours an extended swelling in the seat of inoculation, hot, tense and painful, which continues to enlarge for 24 to 36 hours and does not subside for 4 or 5 days. From the margin of the swelling, swollen lymphatics may often be traced running toward the adjacent lymphatic glands. There is also decided dulness, prostration, inappetence, staring coat and tremors. The body temperature rises 1.5° to 2.5° and upward from the eighth hour after inoculation attaining its maximum from the tenth to the eighteenth hour and subsiding slowly to the forty-eighth to the sixtieth.
Mallein must be used under precautions like tuberculin. It must be obtained freshly prepared from a reputable maker. If preserved for months its force may be largely lost. The animal to be tested should be in his customary environment, and not just arrived from a railroad journey nor other cause of excitement. He must not be fevered as any rise of temperature is then equivocal, and a fall of temperature, which sometimes occurs in the febrile system under mallein, is no sure evidence of glanders. Reaction sometimes fails in advanced cases of glanders, but in such a case other symptoms are usually diagnostic so that mallein is superfluous and should not be misleading. The greatest care should be taken to prevent infection from the syringe, nozzle, skin, hands, etc., as other infections may give rise to local swelling and hyperthermia (see tuberculin test). If a first test leaves the matter in doubt, the animal should be secluded and tested again in a month (some prefer 3 months).
Pathological Anatomy. The colonization of the bacillus mallei in a tissue usually determines a concentration and multiplication of leucocytes, so as to form rounded nests of small lymphoid cells in a scanty fibrous network. These may be miliary or by aggregation they form masses the size of a pea or larger, which bear a close resemblance to the neoplasms of tuberculosis. As in tubercle the central cells of the group, degenerate, forming a granular fatty debris, and constituting an ulcer or abscess. In certain cases with a proliferation of fibrous tissue a cicatricial material is developed. Another characteristic lesion is the occurrence of hyperplasia in the walls of the lymph vessels so as to constitute firm tender cords, and the infiltration of the adjacent lymphatic plexus.
In the nasal mucosa the bacilli form prolific colonies at different points of the membrane and submucosa with the active production of lymphoid cells, followed by granular fatty degeneration and ulceration. Hence may be found different lesions representing the different stages. First there may be miliary deposits with clear contents and standing out like grains of sand. Then there are the larger pea-like nodules with congested vessels and minute hæmorrhages, but made up largely of the nests of lymphoid cells. These may bear on the surface a distinct blood extravasation, or the epithelium may be raised from the corium layer by a liquid exudation. The more advanced nodules show the centre light colored, grayish or yellowish with a distinct granular degeneration of the cells. Later still the degeneration involves the superficial layers and epithelium and an open ulcer is formed with a strong tendency to extend in depth and width. The formation and degeneration of numerous foci of cell proliferation gives the ulcer a very uneven outline. The continuous growth of fresh centres of proliferation may cause marked elevations between the ulcers, constituting extended patches, or the entire nasal mucosa may be thickened as the result of the morbid deposit. The cicatrices resulting from the apparent healing of deep or extensive ulcers or from a fibroid, transformation of the neoplasm consist of condensed connective tissue with small scattered nests of lymphoid cells and bacilli. In chronic cases the bacilli are very scanty.
The mucosa of the Eustachian pouches and tubes, the larynx, trachea and bronchia often present lesions similar to those of the pituitary membrane.
The lungs are usually marked in chronic cases by circumscribed lobular pneumonia, interlobular and peribronchial inflammations and miliary or larger areas of degeneration resembling tubercles. These may begin as a minute congestion and ecchymosis, which later shows in the centre a translucent or gray mass of lymphoid cells, with a surrounding area of congestion. Later still this central mass becomes yellowish and caseated from granular and fatty degeneration and this gradually extends so as to involve the whole area of the nodule. The peripheral portion may condense into a fibroid envelope, but usually this is less smooth and evenly rounded than in the case of an inspissated abscess or bladder-worm. The bacilli are found in the affected tissue but not always abundantly.
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.
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.
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.
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.
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.