Text book of veterinary medicine, Volume 4 (of 5) (part 2 of 3)

Text book of veterinary medicine, Volume 4 (of 5) (part 2 of 3)

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.

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.

There may be various complications as deposits in the lungs with pain in the chest, weak cough, aphonia, bloody expectoration and offensive breath; or the morbid process may take place in the liver or spleen with pain in the hypochondrium and much prostration and even icterus; or the muscles, bones, joints or testicle may suffer and the symptoms may suggest typhoid fever, pyæmia, osteomyelitis, or acute general miliary tuberculosis. The bacillus can usually be detected in the blood.

Acute glanders may prove fatal in three days or it may be prolonged for two, three or even four weeks.

Chronic glanders in man usually confines itself to the cutaneous muscular and osseous systems. It may take on an indolent type with the formation of skin nodules in groups or chains which remain hard and show no tendency to soften nor ulcerate. The adjacent lymphatic glands may become enlarged and indurated and the affection strongly resembles tuberculosis of the skin. Later when the nodules have softened and formed irregular and obstinate ulcers with swollen lymphatic glands, the disease is easily mistaken for syphilis. From pyæmia and septicæmia it is usually to be distinguished by the comparative absence of chills, and by the more sanious character of the pus. From syphilis it may be distinguished by the futility of a course of potassium iodide, and the general history of the case and probable exposure of the patient, and for tuberculosis the same principles will apply. In case of uncertainty, inoculation may be resorted to on the horse in suspected syphilis and on the pig when there is suspicion of tuberculosis. Or conversely the ox may be employed for the latter disease as he is altogether insusceptible to glanders. As a last resort the discovery of the bacillus may be made or the mallein test may be adopted with the concurrence of the patient.

Pathological Anatomy and Diagnosis. This is fundamentally the same as in the horse. The bacillus and its toxic products act on the infected tissues to produce clusters of lymphoid cells in a fibrous stroma after the manner of tuberculosis. Like that disease it also tends to affect primarily the lymph channels and glands, showing a particular tendency to the respiratory mucosa and has a great disposition to early coagulation, necrosis, ulceration, suppuration and abscess. The giant cell of tuberculosis is not a prominent feature in glanders, and the disposition to suppuration is greater especially in the human being so that the disease often resembles pyæmia. As in solipeds, however, the glander abscess has somewhat more sanious or glairy contents and the investing wall is not smooth and regular, but uneven and ulcerous from the successive softening and discharge of the clusters of degenerating lymphoid cells in the adjacent tissue. The pallor of the adjacent tissues from exudation and from the presence of numerous nests of lymphoid cells, the thickening of the efferent lymphatics, and the presence of numerous lymphoid neoplasms in the adjacent glands, and tissues, and often in the internal organs such as the liver and spleen and in the nasal mucosa or lungs together with the history of the patient’s exposure to glanders serve to diagnose from pyæmia. From smallpox and rötheln the skin lesions are distinguished by the presence of a central coagulation necrosis bathed in a glairy seropurulent fluid, and by the infiltration and thickening of the efferent lymphatic trunks. It differs from erysipelas in the same way by the presence in the affected tissues of the small hard lymphoid masses of embryonal tissue, and in a more advanced stage by the granular fatty debris resulting from their fatty degeneration. The presence in the affected tissue of these miliary or pea-like neoplasms in all stages of development from the primary congestion, through the embryonal tissue to the coagulation necrosis and caseation or softening is characteristic of the lesions of glanders. The sanious, sticky or glairy pus is especially noticed in the newly opened abscess, as after exposure to the air it is speedily infected with pus microbes, and the discharge becomes less serous and more creamy. Another characteristic of glanders in man is the frequent implication of the bone marrow, and the formation of the lymphoid deposits in the cancellated tissue until the bone may be reduced to a mere friable shell. Even when the disease is localized in the nasal mucosa it extends rapidly, not only to the skin and muscles, but also to the cartilage and bones of the face, so that deep, wide, perforating and destructive ulcers are common. The enlarged ends of the long bones of the limbs are favorite seats of the lesion, and the synovial membrane of the joints and the articular cartilage often bear centres of lymphoid proliferation. Though usually small the intermuscular neoplasms may form abscesses as large as a hen’s egg. The affected muscle appears pale, degenerated and granular with foci of lymphoid cell growth. The swelling of the lymph glands is usually less than in the soliped though the same in character. The pulmonary neoplasms are histologically almost indistinguishable from tubercle, though the comparative absence of the giant cell, the different staining qualities of the bacillus, and the coincident lesions in the upper air passages, with the cord like infiltration of the walls of the lymphatics may assist in diagnosis. Diagnostic inoculation may be made on the basis of the susceptibility of the ox and white mouse to tuberculosis, and their insusceptibility to glanders; also the partial insusceptibility of the soliped to tuberculosis and his marked susceptibility to glanders.

The characteristic nodules and abscesses may be found in different internal organs such as the stomach, intestine, liver, spleen, kidneys, testicles and brain, especially in acute cases, whereas the lesions of the skin and nose are more common in chronic cases.

PROPHYLAXIS AND TREATMENT OF GLANDERS.

Extinction. Exclusion, in Australia, New Zealand, English army. Occision of infected, and disinfection of stables, harness, vehicles, utensils, manure and other infected things, mallein diagnosis; attendants should avoid handling suspicious horses, except with sound hands, and disinfect latter. Sheep living in horse stables, tested before slaughter, or inspected after. Malleinization on Plains and in high, dry air, in secluded herds: less hopeful elsewhere. Mallein test for all solipeds from glanders districts, and imported horses. Treatment illegal in many states, so that justice would require extinction with indemnities. Successful on high tablelands and mountains. Demands careful segregation and disinfection. Acute cases always hopeless: chronic skin cases more promising. Antiseptic injection of unbroken nodules (carbolic acid, potassium permanganate), also of open sores (mercuric chloride, iodized phenol, cupric sulphate, saturated, zinc chloride), excise nodule. For delicate mucous surfaces Lugol’s solution of iodine or iodized phenol diluted. Tonics: arseniate of strychnia, copper biniodide, baryta nitrate, iron sulphate, sulphites, bisulphites, hyposulphites, phenic acid, open air life at pasture, or thorough ventilation, sunshine, moderate exercise, generous, partly grain diet. Mild cases in separate herd, in secluded, wide pasture with rich diet, including grain, and shelter in clean, comfortable shed at will, under tonics and antiseptics, tested by mallein at intervals, to be restored individually to work after two or more tests without reaction. Serum of immune animals subcutem. Treatment in man: surgically as in the horse, excision, curetting, antisepsis, abscesses opened and disinfected; iodoform insufflations, antiseptic gases, sprays and solutions. Internally: tonics, sulphocarbolates, iron muriate, iodides, phenic acid, quinia, strychnia, arsenite, stimulants, serum treatment, pure air, out door life, rich, digestible food.

Radical efforts at prevention must look to the extinction of the disease in the soliped, and its complete exclusion from Australia and New Zealand shows that such a result is not unattainable. In the English army where every glandered horse is at once killed and all pertaining to him disinfected, the disease is now virtually unknown except in the case of newly purchased horses or regiments operating in the field. In the French army which formerly lost 9 per cent. per annum from glanders, now under similar precautions loses but .5 percent. A law providing for the prompt destruction of every glandered soliped and the safe disinfection of carcasses, stables, harness, vehicles, utensils, fodder, litter and manure that have been exposed to contamination, if enforced, would soon eradicate the disease. But this law should provide efficient machinery for its enforcement, and, under suitable safe guards, an appropriate indemnity for the owner. With the use of mallein in all infected studs, as a diagnostic agent, the campaign can be made sharp, short and effective, instead of waiting as in the past for the slow development of occult cases.

The greatest and most fundamental error in veterinary sanitary legislation is the lack of a guarded indemnity for the animals killed. I strongly urged this fact on the committee of the N. Y. legislature in 1898 but to no purpose. A bill was passed forbidding all indemnity for glandered horses, and an impetus thus given to the spread of the disease is daily bearing fruit in our great cities especially, disastrous to the health of the horses, and a constant menace to that of humanity as well. The law makes it the duty of veterinarians to report all cases of glanders, but in great horse establishments such a report would stop the use of the whole stable, at a loss of thousands of dollars per diem, and put a sudden end to the employment of the reporting practitioner by the firm or corporation in question. The owner of one or two horses can afford to report, the loss of these and their work does not mean absolute ruin, but the owner of hundreds can not safely report. For owner and practitioner alike the alternatives are presented of obedience to the law with personal ruin on the one hand, and the surreptitious dealing with cases of glanders and the preservation of their livelihoods on the other. Whatever may be said as to the constitutionality of the law which destroys private property without compensation under the right of eminent domain, this is certain, that, as applied to animal plagues, this course is unjust, oppressive, and not only useless, but positively injurious, in that it drives the owners of animals to such courses as favor the spread of the plague in place of restricting it. To-day in New York City glanders is extensively prevalent, but large horse owners dare not adopt the legal measures for its extinction, with the certainty of great loss or ruin staring them in the face as the result. It should be further considered that any law is at once bad and vicious in its tendency which places before the citizen the alternatives of disobedience with profit, and obedience with loss or ruin. Such a law is the worst possible economy because in preserving the infection, it not only perpetuates the disease and its attendant losses for all time, but perpetuates forever the official expenses of keeping it in check, when a prompt extinction of the infection would once for all time abolish all loss and all outlay for surveillance.

Until provision can be made for the enforcement of our laws against glanders, all who handle horses should be warned of the danger of working about strange solipeds, or those that show suspicious symptoms, while they have any sores on the hands, and in case they must run any risk of contact with infection, to promptly wash hands and face in a solution of hydrargyrum chloride (1:2000), or carbolic acid (2:100). Animals of susceptible races (sheep, etc.) which have lived with glandered horses should be made to pass the mallein test before they can be put upon the market for human food.

In the high, dry altitudes of the Plains and Rocky Mountains, where most cases of glanders are mild and the majority recover, resort may be had to malleinization provided the patients are kept safely secluded from all other horses. In some horses with a native tendency to immunity, the oft repeated inoculation with 0.5cc. of mallein will render the animal refractory to the infection. Animals that have recovered from casual attacks show the same immunity. Among those who have experimented with mallein may be named: Straus, Schneidemuhl, Semmer, Bonome, and Vivaldi, Mowry and Michel, Schweinitz and Kilborne. Sacharoff apparently secured immunity in the horse by inoculation with virus modified by passing through the cat. Straus found that dogs which had received mallein intravenously could be made immune against intravenous inoculations, but, as Galtier had already pointed out, were still susceptible to cutaneous inoculations. Finger, experimenting on the rabbit, found that immunity only resulted after a long series of inoculations. The frequency of successful auto-inoculations in chronic cases of glanders in the horse would tend to discredit the alleged value of single injections of mallein, so that a long series is necessary if we would aim at good results.

Altogether attempts at immunizing the equine population generally, are not hopeful where it is dense, where they must be kept stabled, where the climate is moist and where glanders is deadly, or tends to persist in the chronic form for years in the same animal.

Considering the prevalence of the disease in a mild form on many of the western breeding ranches it is well to test all horses arriving from the west. The same applies to solipeds imported from abroad.

TREATMENT OF ANIMALS.

In the majority of the states the treatment of a glandered horse is prohibited by statute. Yet without providing definite machinery for the administration of the law, and without indemnities for horses disposed of, such laws are largely inoperative. On the other hand treatment is quite successful on the pastures of our dry table lands and mountains. It can, however, be sanctioned only when careful segregation and disinfection are provided for. Acute cases of glanders are hopeless in any region, but chronic cases and especially such as have the lesions confined to the skin are much more hopeful.

The unbroken nodules may be injected with carbolic acid solution (1:200), or permanganate of potash (1:60). The open sores on the skin may be treated with the same solutions, with mercuric chloride (1:2000 to 1:5000), with iodized phenol, with cupric sulphate (saturated solution), or with chloride of zinc. A primary nodule may be excised and the sore treated with antiseptics. When the lesions are very extensive the less poisonous agents should be made use of, or tincture of iodine may be substituted. The nose lesions may be treated by the weaker solutions of iodine or of iodized phenol.

Benefit also comes from a course of tonics the most successful of which have been arseniate of strychnia, binodide of copper, sulphate of copper, nitrate of baryta and sulphate of iron. The sulphites, bisulphites and hyposulphites and phenic acid are desirable adjuncts. An open air life at pasture is the ideal condition. Otherwise thorough ventilation, sunshine, moderate exercise and nourishing easily digestible food including grain are very important.

When conditions are favorable and an absolutely secluded pasture can be secured, with shelter from storms, and where civic or state authorities do not take effective measures to stamp out glanders, nor compensate owners for animals killed, mild, chronic and cutaneous cases and occult ones that have reacted to mallein without showing any other symptom, may be subjected to treatment. They should have an open air life, a generous diet, including grain, perfect cleanliness and pure air in the shelter-shed, an antiseptic and tonic medication (sulphites, tonics) may be given, and every three months a new mallein test may be applied. If the individual horse passes two successive tests without reaction, and shows no other indication of glanders, if his general health appears perfect and his condition good, he may be returned to work as a sound animal. With effective measures of extinction in force on the other hand, and indemnity for the slaughtered animal, any such measure would be entirely unwarrantable.

Treatment by injecting the serum of immune animal subcutem has given encouraging results. Helman, Semmer and Itzkovitch, Pilavios, Bonome and Vivaldi, Johne, Schindelka, Prieur and others record recoveries in recent cases and there need be no doubt of its value in subjects that are naturally somewhat refractory to the germ. Babes introduced the blood serum of the ox, which is naturally immune, and Prieur speaks with confidence of the treatment of cutaneous glanders in man and certain cases of pulmonary glanders in the horse.

TREATMENT IN MAN.

The surgical treatment of glanders in man does not differ materially from that given for animals. It is more frequently possible to deal with the local lesion in its early stages and then a thorough cauterization of the infected sore, and a little later the complete excision of the primary nodule, or the limited regional infiltration, the curetting of the adjacent parts and the maintenance of thorough disinfection by irrigation, sponging and compress will often be followed by success. Where such radical measures are inadmissible the infected parts should be excised and curetted as far as safe and the adjacent parts subjected to carbolic injections (1:200). Abscesses should be evacuated, fistulæ slit open, and thorough disinfection applied. For the affected air-passages, iodoform insufflations and antiseptic gases, sprays, and solutions should be freely used.

Internally, antiseptics such as sulphocarbolates and tincture of muriate of iron, iodides, and carbolic acid have been largely employed. Whitla recommends 5 grains of quinia in 15 grains of tincture of muriate of iron every four hours. Tonics (arsenate of strychnia), and stimulants, ammoniacal or alcoholic, may be called for. Special symptoms such as pain, rigors, nausea, vomiting, diarrhœa and profuse perspirations must be met by suitable remedies. Finally blood serum from healthy cattle or from immunized animals may be employed subcutem. Pure air and nourishing, easily digestible food are very essential. Every effort should be made to check the disease at its outset, as generalized acute glanders is speedily fatal, and recoveries in chronic cases usually leave a broken down constitution.

LYMPHANGITIS SACCHAROMYCOTICA (FARCINOIDES: EPIZOÖTICA:ULCEROSA.) FARCY IN CATTLE.

Geographical distribution and nature: Japan, Northern Europe, France, Guadaloupe; caseating nodules in skin, subcutem, in mucosæ and internal organs. In horse skin nodules, and glandular abscesses, with thick ovoid refrangent bacterium; saccharomyces (Hitt); swellings first local, then multiple, and general, extending along lymph vessels to glands (Hitt); along air-passages to lungs, from prepuce or scrotum to peritoneum (Hitt), or from conjunctiva to other parts in the orbit (Caparini and Ferner). In cattle, multiple, subcutaneous, nodules—hazlenut to walnut, isolated, hard, painless. Suppurate slowly. Same saccharomyces (Tokishige, Nocard). May invade lungs with fatal result in a year. Mallein test gives no reaction. Treatment: actively antiseptic; open, curette, pack with antiseptic gauze, sublimate bandages; internally, tonics, antiseptics.

Horses and cattle in certain countries (Japan, Sweden, Finland, France, Guadaloupe) are subject to a chronic lymphangitis resembling cutaneous glanders, but associated with the development of bacilli or fungi in the nodular, caseating swellings in the skin, subcutem, in mucosæ and in internal organs.

Nocard describes the affection in the horse as characterized by skin nodules (buttons, boils), which burst and discharge a thick, grumous, or thin, oily, yellowish or bloody pus. The surrounding lymph plexus swells up into corded lines, with at intervals nodules or abscesses. The infection extends to and implicates the lymph glands and general pyemia may follow. The thick ovoid refrangent, pathogenic, bacterium stains in Gram’s solution.

In Northern Europe and Asia, Southern Europe and Guadaloupe an analogous affection is described by Rivolta, Claudio-Fermi, Aruch, Tokishige and Nocard and Leclainche. Hitt attributes this to saccharomyces. The infection attacks horses and cattle, entering by sores and abrasions of the skin of the limbs, or under the harness (back, breast, rump, head). Confined at first to the point of infection it becomes multiple, being conveyed from place to place, through the soil, floor, stall, harness, blankets, brushes, combs, straw, etc., and may extend on the mucosæ. The wounds fester, forming pus and crusts over a more or less considerable swelling. In a variable time, (one to twenty weeks) the surrounding lymphatics become swollen and tender (corded), and nodular swellings appear on their course which fluctuate, burst and discharge a whitish or yellowish pus, sometimes oily or slimy. The disease extends along the lymphatics, invading the lymph glands and even the internal organs.

Tokishige describes cases in which it extended along the respiratory mucosa, causing constriction of the nasal passages and larger bronchi, with dyspnœa, and finally, invading the lung. In other cases it spread from the prepuce, or scrotum, upward along the tunica vaginalis, spermatic cord and testicle. Caparini and Ferner describe it in the orbit, affecting the lids, nictitans, conjunctiva and adjacent parts, with nodules and abscesses. Mazzanti describes the case of a filly which died with pea-like nodules on the colon, and ulceration, with dirty, black, purulent centres, and indurated borders. Tokishige describes the affected cattle as showing a vast number of subcutaneous, hard, painless nodules, varying in size from a hazel nut to a walnut and covered by light colored skin. The nodules were isolated and not connected by swollen, beaded lymph vessels. They encrease and suppurate much more slowly than in the horse. In three cows microscopically examined he found apparently the same branching fungus (saccharomyces), as in the horse cases. The mortality is about 10 per cent.

In the farcy of the ox of Guadaloupe there form subcutaneous nodular abscesses, with cordiform swelling of the lymph plexus and trunks, often proving fatal in a year through extension to the lungs. The abscess breaks, discharging a whitish, creamy or caseous, or grumous contents, containing a bacillus (Nocard). The abscesses usually appear under the sternum or belly and later extend to the thighs and legs. In all such cases the mallein test is inoperative.

The treatment of such cases should be actively antiseptic to destroy the germ while still local. After opening and evacuating the abscesses, excise or curette the diseased tissue, or destroy with the actual cautery, pack the cavities with pledgets soaked in tincture of iodine, iodized phenol creolin, lysol, mercuric chloride, zinc chloride, or copper sulphate, or dusted with aristol, iodoform, or iodized starch. The surrounding swelling, if any, may be painted with tincture of iodine, or covered with cloths wet with a sublimate lotion or other antiseptic. Internally, tonics and antiseptics may be given: arsenite of strychnia, quinia, iron or copper sulphate, sulphites or hyposulphites of soda or potash.

RABIES AND HYDROPHOBIA.

Synonyms. Definition: Acute, infectious, cerebral disease, of domestic and wild carnivora, shown by intellectual, emotional, and aggressive nervous disorder, and extreme nervous excitability. Animals susceptible: canine and feline animals, biting animals and those bitten, of all warm blooded kinds; receptivity greatest in carnivora. Geographical distribution: where population is most dense, trade and movement most active—north temperate zone. Australia, Tasmania, New Zealand, Azores, St. Helena immune—protected by quarantine. Islands in Elbe, places with enforced muzzling. Causes: contagion; inoculation; rutting; skunk bites; absence of flowing robes (men, children). Virulent matters: saliva, bronchial mucus, flesh, blood (not in sheep?), milk, (in advanced stages), nerve tissue. Morbific agent particulate; filtered liquid noninfecting: blastomyces, bacillus, found but not uniformly: claims of brain symptoms from each. Viability; saliva virulent for 11 days; brain 3 weeks at 32° to 63° F., for months aseptic and in contact with carbon dioxide; water 20 to 38 days; body in grave 44 days; virulence lost by drying in thin layer yet kennels remain long infecting; glycerine preserves; robbed of virulence by iodine, citric acid, bromine, chlorine, sulphurous and mineral acid and cupric sulphate. Bites of men effective to 50 per cent., protection by clothes, wool, flow of blood, cleaning of teeth by succession of bites. Infection by licking, sneezing, coughing, inhaling, feeding. Incubation 15 to 60 days in dog, 20 to 45 days in horse, 14 to 60 days in sheep, swine and cattle, 14 to 64 days in man. Prolonged cases doubtful. Symptoms in dogs: change in disposition, more amiable or morose, dull, apathetic, excitable, unwonted silence or howling, restless, depraved appetite, swallowing small objects, searching, tearing sticks or clothes, licking cold stone or genital organs, hiding in dark corner, dull expression, irritation where bitten, hoarse voice, rabid howl, eyes follow unreal objects, snaps at them, listens for unreal sounds, irritability, fury when threatened with stick or shown another dog, bites without growl, bears master’s blow in silence, eyes red, fixed, pupils dilated, squinting, lonely wandering, biting, swimming rivers; restless excitement alternates with torpor and seclusion, slouching gait when worn out; in paralytic form; weakness, paresis, palsy of lower jaw, hind limbs, body, dull, prostrate, apathetic; in lethargic form; no fury nor paralysis, but profound prostration and apathy, no coaxing, threat, punishment not even another dog will rouse. Paralytic and apathetic forms wind up the furious; cases with intermittent attacks. Diagnosis: by marked change of disposition or habit, voice, appetite, any hypersæthesia, strabismus, watching or snapping at unreal objects, taciturnity, fury in presence of other dog or stranger, snapping, biting without giving voice, fury when threatened with stick, open mouth without disposition to paw it, lack of muscular coördination, paresis, paralysis. Distinction from lactation anæmia, bone in palate or throat, dislocation of maxilla, stomato-pharyngitis, cutaneous hypersæthesia, pharyngeal anthrax, epilepsy, pentastoma, cysticercus, filaria immitis, nematodes, and tæniæ, auricular acariasis. Symptoms in cats: changed voice, depraved appetite, hiding, restlessness, irritability, bites, scratches, man or dog. Symptoms in solipeds: trembling, hyperæsthesia, easily startled, ears and eyes alert, dilated flashing pupils, roused by dog or stranger, attacks with teeth and heels, mischievous, pawing, kicking, rolling, rising, straining to urinate or defecate, neighing, sniffling, snorting, everting upper lip, grinding teeth, biting, stiffness or impaired control of limbs, generative excitement, spasms, paralysis, hyperthermia, perspiration. Symptoms in cattle: irritability, restlessness, alert head, ears, eyes, squinting, dilated pupils, loud bellowing, lashing tail, or docility, yet pursues a dog, using horns, heels, (exceptionally teeth), stamps, paws, has genital excitement, anorexia, spasms, weakness, paraplegia. Symptoms in sheep and goat: hyperæsthesia, irritability, genital excitement, fury in presence of dog, stamps, butts, paws, snorts, bleats, grinds teeth, becomes paretic, and paraplegic. Symptoms in camels and deer: camels show furious and paralytic forms, biting and snorting; deer have hyperæsthesia merging into paralysis. Symptoms in swine: extreme irritability, restlessness, start at slightest cause or none, tremors, squealing, jerking, grinding teeth, clenching jaws, bite especially a dog, or not, weakness, lethargy, paralysis. Symptoms in rabbits and Guinea pigs; may be furious, more often paralytic. Symptoms in birds: restlessness, ruffling of feathers, pecking or striking man or dog, or at phantom, palsy. Symptoms in wild carnivora: lose fear of man, approach and attack him, are furious and later paralytic. Skunks bite slyly. Symptoms in man: irritable cicatrix, anxiety, sighing, tremor, insomnia, bad dreams, fever, thirst, spasms of throat when seeing, hearing or taking liquids, dyspnœa, retching, vomiting, spasms, roused by noise, squinting, dilated pupils, mental delusions, reticence, taciturnity, suspicion, mania, exhaustion, paresis, paralysis. Lyssophobia, its detection and cure.

Synonyms. Canine madness; Rabidus Canis; Lyssa; Lytta; Cynolyssa.

Definition. Rabies is an acute, infectious disease, affecting the cerebral and medullary nervous centres and characterized by intellectual, emotional, aggressive and other nervous disorders and by extreme reflex excitability.

Animals susceptible. While the disease is seen most frequently in the canine races (dogs, wolves, foxes and jackals), and in the cat family (cat, lion), it is liable to spread widely among animals that use the teeth as weapons of offense, and such as they can readily attack. When inoculated, all warm blooded animals contract the disease. Thus the carnivora and omnivora (dog, wolf, fox, hyena, jackal, cat, lion, badger and skunk and, to a less extent, the pig and horse) may become active propagators of the infection, which may spread widely among their herbivorous victims (cattle, sheep, goats, deer, rats, mice, chickens and pigeons) through their bites. Man suffers mainly through the attacks of dogs, cats and, in certain localities, wolves or skunks, but he is also liable to become infected from handling rabid domestic herbivora. Different genera differ in susceptibility, the receptivity being apparently greatest in the carnivora.

Geographical Distribution. Rabies is confined to no country nor climate but it attains its greatest prevalence in the north temperate zone, where there is the densest population and where activity of travel favors the propagation of infection. The facility for inoculation is the one determining cause, thus the islands of Australia, Tasmania, New Zealand, the Azores and St. Helena have never suffered and the first three exclude the disease by rigid inspection and quarantine. During the Hamburg epizoötic of 1852–53, the islands in the Elbe escaped though both banks were ravaged. Again, where the muzzling of all dogs has been rigidly enforced, as in many German cities and districts the disease has been practically extirpated.

Etiology. Long before the days of pathological bacteriology rabies was recognized by veterinarians as a disease due to infection alone. Its absence from the various countries above named, and from South and West Africa, its rapid propagation in other countries (La Plata, Malta, Hong Kong) into which it had been introduced for the first time, and its restriction and disappearance wherever muzzling had been strictly carried out, had practically settled this question. The development of the disease in animals which had been experimentally inoculated was no less significant of this truth.

Other alleged causes are based on secondary factors that favor inoculation. The alleged evil influence of the hot season (dog days) is accounted for by the period of rutting of the dog which occurs in spring, and brings together troops of jealous dogs following individual bitches and fighting for their favors. This gives a great impetus to the propagation of the disease which accordingly becomes more prevalent during succeeding months. The statistics of Bouley show, however, that the season of its greatest prevalence in France is March, April and May, that it subsides slowly up to midwinter and encreases again in spring. Boudin’s statistics show the greatest number of cases in man toward midsummer which is explained by the long period of inoculation after bites sustained in the spring, but also because clothing is lighter in summer and infection more likely to reach the skin, and because the heat of the weather tends to cause hyperthermia and encrease susceptibility.

The large preponderance of male dogs among the victims of rabies (7:1) has led to the theory that sex predisposes, but the explanation is rather that the males bite each other in their jealousy while they respect the female, the object of their sexual passion. In inoculated cases, males, females, and castrated contract the affection indifferently and with equal readiness.

The skunk is found to be infected in certain localities, and it has been claimed that the affection is native to this animal, and that the form differs from that which prevails in the dog, but the restriction of the disease to sharply circumscribed areas in Michigan and Kansas, while skunks elsewhere show no such malignant quality, demonstrates that this is but an accidental infection of the family of the Mephitis in a given locality.

Men and children suffer in far greater numbers than women, the difference being mainly due to the protection furnished the female by the flowing skirt, though also in part because of the more frequent contact of men with dogs.

Virulent Matters. In 1813 Gruner and Count Salm demonstrated the virulent properties of the saliva of the rabid dog. This has been many times repeated, though as shown by Pasteur, Raynaud, and others, inoculations with saliva often kill in one or two days by reason of the presence of other infective germs, or suppuration ensues and destroys the rabific virus so that oftentimes not more than one in four develops rabies. Galtier succeeded in inoculating 3 rabbits, 1 dog and 1 sheep with the juice expressed from the salivary glands, and Nocard, Leclainche and Peuch have found this to be very virulent. Paul Bert found the bronchial mucus virulent. Rabies has been frequently conveyed by consuming the bodies of rabid animals, yet Peuch and Galtier have failed to convey infection by the flesh. Eckel and Lafosse successfully inoculated the blood of goat to sheep, of man to dog and of dog to dog. Yet many of the older observers agree with Peuch and Galtier in pronouncing the blood non-virulent. Pasteur, Roux, Bujwid, and Helman failed to obtain virulent cultures from blood. Peuch and Nocard have found the milk virulent, and Bardach found the same to be the case in a woman for two days before her death of rabies. In some partially refractory animals like the sheep, the blood seems to destroy the virus, as intravenous inoculations have been made with impunity. The probability is that the blood is habitually non-virulent in the early stages and in mild cases, but becomes virulent in violent and advanced cases. Pasteur first showed that the virus has a special election for the brain and nervous matter and that the central nervous organs are constantly infecting. Rossi inoculated with a piece of nerve trunk, and Doubouc and Babes advanced the hypothesis that the virus advances along the nerve to reach the brain.

It was formerly supposed that the saliva of omnivora and herbivora was non-virulent but repeated experiment has proved it to be infecting. The blunder was due to the fact that these animals did not often transmit the disease by biting. Some writers even deny that rabies exists at all as an infectious disease. One alleges that the danger of rabies is “less than the gallows.” Experiment shows most conclusively that it is much more certain when the conditions are fulfilled. One may live a long lifetime without seeing a genuine case of rabies, but so he may without seeing leprosy or plague, and he is no more entitled to doubt their existence than he is the existence of Manila, or of the other side of the moon.

Morbific Agent. The actual factor which produces rabies is not certainty known so that we cannot speak of its bacteriology. That it is due to a specific particulate germ is now indisputable. Paul Bert and Nocard filtered the virulent fluid through plaster and found the clear fluid that had passed through non-virulent. Rivolta, Babes, Bouchard and Peuch severally passed a solution of the rabific brain matter through a Chamberland filter and found the clear filtrate harmless. The virulent agent is therefore not a body in solution but a solid (organism) which is held back by the filter. Hallier, Klebs, Galtier, Gibier, Pasteur, Fol, Babes and Dowdeswell have respectively attempted the cultivation and inoculation of organisms found in rabific liquids but none has stood the test of further experiment. Memmo found a blastomyces in the brains of six rabid rabbits and one hydrophobic child. It stains with the aniline dyes but not by Gram’s method; when thrown into the peritoneum of Guinea pigs it produced clonic spasms and death in 24 hours, and in the dog, after an incubation of 8 days caused emaciation, salivation, a disposition to bite, paralysis of the hind limbs and death in 48 hours. Bruschettini using agar or bouillon, containing lecithin or cerebrin and defibrinated dog’s blood, inoculated with pieces of the brain of an inoculated rabbit, obtained in 24 to 36 hours a group of small transparent drop-like colonies at first microscopic, but becoming larger with each new culture on fresh media. These colonies contained a very small, short, thick bacillus, which stains readily in Ziehl’s carbol-fuchsin, and then presents a central clear band giving the appearance of a diploccus. In fluid media spherical forms are produced, but in fresh cultures the diploccus aspect reappears. Injected subdurally in rabbits it gave rise to what appeared to be paralytic rabies and could be inoculated from animal to animal, with similar results. It failed to grow in the usual culture media from which the brain products are absent, thus fulfilling the conditions, of a microbe the point of election of which was the nerve cells. Marx who has sought for Bruschettini’s organism in 60 cases of rabies has only once found anything resembling it and concludes that it was merely a contaminating organism, which caused a paralysis (Centr. f. Bacter. 1896.)

Viability of the poison. Galtier found that the virulent saliva remained potent for 11 days if preserved from drying. It persists for 3 weeks in the brain and medulla kept at 0° to 12° C., for a month in sealed tubes, or for several months if protected against septic microbes and in contact with carbon dioxide.

In water it is preserved for 20 to 38 days so that water soiled with saliva may easily become a means of infection. In graves it has been found virulent as long as 44 days after burial so that in medico-legal cases results may be obtained by exhuming a suspected animal (Galtier).

Haubner found that drying the saliva in thin layers rendered it non-virulent and Pasteur has shown that the rabbit’s medulla loses its virulence in 14 or 15 days when dried in contact with air, and apart from putrefaction. Such laboratory results must however be qualified by the facts recorded by Blaine, Youatt and others in which hound after hound died of rabies from living in a dry kennel in which a rabid animal had preceded them. Until we know something of the living germ itself of rabies, it is unwise to infer too positive results from experiments on that microbe, in what may be but one stage of its existence.

The virus is very resistant to cold, having survived a temperature of −60° C. (−76° F.) for several hours (Roux), −10° C. (−14° F.) for ten months (Jobert). Virulence is destroyed however by a temperature of 48° C. (118.4° F.) in five to twenty minutes (Galtier). Light destroys the virulence in 14 hours at 30° to 35° C. (Celli), but encreased pressure has little effect on it (16 atmospheres, Nocard and Roux).

Glycerine at room temperature preserves the medulla in its full potency for four weeks, but destruction ensues if it is heated (Protopopoff). An aqueous solution of iodine (6:100) destroys the virulence (Galtier), as does also citric acid, bromine, chlorine, sulphurous acid, the mineral acids and cupric sulphate.

Ratio of successful inoculation to bites of rabid animals. As rabies is usually transmitted by the bite, it is well to note that not all the bites of rabid animals are effective. Of 183 dogs confined with and bitten by a rabid dog 91 contracted rabies; of 73 cattle bitten 45 became rabid; out of 121 sheep bitten 51 succumbed and of 890 persons bitten, 428 took hydrophobia. Of 440 persons bitten by rabid wolves 291 contracted the disease. The escape of such a large proportion is variously accounted for. Wolves naturally attack the face, throat or hands where there is no protection by clothing, and inoculation is therefore much more certain. Dogs, especially in cold weather usually bite man through the clothes which wipe off the virus from the smooth conical teeth before they reach the skin. Long haired animals are often protected in the same way. In other cases the bite is sustained on a very vascular part and the free flow of blood washes out the poison. In still other cases the rabid animal making a number of snaps in rapid succession comes to the last with the teeth wiped clean and harmless. Again the prompt washing or cauterizing of the wound tends often to protect against infection.

Under favorable circumstances however every bite infects, and the writer has seen six animals, bitten in the same stable, all contract rabies, while a man bitten through the coat sleeve by the same dog, and cauterized an hour later entirely escaped. If the bites are multiple, deep and irregular, the danger is greater.

The licking of wounds is an occasional mode of infection, the rabid dog in the early stages of the disease sometimes showing an unusual disposition to fawn upon his owner.

Again particles of saliva may be projected by sneezing or otherwise and lodge on sores, or on the mucosa of the nose, eye or lip so as to cause infection. Galtier has conveyed the disease experimentally to rabbits in 11 cases out of 75 by making them breathe the atomized infecting liquid, or by dropping it into the nose. In the same way he infected Guinea pigs and sheep.

Galtier and Bujwid have conveyed the disease, exceptionally, to rabbits and rats by feeding infecting emulsions. Galtier has also produced rabies in ⅒th to ⅓d of the cases operated on by instilling the virus into the eye.

Incubation. The duration of incubation varies with the species, individual, the seat and character of the bite, the amount of virus instilled, the potency of the virus, the age, size and weight of the subject, the excitement of rutting, climatic or weather vicissitudes, fatigue, and nervous or febrile disorders.

In the dog incubation ranges from 15 to 60 days, and perhaps 4 to 6 months. It is claimed to have lasted a year but this is somewhat doubtful. In cats it has varied from 15 to 60 days.

In solipeds it ranges usually from 20 to 45 days. The extremes stated are 15 days and 20 months.

In cattle it ranges from 14 to 50 days (exceptionally 70 days), in sheep and swine from 14 to 60 days. It has been claimed to have lasted 4 months in swine and 5 months in sheep.

In rabbits subdural inoculation has an incubation of 15 days, shortening in 25 removes to 8 days, and finally to 6.

In man incubation is alleged to be even more varied. The rule is from 14 to 64 days, but it is claimed to have been as short as three days and as long as 1 to 12 years (Chabert). In the human being, however, there is always the danger of the disease caused by simple dread (lyssophobia) and until these protracted cases can be verified by successful inoculation on the lower animals, they must be held as extremely doubtful. The Montpellier cadet has been often quoted who left, a few days after he had been bitten, spent ten years in Holland, then returning to the school and learning for the first time that his fellow cadet, who had been bitten by the same dog, had gone mad, he too became rabid without loss of time. Such cases have often been cured by moral suasion and have been seized upon to corroborate the heresy that there is no such thing as genuine rabies in man.

Any incubation, in man or beast which has exceeded 40 days should be considered as doubtful, until certified by the successful inoculation of rabbits or other small animals. For casual inoculations the incubation rarely varies much from the time embraced between 16 and 30 days. It is abridged by a special receptivity; by an overdose of the poison; by the inoculation of a virus of unusual potency; by the youth of the animal inoculated; by great heat of the weather; by all forms of violent excitement; by rutting; and by the inoculation of the virus on the head and above all on the cerebral meninges. By this last method incubation may be reduced to 6 days.

Symptoms in Dogs. In dogs as in other animals rabies is manifested in two great types: the furious and the dumb or paralytic, which, however, usually succeed each other in fully developed cases. Yet the furious phenomena may be entirely omitted, and again the victim may die in the early furious stage so that the paralytic does not appear. The prominence of one form over the other is to some extent determined by the germ derived from a previous case of the same kind or by the family, temperament and habits, bull dogs and hounds being specially subject to the furious type, and house and pet dogs having rather the paralytic form.

The premonitory symptoms are in the main the same for both types, and as these may enable us to recognize the disease before the period of extreme danger, it is especially important that they should be well understood.

Some marked change in the disposition or habits of the animal is the first obvious variation from health, and in a district or country where rabies exists any such change should be the warrant for instant seclusion of the dog before there is any disposition to bite. The unwonted habit may be of almost any kind. The lively, amiable dog may become suddenly dull, apathetic or taciturn; the quiet, unexcitable dog may become unusually affectionate, fawning and demonstrative, licking the owner’s hands and face and perhaps infecting him before any suspicion is aroused. Sudden capricious changes from fawning to apathy or sullenness, or the opposite, should be dreaded. The noisy dog may become suddenly silent; while the silent dog may take to howling without apparent cause. A great restlessness, watchfulness or nervousness, a tendency to start at the slightest sound, and a disposition to move at frequent intervals in search of an easier position or place to lie in, are most dangerous symptoms. A morbid appetite, with a disposition to pick up and swallow all sorts of nonalimentary objects (straw, thread, cord, paper, pins, nails, coal, marbles, pebbles, cloth, earth, dung or urine), in a mature dog is most suggestive. Searching around, scraping, tearing sticks, clothes and other objects to pieces, licking of smooth cold stone or metal, of his penis, or of the generative organs of a bitch, are often early phenomena. The dog may hide in a dark corner, going to sleep and grumbling or growling when disturbed. He may make night hideous with his howls, baying at the moon. He may stand with a dull, melancholy, hopeless expression of countenance, as if beseeching his master for relief from his nameless suffering. But as yet there is no disposition to bite. The dog still responds to the call of the master, but with dulness and apathy, in marked contrast with his usual prompt, alert and loving response. There may be congestion, itching and irritation in the seat of the bite, and it may be licked, scratched or gnawed until raw, tender or bleeding. An early change in the voice may be noticeable. There is at first a certain hoarseness, which gradually develops into the pathognomonic rabid howl which is quite recognizable at a distance. The dog turns his nose upward, and with open mouth, emits a howl which, at first hoarse and low, rises into a shriller and higher note before completion and which may be repeated several times without closing the mouth. It is not an ordinary howl but rather a cry of distress, and, to the educated ear a grave note of warning. Sometimes the dog is dumb from the start.

Close observation will often detect evidence of mental delusions and hallucinations even at this early stage. The apparently sleeping dog suddenly starts up with an air of suspicion and excitement. His eyes may turn after phantom flies or other objects at which he will presently snap. He moves hither and thither with a curious, inquisitive air, searching in dark corners, or under curtains or articles of furniture for some imaginary object. He may stand in attentive attitude listening to fancied sounds, and then bound in that direction in spite of an obstructing wall or utensil. If recalled to reality by his master’s voice his healthy attitude and affection may be completely though temporarily restored. He may compose himself to rest or sleep, and soon again start a victim to further delusions.

The furious stage is ushered in by a more pronounced manifestation of the above symptoms. The rabid howl is more frequent and characteristic. The insomnia and the restless movements, change of place, searching, scratching or tearing are likely to be more prominent. The delusions and the watching or snapping at phantoms are more marked. The causeless sniffing and scraping may imply disorder of the sense of smell. The exalted hyperæsthesia and reflex excitability is usually a most marked feature, frequently modified by a sinister, inimical or malevolent disposition. Some subjects show evidence of intense itching, most marked perhaps in the seat of the wound; others are abnormally sensitive to currents of cold air; they start at the slightest noise, a flash of light, a touch, or the approach of a stranger. A paroxysm of fury may be caused at once by shaking a stick at the patient, but, above all, by the test of presenting a dog before his eyes. He at once rouses himself and, with flashing eyes, dashes himself on his supposed enemy and bites viciously, but without bark or growl. The sudden and mute attack is pathognomonic. But there may be symptoms suggestive of some hypoæsthesia. A blow from the dog’s master is usually borne in silence. The animal shrinks from the blow but does not yelp nor howl. During a paroxysm he will lacerate his gums or loosen his teeth by biting on a stick or iron bar; he will even seize a red hot bar without shrinking. He will often gnaw his limbs or body so as to expose and even lacerate the muscles, driven by the pruritus, or the insatiable disposition to bite. Yet he has still an instinct of self preservation, retiring from a light, or blazing brand, and seeking to evade the tongs used to seize him.

The eyes assume a remarkable expression. They are often fixed, and at times the pupils are widely dilated allowing the reflection of light from the brilliant tapetum lucidum, resembling flashes of fire, and adding greatly to his ferocious appearance, and the sense of terror that he inspires. The conjunctiva is congested, of a dark red and the general expression of the eye is very striking. The soft, trusting, affectionate eyes may still for a moment meet those of the loved master, but there is in them a dull, hopeless, anxious and suffering expression, which appeals for pity and should be viewed with dread. To others there is likely to be less of the affectionate appeal and more of the sinister, suspicious, resentful and malicious expression. To the stranger, therefore, the eye may be a better guide than even to the owner. Squinting of the eyes and closure of the lids for a few seconds are not uncommon. As the disease advances the dilatation of the pupils is more marked, indicating the paralysis of the optic nerve.

In this stage the disposition to wander is characteristic. The rabid dog leaves his home and wanders off a long distance, say ten or twenty miles, snapping in his travels at man or beast that may irritate him, returns dirty and exhausted, and seeks anew his dark place of seclusion, or he may snap at and bite even his master. To those who come in contact with him at this time the dog is especially dangerous from his extreme irritability though weak and exhausted.

If the wandering rabid dog meets a strange dog he attacks him and bites without growling or barking. If the bitten dog does not yelp nor retaliate, but simply flees, the rabid animal moves on, but if he bites back, or howls, he worries him, rolling him over and biting again but always in silence, in marked contrast with an enraged but healthy dog. If he comes up with a herd of cattle or pigs or a flock of sheep or fowls, the result is similar. If they remain perfectly still they may possibly entirely escape, but if they scamper off with noise as usually happens, he rushes at them and bites one after another, so that in a confined yard or park all may suffer. A man meeting the dog increases his danger by making an outcry, whereas if he remains perfectly quiet he may possibly escape. Bouley says that a canine attendant is, in a sense, a measure of protection to a man, as the rabid dog attacks first the animal of his own species, giving the man a chance to escape.

In his wanderings the rabid dog will swim rivers, having no dread of water, just as at home he will plunge his nose in water though unable to swallow. When abroad in this way he exhausts himself by his paroxysms and may perish in one of them, or he may meet his death from man or animal. He may in his exhausted state seek a dark secluded place where he may remain for a time and renew his travel later, or he may pass into the paralytic condition and gradually sink.

When shut up, and his vagrant disposition curbed, the paroxysms are liable to appear intermittently, a period of torpor and quiet alternating with one of restless movement, searching, scraping, howling, biting of any animals within reach and later of men, beginning with strangers. A paroxysm can usually be roused by shaking a stick at him and always by presenting another dog.

There is sometimes a difficulty in deglutition, the dog acting as if he had a bone in his throat which he was trying to dislodge, and fatal bites have been sustained during well meant attempts to remove the hypothetical bone. This bears a resemblance to the pharyngeal spasms which are such a marked feature in the hydrophobic man. But it is not roused, as in man, by the sight or sound of water. On the contrary, water is sought and often swallowed at first and even, exceptionally, throughout the disease. He may even take his usual food for a time. The bowels are usually torpid, and any fæces passed are black and fœtid. Diarrhœa may set in later.

In the early stages the rabid dog walks or trots like any other dog. It is only when exhausted by wandering, or violent paroxysms, or both, that he droops his head and ears, hangs the tail between the legs, and slouches along with arched back, and unsteady, swaying limbs. The appearance of these last symptoms implies advancing debility and paresis, and the near approach of paraplegia. The symptoms may, however, be temporarily relieved by a period of seclusion and quiet.

In dumb or paralytic rabies the striking peculiarity is the omission of the preliminary furious stage, and the disease merges at once into paralysis after the premonitory symptoms. In these cases the early nervous symptoms tend to prostration, weakness and dulness or even stupor, there is no disposition to escape, but rather to seek seclusion and quiet, there is rarely howling and then only at first, and soon there is paralysis of the masseters and dropping of the lower jaw, and there is neither ability nor desire to bite. From this the paralysis extends to the hind limbs and then to the fore limbs and trunk. In other cases one limb is the first to suffer, followed by the face, limbs and body. The most prominent feature is the widely opened mouth, the flaccid, hanging tongue and drivelling saliva. The buccal mucosa, at first red and moist, becomes bluish, dry and powdery. The eyes are dull, mournful, suffering or altogether without expression and the pupils are usually widely dilated. The hind limbs are usually utterly helpless and often the fore ones as well, the prostration is extreme and the patient lies quiet and helpless until released by death in two or three days.

A third form, known as the lethargic, is a modification of the paralytic. There may be neither delirium nor marked paralysis, there is no drooping maxilla, pendant tongue nor stringy, hanging saliva, but only a profound, nervous prostration and complete apathy. The patient curls himself up in some dark, quiet corner and cannot be roused by coaxing or punishment, by hunger or thirst. In this, as in the dumb rabies, the common test of presenting another dog fails to rouse excitement or paroxysm. If left undisturbed, these patients may live to the tenth or fifteenth day.

Beside the typical forms there are all intermediate grades, inclining more or less toward the furious, or the paralytic or lethargic. Galtier mentions cases that showed aphasia, scarcely any disposition to bite, swaying movements of the body and limbs, muscular incoördination, tucked up, tender abdomen, rolling the body like a barrel, and marked dyspnœa. Others show at first a slight disposition to bite which is quickly checked by a very early paralysis of the masseters. In still others the attempts to bite are still seen after dropping of the jaw, but though still moved, it cannot be completely closed.

In exceptional cases rabid dogs have shown intermissions of apparent soundness extending over eight days (Youatt), two months (Pasteur), or even six months (Perrin). Rare as these are they must apparently be accepted, and must qualify to some extent the trust reposed in immunization.

Diagnosis. The early diagnosis of rabies in the dog is of supreme importance as enabling the owner to destroy or seclude the dangerous animal before he has developed the disposition to bite and to propagate the disease. If the dog himself is known to have been bitten, every premonitory symptom should be carefully looked for and critically studied. Any change in the general habit, unusual liveliness or dulness, restlessness, or somnolence, unwonted affection or taciturnity, special watchfulness with vision, or hearing, change in the character or tones of the voice or the disposition to use it, propensity to swallow foreign nonalimentary bodies, retching, vomiting or costiveness, propensity to hide away in a dark corner or to leave home and disappear for a day or more, disposition to gnaw and tear up wood or clothing, or hyperæsthesia affecting any of the senses should be carefully noted. Note especially any exaggeration of the generative instinct, any strabismus, or redness of the eyes, any turning of the eyes or head after imaginary objects or snapping at them, any disposition to anger or attack when another dog or cat is presented and any disposition to growl at or to bite a stranger. This tendency to anger and resentment though not always present is usually a symptom of the very greatest value. If a dog is known to have bitten or attempted to bite any person or animal he should be tied or shut up in a safe place for four days at least, under veterinary supervision, and set free only on condition that no symptoms have developed at the end of this period. A hasty decision that a suspected dog is not rabid must lay a veterinarian open to the most serious charges, in case rabies occurs in man or beast from the bites.

Diagnosis is less difficult after the paroxysmal stage has set in. Then there is the extreme irritability and hyperæsthesia, the appearance of reflex spasms of the pharyngeal muscles and chest under the influence of any peripheral excitement, the derangement of the senses, the dilated pupil, the flashing eye, the squinting, the taciturnity and the propensity to bite. Later still the lack of coördination of movement or the paralysis, especially of the hind limbs and of the jaws.

The symptoms may be simulated by those of some other diseases. Thus the bitch which has been exhausted by lactation may show delirium with taciturnity and a disposition to snap. The dog, which is habitually struck or threatened by passers by, may acquire a sinister look and a disposition to bite on every occasion. The presence of a bone or other foreign body fixed between the upper molars, and various injuries of the jaws, teeth or throat may cause inability to swallow, change of the voice and a morose disposition and expression. In such cases there may be vomiting, rubbing the jaws with the paws as if to disengage something and salivation, but there is neither delirium, fury, muscular weakness nor paralysis. In paralytic rabies on the other hand, along with the open mouth and drivelling saliva, there is no disposition to paw the mouth nor face, the buccal mucosa is not simply red but of a deep violet, and there is attendant weakness or paralysis of the hind parts.

Galtier has seen inability to swallow and dropping of the lower jaw from violent stomato-pharyngitis, and from dislocation of the maxilla.

Great tenderness of the skin from inflammation due to blistering or caustic agents or from rheumatism may cause such alert apprehension and disposition to bite in self defense that it may simulate hyperæsthesia of rabies.

From pharyngeal anthrax and violent angina, rabies is distinguished by the extreme exaltation of the special senses, the marked hyperæsthesia and reflex excitability, and, as in the other diseases mentioned, by the perfectly lucid intermissions. Epilepsy is not to be roused by sudden noise, movement nor attempts to swallow, it is not associated with hyperæsthesia and in the haut mal the spasms affect the muscular system more generally. A disposition to bite, and spasms and other nervous symptoms, resembling to some extent those of rabies, have been seen in cases of pentastoma in the nasal sinuses, cysticercas in the brain, filaria immitis in the blood, nematodes, and tænia in the bowels, and auricular acariasis, but there is no such hallucination nor visual delusion, no alteration of the voice, no cutaneous anæsthesia, no exalted reflex excitability. Cadeac finds rabiform symptoms with disorders of the special senses in animals dosed with various essential oils, but the odor of these essences about the mouth and in the breath would serve to distinguish.

Symptoms in Cats. The disease makes a rapid progress, and often ends in death in three or four days. There is a marked change of voice, the calls being hoarse and bass, having been compared to that of a cat in heat. As in the dog, there is a disposition to pick up and swallow objects that are in no sense food, perhaps even its own urine or fæces. There is a great tendency to hide away under furniture or in secluded corners so that the malady may be far advanced before anything is suspected. If seen the patient shows restlessness and frequent movement, with a marked excitability under noise or other disturbing influence. Any disturbance may arouse a paroxysm, accompanied by occasional wide dilatation of the pupils, with flashes from the bright carpet in the vitreous chamber, and the patient may spring at human beings and bite or scratch the hands, face or other uncovered portion of the body. It shows the same disposition to bite small animals, and especially dogs. A glairy often frothy saliva is found in the mouth and often around the lips. As the disease advances and paresis sets in, the cat usually crawls into some dark secluded corner and there dies.

Symptoms in Solipeds. These may vary much in different cases but the leading characteristics, as seen in the dog, are prominent also in the soliped. There is marked restlessness, trembling, and extraordinary hyperæsthesia, as seen in starting at sounds, sudden flashes of light or other causes of disturbance. The ears are held erect and watchful for sounds; the eyes are red and mostly vigilant with at times pupillary dilatation and flashing. The sight of a dog rouses him instantly to attack it with teeth and heels. A stranger is liable to be similarly treated though the horse is still docile and kind to his keeper. There may be itching of the skin and above all of the seat of the bite. During a paroxysm the movements are usually violent, dangerous and even mischievous. There is constant restless movement, pawing, kicking the ground, the stall or attendants, lying down, rolling, rising, straining to urinate, or defecate, eversion of the rectum, shaking the head, muffled neighing, sniffing, snorting, everting of the upper lip, grinding of the teeth, or biting. In the absence of such paroxysms deglutition may be difficult, and the appetite depraved, the patient preferring earth or manure to the natural food. With spasms or paralysis of the pharynx, the food may be returned through the nose. In some cases a stiffness or impaired control of the limbs has suggested inflammation of the feet. In the uncastrated male and female generative excitement is the rule, the protrusion and erection of the penis, the swelling and rigidity of the clitoris, with frequent straining to pass water, the whinnying of the animal for its mate; attempts at copulation and even ejection of semen may be observed. The seat of the bite may be red, angry and itchy, so that the horse rubs, nibbles or gnaws it, often breaking it open anew. There is usually ardent thirst, and no dread of water, even when swallowing is difficult or impossible.

During a violent paroxysm the horse often bites the halter, blanket, manger, rack or stall, seizes the adjoining horse with his teeth, or gnaws, or tears strips of skin from his own shoulder, breast or limbs. In the same way he uses his feet with the most evident purpose of injuring man or beast that may approach him, or he breaks down his stall.

Even at an early stage there may be spasmodic movements of the eyes, face or body, and later there appear signs of paresis, often commencing in a hind limb and extending to paraplegia and general paralysis. Sometimes paralysis begins in the muscles adjoining the seat of the bite. The temperature, at first normal, may rise to 104° F. in the advanced stages, breathing and pulse are greatly accelerated, and the skin may be bathed in perspiration. Spasms are not entirely superseded by paralysis, and death often takes place during a convulsion, from the fourth to the sixth day. In apoplexy death may ensue in one day.

Cases in which paralysis is not preceded by a furious stage are not uncommon in horses.

Symptoms in Cattle. Cattle are frequent victims of rabies, which assumes mostly the furious type, yet in certain outbreaks the paralytic or lethargic form predominates. There is first a strange irritability and restlessness, very unlike the habitual quiet disposition of the animal. The head is raised, the ears alert, the eyes prominent, red, fixed, with occasionally widely dilated pupils and brilliant flashes from the tapetum lucidum. Sometimes they roll or squint. They may appear wild and ferocious or dull and hopeless. Loud and terrified bellowing is not uncommon, switching of the tail, drivelling of saliva, and exceptionally there are attempts to bite. More commonly the natural weapons of offense are employed, the animal kicks, stamps, paws and, above all, tries to gore man or beast, but especially any dog which may appear. They even make such attacks on purely imaginary beings and without any real, tangible enemy present. The bull, cow or heifer present the usual signs of genital orgasm. Appetite is lost or depraved and rumination arrested. Pharyngeal spasms or paralysis is not uncommon, and signs of colic with frequent defecation may be seen. Violent paroxysms are easily roused by the sight of a small animal and especially of a dog. In these attacks the animal may break his horns or teeth or otherwise injure himself. Sometimes the infection wound becomes irritable, itchy and red or even abraded and raw by licking.

The animal becomes rapidly exhausted and even emaciated by the violence of the paroxysms, and paresis sets in with dragging movements of the hind limbs, which advance to paraplegia and general paralysis. Rolling of the eyes, squinting and pupillar dilatation may be present. Death usually takes place from the fourth to the sixth day.

The purely paralytic rabies is not uncommon in cattle. There may be persistent yawning or other sign of nervous exhaustion or depression, halting on one or more limbs, usually behind, which advances to complete paralysis. In other cases the symptoms are those of mental dulness, and profound lethargy with gradually advancing emaciation. In paretic and paralytic cases the characteristic paroxysms on presentation of a dog may be absent.

Ladague claims to have seen intermittent cases with an interval of 27 and even 36 days.

Symptoms in Sheep and Goat. In these there is the same regular succession of symptoms through intense hyperæsthesia and excitability, fury and genital excitement to the terminal paralysis, or the palsy may set in early without premonitory violence. Among the marked features have been noticed, a change of expression, the pupils dilate, eyes flash, they lick or mount their fellows, they lick or rub the bitten part, snort, stamp or scrape with the fore feet, setting themselves in the attitude of attack, they may butt other sheep, fowls, and other animals, above all dogs, or they may deliver the attack in the air only, at some phantom enemy. They may bleat hoarsely or brokenly, grind the teeth, or work the jaws with the formation of froth about the lips. Galtier says they may even attempt to bite. Sooner or later weakness of the limbs, muscular incoördination, swaying and staggering bespeak enervation, the sheep lies constantly, and if raised stands with unsteady semi-flexed limbs, has trembling or convulsions and dies paralytic in from two to five days. Death has been delayed till the twelfth day (goat) or thirteenth (sheep). In some cases paralysis has been present from the start, the subject lying prostrate from the first.

Rabies in the Camel and Deer. In Algiers camels are often times bitten by rabid dogs and contract the disease showing both furious and paralytic symptoms. They are especially dangerous because of their propensity to bite, and to scatter the virulent product by sneezing.

In England rabies has prevailed extensively in parks of deer, which shut inside high walls have been bitten remorselessly by rabid dogs that had gained admittance. The symptoms of hyperæsthesia and paralysis followed the same general course as in other animals.

Symptoms in Swine. Rabid pigs are usually very restless, excitable and sensitive to all causes of disturbance. They will hide under the litter in the darkest corner but soon start without apparent cause, turn around and lie down again, or they bound up with grunt or scream and rush off as if pursued, push or leap against the wall, stand with ears pricked as if listening, and start violently at any noise or a flash from a lantern, trembling, squealing, or having muscular jerking. The eyes are at times fixed, or may roll, squint or flash from pupillary dilatation. The voice is hoarse, deglutition difficult, there is frequent clenching of the jaws, or grinding of the teeth, and frothing around the mouth. The victim may tear with his teeth the boards of his pen, or gnaw pieces of wood, he may swallow wood, pebbles or earth, and plunge his face in water or other liquid without fear or apparent dread or dislike. The disposition to bite may be viciously shown, and he may strike dangerously with his tusks, while in other cases it may be entirely absent. Peuch quotes cases in which no paroxysm was aroused by the sight of a dog, and others in which the pig would rise and grunt without showing any desire to bite.

Sows will sometimes bite or devour their offspring during a paroxysm, yet nurse and care for the survivors during the intervals.

Emaciation, weakness, exhaustion, lethargy and paralysis appear early, the victim remains down, or, if raised, moves weakly and unsteadily and no longer pays attention to noises nor blows. Death may ensue from the first to the sixth day.

Symptoms in Rabbits. Experimental cases in rabbits are now very common and usually assume the paralytic or lethargic type, there is weakness in the hind parts, advancing in a few hours to paraplegia, the fore limbs may be used for a time while the hind are flaccid and dragged behind, or the animal lies on the sternum and belly with the head sunken and resting on the feet, or he lies extended on his side, in a state of insensibility. In the early stages he may still masticate, with froth collecting on the lips, but there is difficulty in swallowing. If a foot is pinched it is drawn up often with a cry. The bowels are torpid though a few small, round, hard pellets are sometimes passed or a little urine. Incubation is shorter than in the dog, and the virus retains this habit when inoculated on other animals.

In the experimental cases in the Anti-rabic Institute in St. Petersburg, Helman found that the rabbits inoculated with virus from dogs having furious rabies, contracted furious rabies, while those inoculated from the less furious type of street rabies had the disease in the dumb form.

Symptoms in the Guinea-pig. In this animal as in the rabbit the disease has been mainly seen in the experimental form, and has assumed the paralytic type. It trembles, moves stiffly or weakly, lies most of its time and passes rapidly into paralysis. There is usually no tendency to bite, yet Peuch in a case of intraocular inoculation from a rabid cat observed the most violent excitement, loud hoarse screaming, bounding in different directions, biting of the wires of the cage, and other manifestations of violent rabies. In both forms there are liable to be convulsive movements of the jaws, accumulation of frothy saliva, and a free discharge of urine.

Symptoms in Birds. Chickens bitten by mad dogs have been seen to prove restless, erecting the feathers and moving aggressively toward man or dog or phantoms of their imagination and attacking with bill or spurs or both. This, however, rapidly advances to paralysis and death. In cases due to intracranial inoculation on the other hand, somnolence, lethargy, or coma appeared early, and was quickly followed by paralysis. This affects especially the legs and neck. Recoveries are common and the animal is thereafter immune. Subsidence, with complete intermission of symptoms, is more common than in rabbits, the disease reappearing later, and perhaps finally ending in recovery.

Symptoms in Wild Carnivora. The rabid wolf, fox, jackal, hyena, coyote, ferret, polecat and skunk lose their fear of man, and approach and attack him either in field, village or city. The disease has its furious and paralytic stages as in the dog, and the animals attack according to their nature, wolves being dangerous from flying at the face and throat, and skunks from stealing up and biting without warning.

Symptoms in Man. After the period of incubation prodromata may be present, or there may be suddenly and without any premonition, violent spasms of the pharynx and inability to swallow. The premonitory symptoms when present consist in irritability of the cicatrix which becomes red or blue, swollen, itchy or pricking, and an aura or shooting pain may extend from this toward the heart. There is anxiety, sighing, tremor, restlessness impelling to frequent change of place, insomnia, disagreeable or painful dreams, weariness, and gloomy forebodings. The face is pale and drawn, and the eyes wander or have a look of apprehension. There is some fever and often marked thirst, and the attempt to swallow rouses slight spasm or a sensation of tightness in the throat. The fauces, pharynx and eyes are congested, reddened and it may be swollen. Pulse and respiration are both quickened, the inspiration being often prolonged and sighing, and the expiration sobbing. At first the intellect is unimpaired; there is no illusion nor hallucination.

In cases in which premonitory symptoms are lacking, violent spasms of the throat and chest are commonly roused by an attempt to drink and this is so painful that the patient cannot again be induced to try. After this any suggestion of drinking, the offer of drink, the noise of trickling water, the sight of water, the sight of a vessel in which the water was contained, or even of a clear shining surface of glass or metal is likely to bring on a paroxysm. This hydrophobia is peculiar to man being rarely seen in rabid animals. During a paroxysm dyspnœa is extreme, respiration is gasping or sighing, and in the attempt to dislodge the tenacious mucus which is present in the throat, hoarse or shrill inarticulate sounds are emitted which have been supposed to resemble the bark of the dog. There is a sense of closure of the throat and of rising of the stomach, and retching or even vomiting may ensue. Hyperæsthesia, reflex irritability, and exaltation of the special senses, now become extreme, so that a paroxysm may be brought on by the slightest disturbance, a current of air, a bright light, the rustling of a dress, the noise of a footfall, the noise even of talking, or a slight touch. The “tendon reflex” and skin reflex are often much encreased. During a paroxysm there are muscular trembling and clonic spasms,—sometimes opisthotonos. The intervals of complete relaxation, however, serve to distinguish from tetanus. The face is red and drawn, the eyes congested and sometimes squinting, the pupils dilated and the expression one of suffering, apprehension and horror. Mental disorder appears sooner or later, the speech is disconnected, with indication of delusions from which the patient may at first be recalled by the attendant. There is, however, a constant disposition to be reticent, morose and above all, suspicious, as shown by the absence of a direct look, and the frequency of side glances as though in expectation of a hidden danger. This may even rise to mania, the patient charges those about him with having caused his sufferings, or with conspiracy to injure him, and he may seek to defend himself with hands, feet, teeth or any available object. The necessary restraint aggravates and prolongs the attack. On its subsidence the patient collects his scattered senses, regrets, apologizes, and warns against future occurrences of the same kind which he realizes to be beyond his control. Sometimes the delusions continue during the remission as well. Sexual excitement is common in man as in animals.

The convulsive paroxysms may last ½ to 1 hour, and they tend to encrease in duration and force. A violent paroxysm may cause sudden death from asphyxia or apoplexy.

Sooner or later exhaustion and paresis appear. The convulsions become gradually weaker, the reflex irritability and hyperæsthesia abate, and the patient may become once more able to swallow, but an ascending paralysis, beginning in the limbs spreads over the body and death occurs in from one to eighteen hours. In the paralytic stage there may still be slight jerking of the muscles, or tremors, but violent convulsion no longer occurs, and there is extreme prostration, with hurried, rattling breathing, small, weak, irregular pulse and finally, stupor and coma.

Diagnosis in man. The only additional point, to those already stated for animals, is in regard to lyssophobia. This false form of hydrophobia is usually fortified by the fact of a bite, but as a rule it lacks the exaltation of common sensation and of the special senses which characterizes genuine hydrophobia. Very often also there is a flaw in the history, the dog that inflicted the bite is unknown and may still be alive, in which case no medicine is so good as to bring the healthy dog into the presence of the patient. The dog may have been killed by an excited community without any identification of his symptoms as those of rabies or any post mortem examination to throw light on his case. The attack may have come on after a conversation on the subject of the bite, or of rabies, and perhaps, as in the case of the Montpellier cadet, long after and when the patient had for the first time heard that the dog that bit him had been mad. It may be that rabies does not exist in the district and that no other victim in man nor beast can be adduced. It may be that the patient has a nervous organization or is subject to hysteria, and therefore specially predisposed to any disease of the imagination. Such cases cannot be accepted as rabies until a successful inoculation has been made on one or more animals.

RABIES AND HYDROPHOBIA. LESIONS. TREATMENT AND PREVENTION.

Lesions: blood fluid or clot diffluent. Fauces, pharynx and larynx congested, exceptionally ulcerated. In dog, mouth cyanotic, with tenacious mucus, sublingual petechiæ and erosions, stomach contains many foreign bodies, but no food, small intestines and cæcum empty, and like stomach congested: petechiæ on skin and elsewhere, cutaneous and cardiac veins gorged, hyperæmic liver, kidneys and bladder: brain congested, capillaries dilated or blocked, hæmorrhagic, leucocytic collections in lymph spaces, nerve cells swell up with hyaline bodies near nuclei, and neuroglia has hyperplasia, especially near the respiratory centre. Congestion of nerves. Leucocytosis. Therapeutic treatment: Orrotherapy: of little avail. Nerve sedatives; darkness, quiet, nutritive enemata, chloroform, chloral, etc. Prevention: eradicate the virus; muzzle all dogs absolutely, under heavy penalty, for one year; Gower’s view; examples of muzzling; collar with name and owner, shoot all unmuzzled dogs, cage for 6 months bitten dogs and cats, also all imported dogs, shut up in cage for 10 days all dogs that have bitten; treatment of bites, tourniquet, cup, suck through tube, wring wound, cauterize—hot skewer, cautery, mineral solid caustic, mineral acids on pledget or through a tube; Pasteur method: emulsion of spinal cord (of rabid rabbit) after aseptic æration in vitro for 3 to 14 days, injected in graduated doses for 21 days, table of doses, table of mortality; Orrotherapy: by blood serum of immune animal: advantages, disadvantages—technique: Use of sterilized brain matter from rabid animal: experiments; protection by snake venom.

Pathological Anatomy. The blood is fluid or the clot diffluent. Congestion of the fauces, pharynx and larynx is patent during life but may have disappeared after death. Yet I have seen extensive ulceration of the vocal cords in a rabid cow. The congestion may extend to the trachea bronchia and lungs. In dogs the buccal mucosa is often cyanotic, covered with a thick mucus, and may present sublingual ecchymoses and erosions, and wounds of various kinds made by objects bitten or swallowed. The stomach in the same animal is usually almost pathognomonic, being filled with foreign bodies of all kinds—straw, hay, hair, wood, coal, pebbles, pieces of metal, cord, leather, cloth, earth, sand, etc.—the result of the depraved appetite. There is an absence of normal food principles in stomach and small intestines and the cæcum and colon are usually empty. The gastric mucosa is congested, and may be wounded and its contents mixed with blood. Such a condition of the stomach in a dog, that has been bitten, and which after a customary incubation period has shown symptoms like those of rabies, is virtually diagnostic.

The following lesions are common to man and animals: Marked emaciation, cyanosis or petechiæ in skins that are naturally white, early sepsis, cutaneous veins and heart gorged with dark inspissated blood, hyperæmic liver and kidneys, and slightly congested, petechiated empty bladder.

The most important lesions, however are those of the central nervous system. In seven cases out of nine, Gowers found these very distinct. There were vascular disturbance, capillary dilatation, capillary clots, minute hæmorrhages, and accumulations around the affected capillaries of leucocytes occupying the lymph spaces. Benedikt and Babes attach much importance to the formation of hyaline patches in the thickened walls of the vessels and around them, compressing the vessels in some cases to virtual obliteration. The nerve cells swell up, and show small hyaline bodies in the vicinity of the nuclei, and these latter finally disappear. Germano and Capobianco found in addition marked hyperplasia of the neuroglia. Babes, who looks on these changes as pathognomonic, takes a small portion of spinal cord, hardens it in alcohol for 24 hours, stains it with aniline red and examines for the characteristic hyaline nodes.

These brain lesions have been found mainly in the medulla near the floor of the fourth ventricle and the respiratory center, but they are also to be found in other parts of the encephalon and spinal cord. The greater constancy of the medullary lesions serves to explain the characteristic symptoms.

Congestions of the peripheral nerves have also been found. Lüttkemüller found in rabies a moderate increase of the white blood corpuscles and a great number of microcytes.

Therapeutic Treatment. It was long thought that rabies was necessarily fatal, as indeed nearly all developed cases are to the present day. For this reason and much more on account of the risk of preservation and propagation of the deadly germ, the attempts at curative treatment in the lower animals have been looked on as utterly unwarranted or absolutely criminal. Yet it is now known that very exceptionally a recovery takes place, and in that case immunity for the future may be counted on. Yet the frightful danger attendant on the preservation and treatment of a rabid animal, may well forbid the keeping of any of the lower animals affected by rabies unless it be in the safest seclusion and for the production of immunizing or curative products.

Orrotherapy with the blood serum of an immunized animal is of little value, and attended by risk from the rabid animal, but will be noticed below as a prophylactic.

In man when the disease is manifested, palliation has been obtained and very exceptionally recovery, under darkness, quiet, nutritious enemata and antispasmodics or soporifics. Among such antispasmodics and nerve sedatives may be named chloroform, chloral, curare (3 alleged recoveries), eserine (1 recovery), pilocarpin (1 recovery), morphia, datura, atropia, and bromide of potassium. Others have recovered without any medicinal treatment, so that the mildness of the attack must be duly considered in every case.

Prophylaxis. The most effective way of preventing rabies is to eradicate the virus from the country. All immunizing measures resorted to after the infecting bite has been sustained, are of little value as compared with this, they may save the bitten individual, but they do nothing to prevent others from being bitten in the future, and indirectly they contribute to the maintenance of the disease by drawing attention from such radical measures as would rid the country forever of the scourge. In his great work on Diseases of the Nervous System, Gowers puts this not a whit too strongly when he says: “The enforced muzzling of dogs for a period of one year would almost certainly stamp out the disease. That such a measure is not adopted is a national disgrace, which is accentuated by the fact that the Government derives part of its revenue from a tax upon dogs. The opposition to the use of the muzzle is one of the strangest developments of morbid sentiment. There are apparently thousands of well-meaning people who would prefer that hundreds of dogs should perish every year of a painful disease, that many human lives should be annually lost, and scores of persons should be subjected for months to acute mental agony—rather than that dogs should be made to wear an apparatus which causes them a trifling annoyance. This perverted sentiment ought to be met with universal abhorrence as a disgrace to humanity.” Such a statute, backed by a penalty in some degree commensurate to the homicidal criminality of the person who would leave his dog free to inflict this horrible disease on humanity would doubtless be effectual, but some nations have such laws on their statute books, and yet allow them to become dead letters. Others have enforced them to good purpose. Berlin in 1853 had many cases of rabies and muzzling was enforced. In three years the disease was completely eradicated and the city enjoyed nine years of immunity or so long as the law was enforced. Similar successes were met with in Holland, new cases occurring only on the borders or in imported dogs. London in 1889 had 123 cases and muzzling was enjoined. In 1892 the cases were reduced to 3, and the muzzling law was suspended, and a steady yearly encrease resulted, until the 1st three months of 1896 furnished as many as 72 cases.

In the absence of this radical measure muzzling should be enforced for a year in any locality where a case of rabies has occurred, and every dog should wear a collar with the name and residence of his owner inscribed on it. All stray dogs and all unmuzzled ones should be summarily shot. Dogs and cats that have been bitten by rabid animals should be destroyed or shut up in cages for six months under veterinary supervision. Imported dogs should be similarly secluded. Dogs that have bitten animals or men should be shut up for ten days under supervision, when, if rabid, the animal will develop unequivocal symptoms.

Treatment of bites. Absorption from a wound in a limb may be prevented by applying a tourniquet. Wounds on the body may be cupped, or sucked through a tube. Or the wound may be wrung to encrease the flow of blood. As soon as possible it should be thoroughly cauterized. A hot skewer, a Paquelin cautery, a stick of silver nitrate or zinc chloride or caustic potash or a crystal of cupric sulphate will meet this end. If liquid caustics are to be employed they can be applied to all parts of the wound by means of a pipette, a glass tube, or swab.

With thorough cauterization shortly after the bite there is practically nothing to fear, and even if it has not been applied for hours after, it is still valuable in destroying the poison left in the wound from which a continuous infection of the brain, by the transmission of the unknown germ and its toxins, would otherwise take place. It has besides in the human being a good moral effect against lyssophobia by giving the bitten person a certain sense of protection.

The Pasteur Method. This is based on the fact that the spinal cord of the tetanic rabbit when removed aseptically, and kept in vitro in a dry atmosphere, loses in virulence day by day, until on the fourteenth day it is harmless. To render the air more drying, caustic potash is introduced into the flask. The culture of the poison in rabbits intensifies its virulence, until the virus becomes the strongest known and when inoculated subdurally, reduces the incubation to six or seven days.

In Pasteur’s early experiments he began injecting the emulsion of the cord desiccated for 14 days, following with that of the 13th day, and so on to that of the 5th. It was soon found that this was comparatively ineffective when inoculation had been made with a strong virus or in a large dose, and the treatment for such cases was modified to what is now known as the intensive method. The weaker forms of the virus are given at shorter intervals on the first days of treatment, and the stronger forms repeated again and again, and, in place of a 15 days, course of treatment, this is extended to 21 days. The following table illustrates the course:

│ _Number of │ _Day of │ Days that │ Treatment._ │ cord had │Dose Injected. │ been │ │desiccated._│ ───────┬────────┼────────────┼──────────────── 1st day│morning.│ 14 days. │ 3cc. „ │ „ │ 13 days. │ „ ───────┼────────┼────────────┼──────────────── „ │evening.│ 12 „ │ „ „ │ „ │ 11 „ │ „ ───────┼────────┼────────────┼──────────────── 2d „│morning.│ 10 „ │ 3cc. „ │ „ │ 9 „ │ „ ───────┼────────┼────────────┼──────────────── „ │evening.│ 8 „ │ „ „ │ „ │ 7 „ │ „ ───────┼────────┼────────────┼──────────────── 3d „│morning.│ 6 „ │ 2cc. „ │evening.│ 6 „ │ „ ───────┼────────┼────────────┼──────────────── 4th „│ │ 5 „ │ 2cc. 5th „│ │ 5 „ │ 2cc. 6th „│ │ 4 „ │ 2cc. 7th „│ │ 3 „ │ 1cc. 8th „│ │ 4 „ │ 2cc. 9th „│ │ 3 „ │ 1½cc. 10th „│ │ 5 „ │ 2cc. 11th „│ │ 5 „ │ 2cc. 12th „│ │ 4 „ │ 2cc. 13th „│ │ 4 „ │ 2cc. 14th „│ │ 3 „ │ 2cc. 15th „│ │ 3 „ │ 2cc. 16th „│ │ 5 „ │ 2cc. 17th „│ │ 4 „ │ 2cc. 18th „│ │ 3 „ │ 2cc. 19th „│ │ 5 „ │ 2cc. 20th „│ │ 4 „ │ 2cc. 21st „│ │ 3 „ │ 2cc.

Under this treatment the system becomes educated in the production of antitoxins, and perhaps also in phagocytosis so that when subjected to the lethal doses of three, four, five and six days preservation, it successfully resists them. The most conclusive argument in favor of its efficacy is this undeniable fact that the individual escapes death under injected doses which in any unprotected system would prove fatal.

The results as given by the report of the Pasteur Institute are furnished in the following table, from which are excluded such cases only as developed the disease during the course of treatment, which therefore remained incomplete.

Years. Persons Treated. Deaths. Mortality per cent. 1886 2671 25 0.94 1887 1770 14 0.79 1888 1622 9 0.55 1889 1830 7 0.38 1890 1540 5 0.32 1891 1559 4 0.25 1892 1790 4 0.22 1893 1648 6 0.36 1894 1387 7 0.50 1895 1520 5 0.33 1896 1308 4 0.30 1897 1521 6 0.39

The following table gives the number of individuals treated who had been bitten by animals which had been proved rabid by successful inoculation of other animals, and of those bitten by reputedly rabid animals, and their respective mortality.

Died. Mort. per ct. Bitten by animals proved rabid by inoculation 2,872 20 0.69 Bitten by animals pronounced rabid by veterinarian 12,547 61 0.48 Bitten by animals suspected of rabies 4,747 15 0.31 ———— Average mortality 0.46

The Pasteur treatment by its great success in persons who have already been bitten has in a great measure robbed hydrophobia of its terrors, only it must be resorted to as early as possible in the period of incubation. It has also been advocated as a means of immunizing subjects that have not been bitten but are more or less liable to be so, and on this basis a large number of dogs have been passed through it. This is not likely to be adopted in the case of the human being, the more so that a few, although on the whole a very limited number of persons, have developed rabies long after the taking of the Pasteur treatment. This has been attributed to the retention of latent germs in the system, and argues besides a remaining susceptibility to the poison.

In spite of its brilliant success and the great boon it has been to humanity, the Pasteur treatment is not an ideal one. Its success does not consist in an entire extinction of rabies, but merely in the reducing of its evil results; its success is indeed based on a preservation and propagation of the germ and a continuous danger of infection of new subjects; finally, the proposition to end the disease by passing the whole canine race through the treatment, is open to the objections that this would require a fabulous outlay, and that even then some rare cases are not found to be fully protected. To continue the disease, when it may be exterminated, and to palliate its results by the treatment of generation after generation of dogs, must be promptly condemned by the political economist, to say nothing of the consideration of probable human infection.

Orrotherapy. It is not surprising that essays were made in the line of serum treatment. Babes and Lepp in 1889 had some encouraging results in transferring the blood of an immune animal into a healthy one. But Tizzoni, Schwarz and Centanni have especially worked out this method. These have shown that the blood serum of immunized animals destroyed the virulence of the rabic poison, whether mixed with it before injection, or injected with it, or injected within twenty-four hours afterward. A very small amount of the serum is required and though delayed until the end of the first half of the incubation period, it is only necessary to multiply the amount by six or eight times. In this it has a great advantage over the antitoxin of diphtheria or tetanus, the former of which has to be multiplied 20 to 100 times, and the latter 1000 to 2000 times in the later stages of incubation. Further, it is possible by drying to secure the serum in a permanent form which will remain active for a length of time if secluded from air and light.

This has the decided advantages over the Pasteur treatment, (1) that it employs the antitoxin already formed instead of waiting for its formation in the body of the subject injected with the attenuated virus, and (2) that it does not introduce into the system a virulent germ capable of propagating in a favorable medium, but only an agent which is antidotal to that germ.

It has the disadvantage as compared with Pasteur’s method that its action is purely therapeutic in the sense of acting as an antidote, while it produces no permanent immunity. It does not like the toxins educate the cells to produce an encrease of antitoxin, and it can only protect so long as it remains in the system. Whenever it is eliminated or destroyed, the susceptibility to rabies returns. Hence it is important to continue its administration as long as the microbe remains in the system. As in tetanus and diphtheria antitoxin treatment, it is also important to destroy the microbe and its toxins in the infection wound.

The animal which is to furnish the antitoxin is immunized as in the Pasteur method by a succession of graduated doses of rabic virus. After a treatment of 20 days the rabbit or sheep furnishes a serum which is protective when injected in the proportion of 1 of serum to 25,000 of body weight, even though its use be delayed until 24 hours after the introduction of the virus. The sheep can be immunized in 12 days by doses of 0.25 gramme of emulsion of the infected cord to every kilogramme of body weight. To maintain the serum at its highest standard the treatment must be repeated at intervals of 2 to 5 months, as the animal may be able to bear it without loss of condition.

Treatment with Sterilized Brain Matter from a Rabid Animal. In 1886 I sterilized with heat an emulsion of the spinal cord of a man who died of hydrophobia and injected two rabbits with 3 one drachm doses each, and a third with 4 one drachm doses on as many successive days. These rabbits were afterwards inoculated with virulent spinal cord and remained well for nine months, while three control rabbits injected with virulent cord, but which had received no previous treatment died rabid.

Puscarin and Vesesco have shown that the virus is rapidly weakened by heat up to 60° C. at which point the virulence is destroyed. It becomes easy therefore to secure in this way a toxin uncomplicated by any living microbe.

Theoretically the sterilization and use of infecting nervous substance, should share with the Pasteur method the advantage of the selective action of the medullary matter in uniting with the toxins and robbing them to a greater or less extent of their toxicity. It has the additional recommendation that it introduces no living germ, and thus obviates any possible danger of the propagation of disease through the animal operated on.

Fernandez claims an immunity from rabies for dogs that have survived the bite of a viper. Many facts and experiments are adduced in support of this.

TETANUS.

Synonyms. Definition: infectious disease, due to bacillus, and shown by tonic spasms of groups of voluntary muscles. Animals susceptible: warm-blooded animals—dogs and chickens least: ⅔ds solipeds, ⅐th cattle. Pathology and Causes: Bacillus tetani: 4 to 5µ by 0.2 to 0.3µ, often enlarged by spore at one end; anærobic, liquefying, tardily motile, until spore forms, grows in ordinary, alkaline media under hydrogen, death point 60° to 65° C. (140° to 149° F.), for spores 80° C. (176° F.), for an hour, dried it lives for years, in putrid matter 2½ months, stains easily, saprophytic in garden mould, in ingesta of man and horse, abundant in tropics; infection local, killed by oxygen in blood, toxins tetanize: tetanin, spasmotoxin, toxalbumin, diastase; spasms first local near wound, then abruptly general, intravenously causes general spasms first, theory of fermentation in blood; changes in nerve cells, neuroglia, ependyma, peripheral nerves: muscles soft, pallid, red, ruptured fibres, ecchymosis; rigor mortis early, marked: sarco-lactic acid. Accessory causes: traumas and their causes, parturition, umbilical infection, alimentary. General symptoms: incubation 3 to 15 days, minimum 6 hours; tonic contraction of muscle groups of locomotor system beginning near infection wound,—trismus, orthrotonos, opisthotonos, emprosthotonos, pleurosthotonos, ocular muscles; costive, difficult urination, hyperæsthesia, irritability, perspiration, hyperthermia, mastication, deglutition, sucking. Symptoms in horse: neck raised concave above, nose elevated, nostrils wide, eyes sunken, haw protruded, ears rigid, pricked, facial muscles rigid, prominent, mouth drawn back, muscles of back hard, tail elevated, trembles, limbs extended outward, stiff, stilty, jaws clenched or open slightly, stands. Symptoms in cattle; sheep and goat; swine; dogs; birds: Course: violent cases with short incubation are rapid and fatal; mild ones with prolonged incubation hopeful; cattle slow, sheep, goats and dogs acute. Mortality: sheep and pigs 100 per cent.; horses 75 to 85; cows 70 to 80; lambs very fatal. Death from asphyxia, hyperpyrexia, or exhaustion. Lesions: trauma, often healed; congested nerves, gray horns of myelon, increase of cells and granules in nervous matter of cord, corpus striatum, cerebellum; blood extravasations at torn muscle fibres, intestinal and cystic congestion. Diagnosis: from strychnia poisoning by slow advance, and persistence of spasm; from rabies by absence of bite, the continuous masseteric spasms, by absence of resentment, mischief, hallucinations or depraved appetite; from rheumatism by the persistent trismus, hyperæsthesia and excitability; from meningitis by the trismus, perfect mentality, absence of clonic spasm; from tetany by shorter and less perfect remissions, failure to develop under nerve pressure, or improve under thyroid extract; from laminitis by the absence of high early hyperthermia, heat and tenderness of the feet, and advance of hind legs under the body. Treatment: best in slight cases, after long incubation, with slow progress; antispasmodics; rest, darkness, absolute quiet, no litter, nor visitors, slings, sloppy food, gruels, milk, green food, at level of manger; clothing to favor perspiration; excision or antisepsis of wound, carbolic acid, bleeding, opium, prussic acid, potassium cyanide, bromides, physostigma, eserine, chloroform, sulphonal, trional, tartar emetic, tobacco, apomorphia, lobelia, phenacetin, acetanilid, cocaine, chloral, phenic acid, iodine terchloride, iodide of potassium, orrotherapy, antitoxin; best as a preventive, value decreases with development of disease; cerebral injections; brain emulsion; use up toxins in blood; no use if nerve centres are already in combination with toxins, only to ward off fresh toxin. Toxins produce leucocytosis. Prevention: disinfection of all dirty wounds, injections of phenic acid, or iodine; remove foreign bodies, use muriatic and carbolic acids; antisepsis of navel; disinfection of stables, feet, careful shoeing; immunization.

Synonyms. Lockjaw. Trismus.

Definition. An infectious disease of animals and man, characterized by tonic spasms of the voluntary muscles in a given region or more generally, with exacerbations, and dependent on the bacillus tetani.

Animals susceptible. Immunity cannot be claimed for any class of warm blooded animal. Experimentally the dog and chicken prove among the most refractory, in keeping with the comparative insusceptibility of the last named animal to strychnia, but neither can be held to be in any sense immune. Inoculated frogs become tetanic if the temperature is maintained above the normal standard. In 208 cases in domestic animals recorded by Cadiot and Hoffmann, 140 were in horses, 10 in mules, 5 in asses, (solipeds, 155), 28 in cattle, 9 in sheep, 5 in goats, 5 in pigs, and 6 in dogs. Such statistics are liable to prove misleading when we have no means of comparing them with the members of the different genera from which the cases were drawn and the relative exposure of each genus to traumatic lesions (infection atria). Solipeds lead with practically ⅔ds of the entire number of cases, but these were presumably the most numerous of the domestic animals, and preëminently the work animals and therefore the most liable to traumatism. Cattle follow with ⅐th of all cases but here again the large numbers to be drawn upon, and the proportion of work oxen and wounds, are to be considered. The omnivora and carnivora are comparatively little susceptible and among these the chicken may be included. The omnivorous rat is quite susceptible.

Tetanus occurs in 1 per 1000 sick horses in the Prussian army (Friedberger and Fröhner), and in 1 per 3000 sick in that of Wurtenburg (Hering). It is so prevalent in San Domingo that a gelding costs twice as much as a stallion (Wagenfeld). Heat and filth favor its preservation.

In man tetanus is most frequent as the result of wounds (in feet and hands) which are most likely to come in contact with the soil, and it has visibly decreased in connection with the general adoption of antiseptic surgery.

Pathology and Etiology. Sir James Simpson suggested in 1854 that puerperal and surgical tetanus was due to the absorption of a poison produced in the wound (Woodhead). Spinola charged it on infection in wounds in horses. Carle and Rattone in 1884 successfully inoculated 11 out of 12 rabbits with the products from the wound of a man suffering from tetanus. A year later Nicolaier produced tetanus in animals by inoculating them subcutem with garden mould or street dust, and found in the suppurating wounds in connection with various other microbes a minute bacillus longer but thinner than that of mouse septicæmia to which he attributed the tetanizing action. In 1886 Rosenbach inoculated two Guinea pigs with the pus of a tetanic man, and found in the sores of the tetanic pigs the bacillus of Nicolaier in company with another larger spore-forming bacillus. In 1889 Kitasato succeeded in making pure cultures of the bacillus tetani, and successfully inoculated the disease on mice, rabbits, and Guinea pigs producing typical tetanic symptoms and death. This was promptly corroborated by Tizzoni and Cattani and later by a great variety of observers.

Bacillus Tetani. This organism is a minute rod 4 to 5μ in length by 0.2 to 0.3μ in thickness, with slightly rounded ends. In many mature forms the one end is enlarged by the formation of a spherical, refrangent spore which gives the bacillus the appearance of a pin or a “drum-stick.”

The bacillus is anærobic, liquefying, tardily motile, and sporogenous. When spores form the bacillus loses its motility. It grows at room temperatures, in ordinary culture media which have a feebly alkaline reaction, and in an atmosphere of hydrogen, but more actively at a temperature of 36° to 38° C. Below 14° C. growth ceases and the bacillus is killed at 60° to 65° C. The spores, however, can resist a temperature of 80° C., in water for an hour, and 100° C. for four minutes. It was this unusual resistance of the spore to heat that enabled Kitasato to kill off the contaminating organisms and obtain pure cultures from the surviving spores. The spores will survive desiccation for years, retaining their virulence, and may live 2½ months in putrefying material. The addition to the culture medium of 1½ to 2 per cent. of glucose makes the growth much more rapid and abundant, and causes opacity in the medium. The upper portion clears up in 6 or 7 days by the precipitation of the bacilli as a grayish mass. In a glucose culture medium growth is not prevented by the presence of oxygen at the surface. The colonies formed in gelatine plate cultures show an opaque centre with fine divergent rays, and a similar radiating growth is shown in deep stick cultures. At the end of the second week the gelatine begins to liquefy and form a little gas, and finally the whole mass becomes soft and sticky. The bacillus does not liquefy blood serum. Cultures have a disagreeable aromatic odor.

The bacilli stain readily in aniline colors and by Gram’s method. The spores may be stained by Ziehl’s method. To 10 parts of a 10 per cent. alcoholic solution of basic fuchsin, add 100 parts of a watery solution of carbolic acid. Float the cover glass upon this, heating gently for three to five minutes until steam begins to rise, wash well in water, and decolorize in nitric or sulphuric acid, 25 per cent. solution, then in 60 per cent. alcohol to remove color from albuminous background. Wash in water and mount. By placing the specimen for two minutes in a watery solution of methylene blue a contrast is obtained, the bacillus blue and the spore red.

Outside the animal body the bacillus has a saprophytic life in rich garden mould, street dust, stables, yards and drains, and the cracks of floors. Nicolaier failed to obtain it in soil from forests and from the deeper layers of garden earth. Marchesi found it to a depth of two metres but no more. Again it is much more abundant in tropical countries than in temperate and cold ones, and appears to be to a great extent limited to particular localities. It has been found in the intestinal contents of man and horse (Babes, Sormani), and in horse manure, and this mingling with the surface soil and generating an abundance of ammonia determines the anærobic conditions which favor the growth of the microbe. This serves to explain the remarkable prevalence of the disease among those living or working about stables, gardeners, agricultural laborers, soldiers on campaign, and children and others walking with bare feet. The contact with rich infected soil greatly favors inoculation in any accidental wound.

An important feature in the pathology of tetanus is that the bacillus is confined to the seat of the inoculation wound. The many attempts to transmit the infection by blood, nervous matter, and by one or other of the tissues have uniformly failed, though the pus of the infected wound has proved virulent. Similarly, the attempts of Kitasato and others to obtain cultures from the animal liquids or tissues apart from the wound have been futile.

By inoculating the toxins remaining in the pus of the infection wound, however, or in virulent cultures from which the bacilli have been removed by filtration or in which they have been destroyed by heat, all the symptoms of tetanus can be produced (Kitasato, Kund Faber, etc.) In such cases too, the symptoms appear at once, as soon as the toxin is absorbed, and not after a definite period of incubation as in inoculation of the unaltered virus. Kitasato, Vaillard and Vincent reached this conclusion by another channel. They inoculated mice at the root of the tail with virulent tetanus cultures, and at definite intervals after, namely, half an hour, one hour, and one and a half hour, they made a circular incision round the wound and thoroughly cauterized the whole, thus destroying all the inoculated bacilli. They found that tetanus was prevented in those animals only which were operated on at the first half hour. Again, Kitasato injected mice with 0.2 to 0.3cc. of the blood from the heart of a fresh tetanus cadaver, and thereby produced typical tetanic symptoms and death in 1 to 3 days.

Various poisons have been separated from cultures of bacillus tetani. Brieger isolated three substances—tetanin, tetano-toxin and spasmotoxin—which in large doses caused tetanic symptoms and even death. Brieger and Fränkel later isolated a toxalbumin which proved of incomparably greater potency. Again, Brieger, Kitasato and Wehl separated what appeared to be an enzyme or diastase which proved 500 times more potent than atropia. This was in the form of yellow, transparent flakes, soluble in water, but which was not destroyed by drying, nor in the dry state by absolute alcohol, chloroform nor anhydrous ether, but which, like the virulent cultures of tetanus, was easily destroyed by acids, alkalies, hydrogen sulphide, or heat. Like the natural virulent product this may be kept unchanged for months on ice, apart from the light, or with the addition of 0.5 per cent. of carbolic acid, or its own bulk of glycerine. It kills the Guinea-pig in a dose of 0.000025 gramme, and the mouse in a dose of 0.00000025 gramme.

While the propagation of the bacillus in the animal body appears to be local, and the general tetanic symptoms are caused by the absorption of the poison, it remains to be seen on what organ this directly operates, and what accessory conditions favor its efficiency.

In cases due to inoculation the spasms are at first local in the vicinity of the inoculation wound and later become general. Kund Faber shows that there is no gradual transition from the local manifestations to the general, but the latter appear abruptly and in force as a new and independent phenomenon. When we consider further that in inoculation with pure cultures (uncontamininated by pus or saprophytic microbes) the wound often heals promptly, without any sign of remaining local irritation, we may conclude that simple nervous irritation in the sore cannot be invoked as a cause of the early local spasm. It is more likely due to the local diffusion of the poison into the peripheral nerves while the little that has been absorbed is as yet too much diluted in lymph and blood to seriously derange the nerve centres.

When general spasms set in it must be assumed that the poison has reached the nerve centres in toxic quantities, either through the circulation or as is alleged by Babes and others through the nerve trunks. When the poison is injected intravenously the general spasms are the first to appear. Again the section of the nerves of a limb before inoculation prevents spasms in its peripheral muscles when all the body beside has become tetanic (Tizzoni and Vaillard). The removal of the brain from a tetanized frog had no effect, while the removal of a portion of the spinal cord abolished the spasms in the muscles corresponding to that part. Moreover Gumbrecht cut the whole of the sensory nerves of a limb but the spasms occurred in its muscles notwithstanding. It must be admitted, therefore, that the general tetanic spasms are induced by disorder caused by the poison in the spinal nervous centres.

Gumprecht and Goldscheider claim that the poison reaches the spinal centres by way of the nerve trunks basing the conclusion on the observation that the spasms sometimes remain for a time more marked on that side of the body on which the wound or inoculation was made. Absorption through the circulation also is conceded.

Courmont and Doyon claim that the product of the bacillus tetani only operates as a ferment, which produces in the blood the real tetanizing agent, basing the conclusion on an apparent delay in its action, in man, as compared with strychnia, and on the prompt action of the injected blood of a tetanic animal in which this poison is presumably preformed. It should be noted, however, that the disease in man is only seen after accidental inoculation of the bacillus, and that time must be allowed for the increase of the microbe.

Vaillard and Vincent have shown that the promptitude and certainty of the result depend on the age of the culture employed. A culture of 5 days in bouillon at 20° to 22° C. will not harm a Guinea pig in a hypodermic dose of 0.25cc. to 0.5cc. A culture of 20 days old is deadly.

The action on the nerve cell of the spinal cord has been investigated by Goldscheider and Flatau, who found degeneration of the chromatin granules within a short time after inoculation. (Centr. für Allg. Path. Anat. 1897). W. K. Hunter found that the ganglion cell stained more diffusely than normal cells. There were also some capillary dilatation and punctiform hæmorrhages in certain cases (Brit. Med. Jour. 1897).

Péchoutre examined the lumbar enlargement of tetanic rabbits, by Nissl’s method and found the following lesions in the motor cells of the anterior horns: 1st. A partial or total disappearance of the distinct outer marginal line; enlargement of the cell and pericellular space; diffuse coloration of the achromatic substance; a disappearance of the regular concentric disposition of the granules of Nissl which were in part reduced to a fine powder; 2d. Encrease of nucleus and nucleolus.

Others have observed encrease of the cerebro-spinal fluid, thickening of the ependyma, nuclear proliferation in the neuroglia, and softening of the cord, but in many cases no appreciable lesions in the nerve centres have been found, and none can be affirmed as constant. Neuritis in the region of the wound is sometimes found especially if the lesion is a contused or painful one.

The muscles often show lesions the result of the violent contractions. There may be points of ecchymosis and partial rupture of individual fibres, they may be of a deep red, or again pale, soft and as if parboiled. There may be hyperæmia or œdema of the lungs, congestion of the larynx, ecchymosis on the pericardium and other serous and mucous membranes, and congestion of the liver, spleen and kidneys. Rigor mortis sets in rapidly and is usually very persistent. The muscles contain an excess of lactic acid.

Accessory Causes. Whatever contributes to traumas must be classed in this list. Solipeds, work oxen, and dogs are especially exposed in this sense. In all animals castration wounds; in horses and lambs amputation of the tail; in solipeds pricks, bruises and fistulæ of the feet; all kinds of surgical wounds; in females the parturient condition; and in the new born the umbilical sore form infection atria. The tendency to infection in wounds of the feet in animals, and of the hands and feet in man, is easily explained by contact with the virulent earth or dust. Children running barefoot, or injuring their bare knees and soldiers sleeping on the ground are similarly exposed. The contamination of the clothes is the main condition. It has been held that infection never takes place from the gastro-intestinal canal, but the facts that the bacillus is frequently present in the prima viæ and that the mucosa is often perforated by blood-sucking parasites, suggest that some cases (idiopathic) are probably due to intestinal infection. The gland ducts also and the follicles of Peyers’ patches and of the solitary glands offer available fields for the colonization of the bacillus and for infection atria.

General Symptoms in Animals. In experimental cases, in which there has been a large intravenous injection of the blood of a victim of tetanus the symptoms may set in speedily and violently. In casual cases, however, there is usually an incubation period varying on an average from three to fifteen days in the horse while it may be as short as two days in cow and sheep. Hoffmann quotes one incubation in the horse as but six hours after a wound in the neck, and another as twenty-five days, following a castration. The last is rather unreliable as infection may have taken place long after the operation. He quotes cases in the pig and goat, after castration as eight to fourteen days, and one in the dog almost immediately after a bite on the loins.

Following the incubation the marked phenomena are tonic contractions of groups of muscles beginning usually with those near to the seat of the infected wound and extending with varying rapidity to the locomotor muscles generally (limbs, croup, back, loins, neck, tail, abdomen) and those of mastication (jaw) and the eye. The muscles of respiration are only involved at a late date, causing stertorous breathing and it may be asphyxia. Peristalsis is impaired so that there is some costiveness and tardiness in digestion. Urination becomes difficult and infrequent on account of the difficulty of assuming the normal position for the act, and spasm of the sphincter vesicæ and dangerous distension of the bladder may follow. The urine is often albuminous and has a high density and color. Priapism is not infrequent in the male.

The predominance of the spasm in special groups of muscles has been the occasion of giving different names to individual cases.

Trismus or lockjaw is that condition in which the muscles of the jaws are violently contracted so that the incisors can only be separated slightly or not at all.

Orthrotonos is that condition in which the muscles in tonic spasms keep the neck, back and loins rigid, straight and unbending, in one horizontal line.

Opisthotonos is when the muscles of the spine are in rigid spasm, so that the back and loins are slightly depressed, the tail elevated and trembling, the neck drawn upward with a concave superior border (“ewed”), the head extended and the nose elevated.

Emprosthotonos is caused by spasms of the muscles of the ventral aspect of the body, with arching of the back and tucking up of the abdomen.

Pleurosthotonos is when the trunk is spasmodically bent to one side, right or left.

Spasms of the muscles of the eyeball, cause sinking and apparent diminution of that organ, with the protrusion of the membrana nictitans over one-third, one-half or even more of its front surface. This is often referred to by owners as “hooks”.

More striking and pathognomonic than the above is the extreme hyperæsthesia and irritability which rouse into activity or aggravate the symptoms under the slightest cause of disturbance. The effort required to feed from the ground, the stretching of himself to urinate or defecate, the rustling of straw litter under his feet, loud talking, or other sudden noise, banging of doors or windows, hammering in the vicinity, a current of cold air, a flash of light, moving the patient in the stall, attempts at mastication, simple handling, administering medicine, or sudden jerking of the head upward promptly brings on a paroxysm of spasm. Pushing the head suddenly upward or jerking on the halter, is often resorted to as a means of diagnosis, the sudden resulting rigidity of the muscles generally, the rolling of the eye, its retraction toward the depth of the orbit and the protrusion of the membrana nictitans over one-half, one-third or more of the cornea, bringing out the diagnostic symptoms in a striking manner. In very severe cases the head may be drawn upward and backward almost to above the loins (Henry), or one or more of the dorsal or lumbar vertebræ may be broken or crushed (Zundel). A sudden loud noise will sometimes cause the exhausted animal to drop to the ground.

Perspiration is not uncommon. Breathing is usually accelerated, the encrease being in ratio with the violence of the spasms. Pulse and temperature are usually normal at first and may be in slight cases throughout. Even in severe cases the pulse does not rise so much as the respiration. In violent and fatal cases the temperature often rises excessively before death (104° to 110° F.).

When the jaws are not absolutely closed, the tongue is often wounded by the teeth, and, in any case is covered by a tenacious mucus, which may hang in strings from the lips. If the jaws are still movable, mastication is still carried on, but slowly, painfully and imperfectly, and deglutition is more or less difficult. Young animals are unable to suck.

Symptoms in the horse. When the symptoms are fully developed, they are very characteristic. The neck is raised, often concave along its upper border, the nose raised and protruded more or less, the nostrils widely expanded, the eyes sunken, fixed and anxious, with diluted pupils and protrusion of the haw outward and upward from the inner canthus, the ears are pricked, rigid, and drawn toward each other at their tips, the facial muscles may stand out visibly and are firm, the angle of the mouth is drawn back, the veins of the head are full and prominent, saliva froths or drivels from the lips, the tail is elevated and during paroxysms will tremble, and the muscles of the back and limbs are projecting and hard. The limbs are extended outward to give a wider base of support. If moved, the general stiffness is at once seen. The patient cannot be turned round in his stall, he may not even be able to turn the neck to one side, and if backed he resists, or accomplishes the movement only with the greatest difficulty. In walking, the limbs are used as stilts with little or no bending of the joints, and if turned, the body is not bent but moved around with difficulty as if one rigid mass. The pulse is small and hard, the breathing slightly hastened, and the mucosæ congested and reddened. The jaws may be firmly closed, or they may still part for a time half to one inch. In all severe cases the patient obstinately stands, and if he should drop, or lie down, the breathing and spasms are usually encreased and, in the efforts to rise, the respiratory muscles may become spastic with promptly fatal results.

In cattle the same general symptoms prevail. The stiffness of neck and back, the habitual elevation of nose and tail, the stiffness of the legs, propped outward for support, and moved like unbending posts when made to walk, the hardness of the muscles, standing out under the skin, the rigidity of the lips, firmly closed or slightly opened, the general fixity of the erect, retracted ears, and the sunken appearance of the eyes with marked protrusion of the haw, are largely as in the horse. The muzzle is usually dry and hot, the jaws clenched, the tongue firmly compressed against the palate and covered with thick, tenacious mucus, and the flanks are often flattened by the contraction of the oblique muscles, so that they descend almost vertically from the lumbar transverse processes. There is great difficulty in turning and the trunk moves in rather a rigid mass without bending laterally, and the limbs are stiff and stilted. Tympany of the rumen sets in early with oppressed breathing and arrest of defecation and urination, which had been already difficult. The reflex excitability to noises, or other causes of disturbance is often less than in the horse. In cases following metritis, this may be due in part to the depressing poisons absorbed.

Sheep and Goat. Show the same general rigidity of trunk and limbs, the drawing of the head and neck upward and backward, the elevation of nose and tail and the firm closure of the jaws. As the disease advances they may lie on the side with legs straitened and rigid and head and tail raised toward the back. The occlusion of the eye by the haw is the same as in the horse.

In swine the spasms begin with the jaws and face, and extend to the neck, back and limbs with the same general symptoms as in other animals. Champing of the jaws and profuse frothing at the mouth have been noted and the protrusion of the haw is characteristic. As in sheep, the animal may lie on its side with head and limbs rigid and an early death may be looked for. Convulsions are easily distinguished by their transient character.

In dogs tetanus is rare. Möller had two cases in 50,000 sick dogs, Friedberger and Fröhner but one out of 70,000. Cadiot saw two cases in ten years of the Alfort clinic. Labat had several cases in sheep dogs. A slight transient trismus has been noticed as common in puppies. When generalized there is stiffness of the trunk and limbs, abduction of the members. The spine may be straight and rigid or drawn upward and backward, and the loins depressed. The haw covers the eye more or less, the lips are rigid, the jaws clenched, and the skin of the forehead wrinkled. The ears are stiff and drawn toward each other, or backward. The reflex excitability is as great as in the horse, the slightest touch or sudden noise producing violent paroxysms. Inability to bark is a marked feature. Temperature may be normal or up to 107° F.

In birds it is very rare, in keeping with the insusceptibility to strychnia, ergot and other tetanizing agents. Dreymann gives one case in a turkey, and Babes’ experimental cases in pigeons and chickens from a specially virulent bacillus obtained from the horse. The pigeons suffered much more certainly and severely than the chickens, in which there was a marked power of resistance. Dreymann’s turkey moved with stiff limbs and body, had the wings clinging firmly to the body, the head and neck extended and the bill firmly closed. The haw protruded over the eye, and there was hurried and oppressed breathing.

Course. Duration. The course of tetanus varies with the genus affected, with the individual susceptibility and above all with the length of the incubation, and severity of the attack. Cases that set in with great violence after an incubation of two or three days or less are likely to advance to an early death. An early generalization of the spasms, with high temperature (104° F), hurried breathing, congestion of the mucosæ and extreme excitability may end fatally in twenty-four hours or within a week.

If on the other hand the incubation appears to have extended over one, two or three weeks; if the disease is at first equivocal, with some stiffness and firmness of the muscles, but with little or no trismus; if the patient can open the jaws an inch or more and masticate even slowly for a number of days after the onset of the first symptoms; if the haw projects only slightly over the eyeball and the excitability is not extreme the prospect for recovery is much better. Such tardy cases may seem to stand still for a week and then have a slight aggravation and this may be repeated, or a slow improvement may set in and go on gradually to complete convalescence. Improvement may be manifested by a softer or more relaxed condition of the muscles, by a slightly freer movement of the limbs and jaws, by a greater ease in swallowing, by encreasing movements of the ears and eyes, by the lessened projection of the haw, by the freer breathing and circulation and by the permanent lowering of temperature to the normal standard. Convalescence is always slow, but especially slow in severe cases in which time must be allowed for repair not only of the central nervous lesions but also of the ruptures and trophic changes in the muscles.

In cattle the disease is usually slow in its progress and improvement may not set in till the close of the third week. In sheep, goats and dogs on the other hand it is habitually acute, and death may supervene from the third to the eighth day. In the horse all forms are met with and the result will vary according to the severity of the attack.

Mortality. Friedberger and Fröhner sets the mortality in sheep and pigs at nearly 100 per cent.: in horses at 75 to 85 per cent.: and in cows at 70 to 80 per cent. In tetanus neonatorum in lambs, the deaths reach about 100 per cent. In this case the disease usually sets in within forty-eight hours after birth, and with a very high temperature difficult deglutition becomes a marked feature, so that if the patient is not speedily killed by dyspnœa, it soon perishes from starvation and exhaustion.

The cause of death is usually asphyxia, hyperpyrexia, or exhaustion.

Lesions. There are no constant or pathognomonic structural changes in tetanus. Those that are found are inconstant and as a rule secondary. A wound (entrance channel) can usually be made out, often in the region of the foot, or in connection with castration. In the new born there is the unhealed navel, and in parturient cows the catarrhal, septic or injured womb. In the seat of such wound may be found the foreign body (nail, splinter, etc.), and some pus or simple congestion or even necrosis. The nerve trunks leading from such infected wound may be hyperæmic. The presence of the bacillus in the wound may be determined by microscopic examination or inoculation on a small animal.

The changes in the nerve centres may be congestion of the horns of gray matter, and there may be slight hæmorrhage, exudation, especially shown in the encrease of the cerebro-spinal fluid, softening, cell proliferation, and granular invasion of the nervous tissue. In separate cases the myelon, the corpus striatum and the cerebellum have shown lesions. The meninges are occasionally hyperæmic. Spinal lesions have been noted especially in the bulbo-cervical and lumbar regions. Exceptionally in the horse there are blood extravasations from fractures or dislocations of the vertebræ.

In subjects dying of asphyxia the lungs and right heart are congested, and the blood may be black, only loosely coagulable and with free hæmoglobin. There is congestion of the intestinal as of the respiratory mucosa, and also of the liver, spleen and kidneys. The congested bladder usually contains urine contrary to what is the case in rabies.

Diagnosis. From strychnia poisoning tetanus is distinguished by the gradual and progressive approach of the spasms and by the absence of the intervals of complete relaxation which separate the rapidly recurring and violent spasms of strychnia. In tetanus the spasms may be modified but never completely intermitted, and more or less stiffness, trismus and protrusion of the haw constantly persist. In strychnia too, the paroxysm is far more intense than in the early stages of tetanus. The spasms of strychnia are general, while those of tetanus are often most intense in particular groups of muscles often at first in the vicinity of the inoculation wound.

From rabies, tetanus is easily distinguished by the absence of any history of a bite; by the persistence of the tonic spasms especially of the masseters and abdominal muscles during the intervals between the more violent paroxysms (in rabies there is temporary complete relaxation); by the absence of clonic spasms which alone occur in rabies; by the absence of the paralysis which characterizes advanced rabies; by the mental clearness and the absence of hallucinations or mischievous disposition which are marked features of rabies; by the absence of the depraved appetite of rabies; and by the fact that the brain does not contain the infecting germ as is the case in rabies.

From rheumatism of the neck (torticollis) tetanus is easily distinguished by the permanent trismus which is not shown in rheumatism, and by the fact that spasms are easily roused by any artificial excitement, indicating an extraordinary hyperæsthesia and excitability which are nearly absent in rheumatism. The steady unmistakable progress of tetanus is in itself diagnostic.

From meningitis tetanus is to be diagnosed by the presence of trismus without impairment of the mental faculties or fever. In meningitis the spasms are usually confined to particular groups of muscles and do not become generalized under active excitement as in tetanus. Even if the spasms of meningitis affect the jaws and pharynx they are rarely paroxysmal or roused by excitement as in tetanus. They may even be clonic.

Tetany is more commonly localized in particular groups of muscles, and shows longer and more irregular intervals between paroxysms than does tetanus. It is improved by thyroid extract, and may be roused at will to contraction by pressing on the nerve going to the affected muscles.

Laminitis in its most violent form and early stages, may be confounded at first glance with tetanus, but the high fever, the standing on the heels, the advance of the hind legs under the body, the great heat and tenderness of the feet, the impossibility of standing on one fore foot when the other is lifted and the strong pulsation of the digital arteries, are sufficiently distinctive.

Treatment. For fully developed tetanus no known resort of therapeutics can be relied on. In slight cases that have shown a long incubation and a slow increase and extension of spasm and in those having trismus only, a recovery may be expected. Treatment has been conducted largely on theoretic lines and may be divided into antispasmodic, eliminating and antidotal or antiseptic.

Rest, darkness and absolute quiet are the first and main considerations. A dark stall, with no straw litter, the rustling of which often excites the patient, but rather a little chaff, saw dust or even earth to prevent noise from the feet, and the exclusion of all visitors are essential. As a rule slings should be put under the patient so that he cannot lie, nor drop down, and this becomes more imperative as the disease advances. The aggravation of the spasms when down, and the danger of their extension to the respiratory muscles are far more to be dreaded than the temporary excitement caused by the application of slings. Food should be sloppy mashes, of bran, middlings, oat meal, linseed meal, gruels or milk, or green food may be allowed in moderate amount if the jaws are still movable. It must not be forgotten that digestion is impaired and food that is indigestible, especially fermentescible, or in excess, may arouse fatal colics and bloating, yet in a protracted exhausting disease like tetanus, the strength must be sustained by all means in our power. Pure water should always be accessible. Food and water should be furnished in buckets at a level which will not necessitate either raising or dropping the head to get to them (about 4 feet). The food must be given often, in small quantity to avoid fermentation and spoiling. If noise cannot be wholly excluded it may be an advantage to put cotton wool in the ears. I have seen a mare recover when completely covered with cotton wool under blanket and hoods.

Local antiseptic treatment. Theoretically this is of great value since the microbe is confined to the inoculation wound and by the time the first symptoms appear, the spores have developed into bacilli and are in a condition to be easily destroyed by disinfectants. We can, therefore, by caustics or active disinfectants destroy the infecting microbian colony, and prevent the further entrance of any toxins into the circulation and nerve centres. The principle has been shown experimentally successful in cases of inoculation in the tails of cats and Guinea pigs, and the amputation of these members as soon as tetanic symptoms appear (Kitasato, Babes). Unfortunately in too many cases, when first seen, too much of the marvelously potent toxin has already reached the nerve centres, and these have already undergone such changes, that the disease is likely to go on to a fatal issue in spite of the cutting off of future supplies of toxin. Yet the principle is sound and proves helpful in proportion as it is applied nearer to the time of infection. The most thorough method is the amputation of the infected member, if like the tail or ear it can be excised without ruining the animal. In 1875, Barbillon had success in again amputating the tail, in a case of tetanus after docking. Next to this comes the excision of the wounded tissues, but this can too seldom be effectually and certainly accomplished, and we must fall back on caustics and antiseptics. The actual cautery if thoroughly applied may be trusted to destroy the bacillus along with the tissues, but most of the chemical escharotics unite with the albumen to form an impermeable film, which protects the tissues in the deeper part of the wound against the antiseptic action. Of the different antiseptic applications carbolic acid should be especially recommended as being not only antiseptic, but also an antidote to the toxins as shown below. It has the further advantage of acting as a local anæsthetic, and of not coagulating albumen. Creosote, creolin, lysol or other antiseptic may be used instead and should be applied thoroughly to all parts of the depth of the wound on a pledget of surgeon’s cotton or through a tube. When agents so little destructive are employed they may be continuously applied to the sores for a length of time.

Recoveries have taken place after neurectomy, and after stretching the nerve going to the wounded part, the theory being to check the afferent (sensory) nervous current, and arrest the reflex spasms. The new irritation, however, caused by the surgical wound is to be dealt with, and may itself turn the balance against recovery.

Nervous derivation appears to have been beneficial in some advanced, or partially convalescent cases. One horse after 14 days illness (Taffanel) and another after 21 days (Prud’homme), were castrated, bled freely and slowly recovered. Tisserand gives another case without mentioning the stage of the disease. A horse with advanced tetanus was taken to the seashore and shot. He fell into deep water, swam ashore and made a recovery. But whatever virtue may be in elimination of the toxins by bleeding, in nervous derivation or in the shocking of an unbalanced nervous system, these can hardly be recommended as regular methods of treatment. Yet the older veterinary records contain many instances of alleged benefit from bleeding.

Internal treatment. The whole list of antispasmodics have been tried, with no very satisfactory result. Opium has been extensively employed in spite of its tendency to encrease constipation, and morphia given hypodermically has checked spasm and induced sleep. Hydrocyanic acid and potassium cyanide have shown a decided reducing action on the spasms with the same drawback of favoring constipation. Potassium and other bromides are useful in mild and chronic cases, and may be given in full doses in combination with chloral hydrate. Calabar bean and eserine have been given for their physiological action on the nerve centres, and recoveries have followed their use, but they have little effect on the spasms until the system has been saturated to the point of threatening collapse. Chloroform has the advantage that it can be easily given by inhalation, but while it may be pushed to the extent of temporarily checking the spasms, yet these return at once when the action of the drug is exhausted. Chloroform is always dangerous to a weak or exhausted heart and cannot be given for any great length of time continuously. It is, therefore, very unsatisfactory. Sulphonal and trional have similarly checked the spasms. Gelsemium has given good results in certain mild cases, but it must be pushed to the extent of coming just short of poisonous doses, and the fear of an overdose, together with its failure in severe cases, have prevented its general acceptance. The same end has been sought by the use of nauseating antispasmodic agents, as tartar emetic, tobacco, apomorphia, and lobelia, but though useful in individual cases, these are on the whole no more successful than other agents. Phenacetin, antipyrin, acetanilid and cocaine have respectively received credit for some recoveries.

Chloral hydrate commends itself as being at once a most potent antispasmodic and hypnotic, and an antiseptic. It can, moreover, be conveniently given as a rectal injection, thus avoiding the irritation and excitement of administration by the mouth. Given in this way too, it tends to relaxation of the bowels, instead of constipation. Carbolic acid which can be conveniently given by enemata has an anæsthetic action.

Antiseptic and Antidotal or Antitoxin treatment is more promising, yet it has failed to come up to the full measure of expectation, mainly because the nervous changes have already reached a stage which cannot be undone speedily or at all. Under this heading would come phenic acid (½ oz.) and probably chloral hydrate (1 oz.), already referred to, and the various compounds of iodine which may be here noted.

Iodine Terchloride. Iodine. Behring and Kitasato secured immunity of two months duration, by injecting the animal with a filtrate of a culture of tetanus bacillus, and then injecting at the same point 3cc. daily, for five days, of a 1 per cent solution of iodine terchloride. Roux and Chamberland had similar results by using iodine instead of the iodine terchloride, and maintained the full measure of immunity by repeating the inoculation every fortnight. Here it is evident that the action of the iodine is directly antitoxic or antidotal, when introduced along with the toxins and before they can reach the nerve centres.

Iodide of Potassium. In an experimental case of general tetanus in the dog, Babes had a recovery in ten days, by injecting subcutem 5cc. of Lugol’s solution and thereafter for eight days 10 to 30cc. daily. This suggests the use of this agent along with phenic acid, or as an alternate, in any case in which phenol appears to be losing its effect by use. It may be used hypodermically, or in the drinking water or by rectal injection. It has an advantage over phenic acid in being actively diuretic and eliminating, while phenic acid has the recommendation that it tends to lower nervous excitability and moderate the reflex spasm. Theoretically the combination of the two agents, which do not mutually decompose each other, should give the best results.

These experiments have been often repeated showing clearly the antidotal action of the iodine compounds when mixed with the virus before inoculation, or injected with the virus into the seat of the wound. When employed later when the symptoms have developed, everything depends on the changes already accomplished in the nerve centres, and the severity and generalization of the spasms.

Serum Antitoxin Orrotherapy. Babes appears to have been the first (1889) to use the serum of animals (rat) recovered from tetanus in mitigating and curing tetanus in experimental cases. An attempt on a well developed case in man failed. His method of preparing the serum is as follows: A horse of 900 lbs. (461 kgm.), is inoculated with a mixture composed of 0.5cc. toxin (of which 0.001 mgm. kills a mouse) and 0.5cc. iodo-potassium iodide, and then at intervals of four or five days of 2.5cc., 4, 5 and 10cc. of the iodine mixture. Then stronger mixtures are used: first 2 parts of toxin to 1 part of the iodine mixture; dose 10cc.; then 3:1 dose 10cc.; then 4:1 dose 5cc.; then 15:1 dose 10cc.; then 30:1 dose 25cc.; and finally virulent cultures in progressively encreasing doses 10, 20, 30 and 50cc. One week after the last injection 1cc. of the blood serum will antidote 50cc. of toxin. Injection of toxin is however continued and the dose is gradually raised to 200cc. Eight or fourteen days after the last injection the blood serum may be taken for protective purposes. He has prepared antitoxin from cows in the same way, and Brieger and Ehrlich have prepared it from the goat. Chickens being naturally refractory to tetanus toxin can bear large doses and a potent antitoxin is more speedily secured from them. In the case of the cow the milk is rich in antitoxin.

Other methods of preparing an animal for producing the antitoxin have been resorted to as injecting it with a mixture of toxin and antitoxin in increasing doses, or again injecting with a mixture of toxin and thyroid extract in increasing doses. The extract of the normal thyroid contains a natural antitoxin.

It may be fairly inferred that the antitoxin is not formed in the nerve cells alone in their resistance to the toxin, but also in the thyroid, the liver (bile having an antitoxic action), and perhaps in other organs or liquids.

The blood of the immunized animal drawn through the sterilized cannula and aspirating syringe is coagulated in vessels set on ice, and the serum when separated is mixed with 0.5 per cent. carbolic acid and 1 per cent. chloroform, and kept in the dark in well closed bottles. It will usually keep for years.

Early experiments with antitoxins showed that when mixed with the toxin before injection it could be trusted to neutralize it. Ehrlich, Tizzoni and Cattani even claimed success in all experimental subjects if employed as soon as the slightest symptoms of tetanus were shown. They found, however, that it required 1000 to 2000 times the amount of antitoxin in such cases than was required when it was mixed with the toxin prior to injection. They found, moreover, that when the disease is fully developed the dose must be 150 times more than is required when the first symptoms are shown. It should be added that when the disease has developed rapidly, after a short incubation, and is well advanced the antitoxin treatment is usually of little avail. The changes in the nerve centres are already too great to allow hope of recovery. In man the ratio of recoveries are about as follows: After incubation of 10 days or under, 3 to 4.5 per cent. recover. After an incubation of 11 to 15 days 50 per cent. recover (Woodhead). Lambert claims 46 per cent. recoveries in 114 cases, and 38.71 per cent. recoveries in acute cases with an incubation of 8 days and under.

On the whole the ratio of recoveries is greater under the antitoxin treatment than before, though far from sustaining the optimistic views of Behring and other early experimenters. Babes draws attention to the fact that spore laden splinters of wood, in the wound render the antitoxin useless as a continuous succession of fresh spores, bacilli and toxins are thereby supplied. As this is one of the most common forms of casual infection it interferes seriously with the success of antitoxin treatment.

Roux and Borrel found that in animals, intracranial injection of the antitoxin was the most effective method. Recovery also followed its injection into the cerebrum of a tetanic boy. Babes had recoveries in two cases out of three with cerebral or intracranial injections. As the reflex spasms depend on the spinal centres these would seem to be the ideal points of injection.

Babes who has done a large amount of subcutaneous and intraperitoneal injection of antitoxin, employed for man doses of 300 to 500cc., which would represent 8 to 10 ozs. as the dose for an ordinary horse. As the antitoxin is rapidly eliminated from the body, these should be repeated daily or every other day. Nor should this supercede other curative measures. The leading principles may be thus stated: 1st. Antitoxin should be used at the earliest possible moment. 2nd. The infected wound area must be thoroughly disinfected or destroyed by caustics, and that at once. 3rd. The antidotal treatment by phenol and iodine must not be omitted. 4th. Palliative treatment by antispasmodics, narcotics or soporifics must go hand in hand with antitoxic treatment. 5th. Measures should be taken to secure elimination of the toxins present in the blood.

Treatment by brain emulsion. Wassermann and Takaki (Berlin Klin. Woch. Jan. 3d, 1898) have in a number of cases, mixed 1cc. of brain substance of a warm-blooded animal with ten times the lethal dose of tetanus toxin and injected without producing any symptoms of tetanus. They obtained a similar immunity by injecting the brain emulsion 24 hours after the injection of three times, and in other cases of five times the lethal dose of tetanus toxin. Control cases uniformly died of tetanus. The brain matter was obtained from Guinea pigs, pigeons, rabbits, horses, and men. They accordingly advanced the theory that brain matter is a direct antidote to the tetanus toxin, uniting with it chemically and rendering it innocuous. The liver, spleen, kidney, bone marrow and blood serum gave no such protection.

Marie, in a series of experiments, injected the brain emulsion and tetanus poison at different parts of the body of Guinea pigs and found that fatal tetanus ensued. It would appear, therefore, that the brain emulsion acts by direct contact, and that it is only by its meeting and combining with the toxin before the latter reaches the spinal cord that tetanus can be prevented.

Roux and Borrel (Ann. de l’Instit. Pasteur, 1898) demonstrated this union between the poison and brain matter, by making an emulsion of the two, and putting in a centrifuge, which will separate the brain substance from the clear liquid. The fluid obtained in this way was shown by injection on the living animal to contain almost no toxin. Knorr and Blumenthal reached the same conclusion as to a chemical union with the brain matter which robbed the toxin of its toxicity.

Knorr, and Tizzoni, and Cattani and Morax showed indeed, that if the tetanus toxin is injected subdurally or into the surface layers of the cerebrum, it produces not tetanus, but a characteristic cerebral disease. A dose of ¹⁄₂₀th or ⅒th cc. of tetanus toxin produces in the rabbit, in 10 to 12 hours, restlessness, constant change of place, and signs of great fear like hiding the head, turning rapidly round, attempting to escape, polyuria, grinding the teeth, epileptoid convulsions. The toxin in this case had manifestly united with the brain substance while the cord suffered little.

Metchnikoff (Ann. de l’Inst. Past., April, 1898) holds that the brain matter is only valuable in holding the toxin until it can be destroyed by the leucocytes. He showed that the injection of the tetanus toxin in chickens or Guinea pigs greatly encreased the production of leucocytes. He injected tetanus toxin into the aqueous humor of the rabbit without producing much effect, but when the same agent mixed with cerebral substance was injected, the result was a great accumulation of leucocytes, and hypopion. If the mixture of brain substance and tetanus toxins were injected on the brain, little encrease of leucocytes occurred, but if thrown into the peritoneum, a most remarkable leucocytosis took place. In twenty minutes after the injection the fluid withdrawn from the abdomen showed large numbers of leucocytes filled with brain substance, but no free cerebral matter.

The present status of the treatment by brain substance is therefore somewhat uncertain. The value of that agent in holding the toxin is allowed, but like the antitoxin it must be employed before the toxin has reached the nerve centres and united with the living ganglion cells. Its use would be called for therefore at the earliest possible moment and it should be continued so long as there is reason to suspect the production of fresh toxin in the wound. Its direct action on the toxin would suggest its injection around an infected wound, or even as a dressing for the wound in connection with antiseptics. When tetanus has already set in it cannot be expected to undo the evil already accomplished by the union of the toxin with the cells of the cord, though it might in part arrest and hold new supplies of this poison coming from the wound to the nerve centres.

Prevention. In a disease so deadly as tetanus and so refractory to treatment even by antitoxin when it is once developed, prophylactic measures are of the greatest importance. With the extensive adoption of antiseptic surgery there has already been a material diminution in the number of cases, yet a greater attention is demanded to the prevention of casual cases which result from ordinary wounds. Dirty, grimy wounds filled with the dust of stable yard or garden soil, and such as contain splinters of wood, stones, thorns, straw and the like can only be considered quite safe after thorough disinfection. It has been shown that the toxin is easily neutralized at the time of infection, whereas, after the disease is developed it will require 1,000 or 100,000 times as much antitoxin to produce the same effect. In the case of soiled wounds, therefore, in a valuable animal, a harmless injection of antitoxin or of phenic acid or iodine solution before the development of tetanic symptoms is not an unwise precaution. A succession of such injections might be given to ward off the disease until after a lapse of time exceeding the short and dangerous incubation.

Much more important is the disinfection of the wound itself. All foreign bodies must be removed, but especially those that like splinters of wood and straws are likely to harbor the spores of the bacillus. Then the wound may be thoroughly cauterized thermically or chemically, or it may be irrigated with a strong antiseptic solution and then dressed with some agent that will prove destructive to the spores, and antidotal to the toxin. Strong carbolic acid may be applied to the whole raw surface including the uttermost recesses of the wound, and after a few seconds or half a minute this may be neutralized by filling the wound with dilute acetic acid or alcohol, after which a dressing of Lugol’s solution may be applied. Lambert advises a combination of hydrochloric and carbolic acids.

Weaker antiseptics, like a 5 per cent. solution of carbolic acid, do more harm than good, as they destroy the pus and saprophytic microbes and even the tetanus bacillus in the wound, without affecting the tetanus spores, which finding no other microbes to contest with them the possession of the field may find themselves in a better position than before to develop into bacilli and cause tetanus.

Tetanus neonatorum may be certainly prevented by the application of a disinfectant plaster on the navel at birth. Over 50 years ago in Scotland this desideratum was met by applying on the navel of the new-born child a soft and immaculately clean piece of cotton cloth which had just been flamed over a light. On the island of St. Kilda the former mortality of 67.2 per cent. of new-born infants, was promptly abolished by dressing the navel daily with iodoform. For new-born animals a cheap and convenient application may be made by incorporating 1 oz. powdered iodine and 2 lbs. wood tar, and smearing this on the navel.

Much may be done by disinfection of stables and yards where the victims of tetanus have been. The anærobic germ soon loses its virulence in free air and sunshine, and one has to dread especially, filthy stables, collections of manure, contaminated litter, wood, combs, brushes and buckets. In unpaved yards remove the infected surface soil and replace by fresh disinfected earth, or still better, well burned brick.

For horses which are necessarily exposed to manure or contaminated soil, it is commendable to wash the hoofs and pasterns on returning from work and then sponge with a weak solution (5 per cent.) of phenic acid. Another resort is to smear the hoofs daily with an ointment of tar and lard, equal parts. This cannot protect from infection by splinters of wood containing the spores, but is to a large extent preventive in the case of bacilli that might have been otherwise lodged on the surface and which could have been carried into the wounds inflicted by nails and other noninfected bodies. Careful shoeing is all important, to avoid the bruises, suppurating corns and gravelling which make openings for the ready entrance of the spore.

Roux and Nocard recommend immunization by protective inoculation. This is not only possible, but would be justified economically in the case of valuable animals, or in all animals in a district where the bacillus tetani is universally spread. The method is the same as advised above for the immunization of animals, for the production of antitoxin.

In districts where tetanus is rare, the cost of universal immunization against the disease would very far exceed the losses front casual cases. Under such conditions it would be an economical blunder.

FOOT AND MOUTH DISEASE.

Synonyms. Definition. Susceptible animals: cloven footed, all warm blooded animals. Historic notes; Geographical distribution; English invasions in 18th and 19th centuries; North and South American invasions in 1870; In Asia from immemorial times. Causes: infection in liquid of vesicles, saliva on pastures, roads, feeding and drinking places, halters, etc.; from feet on pastures, buildings, yards, roads, cars, boats, etc.; from teats through milk. Microbe not certainly known, micrococci, streptococci and bacilli found. Virus inert when dried 24 hours at 88° F.; survived 9 months at 32° F., attack immunizes for 5 months; injection of 1 lymph and 2 of blood of immune renders refractory; filtered lymph still virulent; microbe probably infinitesimal; accessory causes: movement, mingling of cattle, sheep, swine, etc., war, trade, common pasturage, infected roads, ships, yards, halters, etc. Symptoms: incubation 36 hours to 6 days; slight fever; redness, tenderness of buccal mucosa and teats, grinding teeth, smacking tongue, tender feet, shaking them backward, bullæ on mouth and teats, not nodular, nor chambered as in variola, salivation, bloody, circular or irregular raw sores, vesicles and erosions in interdigital space, shedding hoofs, sheep walk on knees, gangrenous mammitis; intestinal eruption and diarrhœa in sucklings. Mortality. Prognosis; recovery in 15 days, deaths rare if cared for. Losses from destruction of product and emaciation—occasional abortion. Diagnosis: based on infection of all exposed bisulcates, localization on mouth, teats and feet, inoculability on other warm blooded animals, unchambered vesicles, slight fever, and prompt recovery. Notes of affection in man. Symptoms in man. Prevention and treatment in man. Prevention in animals: exclusion of contagion, immediate and mediate; close infected pastures and roads, stop all movement of bisulcates, disinfect all boats, cars, places and things exposed, exclude visitors, guarantees with strange animals, quarantine and disinfect arrivals, exclude fresh animal products, fodder and litter, wash, disinfect soiled clothes. Inoculation undesirable. Treatment in animals: cleanliness, dryness, disinfection, segregate sick and well, gaseous antiseptics, liquid ointments. Gruels, mashes, sliced, boiled, or pulped roots. Local dressings for mouth, teats and feet. Evulsion of hoof. Mammitis.

Synonyms. Aphthous fever: Aphtha Epizoötica, Eczema Epizoötica.

Definition. An acute infectious disease of the lower animals but especially of ruminants, characterized by a slight fever and the eruption of vesicles, or ballæ on the skin and mucosæ, and usually those of the mouth, feet and teats.

Susceptible Animals. The animals that prove the most obnoxious to the disease are the bisulcates—large and small ruminants and swine. Man however is susceptible as are also horses, dogs, cats and fowls, when they are inoculated or fed upon the infected milk or other products. It is doubtful if any warm-blooded animal enjoys an immunity.

History, Geographical Distribution. Toward the middle of the eighteenth century this disease prevailed in Central Europe and England. The latter country stamped out both this and the Rinderpest, but it continued to prevail on the Continent and was re-imported into England in 1839. It reached America through an importation from England to Montreal in 1870, but owing to more or less effective quarantine, to the absence of cattle traffic from east to west, and above all to the prolonged confinement in yards and stables during our northern winter, it burnt itself out in the course of the year. In Asia it has prevailed from time immemorial, and it was imported into South America in 1870.

Etiology. This disease has long been known as caused by infection alone. Excluded from England in the middle of the eighteenth century it did not appear again until re-imported in the middle of the nineteenth, and then speedily overran the whole island except the breeding districts into which strange stock were never taken. In South America it was unknown until imported from the Old World into the Argentine Republic and then it made a wide extension and maintained itself where the stock was kept on unfenced ranches. In our fenced Northeastern states it died out and has not reappeared.

The infection is especially resident in the vesicles or aphthæ. From the mouth this is distributed, with the abundant drivelling saliva, on pastures, roads, feeding and drinking troughs, ponds, streams and halters, and readily communicates the disease to healthy stock following in the same places. From the feet and especially the interdigital space, it is left on the vegetation, buildings, yards, cars, boats and all other possible media to infect other stock in turn. From the teats it mingles with the milk so as to infect the young suckling and all animals and men to whom the milk may be given. It may become dried on litter and other light objects and carried by the winds, or it may be carried on the feet of men or animals including birds, but apart from this it is not readily diffused and oftentimes a broad highway may set a limit to its propagation.

The infecting microbe is not definitely known. Nosotti found a micrococcus in the lymph of the vesicle, which stained readily in aniline colors, was easily cultivated and pathogenic. Klein found a streptococcus which, similarly tested, presented an equal claim to be the causative factor. Bassianus and Siegel found in the blood and tissues of a person who died of foot and mouth disease a small oval bacillus, which they later obtained from the vesicles of three children who were suffering from the disease, and from animals attacked in two successive epizoötics. With this they first successfully inoculated a calf and from the pure cultures obtained from its blood, inoculated three calves and a young pig.

Löffler and Frosch, the recent commission on foot and mouth disease in Germany, report that no organisms could be seen nor cultivated from the lymph found in recent bullæ of the buccal mucosa, though this lymph proved virulent when inoculated on calves.

They found that the lymph became inert when dried for 24 hours at 31° C. (88° F.), while it retained its vitality and virulence after exposure for 9 months to a temperature of 0° C. They concluded that it could not penetrate through the unbroken skin nor mucosa, and that it was most effective when injected into the blood or peritoneal cavity. One attack conferred immunity for 5 months. Blood from immune animals, injected into susceptible ones, does not confer immunity, but 75 per cent. could be rendered immune if injected with a mixture of the lymph from the vesicle and double the same amount of the blood from the immune animal. Animals so treated become immune to 100 times the infecting dose. Filtered lymph was still virulent and the commission suggests that the microbe may be so small as to pass through the filter, and escape discovery by the most powerful lenses. An object one fifth the size of the smallest known bacillus—that of influenza—would be invisible under our best microscope.

By actual experiment the virus has been found in the nose, larynx, bronchia, stomach and intestines, but into all these the virulent lymph of the bullæ can find its way. In the intestines, indeed, in cases caused by feeding, bullæ have been found on the mucosa.

A most important question would be that of the virulence of the milk, but inasmuch as the vesicles appear on the teats and even on the openings of the milk ducts, and in bursting discharge their contents with the milk into the pail, the milk becomes per force infecting. The experiment of Hertwig and his students who infected themselves by drinking the warm milk by way of experiment, has been often repeated unwittingly by unwilling victims, and the many cases of calves, pigs and chickens contracting the disease by consuming the otherwise discarded milk leaves no room for doubt that this product is often infecting.

Among conditions contributing to a spread of infection, nothing is more potent than a free movement of ruminants, and swine whether determined by war, trade, or the intermingling of different herds on commons or unfenced ranges. In infected countries, in which cattle are distributed through large central markets there is always a wide extension after one of these fairs, the infection being narrowly circumscribed to herds receiving cattle from the fair, or those that have travelled on the same roads or fields after the market cattle. It has repeatedly happened that cattle shipped from the United States, where this disease has long been unknown, have been found diseased on their arrival at a British port, simply because they have been tied upon the passage with halters formerly used on infected Irish or Continental stock.

Symptoms in animals. There is first a period of incubation shorter in hot than in cold weather and varying from 36 hours to 6 days (exceptionally 15 days). It is altogether probable that prolonged incubation is really delayed infection, the virus having been attached to the feet for some time before it entered the tissues. Cattle usually show the disease two days after exposure in a public market, building or conveyance.

There is first moderate hyperthermia (102° to 103° F.), indicated by the clinical thermometer before there is any outward sign of ill health. There may be erection of the hair, tremors or distinct shivering, dryness and heat of the muzzle, redness and even tenderness of the buccal mucosa and teats, saliva drivels from the mouth or may show as a frothy mass at the commissures or margins of the lips, and there may be grinding of the teeth and a peculiar smacking of the tongue and hard palate which may be heard at a considerable distance. There are greatly impaired appetite and rumination. Tenderness of the feet is shown by halting or lameness and by the extension backward and shaking of the hind feet in turn.

With the appearance of the eruption, usually on the second day of illness, the fever as a rule moderates, and on examination of the mouth bullæ of ⅓d. to 1 inch in diameter may be found on the inside of the lips, and cheeks, or on the palate and tongue, with, in many cases, a congested areola, but showing no nodule as in variola. These bullæ may extend to the muzzle, pituitary membrane or pharynx. They burst very soon after their formation, exposing a red base of inflamed corium, with a clearly rounded margin, or, at first, with shreds of the torn epithelial covering. The salivation now becomes more profuse, glairy and even bloody, and there is more active movement of the tongue. When the bullæ have been confluent there are formed extensive red patches denuded of epithelium, and the suffering causes a complete but temporary dysphagia. The renewal of the epithelium, however, takes place promptly and may be well advanced in four or five days. Upon the teats the bullæ appear at about the same time but are usually smaller than the buccal, and do not show the thickened base of cow pox. They burst in 36 to 48 hours unless broken earlier by the hands of the milker, forming sores comparable to those of the mouth, which are liable to be kept up by the necessary manipulations in milking.

Upon the feet the eruption shows especially in the interdigital space, at first as vesicles smaller than those of the mouth and teats, leaving erosions and ulcers which extend under the adjacent horn, and upward on the front and back of the pastern. From exposure to mud and filth these are liable to be kept up even longer than those of the mouth and teats, and under neglect the entire hoof is often shed. In sheep and swine the disease may be localized almost exclusively in the feet. Sheep will even walk on the knees.

In young animals and those fed on the milk, the eruption may take place on the intestinal mucosa with violent congestion, diarrhœa and a fatal issue. Aggravated cases may show gangrenous mammitis or abortions.

Mortality and Prognosis. While there are seasons of special pathogenic severity, yet as a rule, the foot and mouth disease is a mild affection and unless neglected, the patients entirely recover in about fifteen days. The pecuniary loss in dairy and feeding cattle has been found to average in Great Britain about $10 per head, and as few animals escape, the consequences are usually very serious. In England the losses from this disease in 1883 reached $5,000,000, in France, those of 1871 were $7,500,000 and in Switzerland, $2,500,000. In Germany, over 7,000,000 animals suffered from 1889–94.

Differential Diagnosis. While a mistake might be made in an isolated case, such a thing should be absolutely impossible where cattle and other animals are collected in herds. The rapid infection of the whole herd, the implication of sheep and swine along with the cattle, and the eruption of the characteristic bullæ on the mouth, feet and udder or on two of these locations to the exclusion of the rest of the body, is not likely to be counterfeited by another disease. An outbreak of gangrenous ergotism in Kansas, Missouri and Illinois in the spring of 1884, was pronounced to be foot and mouth disease by a number of veterinarians, including an expert sent by the Government of Canada. On behalf of the U. S. Treasury I investigated the disease, which caused in many cases sores on the mouths and feet, but it spared all sheep and swine, could not be conveyed to them nor to new born calves by inoculation, and in many cases it caused gangrene of all the tissues, soft and hard, and separation of the limb at a given point, often near the tarsus. The quarantines were raised, the disease made no further extension, and the existing panic subsided.

Infection of Man. The first authentic record of this affection in man we owe to Valentin, who records that during the outbreak in Hesse in 1695 men suffered from inflammation of the gums, tongue and mouth. Michel Sagar says, that in 1764 men who drank the milk were affected with aphtha. In 1828 it was conveyed from animals to men in Bohemia (Nadberny), in Styria (Levitsky) and Wurtemberg (Kolb). In 1834, three veterinarians, Hertwig, Mann and Villain, voluntarily drank a quart each of the warm milk of a cow suffering from this affection. On the second day Hertwig suffered from fever, headache and itching of the hands and fingers. Five days later bullæ formed on the hands and fingers, the tongue, cheeks and lips. In the two others the eruption was confined to the buccal mucosa. Since that time records of the infection of human beings have been very numerous. During the American epizoötic of 1870 I met with the case of a farmer at South Dover, N. Y., who suffered from sore mouth and blisters along the margin of the tongue from drinking the milk. The danger is greatest in children on an exclusive milk diet and who drink it warm. Kolb in 1828, noticed acid vomiting and diarrhœa in such subjects, Hübner observed that beside the buccal eruption such children often suffered from inflammation of the stomach and bowels and that very young children fed on the milk of the diseased cows died. Balfour, Watson and others have noticed similar results in Scotland.

Allbutt saw the buccal eruption in three children in Yorkshire, England, during the local prevalence of the English epizoötic in 1883, and secured information of a number of other cases in the same district.

A number of cases were recorded during 1893 in Germany. A shepherd infected himself by holding in his mouth the knife with which he had pared the diseased feet of sheep, and another workman and a veterinarian had extensive eruptions on the hands after dressing the affected feet. A number of milk-maids were infected by milking, the eruption appearing on the hands, and in one case on the breast. A child fed on the milk of diseased cows, had chill and fever with gastric disturbance, and later an eruption of vesicles on the lips and tongue and between the fingers and toes.

Again, in 1895, during the prevalence of foot and mouth disease in the southern part of Berlin, a considerable number of the milk consumers suffered from fever with the eruption of bullæ on the tongue and buccal mucosa generally, which on early bursting left very painful ulcerations. The acute disease did not last more than five days, but left a sense of great weakness for a time. Virchow, who made an investigation, unhesitatingly pronounced it to be foot and mouth disease.

Cases of infection through butter made from infected milk are on record. A Berlin veterinary student suffered from the buccal eruption and erysipelatoid swelling of the ear, and a German clergyman had in addition a period of chilliness, fever, diarrhœa and pruritus. Similarly Schneider quotes cases determined by infected cheese, and Friedberger and Fröhner, cases caused by virulent buttermilk.

Symptoms in Man. In man there is observed the tendency to localization on the same points as in animals. As the hands are naturally exposed to infection by milking or treating the diseased animals, they are especially obnoxious to the eruption, and the same is true of the mouth when the infected milk or other dairy products are consumed. The bullæ on the buccal mucosa are generally confluent, and often extend to the fauces and pharynx, rendering speech difficult and swallowing painful, and leaving extensive and painful sores which, however, soon heal up. In women the bullæ have been seen around the congested nipples, and in exceptional cases they have been generally diffused over the body.

In cases due to drinking the milk, the early febrile symptoms are liable to be accompanied or followed by nausea, anorexia, abdominal pain and diarrhœa, and still later by the cutaneous and buccal eruption.

The duration of the disease is from 10 to 15 days and as a rule no permanent scars are left on the skin or mucous membranes.

The diagnosis is assisted by the knowledge of the prevalence of the disease in herds in the district, and that the patient has handled the diseased animals, or drunk their milk, or eaten their butter or cheese products. The predilection of the eruption for the fingers, the roots of the nails and the mouth is very significant. The disease follows an acute course and convalescence is complete in ten or fifteen days, which serves to differentiate it from most skin eruptions. From variola which pursues an equally rapid course it is distinguished by the absence of the primary nodular swelling, and of the septa or pillars that divide the mature pock into independent chambers.

Prophylactics. The best prevention for man is to exclude the disease from the country and its herds as is now the case in the United States. When the disease does exist in herds the attendants should cauterize any sores on the hands, and wash the hands with an antiseptic, such as a 10 per cent. carbolic acid solution, after handling the diseased. The milk and its manufactured products—butter and cheese—should be withheld from consumption until after the herd has recovered. Infection can be obviated by boiling the milk.

Treatment. The disease follows a rapid course and is self-limiting, and usually benign so that active treatment is not urgently demanded. The local lesions are best met by non-poisonous antiseptics, such as: borax in powder or strong solution; boric acid (4:100); sodium hyposulphite (½ oz. 1 qt.); chlorate of potash (½ oz. to 1 quart); salicylic acid (1:100); or salicylate of soda. Pounded ice may be used as a soothing agent. The cutaneous lesions may be wrapped in cloth wet with one or other of the antiseptic lotions. Any disposition to ulcerate may be met by the stick of silver nitrate.

Slightly laxative or diuretic agents may be employed for their febrifuge and eliminating properties and the food should be light, easily digestible and given cold.

Prevention in Animals. When the disease exists in a country or district this includes all measures preventive of immediate or mediate contagion. Arrest of all movement of cloven footed animals in infected districts, disinfection of cars, boats and other conveyances, of markets, yards, highways, seclusion of infected herds and pastures, exclusion of visitors, disinfection of products, certificates of soundness of origin, thorough disinfection after recovery of the herd, such are the leading points to attend to. Inspection or closure of fairs and markets is desirable and any exposure of diseased or infected animals should be visited with heavy penalty, in addition to the cost of detention and supervision. For a noninfected country a certificate and guarantee of non-exposure with each cloven-footed animal imported, and of thorough disinfection of the cars, boats, halters or other objects used upon them, and of the places, fodder and litter supplied, together with a quarantine (1 week) and surface disinfection should be required under penalty. Exclusion of fresh hides, bones, guts, hair, bristles, wool, horn, as well as of fodder and litter is essential. Cattle attendants, drivers and others whose clothes are soiled with the products of the barn, should have the same washed and disinfected.

Inoculation has been proposed, and even practiced to pass a whole herd promptly through the malady, but as immunity lasts but three months, and the attendant risks to other herds are greatly encreased it is at once an economic blunder, and a great injury to adjoining owners. Any resulting extension to other herds should be an occasion for a verdict for damages at common law.

Treatment in Animals. Provision is first made against extension of the infection. The floor should be kept clean, dry and covered with sawdust, tan bark, gypsum or litter sprinkled with these or with phenic acid. The herd should be divided into two lots—the apparently sound, and unsound kept strictly apart under separate attendants, above all separate milkers. As soon as any symptoms are shown by an animal in the sound enclosure it must be instantly transferred to the other and its stall disinfected. Antiseptics such as gaseous iodine (two tablespoonful of tincture of iodine, thrown into a quart of boiling water twice daily), sulphurous acid, salicylic acid, creolin, lysol or other ointment on the feet and teats, may also be used. In this way it may be possible to save a number from an attack, yet most commonly the exposure is common and universal and the malady develops in all simultaneously. For those already attacked, gruels, mashes, and cool pulped, finely sliced or boiled roots may be all that is required, the disease runs its course and recovery ensues in 15 days. As local dressings the following may serve as examples: for the mouth, borax, chlorate of potash, salicylate or sulphite of soda 2 drs. to 1 quart water; phenic acid, creolin, or lysol, one or two teaspoonfuls to a quart; for the foot, clean the interdigital space and apply tar and carbolic acid with bandage, or use solutions of creolin, lysol, pyoktanin or blue-stone; in aggravated cases strong mineral acids with tar; for the teats, ointments of boric or salicylic acid, creolin, lysol, naphthalin or napthol. Separation of the hoof or mammitis will require treatment according to indications.

MILK SICKNESS. “THE TREMBLES.”

Geographical distribution: timbered lands in the United States; different altitudes, and geological formations; on hills and wooded bottoms; known to Indians and pioneers; now unknown where formerly prevailed. Contagion: through milk; no specific microbe found in every case. Alleged causes: rhus; nickel; spirillum; bacillus. Prevails in dry seasons; contracted under night exposure; confined to given enclosures; to late summer and autumn. Not conveyed by contagion, indefinitely, as are plagues. Men show very varying susceptibility; young children may be relatively immune. Fatigue, debility, ill health, predispose. Exertion to fatigue rouses symptoms in animal affected. Cow in full milk eliminates toxins and does not show symptoms; the milk infects. Steers, bulls and heifers, show marked symptoms. Calves suffer through milk; swine through veal; dogs through pork; buzzard through dead dog. Incubation 8 to 12 days. Symptoms: tardy, lazy gait, drooping, anorexia, ardent thirst, inactive bowels and kidneys, milch cows when driven or excited, tremble and may suddenly die. Muscular debility, constant decubitus, complete apathy, neither evades nor resents injury. Bloodshot, fixed, glazed, unwinking eyes, pulse and breathing slow, temperature low, hebetude, torpor, coma; death 8th to 10th day. Sheep very prostrate. Calves tremble when sucking, vomit and perhaps die suddenly. Pigs and dogs vomit, and show costiveness, remarkable debility and weariness. Man is weary, languorous, weak, apathetic, loathes food, is nauseated, retches. No fever; but ardent thirst, tremulous tongue, mawkish breath, soft flabby belly, careless of own or family interests, forgetful of decency. Nausea, vomiting of blueish liquid, hebetude, inactive bowels, coma. Lesions: gastro-intestinal congestions; ingesta like hard balls of sawdust. Treatment: charcoal, mild laxatives, elm bark, egg nog, potassium permanganate. Prevention: clear timber land, let in sunshine, cultivate. Insects. Sterilize the milk.

This is an infectious disease which has been found enzoötic in certain unimproved, timbered lands of North Carolina, Georgia, Tennessee, Kentucky, W. Pennsylvania, Ohio, Michigan, Indiana and Illinois. Beach says it has never been reported on any of the Western prairies, at any point west of the Mississippi River, in New England, in the Canadas, in any islands, or in any part of the Old World. Altitude appears to have no effect in its production, nor geological formation; it has been found in the wooded mountains of the Blue Ridge of N. Carolina and Georgia (Kerr, Salmon, Phillips); in the hills of Pennsylvania and Kentucky; (Beach, Phillips); on timbered uplands (Phillips); and on the wooded bottoms of the Scioto and Miami in Ohio (Phillips, Schmidt); in the timbered bottom lands of the Wabash and White Rivers in Indiana (Phillips); and in the wooded bottoms (Beardsley), and Indian Grove in McLean, Co., Ill. (Beach). The constant conditions are the heavily timbered and virgin condition of the soil.

It was much more prevalent in the time of the early settlers, than it is to-day, many infecting localities having become salubrious in connection with the clearing away of the forests and cultivation of the soil. The disease was well known to the Indians and often proved disastrous to the pioneers, whole communities being swept off as recorded of Pigeon Creek, by Nicolay and Hay in their History of Abraham Lincoln. According to these writers it was “a malignant form of fever—attributed variously to malaria, and to the eating of poisonous herbs by the cattle—attacking cattle as well as human beings, attended with violent retching and a burning sensation in the stomach, and often terminating fatally on the third day.” Even in these early days settlers were loathe to acknowledge the existence of the infection on their lands, doubtless because it depreciated them, and to-day with a better knowledge of the necessary precautionary measures, it has literally disappeared in many places, so that it is now difficult to find a case.

Contagion. That the disease has been transmitted through the milk from animals to man and other animals has been too painfully evident from the first, but no specific microörganism has been found to be constantly present, capable of pure culture in artificial media and of causing the disease when transferred from such media to a new victim. Naturally all sorts of theories have been advanced, no one of which has been demonstrably proved. It has been attributed to eating of poison ivy (Rhus toxicodendron) by the cattle, as this plant was usually found on the infecting lands, but rhus is also common throughout New England and the Eastern States where milk sickness is unknown. It has been claimed that it was due to mineral agents, especially nickel, in the water but the mineral salts in the water are not removed by culture of the surface soil, which puts an end to milk sickness. Phillips (1876) claimed to have found the cause in an actively motile spirillum in the blood, but he had examined the blood of but one patient, and it has not been found in other patients by subsequent observers. Bitting found a bacillus but further research has not determined its constancy.

Beach furnishes a series of observations which should be useful in seeking to estimate the value of any theory propounded. 1st. Milk sickness is a disease of dry seasons. 2. In unusually dry seasons it is dangerous to leave domestic animals out over night in the localities where the disease is prevalent. 3d. It has never been considered dangerous for animals to pasture on such lands in the day time. 4th. Cattle in one field will habitually escape, and in another with apparently exactly the same conditions and the same flora they are attacked. 5th. The disease is unknown on the open prairies of the Western States, where the domestic animals are not allowed to remain over night in the timber belts. 6th. With occasional exceptions, it is a disease of late summer and autumn. The dangerous lots can, as a rule, be safely depastured in winter and spring. 7th. The pioneers found that they could protect their stock by keeping them corralled on a “tame” piece of land from before nightfall until the fogs and dews became dissipated on the following morning.

For the land to become “tame” it was only considered necessary to cut off the timber and let the sunshine act freely on the surface. Plowing and cultivation did not seem to be requisite in all cases.

A great drawback to research is the difficulty of securing cases to study. Many lots, formerly dangerous, are no longer so, and others still infecting are kept so secluded that casual cases cannot be found, without much expense for experimental animals. Again, owners do not care to depreciate their land by acknowledging that it is infecting. The experiment stations naturally enough look askance, on the proposal to institute expensive experiments on a disease which dies out when the soil is improved. Deadly as the disease is to the individual attacked (man or beast), it is not propagated indefinitely from non-milking subjects, by simple contact or proximity after the manner of plagues. It usually comes to an end by the death or recovery of the subject that has contracted it by consuming meat, milk, butter or cheese, the product of an infected animal. The demand for sanitary police measures is, therefore, less urgent. Different observers claim that cases occur in the large cities, through the consumption of meat, butter or cheese, sent from infected localities, but that the city physician fails to make a correct diagnosis. These must, however, be comparatively rare.

In addition to ingestion as a cause, certain accessory causes ought to be noted. Some men eat the infecting material with impunity, while others succumb to the deadly disease. As the observations have all been made in or near the infecting localities, individuals may be immune through a previous attack and recovery, or there may be a native immunity through unknown conditions. Young children often suffer less than adults, possibly because of the greater activity of their emunctories and consequent elimination of the toxic products and the comparative absence of exhausting or depressing conditions. Their purely animal food (milk) may exercise an influence, and this may assist in explaining the fact that certain adults appear to be refractory.

Fatigue, debility and ill health are said to predispose the system. Milk sickness attacks most violently those that have been subjected to overwork or severe exertion of any kind, especially in hot weather, those suffering from want of sleep (sitting up with the sick), those having a special cause of mental depression, those suffering from some illness—constipation, indigestion, malaria, etc.

Milch cows are probably more open to the attacks of the germ because their systems are reduced by simultaneous milking and breeding through a number of years. Exertion or fatigue has a potent influence in developing the symptoms, so that it is a common practice in the vicinity of infected localities to subject animals to a good run before purchasing. Paradoxically enough the infected milch cow which is distributing the infecting element freely in her dairy products usually shows, in herself, no distinct symptoms of the disease. If she is dry or farrow she suffers like any other animal, but if in full milk, the toxins, and even the hypothetical microbe, seem to escape in that secretion, which proves highly poisonous to other animals, while the cow retains her spirits, vigor and outward appearance of health. Steers, bulls and heifers, on the other hand, show violent symptoms.

Calves suffer so long as they suck the milk. The dead calf is eaten by swine, which suffer in their turn, and the dog contracts the disease by eating one of these animals, or by taking infected milk or cheese. The buzzard eats the dead dog and dies as the result.

Incubation is from 8 to 12 days, though it may be reduced to two. (Beach.)

Symptoms. In the domestic animals the first indication of illness is a lazy, tardy disposition, The subject stands apart from the herd, with drooping head and ears, listless, indifferent to all around him, and often without appetite; or, in cattle or sheep, rumination. There is usually extreme thirst, but without correspondingly free urination or defecation. Peristalsis is virtually abolished and nothing whatever passes from the bowels. The patient is likely to be found lying down and it is difficult to get him up, and when raised he moves stiffly and with reluctance.

In milking cows there may be no symptoms until the animal is excited or fatigued by violent or continued exercise, as a hard run, or a drive of four or five miles. This developes the tremors alike in milch cows and in the mild cases in dry cattle or sheep. The subject stands still and trembles in a striking way, the action resembling the muscular contractions seen after the removal of the hide in an animal newly killed. The head and ears are drooped, movements are uncertain and stiff, and the animal may even drop dead on the spot.

As the disease advances the muscular debility becomes so great that the animal lies down if possible, and if once down he seldom rises again. The decubitus is extended, the head being stretched on the ground. There is a most complete apathy, the subject showing no fear, no apprehension, no disposition to escape or resent injury. The wildest or most timid steer can be freely handled, and there is no disposition to flight or retaliation. The eyes are bloodshot and become fixed and glazed, winking ceases, the breathing is slow, pulse infrequent, and temperature often subnormal. The extremities and surface of the body are cool, the muzzle dry, the coat usually stares, the apathy merges into a complete hebetude, torpor and coma, in which condition the animal often dies on the eighth or tenth day. Violent exercise precipitates the death at once. Recoveries are infrequent and attended by no critical discharge from bowels or kidneys, only by a slow, at first almost imperceptible, resumption of natural action.

The milder cases, those that show no appreciable symptom when at rest, are seized with trembling or rigor when made to undergo the slightest exertion; they appear haggard, stupid and spiritless, drag their limbs slowly and stiffly and quickly stop from pure weariness and debility.

The prostration is even more marked in sheep, which often seem unable to rise, or lack the nervous energy to do so.

Calves tremble while sucking, and will sometimes leave the teat, vomit the contents of the stomach, fall down and perish.

In Vomiting Animals (pig, dog,) emesis usually occurs, and torpor of the bowels or obstinate constipation is present. Pigs burrow under the litter and are driven out with difficulty, and dogs when called on to follow, do so reluctantly, slowly and stiffly and fail to keep pace with their master (“the Slows”).

In all animals alike active or continued exertion rouses or intensifies the symptoms.

In man there is at first extreme langour, weariness and weakness, the patient cannot be troubled to move, he loses appetite, loathes food, and soon has nausea and retching—often from the first. There is no chill, rigor nor violent headache as in other fevers; but insatiable thirst; large, flabby, tremulous, moist tongue, coated a dirty white; cold nose, ears and general surface; dry skin; sweet, mawkish or offensive breath; flat, flabby empty belly; without peristalsis or defecation. Respiration becomes very slow, pulse weak and compressible, heart action tumultuous and labored, temperature often below normal, and though sometimes 99° or 100° F., never higher. The patient takes to bed in four or five days, or, after exertion or fatigue, in a few hours becomes profoundly apathetic, expresses no concern for his business, his own future or that of his family, is intolerant of bed clothes or other covering and utterly oblivious of the demands of decency. Nausea continues, but retching becomes weaker, and comparatively ineffective, or brings up a little liquid which has been compared to blueing water of the laundry. The apathy merges into a state of hebetude and this into coma, with fixed, glazed eyes, absence of all winking, and insensibility to irritants and death takes place quietly without a moan or struggle.

Recovery is slow, and improvement for a time is almost imperceptible. In some cases there remains a nervous atony, and in man, a lack of mental and bodily vigor, and a disposition to relapse under exposure to intense heat or fatigue has been noted, but in many cases recovery is complete and permanent without lasting weakness.

Lesions. Both in man and animals, congestions of the gastric and intestinal mucosæ have been noted, usually with a dark firm condition of the membrane, but in some cases with capillary stasis, and sloughing. Beach never saw indication of tenderness in the abdomen or elsewhere, nor did he ever find blood nor stercoraceous matter in the vomited material. The contents of stomach (paunch in cattle) and bowels formed hard balls like cemented sawdust, firmly adherent to the dry mucosa.

Treatment and Prevention. Treatment by the Indians consisted in giving large doses of powdered charcoal suspended in milk. The early physicians attempted to open the bowels by calomel and jalap, olive oil, magnesia citrate, and even croton oil, but the last generally with fatal results. Milder and hardly less effective treatment consisted in large doses of elm bark. Beach believed he got better results with quinine and egg nog. It might be suggested to try such antiseptics as potassium permanganate, peristaltic stimulants like eserine or pilocarpin, as an eliminating agent pure water or weak diuretics, and nerve stimulants nitroglycerine or ammoniacal preparations.

Prophylaxis. The time-honored resort of clearing the timber and brush land so as to let the sun act freely on the soil, and the putting in of cultivated crops, is proved reliable and permanent. The other precautions in use are valuable in protecting the herd, but lack the merit of thoroughness and permanence and thus fail to strike at the root of the trouble. They are: 1st. the exclusion of domestic animals from the infected woods in late summer and autumn and in very dry seasons; and 2d. the exclusion of stock from such pastures from before nightfall until after the dews have evaporated on the following morning.

The danger which attends on passing the night in the forest, strongly suggests the intervention for the transfer of the poison of some nocturnal animal, perhaps a night-flying insect, like the anopheles, which transmits the plasmodium of malaria. If the germ and its intermediate bearer (if any) were demonstrated, probably other and simpler means of prevention could be adopted.

The fact that the propagation of the disease is not constant and wide spreading, like a genuine plague, lessens the urgency for a rigid sanitary police, yet animals kept on such infected farms, should be tested by long or vigorous driving before they are killed for food, and all milk devoted to the production of butter and cheese should be Pasteurized or sterilized before use. It might well be questioned whether the clearing and exposure of infecting places should not be undertaken by the state as a sanitary measure.

In view of the fact that a milch cow may not show symptoms of the disease, and yet yield deadly milk, and considering that the owner cannot always tell whether she has been in the infecting woods, or having been in, whether she is infected, it becomes an important public health question whether such a source of deadly disease should be perpetuated, where human food is open to contamination.

VARIOLA: POX.

Definition: Structure of lesion. Nomenclature. History, smallpox, sheeppox, cowpox, horsepox. Animals susceptible: Man, sheep, cow, goat, horse, pig, dog, buffalo, camel, monkey. Microbiology: A pure contagium, particulate contagium, cocci, sporidium vaccinale. Horsepox: Early history, means of infection. Symptoms: Vesicles on lips, on heels, concretions, treatment. Cowpox: Relation to horsepox. Causes. Relation to smallpox. Observations of Ceely, Fletcher, Thiele, Klein, Martin, Reiter, Chauveau, influence of vaccination, of spring parturitions, of infected stables. Symptoms: Incubation, seat and nature of vesicle, inoculations for vaccine. Diagnosis from aphthous fever, rinderpest, eruption of mastfeeding, false cowpox, streptococcus eruption. Duration. Course. Prognosis. Treatment. Sheeppox: Synonyms. Definition. Pathogenesis: Sheep, goat, ox, dog, pig, horse. Forms: Discrete, confluent, hæmorrhagic. Distribution. Causes. Contagion; extends on air; experiments on blood; wool, hides, litter, buildings, yard, parks, railway cars, boats, clothes, manure, wine, milk, men, dogs, cats, birds, vermin, flies. Receptivity. Overcrowding, filth, starvation, neglect, wars, commerce. Recovered sheep. Disinfectants. Incubation 4 to 7 days; conditions affecting. Symptoms: Hyperthermia, general disorders, rigors, anorexia, skin blush on parts devoid of wool, red points, papules, vesicles, pustules, desiccation. Successive crops. On eye, nasal mucosa, mouth, pharynx, intestines, lungs. Confluent cases. Lesions. Prognosis. Mortality. Depreciation. Treatment. Prevention: By segregation, slaughter and disinfection; by ovination. Technique of ovination. Resulting immunity. Sheeppox in Goat: Danger of infection to sheep. Goatpox. Swinepox: From man, sheep, goat. Symptoms. Forms: Discrete, confluent. Susceptibility of young. Treatment. Prevention. Dogpox: From man; from sheep. Other eruptions in dog. Symptoms: Fever, flushed skin, red points, papules, vesicles, pustules. Discrete. Confluent. Treatment. Prevention of infection of man and sheep.

By the generic name Variola is understood a febrile malady attended by a characteristic eruption on the skin, at first papular, then becoming vesicular and finally pustular. The structure of the vesicle is so characteristic that it may be taken to indicate the variolous eruption as found in man and a variety of the domestic animals. The first indication of the lesion is the appearance on the skin of fine points of congestion like fleabites. This is followed by active diapedesis and proliferation of cells in the papillary layer and rete mucosum, constituting the nodule or pimple stage. In smallpox this is so firm and definitely outlined that it has been compared to the presence of a shot in the skin. As the proliferation of cells increases these form in separate clusters or groups, isolated from each other by septa or walls largely made up of the epidermic cells. In the next stage, therefore, when exudation takes place the lymph accumulates in the spaces occupied by the clusters of growing cells, and is found in a series of chambers more or less perfectly separated from each other, so that to evacuate the whole vesicle, each minute sac must be punctured independently. The vesicles thus differ from others caused by ordinary irritants in that each is chambered, instead of forming one common undivided sac, which may be emptied by a single puncture. In the next stage, when suppuration ensues, the septa usually undergo liquefaction, so that the liquid occupies one individed cavity in each pustule. For this reason the central depression seen in the larger vesicles (cowpox) in their early stage tends to disappear in the pustule. It may reappear later in the resulting scab. Desiccation, scabbing and desquamation complete the course of the affection, a distinct pit being left as a result of the destruction of the superficial layer of the dermis.

Nomenclature. The term variola is believed to come from the Latin varius (variegated, spotted) and pox from the Saxon pock (pouch). The specific names, drawn from these tongues sustain this view: As, variolæ vaccinæ, cowpox, kine-pox; variolæ equinæ, horsepox; variolæ ovinæ, sheeppox; variolæ caprinæ, goatpox; variolæ suillæ, swine pox; variolæ caninæ, dog pox. The term smallpox, (petite verole) is deduced from the small size of the vesicle as compared with that of cowpox, just as the same has originated the term smallpox in sheep.

History. Variola has undoubtedly existed from very ancient times. Moore found it referred to in Chinese records of 1122 years before Christ, but it was only clearly described early in the tenth century by Rhazes an Arabian physician. Gregory, however, found the name variola in Latin manuscripts in the British Museum of a much earlier date. The early epidemics of small pox have usually extended from the east, and the disposition has been to refer its origin to the crowded communities of central Asia, but nothing is certainly known as to such origin and the lack of definite recognition and description cannot be taken as implying that the disease did not exist. The extension of small pox to America in 1520 was distinctly traced to a sick negro slave landed in Mexico, and the way in which it swept the continent killing the Indians by tens of thousands, speaks strongly for its prior absence and the extraordinary susceptibility of the hitherto unaffected Indian races.

The variolæ of animals are not recorded until later, the mildness of the forms attacking cattle and horses, and the lack of close observation of the diseases of sheep furnishing a reasonable explanation. We must pass over as uncertain the lues ovium of Thomas Wallsingham, (Historia Anglicana), imported in a rotten Spanish ewe in 1274, and which prevailed for 25 years destroying nearly all the sheep of the kingdom, also the reference to the “pockes” of sheep in Chaucer’s “Pardoners’ tale” as highly uncertain. Laurent Joubert in his work on the “peste” mentions sheep pox as prevailing in 1567, and Rabelais speaks of it as prevailing in France in 1578. It prevailed in Padua in 1649, in Venice in 1664, 1672, and 1674 (Bottani), in Italy in 1690 (Ramazini), in Germany in 1687–8 (Stegman), in England in 1711, in Hungary in 1712, in France, Italy, etc., in 1714 (Kanold), in Venice and Bohemia in 1719 (Bottani), in Saxony in 1720, in Venice and France in 1723–24 (Bottani, Astruc), in Thuringia in 1725, in Siberia in 1771 (Pallas), and in Persia generally at the beginning of the 19th century (Bruce). Great Britian, long protected by her insular position, was infected by sheep from Germany in 1847 and again in 1862. Under ovination the first invasion prevailed for four years causing wide spread destruction; under strict separation based on thermometry, the second lasted but four months.

Cowpox has existed in England for centuries, but it has only attracted general attention since the introduction of vaccination by Jenner in 1796. Horsepox has existed concurrently with cowpox, the infection being habitually transferred by the hands of the milkers from horse to cow and vice versa. Jenner found it so common in the Valley of Gloucester, that he considered it as the habitual source of cowpox. Sacco recognized it at the beginning of the 19th century, Hertwig in Berlin in 1830, Röll in Vienna in 1855, and Bouley and others later in different parts of Europe.

Animals Susceptible. Variola in some form affects man, sheep, cattle, horses, goats, pigs, dogs, buffaloes, camels and monkeys.

Microbiology and Infection. It has long been well established that variola is due to contagion alone. The habitual dread of contact with a smallpox patient, shows the general appreciation of the danger of contagion, and the many epidemics, started by the introduction of a smallpox patient and thereafter spreading from that as a centre, together with the long continued immunity of certain insular or trans-oceanic countries illustrate this. One of the most striking examples is the immemorial immunity of the New World until the landing of the variolous slave in Mexico in 1520, and the immediate, rapid and destructive spread of the disease among the native tribes. Sheeppox offers a no less striking example. Prevailing for centuries in Asia and Europe, its extension to a new district was always the manifest result of the movement of infected sheep; England remained immune until her first invasion in 1847, and the second in 1862, in both cases the source was easily traced, and the disease completely extinguished by the destruction of the infection in its circumscribed area; the more distant sheep raising countries, America, North and South, Australia, Tasmania, New Zealand, South Africa, in the absence of importation of infected sheep remain free to the present time. For horsepox and cowpox the demonstration is more difficult as limited outbreaks, have occurred at intervals in different localities, traceable more or less clearly to infection from vaccinated persons, yet often mistakenly attributed to spontaneous developments of the disease. Before the days of Jenner however it prevailed habitually in certain dairying districts (Gloucestershire), and I can point to localities in New York, in which the infection is manifestly laid up in the stables, and the disease develops yearly in the heifers coming into milk for the first time and in newly purchased cows, that have not been previously exposed.

The contagion varies greatly in force in the different forms of variola, the milder horsepox or cowpox, requiring actual contact (inoculation) while in smallpox and sheeppox, infection may take place at some distance from the patient (in sheep over 200 yards).

A particulate infecting material was demonstrated by Chauveau, who filtered the virus and inoculated the filtered liquid without effect, while the solids retained on the filter invariably produced the disease.

The identity of the microbe of variola has been much discussed. Guttmann and Grigorjew found in the lymph a coccus (Staphylococcus albus variolæ), Ruete a very motile diplococcus, and others streptococcus, but in cutaneous lesions it is very difficult to exclude such elements. Pfeiffer, Guarnieri, Van der Loeff, Wasielewski and others have drawn attention to small protoplasmic bodies (manifestly protozoa) found in the vaccine lymph, and which appear to be the infecting agents. Wasielewski cultivated these on a rabbit’s cornea to the 48th generation, and from the last successfully inoculated a calf and several children.

Funck finds this sporidium vaccinale constantly in the vaccine lymph and surrounding tissue, as a refractile, amœboid, spherical organism (spore) 1 to 3μ in diameter, and, less abundantly, a round or ovoid spore cyst 25μ. These cysts are either smooth or uneven like a raspberry, and have a single or double contoured membrane. They are easily stained with Sudan III. Examined in hanging drops they are seen just under the cover glass, not on the surface of the drops. Larger flattened bodies found in the lymph, with many included spores are manifestly epithelial cells. Copiman cultivated the organism in glycerinated collodion capsules in the peritoneal cavity of rabbits and dogs, producing zoöglœea masses staining peripherically with methylene blue, and which caused typical vaccinia in calves. He found the same elements in variola of man.

HORSE POX. VARIOLA EQUINÆ.

This was recognized toward the end of the 18th century, in the valley of the Severn, England, by Jenner, who believed it to be the origin of cowpox, but failed apparently to distinguish it from ordinary “grease”. To-day, when we must trace each case to a preëxistent one in some animal, and ignore the question of primary origin, we must still recognize that it passes readily from horse to cow, and from cow to horse, through the hands of milkers and stable-men, but that it also has the source of vaccinated persons in the families of those handling the horses. Whether it was also often derived from the very prevalent small pox in past times is doubtful, yet it appears to have been much more common about the year 1800 than it is to-day. When once started in a stable it passes readily from horse to horse, through the hands of shoeing-smiths and grooms, including of course their aprons, brushes, sponges and rubbers, and also through blankets, bandages, litter and other things on which the virus has been received. The susceptibility of the skin in the hollow of the pastern depends mainly on the frequency of chaps and abrasions, and to a certain extent on contact with the road-mud infected by other passing animals. At times the suffering animal licks the affected part, and determines the eruption on the mouth, lips and nose (see contagious pustular stomatitis). Megnin saw cases affecting the external generative organs and transmitted between the sexes by coition. (See vesicular eruption on the genitals). All such cases should be identified by inoculation.

Hertwig, as early as 1830 recorded the existence of horsepox in Berlin, where it has been seen frequently since, and noted its transmission to man. Bouley gave evidence of its special prevalence at Paris, and of the production of typical vaccine vesicles in man by its inoculation. More recently it has been frequently observed and studied by inoculation and otherwise.

Symptoms. These, whether seen in horse, cow or man, do not differ from those of cow pox, with which it may be held to be identical. The observations of Chauveau, Warlomont, and Pfeiffer that experimental infection, intravenous, subcutaneous, intratracheal (inhalation), or by feeding almost always failed to give the general eruption which characterizes small pox and sheep pox. It remains strictly local except when inoculated on other parts of the skin or mucosa. It must be added, however, that small pox or sheep pox, when inoculated successfully on the horse, as a rule remains confined to the seat of inoculation. The constitution of the horse, like that of the cow, tends to resist its virulence.

The affected horse may show preliminary febrile symptoms, but these are usually too slight to be noticed. They are followed by heat, tenderness and swelling of some part of the skin, usually in the hollow of the pastern and perhaps the back part of the metatarsal region, with more or less (sometimes extreme) lameness. On the swollen skin may be detected nodules, which may pass early into vesicles and pustules. The eruption varies, however, as developed on the comparatively hairless lips or nose, or on the densely pilous pastern.

On the lips, or other part lightly covered with hair, one can easily follow the successive formation of the round nodule, the distinct (sometimes umbilicated) vesicle, with its clear translucent straw-colored contents, and the pustule, which bursts, forming a sore, or dries up forming a dense scab, like that of cowpox.

On the heels, or on any part thickly covered with hair, the vesicle or pustule is rarely recognized, the exudate on the contrary takes place mainly on the surface, which becomes encrusted with an abundant yellowish concretion, matting the hairs together, and sometimes literally covering them. This may be very misleading to the practitioner who expects to see the succession of fully developed vesicle and pustule, and overlooking the true nature of the malady he may allow it to spread widely in a stable.

Describing his inoculation cases, Chauveau gives the following successive phenomena:—

“From the fifth to the eighth day the points of inoculation become distinctly papular. As far as about the tenth day, the papules encrease, and become more prominent, taking the form of an extremely wide cone, with a base of ⅓ to ½ inch. During this period these large conical papules are resistant and painful on pressure, but show no elevation nor change in the epidermis, save a slightly reddish reflection in animals with white skins. Afterward supervenes a new stage which may be called the period of secretion. This commences from the ninth to the twelfth day. The epidermis, slightly raised upon all the papule, sweats out numerous drops of a limpid, very slightly yellow serosity. These drops soon concrete into yellowish, transparent crusts covering the whole surface of the pustule:—a species of characteristic crystallization, very different from the crusts that succeed the vaccine pustules in mare and cow. The secretion, which continues several days, is terminated from the thirteenth to the seventeenth day after inoculation. If then the crust is raised there is exposed a humid, pink, granular surface not projecting beyond the surrounding skin. This surface is hollowed out by a very deep central cavity, a sort of umbilicus, in which is inserted, like a nail, a projection from the deep surface of the crust.”

I would add that after recovery the hair in the seats of the nodules has a lighter color and, on the shanks and higher, remains dappled for the season.

No treatment is demanded. The application of a solution of sodium bisulphite once or twice a day, or continuously on a bandage, will greatly modify the intensity of the inflammation, and ward off complex infections. If the skin is left tender or with a disposition to crack, treat it as advised under chapped heels.

COWPOX. VARIOLA VACCINÆ.

This is manifestly the same disease, and due to the same microbe as horse pox. The disease of the one genus is easily transmitted to the other and the lesions and symptoms are the same, as if the virus were derived from an animal of the same species. Differences in the local manifestations appear to be due rather to the varying conditions of the skin and hair follicles, than to any material distinction in the virus.

Causes. Aside from the germ (Sporidium vaccinale) the conditions which favor infection are: the milking of susceptible cows with imperfectly washed hands, after dressing legs, the seat of horse pox eruption; the milking of healthy cows after those affected with cowpox; and the milking with hands contaminated with the exudate in cases of vaccination of man. That susceptible cows may also be inoculated successfully from smallpox patients, under given conditions appears to be true, but in Western Europe and America this is very uncommon, and would be much more so if vaccination were universally carried out. Among those who claim the identity of small pox and cow pox may be named Ceely, Reiter, Babcock, Thiele, Voigt and Klein.

Ceely alleges the infection of five cows and one heifer, in 1839, in England, from chewing the flock of a bed on which a small pox patient had died. In 12 or 14 days they had tender congested udders, with hard pimples imbedded in the skin, followed by blisters, and brownish scabs. The milk diminished, saliva drivelled from the mouth, the cheeks were inflated and retracted, the coat stared, their feet were drawn together, and the back was arched. The disease was communicated to the owner. This was clearly an outbreak of aphthous fever, which invaded England in that year, and was still an unknown disease to medical men. The implication of the heifer which would not have been inoculated with variola through the hands of the milker, and the salivation which is unknown in cow pox, but points directly to the buccal vesicles of foot and mouth disease, are conclusive on this point.

Ceely later, after many fruitless attempts to convey smallpox to the cow, at last met with results which indicated cowpox, and which he thereafter passed from cow to cow with the characteristic cowpox eruption.

Fletcher further reports the transmission of smallpox through the horse to the cow, and thence to the child in the form of cowpox.

In 1836, Thiele, Kasan, S. Russia inoculated some cows on the udder with smallpox lymph, and conveyed the lymph of the resulting vesicles back to man, and from man to man for seventy-five generations of the virus without finding any variation from the type of the true vaccine disease. He repeated the experiment with equal success in 1838.

Such experiments, made before the days of careful antiseptic, or aseptic, laboratory methods, by men who were daily engaged in making vaccinations, cannot be very implicitly relied on, yet the success of Thiele in Central Asia, the early home of variola, may indicate the possibility of a transition, under given eastern conditions, which, to say the least, is exceedingly rare in Western Europe or America.

The experiments of Klein, conducted under modern methods, are more conclusive, and seem to imply the possibility of smallpox passing into cowpox, in the bovine system, under some not yet clearly defined conditions. Until such conditions are sufficiently well known, so that they can be controlled at will, no one can be justified in attempting to produce lymph for vaccination by simply passing smallpox virus through the system of the cow.

It seems important to note one or two instances of the evident transmission of smallpox from man to man through the bovine system.

In 1860, Martin inoculated variolous matter, from a man who had just died of smallpox, on a cow’s udder, and subsequently inoculated about fifty persons from the eruption caused in the cow. Most of those so inoculated had unmistakable smallpox and three died.

Reiter had a very similar experience.

Chauveau (French Commission) inoculated twelve susceptible cattle with smallpox virus and produced, in all but one, small conical (smallpox) papules and vesicles, and in ten of these, on subsequent inoculation with cowpox, six proved immune, three had rudimentary pustules, and one had a distinct cowpox eruption.

A milch cow and two heifers were inoculated with smallpox and cowpox on two sides of the vulva, with the result that each disease appeared in the seat of its inoculation, with its characteristic vesicles, and the two developed side by side. The smallpox vesicles were by inoculation conveyed from ox to ox with steadily decreasing activity. Inoculated from the cow on a child, it caused great hyperthermia, vomiting, one large vesicle like vaccinia and a general eruption like varioloid. Inoculation from this child upon another produced a mixed eruption of cowpox and varioloid. Inoculation from the second child on a bull and heifer produced papular eruption only.

Smallpox virus, inoculated on a horse produced a papular eruption, but failed to affect another horse that had been previously vaccinated. Cowpox virus inoculated on the first horse which had had the papular eruption, caused a second papular eruption (not cowpox). The virus from a vesicle in the first horse caused a similar eruption in another horse, on which it was inoculated. The lymph from the papular eruption led to a similar eruption in cattle, on which it was inoculated, but did not protect against cowpox, subsequently inoculated.

The lymph from the papular eruption in the horse, inoculated on two children, produced fever, vomiting, a general papular (smallpox) eruption, in which a few of the pustules only showed a tendency to umbilication. A child and its mother in the same ward contracted varioloid. A child inoculated from one of the first named children, had six large umbilicated vesicles like cowpox and a general papular (smallpox) eruption. Another child inoculated from the last had six large umbilicated vesicles, and a general papular (smallpox) eruption. From the papular eruption of one of these children a horse and seven cattle were inoculated and in all a varioloid eruption resulted.

The rational conclusion is, that while there is every indication of a primal identity of the two diseases, and indeed of all forms of variola, as shown by a disposition of the virus from one genus, when inoculated upon a totally different genus, to show some indication of the characteristic eruption of the latter, yet the generic type, which comes from the long continued growth in the one class of animal, becomes so fixed, that it cannot be overcome at once, and sometimes apparently not at all, by transferring it to an animal of another class.

If the unfortunate results obtained by Martin, Reiter, and Chauveau, are insufficient to deter from the use of smallpox lymph which has been passed through the cow, the long experience with humanized vaccine, which in its inoculation from man to man for a century has shown no tendency to revert to smallpox virus should be a sufficient warning against such dangerous optimism.

No deduction can be safely drawn from the comparative mildness of most of the cases caused by reinoculation from cow or horse to man, inasmuch as that all forms of variola can be rendered less severe by resorting to inoculation, which was extensively practised to limit the ravages of smallpox before the days of vaccination, and is still largely resorted to in the case of sheeppox in Europe. In each of these diseases the mortality can easily be reduced to 2 per cent. instead of the 20 to 50 per cent. which are lost when the disease is contracted casually.

As occurring casually, cowpox like horsepox is rare. Yet in Denmark, a dairying country, 1,037 cases were reported in 1877–8, and 878 cases in 1888–9. I have found some outbreaks explainable, through the existence of vaccinations in the families of the milkers, and Bollinger says that in Germany, most outbreaks take place in spring, the time when children are vaccinated. He should have added that this is the usual time of parturition in the cow, the time when primipara are first subjected to the danger from the hands of the milker, and when the cow from the noninfected district is brought into an infected stable for the season’s milking. In a dairying district in Tompkins Co., N.Y., the affection appeared every spring, in the same barns, in heifers with their first calf and in newly bought cows. All older cows, bulls, steers and unimpregnated heifers escaped.

Symptoms. The period of incubation is two days, after inoculation, and though it may appear to extend to a week when the disease is contracted accidently, it is impossible in such cases to state the exact date of infection. The preliminary fever is not always present, or recognized, yet there may be slight encrease of temperature, partial impairment of appetite and rumination, extra firmness of the fæces, a higher color of the urine, and above all a slight diminution of milk, which is a little more watery and coagulates more readily, than the normal.

This is followed by heat and tenderness of the udder and the appearance on the teats of small, pale red nodules the size of a pea or larger. In one or two days more the nodule, largely encreased in size, presents in the centre a depressed or umbilicated bluish white portion, with a firm yellowish, reddish or reddish blue margin, and outside this a soft pink areola, shading off into the white skin. The epidermis is raised at points by a viscid, yellowish lymph, enclosed in a series of saccules (multilocular vesicle). The vesicle encreases to 8 or 10 lines in diameter by the eighth or tenth day, and exceptionally, the umbilication is effaced by the excessive production of lymph. If left unbroken a brownish shade appears in the centre and gradually extends toward the periphery, the contents becoming purulent, and the pustule gradually drying up to form a crust. The drying and thickening of the crust goes on until the fourteenth day and the crust is usually detached by the twentieth, leaving a pale rose colored, smooth, shallow depression, which forms the permanent pit left after the skin has healed. The primary scabs usually show the central umbilication, and always the conical projection in the center of the deep aspect, and corresponding to the pit.

Vesicles on the mammæ may pass through the above stages, but those on the teats are usually ruptured by the hands of the milker as soon as the liquid is thrown out, and this gives rise to troublesome sores, with complex infections, at times implicating the gland tissue so as to cause destructive mammitis with loss of one or more quarters, and in any case abraded and irritated at each milking, so that the animal resists handling, the milk is drawn off imperfectly, and dries up or the cow becomes an inveterate kicker. If the milker has not been vaccinated he is liable to contract the disease.

A succession of vesicles often appear on the same animal, so that they may be found in all different stages of vesicle, pustule and crust on the same bag at one time. The later eruptions may be the result of inoculation from the earlier ones, and tend to prolong the attack materially.

In inoculation of the bovine animal for the production of lymph for vaccination, the skin of the abdomen from the symphysis pubis to the umbilicus is shaved, or in other cases the skin between the thighs, or in still others the skin on each side over the loins, and the virus applied in 50 to 200 points, by preference scraped until liquid oozes, but without any escape of blood. In a warm room the eruption matures in four or five days, its form taking on an appearance approximating that seen on the hairy skin of the horse. The individual lesions are somewhat extended corresponding in form and size to the abrasion on which the lymph was applied, and usually present the appearance of a raised patch, covered by a grayish film of epidermis, on the removal of which there is seen a raw alveolated surface filled with the amber-colored lymph.

Differential Diagnosis. From aphthous fever, cowpox is clearly distinguished by (a) the multilocular structure of the vesicle, while that of aphthous fever is a single undivided cavity which can be drained completely by a single needle prick; (b) by the pitting or umbilication, the aphthous vesicle being uniformly rounded and convex; (c) by the absence of vesicles or sores on the mouth and feet, which are rarely wanting in the aphthous eruption; (d) by the comparative absence of hyperthermia and constitutional disturbance, which is better marked though still slight in aphthous fever, and (e) by the absence of the intense and subtle infection of aphthous fever, which quickly attacks a whole herd and extends with equal rapidity over sheep, goats and pigs, attacking all cloven-footed animals virtually without exception. The cowpox patient, on the contrary, does not necessarily attack the cow in the next stall unless milked by the same hands, and spares heifers, bulls, steers, sheep, goats and pigs.

From the rinderpest cutaneous eruption it is easily distinguished by the presence of lymph in the lesion, that of rinderpest being a mere epidermic concretion; by the absence of the intense fever, anorexia and general constitutional disturbance, and of the early and high mortality which characterize that disease; by the absence of rapid and uniform infection of other cattle irrespective of a common milker; by the immunity of heifers, steers and bulls, which are speedily prostrated by rinderpest, and by the absence of the congestions and epithelial concretions of the mucosæ which characterize rinderpest.

From the leg irruption found in animals feeding on distiller’s swill and grains, or on the mast of beet sugar factories, by the history of the outbreak, of the dietary, of the seat and nature of the disease, and by the escape of animals living on a different aliment.

From the false cowpox (varicella) it is distinguished by the unilocular lesion of the latter, its absence of areola, and its rapid pustulation and drying, in five or six days into a thin papery crust instead of a thick, firm, umbilicated scab, as in cowpox. Varicella is further liable to appear in successive crops and thus last for several weeks.

The streptococcus eruption on teats and udder, is marked by the formation of abscesses of various sizes from a simple pustule upward, by the unilocular condition of the pus sac, by its tendency to invade the deeper tissues, and by its rupture and granulation without the formation of the thick umbilicated scab of cowpox.

The hard warty growths on the teats which last for weeks or months should never be mistaken for cowpox.

Cowpox usually lasts for some weeks in a herd, the duration depending on the number of susceptible animals and, whether these are habitually milked by the same person.

Course. Prognosis. It is a mild affection, which does not endanger life, yet it causes considerable loss through diminution of the milk secretion and, it may be, altered character of the milk, through the persistent sores and ulcers of the teats, through inflammation of the mammæ, and through an acquired habit of kicking.

Treatment is rarely needed. Any costiveness should be corrected by a cooling saline laxative (½ to 1 lb. Epsom salts) or by soft food, and milking should be done with great care to prevent rupture of the vesicles and the formation of sores. A teat tube may be used if necessary. Sores may be dressed with bland ointment. An ounce each of spermacetti and sweet almond oil with half a dram of gum myrrh. Or the vesicles or sores may be washed after each milking with a solution of 2 drams hyposulphite of soda in 1 quart water.

SHEEPPOX. VARIOLA OVINA.

Synonyms. Pocks; Peltrot; Clavelee, Picotte, (Fr.).

Definition. An acute febrile affection, eminently contagious, prevailing epizoötically in sheep and goats, characterized by early and marked hyperthermia, and general constitutional disorder, followed by the appearance on the bare or merely hairy portions of the skin, of diffuse redness becoming intensified in points, a rounded papular eruption, passing into vesicles, pustules and scabs, which latter dry up and drop off in 15 to 20 days.

Pathogenesis. Beside sheep and goats which contract the disease by exposure, the following genera have been successfully inoculated: ox, dog, pig, horse.

Forms. Two typical forms are recognized: (a) the discrete, regular or benign, in which the vesicles remain relatively few, and well isolated from each other, and (b) the confluent, irregular or malignant in which the vesicles are generally diffused over the body, even on the parts covered by wool, and set so close together that they merge into each other forming extensive continuous lesions. Other forms are the hæmorrhagic, purple or black sheeppox, the volante or intermittent kind, etc.

Geographical Distribution. Formerly common in Central and Western Europe, it still prevails continuously in the Balkans, the Danubian Principalities, Italy, Spain, the South of France and Algiers. Like other forms of variola, its permanent home is in Asia.

Causes. Long before the advent of modern bacteriology, sheeppox was held to be always and everywhere the result of contagion alone. Whenever it entered a new locality it was as the result of the importation of an affected sheep or one of its products; insular places like England maintained a permanent immunity, though the disease prevailed on the other side of the narrow straits or channel; yet when imported (1847 and 1862) it demonstrated a general susceptibility of the flocks on exposure or inoculation; more distant lands (America, Australia, Tasmania, South Africa, etc.) in the absence of imported infection remain clear to the present day.

The infection is more intense and diffusible than that of cowpox and horsepox following in this the smallpox of man. Absolute contact is not necessary, in either case the infection is carried in the air either on dust or otherwise, and above all in a confined building, a crowded sheep fold or a dusty highway.

In all forms of variola the virulence is concentrated in the lymph of the vesicle, and in horsepox and cowpox it is largely confined to this, whilst in sheeppox in severe cases it must also at times infect the blood, as lambs are occasionally born with sheeppox. On this basis the infection of the secretions generally has been advocated, but it is to be supposed that in moderate cases these are contaminated after secretion. Nocard and Roux produced immunity by the transfusion of blood from the sick to the healthy, but in no case a variolous eruption. Even the serosity from the swollen lymph glands failed to convey the disease.

In view of the diffusible nature of the germ, however, we must recognize that all secretions may be quickly contaminated as soon as they are exposed, and therefore no product of a sick or suspected sheep can be held to be safe, and all should be treated as presumably infected. The most dangerous products and those most liable to convey the disease are wool, hides, litter, buildings, yards, covers, parks, railway cars, boats, manure, urine and milk.

Living creatures like men, dogs, cats, birds, vermin, flies and other predacious insects are occasional bearers of infection.

Receptivity must be considered in every case. In countries and districts habitually immune from sheeppox, all breeds appear to be equally susceptible, the only refractory specimens being sheep that have survived a first attack, and lambs born of ewes that had the disease (naturally or inoculated) during the later stages of gestation. New born lambs, on an exclusively milk diet, are alleged to be somewhat refractory. In a country where sheeppox has prevailed long and extensively, as in Algiers and Brittany, certain breeds of sheep seem to have attained to a large measure of immunity (Nocard). This is doubtless largely due to the survival of the more insusceptible strains of blood, as Algerian sheep carried into France lead to most virulent outbreaks among the native animals (Galtier).

This relative immunity is still more decided when we come to animals of other genera. Though the latest results of research seem to identify the sporidia found in the different forms of variola, yet the long habit of living in an environment found in the ovine race unfits the germ for pathogenic life in various other genera that have their own variolæ. Sacco and Villain reported inoculations from sheep to man, but as the first was experimenting with variola at the same time, and the second did not test his pustules by reinoculation the results are not convincing. Küchenmeister had a general eruption in sheep after intravenous injection of variola of man, but failed to test it by reinoculation. Voisin and Nocard on the other hand were uniformly unsuccessful in attempts to convey sheeppox to man, and the handling of variolous flocks from time immemorial must have led to many cases in man, had he been appreciably receptive. It is virtually the same with cowpox. Huzard vaccinated 2,000 sheep without producing immunity from sheeppox. Voisin had precisely similar results. He further inoculated infants with sheeppox, and later, successfully, with vaccine lymph.

It does not follow that these genera would be insusceptible under all conditions. Yet the failure to immunize against each other would argue a wider divergence of sheeppox and cowpox, than of smallpox and cowpox, or than of bovine and avian tuberculosis.

Galtier failed to inoculate sheeppox on rabbits or Guinea pigs, yet Jourdan, records a destructive outbreak in the Alps, in hares, kept in the same places with variolous sheep.

Accessory External Causes. All unwholesome conditions of life, and especially overcrowding, filth, starvation, and neglect contribute to the extension of the infection. Still more so, the importation of sheep, whether in the parks of armies, or in the channels of trade, by rail, or steamboat, through stockyards or markets.

The virus is possessed of unusual vitality, and in the dried condition, secluded from air and light will remain virulent for an indefinite period. Hence the danger of wool, and dried sheepskins. Even in the moisture of an ordinary shed it has retained its infectiveness for five or six months. The sheep that has recovered from the affection may transmit the disease to others for a period of six weeks. The virulence is rapidly destroyed by exposure to free air and sunshine, by a high temperature (140° F.), by dilute HCl (2:100), by carbolic acid (2:100), by zinc chloride (5:100), by potassæ permanganas (10:100), by lime chloride (4:100), or indeed by any of the strong antiseptics.

Incubation. This extends from four to seven days on an average, with a minimum of two and a maximum of twenty days. The conditions favoring an early eruption are youth, high condition, and a hot season, or close warm building, with overcrowding. Those favoring a tardy eruption are old age, debility, and above all a cold or wet season with exposure in the open air. Simonds, who inoculated in England in the cold months (October and November) never saw it exceed 13 days. In certain cases, however when the eruption had already commenced in mild weather, the sudden occurrence of a week of cold and wet, would stop it short to start anew on the return of warm weather a week later. In inoculated cases the incubation is shortened, while it is prolonged when the virus is introduced by the digestive or respiratory passages.

Symptoms. During the last two or three days of a prolonged incubation and especially in old sheep, there may be some impairment of appetite and rumination, dulness, a stiffness of movement of the hind limbs, and a disposition to lag behind the flock. The temperature may even have risen (104.5° F.), yet Simonds has never seen the febrile symptoms precede the eruption.

There follow, trembling, or rigors, accelerated pulse (80 to 90) and breathing, arched back, anorexia, suspension of rumination, costiveness, redness of the eyes, epiphora, a watery discharge from the nose, gradually becoming more viscid, and a marked hyperthermia (105°, 106° or 107° F.) If the skin is white, a blush, with some heat, is shown in the seat of the future eruption, usually on the parts uncovered by wool, the axillæ, sternum, abdomen, udder, inner sides of the thighs, lower surface of the tail, and the face—especially the eyelids, nostrils and lips.

In two days more, deep red points, like flea bites, appear more or less numerously, in the congested parts of the skin, and in twenty-four hours these have increased to firm rounded papules which are felt to extend into the true skin. These vary in size from 3 to 12 mm. or more. In two or three days the papule has become firmer and less tender, and shows in the centre a paler area where the exudation has resolved it into a vesicle. The characteristic sheeppox vesicle is rounded or flattened on its summit, being rarely pointed as in smallpox, or umbilicated as in cowpox. It is usually surrounded by a pink zone, which is at times infiltrated, firm and resistant. After about the sixth day, the vesicle becomes yellowish from the formation of pus. The pustules, with the surrounding tumefaction, encrease for about three days, when if they have not become confluent nor infected, they begin to dry up, acquiring a grayish crust on the surface which gradually encreases to a thick scab, which in five or six days more is detached leaving a pink, pitted spot covered by forming epidermis. Sometimes no distinct scab forms, but the crust dries, cracks up, and falls off in scales.

All the vesicles do not appear at once, but some earlier and some later, so that the successive stages of the eruption may be often seen together on the same subject, and the case is thereby materially prolonged.

As in other forms of variola the hyperthermia usually subsides with the appearance of the eruption, but as often reappears in some measure with pustulation (secondary fever of reaction), and becomes more severe in proportion to the extent and confluence of the eruption and the occurrence of complex infection.

The eruption may invade the conjunctiva, the cornea (inducing blindness), the nasal mucosa (causing difficult breathing), the mouth (salivation, difficult mastication), the pharynx (difficult deglutition), the stomach and intestines (diarrhœa), the bronchia (cough), or the vulva.

With the occurrence of desiccation, in discrete cases, the fever subsides, the swelling of the skin and head disappears, the discharges from the nose and eyes cease, and the animal is restored to health.

A secondary eruption will sometimes take place, but only papules form, which disappear without reaching maturity.

The duration of discrete sheep pox is usually about three weeks, but it may reach four in cool weather. It is more rapid and more prone to dangerous complications in hot weather. As the members of a flock are usually attacked in succession, it may take three months to pass through a flock.

In confluent or complicated cases the fever of invasion is very high, the sheep dull, prostrate, tender to touch along the back and loins particularly, with hurried, labored, panting, breathing, and mawkish, fevered breath, the weakness increases rapidly, standing even may become difficult, the wool is loosened and falls off in patches, the exposed skin is red, shading, it may be, into a violet hue. The head droops, the lips and nostrils swell, saliva drivels abundantly, anorexia is complete, though thirst may be ardent, a yellowish and even reddish, fœtid discharge may flow from the nose, respiration is difficult, the eyes are watery and deeply sunken, and the head, limbs, breast and abdomen are extensively infiltrated and œdematous.

Fever does not subside with the occurrence of eruption, which may appear thickly over the whole body, the woolly parts as well as the bare or hairy. The vesicles, which have often a dark, unhealthy look, tend to become confluent, and instead of proceeding regularly to maturity, they may remain hard or indolent papules or nodules or blacken and dry up. The secretion, when it takes place, is liable to be a thick, yellowish, fœtid pus. The eruption has much more tendency than with the discrete form to invade mucosæ, and not infrequently the serosæ are involved, especially those covering the lungs, liver and spleen. In the worst cases death may result from the fever before any eruption has taken place, in other cases the extent of the internal lesions tends to hasten a fatal result. With the amount of care that can be given to a flock, confluent cases are usually fatal.

In connection with the itching and scratching of the nose, abrasions and complex infections ensue, resulting in extensive ulceration and gangrene implicating the nasal cartilages and bones. The eruption around the pasterns may lead to shedding of the hoofs, and sloughing of the whole digital structures. Suppurating and gangrenous swellings form subcutaneously and in the lymph glands with fatal results. Blindness is especially liable to happen from the formation of the eruption on the conjunctiva and cornea. Ulcerations and sloughs are common on the internal mucosæ, and even on the serosæ. In implication of the abdominal organs, a fœtid diarrhœa is usually present, and in pregnant ewes abortion is the usual result.

Lesions. The cutaneous lesions are in their multilocular structure, the same as in cowpox, but differ materially in size and form. The typical vesicle is small (5 to 12 mm.), and neither broad and umbilicated like cowpox, nor conical and pointed as in smallpox, but round with a slight flattening on the summit. On the same animal may often be found all the successive stages at once, red points or hæmorrhagic spots, vesiculation, pustulation and even desiccation. The early changes are seen in the papillary layer and rete mucosum, in the form of swelling and congestion of the papillæ, exudation, active proliferation of the epidermic and tissue cells, and migration of leucocytes, (embryonic cells polynuclear) vacuolation of the papule, the spaces being filled with a straw colored exudate, and finally, the replacing of this by pus. If the local inflammation is very acute, the pustule may be resolved into a small abscess. On section of the skin the affected parts are found to be the seat of congestion and gelatinoid exudation, extending into the subcutaneous and intermuscular connective tissue, and even the muscles themselves are blackish and their capillaries engorged. The exudation is especially abundant in the dependent parts (head, neck, sternal and abdominal regions, legs). In proportion to the severity of the attack there are congestion, exudation, swelling, and blood extravasation in the lymph glands.

The nasal mucosa is congested, thickened or even ulcerated with abundant, tenacious, muco-purulent secretion and the nasal chambers narrowed or obstructed, and similar changes may be present in the larynx, trachea and bronchia. Spots of ecchymosis and even distinct variolous vesicles are to be expected. The pleuræ are often the seat of congestion, petechiæ, exudation, and discoloration (red or pale). The lung may show congestion and hepatisation in circumscribed areas, or there may be on the surface of such hepatised portions red or grayish foci, like a lentil, pea or bean, the seat of degeneration or forming minute abscesses. The pericardium and myocardium may be involved to a limited extent.

The buccal and pharyngeal mucosæ may be the seats of vesicles, or erosions or ulcers the result of their destruction, and the gastro-intestinal mucosa presents ecchymoses, vesicles, abrasions, and open sores in the midst of inflamed catarrhal patches. The mesenteric and other lymph glands are congested, swollen, softened and friable. Congestions and petechiæ are found on the peritoneum, liver, spleen and kidneys, with, at times, nodular foci. In certain cases congestions and effusions have been found on the pia mater and arachnoid, in the cerebral ventricles and the brain substance.

Prognosis. Mortality. Mortality varies much with the severity of the special outbreak and the conditions of life, favorable or otherwise, in which the flock is placed. In the milder forms the mortality may not exceed seven per cent, while in the more violent the whole flock almost may perish. A fatality of 20 to 30 per cent is the general average. Yet the inoculated form kills but 2 per cent.

If at the outset there is great weakness and prostration, complete anorexia and high fever, the prospect is discouraging. If the fever is moderate and strength and appetite retained, the case is very hopeful. On its first advent into a new country it causes a far greater mortality than after it has been long domiciled there, and frequent outbreaks have killed off the more susceptible strains of blood. Again very hot weather, or, still more, the prevalence of cold, drenching rains aggravates an outbreak and greatly encreases the fatality.

The loss is not to be measured by the deaths alone. The failure of the crop of lambs, through abortion, the shedding of wool, the loss of sight, hearing, hoofs, digits, flesh, stamina, etc, render recovery far from desirable, in the worst cases, as the animal fails to thrive or pay for its keep. On the contrary it is immune from any future attack, and if left in a thrifty condition it becomes especially valuable in a district where sheeppox prevails.

Treatment. Once established in the system the disease will follow its regular course, through all its stages. Yet we can, by dieting, pure air, cleanliness, shelter and even by medicinal measures, do much to render that course a safe one. Cool sheds, pure air, clean floor, dry clean litter and shelter from rain are above all important. The sheep may be separated in different enclosures in small lots of 5 or 6 to prevent crowding, heating, and excitement, and in any case the infected should be removed from the noninfected, and even from each other to avoid infection and reinfection. This is especially requisite in hot weather.

For the strong and vigorous, a diet of sliced roots and meal (oat, bran, linseed, barley, wheat middlings) is good, while for the weak, gruels of oat meal, barley meal, linseed meal, or the same agents dry, may be given. Powdered saltpeter may be given in this (1 oz. to 8 or 10 sheep) and common salt allowed to be licked at will. Drinking water may be given pure, or slightly acidulated with sulphuric or hydrochloric acid, or hyposulphite or bisulphite of soda may be used as a substitute for the latter. The bowels are usually costive, and may be relieved at first by 3 ozs. of sodic sulphate, and later, if need be, by soapy injections. Often during the course of the disease a sudden access of fever may be cut short by a mild laxative, if that is not contra-indicated by existing diarrhœa.

Avoid giving heating agents to bring out the eruption. The severity of any case and the danger of complex infection are usually in ratio with the extent of the eruption.

Lotions of hyposulphite of soda may be applied to the affected parts from the first, and even weak lotions of chloride of zinc after the maturation of the pustules. For the eyes, nose and mouth antiseptic lotions may be called for.

In the advanced stages, in weak subjects, tonics and stimulants may prove useful. To the mineral acid, quinine (10 grain doses) or gentian (drachm doses) or other bitter may be added for valuable stock.

Treatment is only permissible in the case of very valuable animals and when they are surrounded with the most perfect antiseptic precautions, to prevent the escape of the infection.

Prevention. As in all dangerous infections this must be the preëminent object, and when a new country has been invaded by the disease, no sentiment nor alleged value of affected or exposed animals should be made the warrant for treatment, nor stand in the way of the extinction of the plague by the most rigorous measures. The recovery of an individual flock is never to be put in the balance with the danger to which other flocks are thereby exposed. To avoid smuggling away of exposed animals, and consequent spread of the disease, the loss should be met by the commonwealth and no foolish idea of administrative economy, should tempt a stock owner to endanger the flocks of a whole nation.

Sheep and goats from countries where sheeppox exists should be absolutely excluded. If, in exceptional cases they are allowed to land on our shores, they should be guaranteed by a veterinary certificate as coming from a noninfected district, by a route free of infection, they should be critically examined by an expert on arrival, and if passed, should still with all clothing and utensils, be subjected to thorough disinfection. The clothing of attendants should be similarly dealt with. If importation is merely across a frontier, a quarantine of 21 days followed by a disinfectant bath should be enforced.

If sheeppox has gained a footing in a flock in a new country, the flock should be at once appraised and destroyed, and the place thoroughly disinfected and shut up for three months. All cars, ships, wharfs, landings, chutes, yards, buildings, parks, roads, etc., used by them should be closed and thoroughly disinfected. All flocks exposed to any such place or thing should be placed in strict quarantine for three weeks, under official veterinary supervision and disposed of, should they become affected.

As an alternative each infected and suspected flock should be secluded in a well fenced place or shed from which all men except the necessary attendants, all dogs and other mammals, including vermin, all birds and as far as possible all flies are excluded. They should be divided into small lots of 5 or 6 placed in separate pens, their temperatures should be taken 3 or 4 times a day, and any one showing a temperature of 104° or 105° F. should be instantly removed to a separate pen, and destroyed as soon as the disease can be identified. In this way a diseased sheep can usually be removed before it has infected its fellows, and at the worst the infection will rarely spread beyond the 5 or 6 animals enclosed in the pen where the first case appeared. It is well to sprinkle the wool of all the flock with a 5 per cent solution of carbolic acid, and the floor or ground with chloride of lime. The diseased carcasses should be thoroughly sterilized by burning, boiling, or immersion in strong acids, or they should be deeply buried, the infected pen disinfected on each occasion, and the hands and clothes of the attendants purified.

Careful treatment in this way will usually cut short the disease with the loss of those only that were already infected when the outbreak was taken in hand, but it must be in the hands of men who are at once experts and vigilant and trustworthy. The English invasion of 1862, under the direction of the late Professor Gamgee, was completely stamped out in four weeks on this plan, whereas the invasion of 1847, met by the expedients of inoculation and quarantine, lasted for four years, with great losses in a number of flocks, and a very heavy bill for continued expert supervision. This should be a wholesome lesson to the American legislators who consider the prompt extinction of infection, by abolishing this source of its increase in the living body, as a wasteful outlay.

Preventive Inoculation, Ovination. If it were possible to give immunity against sheeppox by inoculation with the exudate of cowpox, and without danger to the sheep from fatal cowpox, or from its transformation into the more destructive sheeppox, it would be a most desirable resource. But experiment goes to show that vaccination is useless, in the temperate climates at least. Sacco, Hussan, Buniva and others in Italy vaccinated sheep extensively and claimed to have obtained good results, but this has not been endorsed by subsequent observers. D’Arboval vaccinated 1,523 sheep, of which 1,341 contracted cowpox, and out of 429 of these exposed to sheeppox later, 308 contracted the latter disease. Ceely vaccinated two sheep, both of which afterward had mild sheeppox through inoculation. Simonds and Marson vaccinated 306 sheep, 112 of them successfully, and of these last two-thirds contracted cowpox a second time on re-vaccination. Twenty-nine of the successfully vaccinated sheep were inoculated with sheeppox lymph, and in every case successfully. It is obvious that vaccination, as a protective measure, is absolutely untrustworthy in France or in England. Under the warm skies of Italy, as in Persia, there may be a close relationship between the two diseases, yet in Italy sheeppox was constantly prevalent, and it is to be feared that the immunity in a number of cases was due to a previous attack of that disease rather than to the vaccination. It should be noted that in Persia sheeppox is said to be communicable to man, while in England, Ceely failed to transmit it.

Ceely suggested variolisation with human smallpox as a preventive of sheeppox, but Simonds and Marson failed to convey smallpox to the sheep, though the same animal readily contracted sheeppox. One can hardly contemplate Ceely’s proposal with equanimity. Immunity for sheep would be dearly bought at the cost of a general diffusion of smallpox virus.

Ovination or inoculation with the lymph of sheeppox is the only available method of immunization. It entails, however, an extraordinary multiplication of the virus in each inoculated animal, and considering the numerous loopholes for its possible diffusion it can only be looked on as a very dangerous and usually, in the long run, a very expensive resort. The experience of England, above referred to, is eloquent in witnessing against ovination, and “in Prussia and Austria the dissemination of sheeppox went hand in hand with inoculation.”—Friedberger and Fröhner.

On the other hand ovination is not fatal to the flock operated on. The mortality is often below 1 percent., and virtually never exceeds 4, with a general average of about 2 per cent. It is this comparative impunity of the inoculated flock which closes the eyes of most persons to the great danger to a whole country and the wasteful prodigality of the operation.

Ovination further shortens the duration of the outbreak in a large flock, passing all through the disease in 21 days, whereas as contracted by simple exposure, the duration of the outbreak may last 90 days or more. It further enables the owner to give such protection, shelter and care as will guard the flock against exposure and dangerous complications. But while preferable to the abandoning of the disease to its natural course, it is always to be strongly condemned, where it is possible to adopt the method which detects the sick animal in the incipient stage by thermometry, and does away with the infection by its removal, followed by disinfection. The only excuse for ovination is the general prevalence of sheeppox on an island or other secluded district where there is no great added danger from the further diffusion of the virus, and when its simultaneous practice over the whole region can be made the basis for universal disinfection and the definite extinction of the contagium.

Technique of Ovination. The lymph (“ovine”) should be taken from a mild case of the disease, and from a vesicle at full maturity (about the 6th day), but containing as yet a clear, translucent exudate, without turbidity or other indication of formation of pus, or other infection. Inoculation is made by preference on the bare lower surface of the tail near its tip or 3 to 4 inches behind the anus. If this is unsuitable, the inner side of the ear, an inch from the tip is usually selected, though there is here an added element of danger, owing to its proximity to the eye. The insertion is made with an ordinary suture needle, which is introduced obliquely under the epidermis about one line, and pressed upon with the thumb as it is withdrawn. A still better instrument is the inoculation needle or lancet with a groove or spoonlike hollow on one side. Or the skin may be scratched or abraded with the lancet, as in vaccination, until serum oozes, when the virus is rubbed on and the part is covered with a piece of sticking plaster. On the third or fifth day the flock is again examined and those that have failed to take are ovinated anew.

The virus is most conveniently taken direct from the affected sheep, but it may be preserved in capillary tubes, or on glass or ivory points, or mixed with glycerine between glass plates, or finally, the first scab well dried may be preserved and utilized, a minute portion being inserted with the lancet in a pocket made under the epidermis.

Attempts have been made to secure a mitigated and safer virus, by diluting the lymph with water or normal salt solution (1:50–150) (Peuch), by amputating the seat of inoculation (the tip of the ear) on the 4th or 7th day, when the vesicle is formed (Galtier), by taking a susceptible sheep and inoculating it with sheeppox virus for ten consecutive days, and then selecting for use the lymph from the papule of the sixth inoculation. The inoculations of the seventh day and later give rise to no papule even (Pourquier). By this means it is claimed that the inoculated disease remains strictly local, passes through its successive stages in a shorter time (15 days or less), and is perfectly harmless to the sheep inoculated. Nocard and Mollereau sought the same end by mixing the virus with oxygenated water, and Semmer and Raupach by heating it to 130° F. In view of the facts that it is only under extraordinary conditions that ovination is permissible at all, and that the mortality, resulting from it can be kept down to about 1 per cent., it seems hardly worth while to attempt to obviate this loss, by any method which may come short of the full measure of immunity.

Ovination confers immunity for a year or longer.

The care of the flock during eruption is the same as in sheeppox contracted in the usual way.

SHEEPPOX IN GOAT. VARIOLA CAPRINA.

The goat can be successfully inoculated from the sheep, the resulting vesicles being smaller and less prominent, and the disease assuming a milder type. It is alleged to pass naturally from sheep to goat, and from goat to sheep, as well as from goat to goat but, on the whole, it is a rare disease and goats have been known to live in flocks of sheep attacked with sheeppox, without themselves contracting the disease. The malady seems to be of little account to the goat, yet in sheep countries, the interests of flockmasters would demand that it should be stamped out as vigorously as the same disease in sheep.

GOATPOX; VARIOLA CAPRINA.

In Persia according to Bruce goats suffer from a form of variola, having larger vesicles, umbilicated and approximating to, if not identical with cowpox. In Algiers there is found a goatpox from which sheep are alleged to be immune (Nocard, Peuch, Bremond, Galtier) so that further observations are wanted to put the different forms of variola of the goat in their proper places. In a country where sheeppox is constantly present, there is of course the possible source of fallacy of experimenting with animals that have already had the disease, therefore it would be expedient to put all forms of goat variola under police control.

SWINEPOX. VARIOLA SUILLA.

Variola appears to be rather more frequent in swine than in goats. Ficanus as quoted by Joubert saw it in 1567, contracted it was supposed from smallpox patients. It was noted by Ramazini in 1690, by Stegman in 1697, and later by Gerlach and others. In 1891 517 cases were reported in Hungary. It is said to be derived from man by the use of bed straw for litter and from sheep by occupying the same stall. It can be transmitted experimentally from pig to pig, from pigs to goats, and from goats back to pigs (Gerlach). It is also claimed to pass from the pig to man (Freidberger and Fröhner). Young pigs are especially subject to it and one attack confers immunity for the future.

Symptoms. After a febrile condition of variable length, but usually of a high intensity, red spots appear on the head, neck, chest, belly or inside the arms and thighs, at first like flea bites, but passing through the stage of papule to become vesicular on the sixth day. About the ninth or tenth day they become purulent, and in two or three days more a black, concave, circular crust has formed which is soon detached. The eruption may be local or general, discrete or confluent and the issue of the case will depend much on this character. In exceptional cases the eruption invades the mouth, eye, throat, stomach, or intestines. Croker notes the accompaniment of a fatal lobular catarrhal pneumonia.

It must be carefully distinguished from urticaria, eczema, and eruptions due to pustulating irritants.

Treatment is in the main the same as for sheep, care being taken to secure perfect cleanliness, pure air, dry clean litter, easily digested food, and protection from crowding, undue heat, cold or wet. Buttermilk and other acidulous and diuretic drinks are recommended, and careful attention to the state of the bowels throughout.

Prevention is still more important, and better than any treatment would be the most rigorous measures for its extinction along the lines laid down for sheep pox. Whether the infection has been derived from man or sheep it must be looked on as eminently dangerous to the class of animal from which it originated, and every available means used for its extinction.

DOG POX: VARIOLA CANINA.

Dog pox is rare, the affection occurring especially in the young. It is said to be derived in certain cases from smallpox patients (Weiskopf), and in others from sheep pox (Röll). The latter claims that the dog has also its own specific form. Dupuis and others claim experimental transmission from man to dog. At the same time eruptions connected with gastric or hepatic disorder, distemper, eczema, or aphthous fever are liable to be mistaken for it.

Symptoms. The young animals suffer from fever for a day or two, followed by heat and redness on the sides and belly, and points of deeper red, like flea bites, which gradually evolve through papules and vesicles to pustules, and terminate in crusts, that drop off leaving round bare spots. The vesicles may appear locally or generally and may be discrete or confluent. Sucking puppies, when attacked usually perish.

In treatment the same hygienic measures are demanded as for other animals, special care being required to keep the bowels and kidneys acting in a healthy manner. Perfect cleanliness must be secured, and nonstimulating easily digested food. Excessive fever would demand tepid baths, cold sponging, or acetanilid, and undue warmth, crowding and cold exposure must be alike guarded against.

In view of the alleged sources of the disease in man and sheep, the strictest seclusion of the affected dog, in disinfected surroundings will become absolutely essential and when this cannot be carried out he should be summarily destroyed.

VESICULAR EXANTHEMA OF HORSES.

Definition: Vesicles usually on external genitals, with fever and infection. Causes: Contagion by coition, clothing or stable utensils; inoculated on man or cow, resembles cowpox, but a first attack does not always immunize a stallion; inoculable on sheep, goat and pig. Symptoms: Incubation one to six days; local redness, heat, swelling, tenderness, papule, vesicle, pustule, scab, desquamation, depigmentation on genitals or in sucklings on mouth, lips, nose; may extend to mammary and inguinal regions, with swelling, stiffness and constitutional disturbance. Diagnosis from dourine. Treatment: Cleanliness, astringent, antiseptic lotions; open and disinfect abscesses; laxatives or diuretics. Prevention: Withhold from breeding.

Definition. An acute infectious disease, manifested by hyperthermia, hyperæmia, and the formation usually on the external generative organs of a crop of papules rapidly progressing to vesicles, pustules and open sores, and attended by great local irritation and itching. It runs a mild course and recovery ensues spontaneously in about fifteen days.

Causes. The disease is only known as a contagious affection, propagated from animal to animal by breeding together, or by using the same comb, brush or rubber, or by sucking, and in rare cases by other accidental or experimental inoculations. To make a successful inoculation the virus must be taken from the vesicles or pustules. When transferred to man or ox it develops an eruption which is indistinguishable from cowpox (Trasbot, Peuch, Galtier). Still a first attack does not always confer immunity, as stallions may have two successive attacks within a few weeks (Steinhoff). This implies that either this is not genuine cowpox, as claimed in France, or that two different exanthematous affections have been classed as one. Inoculation with the virus has produced a characteristic eruption in sheep, goats and pigs.

Symptoms. After a period of incubation of from one to six days there appear heat, swelling and tenderness of the affected part, followed by the formation of papules, gradually passing into vesicles, pustules and scabs which scale off, leaving a white depigmented surface. In stallions and mares the usual seat of the eruption is the external generative organs; in young sucking animals the mouth, lips, nose and quarters, and in inoculated cases wherever the virus has been implanted.

In the mare there is swelling of the lips of the vulva and redness of the vaginal and vulvar mucosa with points of a darker red, which become firm, papular, vesicular and finally pustular. A similar eruption shows on the skin of the swollen labiæ, on the lower surface of the tail and on the hips, though on these points the phenomena are obscured somewhat by the abundance of pigment. The contents of the vesicles are at first limpid but gradually change to opaque yellowish white, brown, or even red from slight blood extravasation. It causes not only marked tenderness but great itching so that the patient rubs the tail and rump, rupturing the vesicles, causing blood extravasations and retarding healing. The sores are primarily two or three lines in diameter but may widen and deepen under the friction. The surface may be red and angry and covered by a yellowish viscid discharge. When they heal they leave on the dark skin, round spots white and devoid of pigment. The itching during the acute stage of the disease, leads to generative excitement, frequent straining, contractions of the erector clitoris and ejection of urine. The animal appears to be constantly in heat, yet the absence of hyperthermia shows that there is no constitutional disorder nor central nervous affection. The disease appears to be purely local.

In the stallion after a similar incubation, the penis and usually the sheath become swollen and congested and if free from pigment there are dark points as described in the vulva. These points become firm, prominent, and finally vesicular and pustular. If continued in service the resulting sores may extend and prove protracted. In the absence of service they tend to heal about the fifteenth day. The eruption may extend on the scrotum, the inner side of the thighs, the throat, the lower surface of the neck, and the inside of the forelegs; on any parts indeed that may become soiled on mounting the mare. The meatus urinarius is red, swollen and angry, and shows a muco-purulent discharge. Generative excitement is shown by the more frequent rising and falling of the testicles, protrusion and retraction of the penis, and the frequency of urination.

In bad cases in both sexes the eruption encroaches more widely on the skin, and subcutaneous abscesses may form on the vulva, anus, tail, between the thighs or on the scrotal, mammary or inguinal regions. These are attended by extensive local swellings extending on the croup, or down to the hock, or forward to the hind limbs. In such cases there is more or less stiffness or lameness, with constitutional disturbance, hyperthermia, gastric disorder and emaciation.

Diagnosis. This disease is distinguished from dourine by the known absence of the latter from the locality, by the ready transmission, of the benign exanthema to cattle, by the entire absence of paresis or mental hebetude, by its rapid progress and early recovery, usually in fifteen days.

Treatment consists in thorough cleanliness, and the application of cooling, astringent, antiseptic lotions to the affected parts. Solutions of borax, boric acid, sulphate or chloride of zinc, permanganate of potash, corrosive sublimate, chlorine water, creolin, lysol, carbolic acid, or other such agent with glycerine will act promptly and well. In the severe cases with secondary abscesses the latter must be opened and the cavities treated antiseptically. Cooling laxatives and diuretics with salicylates or hyposulphites may also be desirable.

Prevention. No animal having sores nor discharge from the generative organs should be used for breeding. The owner of the animal infected by breeding has a good claim for damages.

VESICULAR EXANTHEMA IN CATTLE.

Definition: acute infections, eruptive affection, usually of the genitals, in cattle, transmitted by breeding, and marked by congestion, papules, vesicles and pustules. Cause: infection by coition; by contact, by gutter, by tail, by licking, in sucklings. Oxen and non-pregnant cows suffer. Symptoms: incubation 1 to 6 days, cows have swelling, red points, papules, vesicles and pustules on vulvar mucosa and adjoining skin, with profuse glairy discharge, and it may be fever: bull has matting of preputial hairs, frequent micturition, swollen sheath, red penis, vesicles, even necrotic ulcers and distortion. Immunization short, uncertain. Treatment as in horse. Prevention: seclusion and disinfection of animals, disinfection of stalls, gutters, rubbing posts, trees, complete segregation of sick from healthy.

Definition. An acute eruptive affection, attacking particularly the generative organs of breeding cattle, manifested by congestion, papules, vesicles and pustules of the mucosa and skin and transmitted largely by copulation.

Causes. The one known cause is infection and the most common mode of communicating it is by the generative act. In this it agrees with the mild coital exanthema of horses, and the two affections have been considered as identical with each other and with cowpox (Trasbot). The similarity of the symptoms and the duration of the disease sustain this view, but, if correct, it is probable that the affection has undergone a distinct modification which adapts the microbe especially to life in the genital canal, and to the maintenance of its virulence for a longer period, and finally, robs it of the power of producing any permanent immunity. Cowpox, though raised on the lips of the vulva, the inner side of the thighs and the abdomen where it can be easily reached by the tail does not tend to implicate the genital canal, and it so quickly secures immunity, that neither male nor female would be likely to long convey the disease. Yet in both horses and cattle experience shows that the acquired immunity of vesicular exanthema is very short lived.

Cattle, much more than horses, are liable to transmission of the disease by other channels than coition. Contact with the same soiled stall and gutter, the direct transference to adjoining animals by the soiled tail, and the greater frequency with which they lick themselves and others doubtless contribute to this. The frequency of non-coital infection is shown in Numann’s cases affecting the anus and sheath in oxen; also in Fenner’s long list of cases in 669 non-pregnant cows, in a number of cows in advanced pregnancy and in calves of a few weeks old (Friedberger and Fröhner).

Symptoms. In Cows. After an incubation of one to six, (or exceptionally ten) days, there occur swelling and redness of the lips of the vulva, and the vaginal mucosa with here and there dark red points, and an abundant clear, glairy discharge. The red points may become firm and papular, and an exudate beneath the epithelium transforms them into vesicles at first translucent but later yellow or brown as pus cells accumulate. The clear mucous discharge meanwhile becomes opaque and, as the pustules open, forming sores, yellowish and purulent. This discharge soils the tails and hips, drains out on the back part of the stall and the gutters and is carried by the tail to the udder and to other stock. Itching may be severe and the constant rubbing and switching of the tail, may irritate the sores and cause them to deepen or extend, beside favoring septic infection and local necrotic processes. In such cases there may be more or less fever, impairment of appetite, rumination and digestion, and of the secretion of milk. Abortion is not unknown though exceptional.

Symptoms. In Bull. The matting together of the long hairs of the prepuce may be the first indication of the disease, attended or followed by frequent micturition, or by standing with the tail raised and the accelerator urinæ pulsating over the ischiatic arch as if passing urine. The sheath appears swollen, the penis red granular, and angry, with red spots, and even the scrotum may be involved in the enlargement. The red points advance as in the female through the different forms of papule, vesicle and pustule to the formation of sores which are more or less red and angry. There may be an indisposition or even inability to protract the penis, and the bull may be tardy to serve, or in case the organ is erected and used, blood may ooze from the respective sores. The disease usually lasts about two weeks, but may recur a few weeks later in connection with a new infection. In aggravated and prolonged cases there may be local septic and necrotic processes, and general fever and digestive disturbances. Distortions of the penis may render the subject permanently useless as a sire.

Treatment is essentially the same as in the horse. Antiseptic and astringent solutions (sulphate of zinc, iron or copper (2:100), nitrate of silver, carbolic acid, corrosive sublimate, lysol, creolin, etc.) may be used to advantage. Laxatives and diuretics may be called for.

Prevention. This would require the temporary seclusion and final disinfection of all animals attacked, the thorough cleansing and disinfection of the stalls and gutters, as well as all posts, trees and fences on which the animals rub themselves. The attendants should use no combs, brushes, sponges nor rubbers indiscriminately on the sick and healthy. They should disinfect their hands and, if necessary, their clothes after having handled the sick and before handling or milking sound animals. An obvious precaution is to place the sick and healthy in separate buildings and yards.

INFECTIOUS GENITAL CATARRH IN RABBITS.

Freidberger and Fröhner record a very contagious catarrhal affection of the vulva and prepuce in high bred rabbits, and conveyed from animal to animal by sexual congress. The characteristic symptoms were extensive swelling of the parts and an abundant muco-purulent discharge.

Injection of the genital passages with a sulphate of copper solution (1 to 2 per cent) for several weeks in succession effected a cure.

INFECTIOUS ULCEROUS STOMATITIS IN LAMBS AND KIDS.

Prevails in France. Predisposing causes, bad hygiene. Specific cause, streptococcus. Pathogenesis, to lambs and kids through sucking, drinking, feeding; inoculable on Guinea-pig, not rabbit. Lesions: like thrush, congested patches, with curd-like concretion; epithelium, leucocytes, microbe; in bad cases gastro-enteritis, hepatitis, or pneumonia. Symptoms: hyperthermia, refusal of teat, froth on lips, dulness, debility, emaciation, death in 15 days; in mouth, concretions and red raw sores; cough, hurried breathing, diarrhœa; subacute cases have little fever, or infection. Mortality 8 per cent. in acute cases, none in subacute. Prevention: separation and disinfection of fold. Treatment: antiseptics to mouth; borax, sulphites, chlorate of potash, sodium salicylate, iron chloride, copperas, silver nitrate. Feed through tube or syringe. Internally, sulphites.

This is found in all parts of France, as described by Besnoit.

Causes. The predisposition, as in the case of many other fatal internal inflammations, depends largely on faulty hygiene, foul, ill ventilated, hot, close, damp, overcrowded folds, without sunshine, drainage or free access to the outer air.

The specific cause is a large coccus, isolated or in chains of 2, 3, 4 or more (streptococcus), and found abundantly in the pultaceous buccal exudate, and in the internal lesions developed by autoinfection. It grows readily in bouillon in the form of a precipitate in the bottom of the liquid, in gelatine and glucose in very small, thin colonies, and on potato in creamy masses. It is stained by anilin and by Gram’s (iodine) preparation.

Pathogenesis. Inoculable on the Guinea pig, it is harmless to the rabbit. It is readily conveyed to lambs and kids by inoculation, or through the teats, by licking, drinking, feeding, etc. Acute cases are very virulent, subacute very little so. Isolated cases of the latter are not uncommon.

Lesions. The buccal lesions are like those of thrush (muguet). The mucosa is more or less congested and reddened with raised patches, of varying extent, of white, curdy looking concretions, composed of excess of epithelial cells and leucocytes with an abundant exudate. The specific coccus is present in great numbers and often in almost pure cultures. The internal lesions found in the more acute and fatal cases are mostly in the form of gastro-enteritis, hepatitis and pneumonia, containing the specific cocci, and due to the inhalation or swallowing of the virulent buccal products.

Symptoms. In the acute cases an intense hyperthermia is the first symptom, speedily followed by refusal to suck, the accumulation of froth around the lips, great dulness and lassitude, prostration, rapidly advancing debility, and emaciation, and death in 15 days in a condition of marasmus and inanition. When the mouth is opened the curdy white or yellowish white patches of exudation are seen with an abundant glairy mucus, and occasionally red, raw, angry patches from which the morbid growth has been detached. The symptoms of pneumonia or of muco-enteritis are usually in evidence, with or without diarrhœal or dysenteric discharges. Acute cases are extremely contagious.

In subacute cases the lesions are confined to the buccal mucosa, as curdy white, raised concretions with ulcerous surfaces, frothy lips and refusal of the teat, but without marked hyperthermia or constitutional disturbance. Contagion is little marked, the disease appearing enzoötically in flocks, or even as but one case in each of several flocks.

Mortality. Eight per cent. of acute cases may perish, but the subacute nearly all recover.

Prevention. When the disease has appeared in a flock, or in its vicinity, the mouths of the lambs should be examined daily and affected subjects and their dams carefully separated. A thorough disinfection of the fold is imperative.

Treatment. Use antiseptics on the mouth, selecting the non-poisonous articles. Borax may be rubbed freely on the patches. Solutions of sulphite, bisulphite or hyposulphite of soda (1 oz. to 1 qt.) may be used at frequent intervals on the mouth; chlorate of potash (5:100), sodium salicylate (1:100), iron chloride (1:100) may be used. Ulcerous patches may be cauterized by iron sulphate, silver nitrate, or the potential cautery. Besnoit advises mercuric chloride (1:1,000) for cutaneous lesions, but this would be unsuitable for either mouth or lips. The strength must be sustained by the dam’s milk given through a tube or syringe. For gastric lesions the sulphites may be given.

CONTAGIOUS ABORTION.

Definition: Premature expulsion of non-viable fœtus. Synonyms. Susceptible animals: cows, goats, sows, mares. Accessory causes: Ice cold drinks at periods of ovulation, frozen aliments, ice cold bath or rain storm, mechanical injuries, unwholesome fermentescible food, indigestible foods, close stabling, heavy milking, early breeding, inbreeding, stagnant water, ergot, smut, vegetable irritants or ecbolics, constitutional diseases, irritation of generative organs, death of fœtus, urinary calculi, odor of carcass or carrion, contagion, experimental infection between cows, between mare and cow, relation to omphalitis. Nocard’s streptococci and bacilli, Bang’s bacillus with best growth in two distinct grades of oxygenation, Galtier’s observations, bacterium of the Colon group in America, infection of the calves (pneumonia). Various kinds of infectious abortion. Acquired immunity, variable in different forms. Immunized cow still infecting. Symptoms. Lesions. Abortion in mares. Therapeutics. Prevention: Protection of a sound herd, guarantee with purchase, government control, precautions with male or unimpregnated female, with pregnant. Extinction in a herd, separation, disinfection, disposal of abortion, manure, urine, disinfection of animal, of genital organs, precautions as to service, new born, fields, ewes. Disinfectants, subcutem or in muscles.

Definition. The premature expulsion of the product of conception before it is viable out of the womb. Strictly speaking, a parturition in which the offspring is so far matured as to be viable is a premature parturition, while if it is non-viable it is an abortion. Vulgarly, however, as applied to herds, the term is used for any early parting with the fœtus. In this wider sense infectious abortion is the premature expulsion of the fœtus owing to an infectious catarrh of the womb, transmitted from one animal to another by the transference of the microbe.

Synonyms. Infectious Abortion, Enzoötic Abortion, Epizoötic Abortion.

Animals Affected. Abortion is most common in cows, and less frequent in ewes, goats, sows and mares.

Forms and Accessory Causes of Abortion. It was formerly supposed that abortion in herds was mainly due to mechanical and chemical agencies acting injuriously on the system, and in adopting the explanation of a particulate, transferrable, infectious agent for the habitual widespread forms of the disease, we should not forget these accessory causes, many of which by themselves cause sporadic abortions without the intervention of an infectious element.

The free consumption of ice cold water by the healthy dam causes active gastro-intestinal peristalsis and vigorous movements of the advanced fœtus, which can be seen or felt in the right flank, so that this is often resorted to, to determine whether the animal is pregnant or not. If this is frequently repeated or carried to excess in susceptible animals it will at times cause abortions. As in all other cases of mechanical or physiological disturbance, this is most operative at those periods of constitutional changes, which if the animal had been unimpregnated would have brought about ovulation and œstrum.

The greedy ingestion of cold aliments, like frozen roots, or green vegetation covered with hoar frost, may have a similar action, the more so that such aliments are extremely fermentescible and liable to cause tympany and undue pressure on the gravid womb.

Even without ingestion, exposure to cold rain or snow storms or the plunging in ice cold water tends to produce excessive peristalsis and fœtal movements and thereby prove injurious.

Mechanical injuries to the abdomen as crushing by a gate, kicks, hooking with horns or tusks, hounding with dogs, riding of each other when a cow is in heat, are liable to produce congestions, detachment of fœtal membranes, and even death of the fœtus.

Very fermentescible foods like those following a wet season or bad harvest, or those made of the leafy albuminous plants like lucerne (alfalfa), sainfoin and clover, act injuriously in the way of causing tympanies and compressions, but it must also be recognized that we are here dealing with fodders abounding in bacterial ferments, and that some of their products may act physiologically as ecbolics, even if the bacteria themselves do not colonize the genital passages as infections.

Insufficient food or very innutritious forage, too close stabling, heavy milking, early breeding (dam or sire), inbreeding, are liable to lower the general stamina and throw the system more open to the action of other factors.

Stagnant, corrupt drinking water has been charged with causing abortion, and the trouble has ceased when it has been withdrawn, but it is difficult to estimate its value in different cases—disturbing digestion, fermentation, poisoning, or introducing of actual infection.

Ergoted grasses and smut in maize, wheat or oats, have been often charged with wide spread abortions, and though each has in turn been administered in large and continuous doses without causing abortion, this does not invalidate the many cases in which it manifestly had that effect, nor does it show that obstetricians have been mistaken in their almost immemorial trust in ergot as an ecbolic. It must be recognized, however, that grown under different conditions, of sunshine and shade, and harvested at different stages of its development, ergot varies greatly in its physiological action, as it does also from having been overkept and thus one specimen is effective or dangerous while another is absolutely ineffective. The specific action of the alkaloids in determining contraction of involuntary muscular fibre, is seen alike when used medicinally and when acting as an accidental toxic agent in causing spasms, nervous torpor or paralysis, delirium; gangrene of the feet, tail or tip of the ear; or contraction of the womb and expulsion of its contents. Like other agents mentioned ergot is at times an active ecbolic when coöperating with other similarly operating agencies.

Irritant vegetables of various kinds are to be dreaded. Such as act on the bowels and kidneys, keeping up a constant diarrhœa and diuresis, are quite liable to cause abortion in susceptible subjects. Savin, tansy and rue have obtained a bad reputation in this sense.

Cotton root bark is an active ecbolic, but is not likely to harm animals unless deliberately administered.

Impaction of the rumen or manifolds, and obstinate constipation with the resulting straining or compression must be named as an accessory cause.

Severe constitutional diseases, especially the infectious fevers, aphthous fever, lung plague, rinderpest, etc., are occasional causes of abortion.

It may be brought about by direct irritation of the womb, as in ovariotomy or dilatation of the cervix, or again by death of the fœtus through twisting of the umbilical cord.

Where cattle are subjected to dry winter feeding, in the absence of ensilage or roots, on the magnesian limestones, small calculi in the kidney are almost the rule in winter and the irritation caused by these conduces to abortion.

Nor must mental influence be altogether ignored. Cows and even mares are exceedingly sensitive to the smells of decomposing animal matter, as seen every day in the vicinity of abattoirs, or in case the carcass of one of their fellows has been opened, and not infrequently in connection with carrion, and the occurrence of abortions after such excitement has been frequently noticed. Cases are on record of specially susceptible cows having had active labor pains, from being with another cow at the time of parturition. Shepherds have noticed that violent thunder storms have been followed by numerous abortions in the flocks.

The Contagious Form. Any of the usual causes of sporadic or accidental abortion may coöperate with the true infectious element and give unusual energy to it, yet it is of the utmost importance to recognize the contagion as the essential cause in all cases in which it is present. This can usually be done by a careful inquiry into the history of the outbreak.

When a herd has been continuously healthy up to the date of the introduction of a cow brought from a herd where abortion has been prevailing, and when following her arrival, one after another of the original members of the herd abort, without any apparent cause in the way of change of feed, water, barn, stalls, or general management, the evidence of the introduction of contagion by the cow in question is very circumstantial and forcible. If pregnant cows standing next to the new cow, or near to her, abort, the argument for contagion is still further corroborated. If the trouble continues in the herd year after year, attacking fresh animals some months after their purchase, the case becomes still stronger.

Or if a cow from a healthy herd is sent to a bull, that has been allowed to serve an aborting cow, and if the resulting pregnancy in the first cow is terminated by abortion, and if this is followed by successive abortions in the previously healthy herd, we may reasonably conclude that we are dealing with the infectious form. If no other appreciable cause for the trouble can be found we may reasonably conclude that this was the channel for infection.

Or a bull is brought from a herd where abortions have taken place, and some time after his arrival, the cows of the previously sound herd begin to abort, the first cases being in those that the new bull has served. The occurrence is manifestly the result of contagion.

Or a newly purchased cow aborts, and is disposed of in consequence, and another cow, placed in the same stall, in due time aborts also, and others follow in succession, especially those that stood next or near to the stall in question. Everything points to an introduced infection.

An indefinite number of other exemplary cases might be adduced, each varying from the last, but all agreeing in this, that the evidence of infection stands out prominently and unmistakably. The infecting material may have been carried by the tail, tongue, soiled stall, gutter, rubbing post, fence or other object, yet the fact of contagion can be demonstrated with reasonable certainty.

These conclusions have been repeatedly affirmed by actual experimental transmission. The Scottish abortion committee found that healthy pregnant cows often escape, though standing near or even next to an aborting one, but that when a piece of cotton wool was inserted into the vagina of an aborting cow for twenty minutes and then transferred to that of a healthy one, the latter invariably aborted. Galtier found that when the infecting vaginal mucus of the aborting cow was transferred to the same passage of the healthy pregnant one, abortion took place in the latter. He succeeded in conveying the disease in this way from cow to sow, ewe, goat, rabbit and Guinea pig, and found that growth in the body of the rodent intensified its virulence, so that it could then be successfully inoculated on the mare, bitch and cat.

Bang subjected two cows, from healthy herds and three months pregnant, to repeated injections of the products of the culture of his abortion bacillus in serum glycerine bouillon. Three injections were made on April 14, May 23 and June 4, and on June 24 one cow aborted. The other sickened and when killed was found to carry a dead fœtus. Pure cultures of the abortion bacillus were found in the fœtal membranes and liquids of both animals.

Casual Infections. In a case which came under the observation of the present writer, a family cow kept in a barn where no abortion had previously occurred, was taken for service to a bull in a herd where abortion was prevailing, and though she was only present at the latter place for a few minutes, she aborted in the sixth month.

Another cow from the same aborting herd, was taken into another herd at a distance of two miles, where abortion had been unknown up to that time, and some months later the cow standing in the stall next to her aborted. The remainder of this herd was sold soon after, so that the further progress of the disease was not traced.

Tobiassen quotes the case of a cow from an aborting herd, which calved a fortnight before the regular time. The calf was at once sent to another farm where no abortion had occurred, and placed in the same building with the pregnant cows, all of which later aborted. The outbreak thus started lasted for several years.

Jansen as quoted by Sand, reports the case of a cow from an aborting herd having been taken into a herd that had been previously quite free from the disease. Soon after her arrival she aborted, and later, cows in the same herd aborted. The owner kept the matter secret and sent his cows to a neighbor’s bull for service, with the result that for two years abortion prevailed among the cows served by this bull.

J. R. Jansen reports that a cow brought from an infected farm, for fattening purposes, proved to be pregnant and finally aborted, and that 24 of the pregnant cows on the same farm aborted in the same year.

Mörck relates how a cow that had aborted a fortnight previously was taken to a farm where abortions had never been known. She aborted during her next gestation and so did the rest of the herd, 9 in number.

Christensen records the occurrence of a general abortion in a previously healthy herd, members of which had been sent for service to the bull of a neighboring aborting herd.

Nygaard reports that a bull from a healthy herd, but which had been allowed to serve some cows from a neighboring infected herd, was sold to go on a previously healthy farm, where he was put to 14 cows only. Of these 12 aborted, and the complement of the herd, beyond the 14 cows, put to another bull, remained well.

In each of these cases the environment of the animals and the conditions remained the same, the one appreciable cause of the outbreak being the contact with an animal from an aborting herd.

Experimental Infection. Braüer led the way by transferring in 11 instances the vaginal mucus of aborting cows to the vagina of healthy ones. The resulting abortions occurred from the 9th to the 21st day after inoculation. Lehnert repeated this on two cows, the abortions taking place on the twelfth and twentieth days respectively. Trinchera transferred the purulent vaginal mucus of an aborting cow to the vaginæ of healthy ones, determining in the latter, in 9 to 13 days, abortion attended by suppurating vaginal catarrh. He secured similar results by using the material scraped from the surface of the chorion of an immature fœtus.

The Scottish Commission (Woodhead, McFadyean and Aitkin) placed a healthy pregnant cow in an aborting herd, and on two successive days lodged in her vagina for twenty minutes a piece of cotton wool soaked in the vaginal mucus of a recently aborted cow. Within a month abortion threatened, and on the seventieth day a seven months calf was dropped.

In a second experiment a cow, six months in calf, was taken from a healthy herd and placed in an aborting dairy herd and a quantity of vaginal mucus from a cow that had recently aborted was injected under the skin of the vagina. She calved prematurely at the end of the eighth month of gestation.

Williamsen, while treating a herd for abortion, took a piece of the afterbirth of one of the aborting cows and rubbed it on the vagina of a healthy cow of his own, which had a habit of carrying her calf fourteen days over time. Five days after she had premature parturition.

He took a fragment of the fœtal membrane from the cow just named and rubbed it on the vagina of a pregnant cow condemned for tuberculosis. In seventeen days the cow aborted.

Though not started as an experiment, the writer may name the general extension of abortion from one or two cows in a tuberculous herd after they had been tested with tuberculin. Cases of this kind are doubtless much more common than has been supposed.

Kilborne and Smith developed suppurating vaginal catarrh in cows and mares by inoculating them with the artificial cultures of bacilli obtained from the vaginal secretions of aborting mares.

Turner made cultures from the ovaries of aborting mares, and others from the genital organs of foals suffering from omphalitis, and produced abortions in pregnant mares by injecting with the same.

Pathology. Bacteriology. Franck attributed the disease to leptothrix vaginalis, but subsequent observers failed to substantiate this.

The Scottish Abortion Commission isolated five different bacteria from the abortion membranes and vaginal mucus, but failed to identify any one of these as, by itself, capable of causing the disease.

Nocard found in the fibrino-purulent matter between the chorion and womb in aborting animals a micrococcus occurring singly or in chains, and a short, delicate bacillus isolated or in pairs. From the absence of evil effects between pregnancies he opines that the germs grow in the membranes only, and do not affect the womb nor the general system. He recognizes, however, that they survive in the womb from one pregnancy to another in the complete absence of these membranes.

Galtier, on the contrary, conveyed the disease variously by the inoculation or feeding of the milk or abortion membranes to sheep, goat, pig, rabbit and Guinea pig, and accordingly claims that the general system of the pregnant animal is infected, and that the germs can be conveyed through the blood to the womb. In deducing this from feeding experiments he appears to make too little account of the ready infection through proximity of the anus and vulva.

Chester, of Delaware Agri. Experiment Station, found in the fœtal membranes of aborting cows a bacillus, which in form and habits of growth closely resembled the bacillus coli commune. In the fermentation test, however, it showed a marked difference.

Inoculated on rabbits it did not prove fatal. Injected into the vagina of a healthy pregnant cow it caused slight catarrhal discharge for four or five days, but the calf was carried to full time six and a half months later.

Bang found in aborting cows, between the womb and fœtal membranes, a considerable odorless, gelatinoid, liquid exudate, and some pus cells. There was active catarrh of the uterine mucosa which often carried the disease over into the next pregnancy. In the exudate he found a number of very minute nonmotile bacilli (1 to 3μ), which stained readily with aniline colors, excepting in a vacuole or nucleus which was less deeply pigmented. This bacillus grew well in serum glycerine bouillon, and more sparingly in serum-gelatine agar. In the latter it showed a remarkable peculiarity which serves to identify it readily from other microbes, in two successive zones of luxuriant growth at two different depths, with an intermediate clear zone, in which little or no growth took place. It seems to prefer a greater or lesser supply of oxygen (21 or 90:100) without being able to adapt itself to the intermediate condition. As already stated it produced abortion in the cow in 21 days after injection into the vagina. It also induced uterine catarrh and abortion in ewes, goats, rabbits, Guinea pigs and mares when injected into the vagina. From the vagina it usually reaches the womb, but not always. In several cases in which it was injected subcutem or intravenously it caused hyperthermia, and was later found in abundance in the interior of the womb and fœtal membranes, and in the bowels of the fœtus. The microbe is, therefore, capable of living in the blood and affecting the womb by whatever channel it may enter the system.

V. A. Moore and the present writer made a series of experiments at the New York State Veterinary College. In the fœtal membranes and uterine mucus of a number of cows, aborting in different parts of the State and therefore long distances apart, we found a bacillus that in form and culture-experiments closely resembles bacillus coli commune. This was nearly always in pure cultures, and in the few cases showing other microbes, these were only such as inhabit the healthy vagina. Our bacillus was never found in the womb nor fœtal membranes of cows that had calved at the full period in healthy herds. It agreed in most respects with the bacillus found by Chester, but differed somewhat in fermentation tests. It differed also in proving fatal to rabbits when inoculated on these animals. Injected in the form of cultures into the vagina in three old pregnant cows it continued to live on the mucosa, producing more or less catarrh and muco-purulent discharge in the different cases, yet all three carried the calf to full time, one having calved on the 123d day after injection, the second on the 167th, and the third on the 190th.

The results obtained at the Delaware College Experiment Station and the New York State Veterinary College, do not differ so seriously, as either one does from those obtained in Europe, by Nocard, Bang, and the Scottish Abortion Committee. The facts that the same germs were found, either in pure cultures, or exceptionally, along with the normal microbes of the healthy vagina, in the womb, and fœtal membranes of every aborting cow, that they were never found in the healthy cow which had calved at full time, and that the generative passages were the seat of a catarrh, alike in the cows that aborted and in those that were inoculated with the abortion discharges, but did not themselves abort, are all but conclusive that this microbe is the essential cause of the abortion.

The single objection to this view, namely that the inoculated cows did not abort is explained by the fact that in the New York abortions it is the rule that the calf is carried six or seven months from the date of impregnation (the date of the presumptive infection) to that of abortion. It is to be further borne in mind that our experimental cows were old, and may have passed through the disease before and become in some measure immune, that they were dry during the experiment, and were subjected to no extraneous excitement that would predispose them to abort. The presumption is that had the experiments been started earlier in the gestation, the abortion would have come in due time. The microbe maintained its hold on the mucosa and continued to advance up to and beyond parturition.

Another distinction of the European abortions, is in the presence of the microbe in European form in the digestive organs of the calf, and that the viable calves of infected cows are liable to die of intestinal disorders a few days after birth. Galtier, the Marquis de Poncius and Pry insist strongly on this. On a farm on the estate of the Marquis, where abortion had prevailed for twenty years, the calves of infected cows show at birth, or very shortly after, symptoms of broncho-pneumonia and of a complication of nervous disorders. They are breathless, wheeze, discharge from the nose, cough, scour, have convulsions or other nervous trouble. A large proportion of such calves die; and their lungs are found in part red, consolidated and devoid of air and the bronchia contain a muco-purulent product. Lesions denoting inflammation of the serosæ of the lungs, liver and intestines are common. This coincidence of a fatal disease in many of the surviving calves is exceptional among the aborting herds of New York.

In noting the evidence of a wide difference between the prevalent American and European forms of abortion in cows, one should be prepared to go farther, and accept if need be, still other distinctive forms in each of the two continents. Any catarrhal condition of the uterine mucous membrane, is a recognized hindrance to conception, and cause of abortion, and we must recognize that the forms of invasion of the womb by pus microbes are as numerous as there are irritant germs capable of living in the membrane. The question as to how many of these can produce contagious abortion is to be determined by the susceptibility of the membrane to irritation by each germ, and whether the latter can retain all its power of survival and virulence in passing from one animal to another. The presumption is, therefore, in favor of a variety of forms of contagious abortion, each due to its own specific microbe or microbes, rather than of a single unvarying type of the disease. In some the affection appears to be a purely local one (American), the microbe being confined to the genital or genito-urinary mucosa, whereas in others the microbes (Bangs’, Galtier’s, etc.) live also in the blood producing a general infection.

Two great types at least have been demonstrated in Europe and America. Whether future investigation shall show the presence in one of these continents of the types as yet only known in the other, remains to be seen. If the particular forms should turn out to be limited to different continents we are at once confronted with the necessity of an international sanitary quarantine, and inspection. Matters are bad enough now in our dairying districts, but if we are to be open to the importation of new types of abortion, which do not mutually immunize against each other, but which may be taken one after another in succession through a series of years, they may easily become incomparably worse.

Acquired Immunity. The question of persistent abortion year after year, in the same animal, is most important. If a first contagious abortion entails a second, a third, a fourth and a fifth in the same animal, in as many successive years, then manifestly the preservation of such animal is a most wasteful economy, altogether independently of the danger of her transmitting the infection to healthy stock. If, however, she herself becomes immune after a first or second abortion, it may be profitable to retain her for milk production or breeding, provided that she can no longer infect susceptible cows with which she must come in contact.

Acquired immunity of the individual cow is the rule after one or two abortions caused by the microbes with which we are at present most familiar. There are exceptions to this rule due to special nervousness and excitability of given cows, which tend to an indefinite repetition of the abortion, under the stimulation of pregnancy, of the continued presence of the microbe, or of some local disease (tubercle, tumor, parasite, etc.) of the ovary, womb or peritoneum. Yet statistics show that this only applies to a small proportion of cows and these the most nervous and excitable. The tendency toward insusceptibility to the deleterious action of the germ, which may still be present, is in the cow as a rule greater than the disposition toward a nervous encrease of the susceptibility. The difficulty of reaching a conclusion on this point depends on the fact that stockowners very commonly dispose of aborting cows, and as the freshly bought cows are usually attacked sooner or later, it is too confidently assumed that the old cows also would have continued to abort had they been retained. Many years ago, however, observant New York dairymen had noticed that the same cow rarely aborted over three years in succession, and in the great majority of cases not over two. The owner of a large herd, who has had much experience with the disease, assures me that the rule has been, that a cow did not abort with him a second time. The continuous abortion in a herd was mainly among newly purchased cows and others that had not been previously attacked, including heifers carrying first calf. The same is in a measure true of the European abortions.

Nocard says that after three to five years there is an acquired immunity. Only heifers and the cows that have been recently bought in, abort.

Penberthy, speaking of England, says that in case of repeated abortion in the same cow, the calf is carried longer each successive year until it comes to its full term.

Sand, in his symposium of the experience of Danish veterinarians, says it is quite exceptional that a cow should continue to abort, but outbreaks of abortion disappear spontaneously if no new cows are brought in.

Bang refers to a herd of 200 head of which 83 aborted in their first pregnancy, and of these only 20 aborted in the second, while 7 failed to breed. Counting the latter as having aborted, this amounts to less than one-third, while over two-thirds of the cows that aborted in the first gestation carried the calf to full time.

Paulsen quotes the case of a herd of 16, 7 of which aborted after service by a bull in an aborting herd. One of the seven was sold, but the remaining six all went full time in the following year.

Mörck records the case of a herd of 16 cows, the majority of which aborted in the same year. All the aborting cows were sold and fresh ones purchased. Next year the new stock aborted together with some of the cows that had been held over. He continued this course for eight years without any improvement, and then decided to keep the aborting cows as well as the others. In two years the affection disappeared from the herd.

Such small herds, in which all become early infected, and in which there is no further opportunity for the infection of susceptible animals (cows not yet infected, heifers in first gestation, new purchases), furnish a better opportunity than do large herds, to trace the acquirement of tolerance.

In a question of this kind, one must allow for variations in the different types of abortion caused by various microbes, but in the forms with which we are familiar in Europe and America, the acquired tolerance of the individual can be counted on with great confidence. It has indeed been largely traded upon by purveyors of antiabortion nostrums who promise to cure the individual cow, to which alone their drugs are administered. Two evils result: the stock owner’s money is paid for that which unaided, nature would have accomplished for him; and attention is withdrawn from the real necessity of the case, the prevention of the infection of freshly introduced animals. The nostrum vender thus secures for himself a growing market, as the yearly production of fresh cases in the same herds, appears to demand a constant use of the agent which appeared to work so well in the earlier ones.

Immunized animal still infecting. The cow that no longer aborts is not, therefore, a safe member of a herd. As an individual animal she has become resistant to the pathogenic influence of the germ, she is invulnerable to it to the extent that she no longer aborts, but her system and generative passages have acquired no such active bactericidal power over the microbe as to lead to its speedy destruction. The genital passages, once colonized, continue to be a field of growth of the bacillus long after its power to cause abortion in that particular animal has passed. Analogous cases can easily be quoted from the field of pathology. The horse that has apparently recovered from dourine still conveys the disease to others with which it has sexual congress; the recovered syphilitic person is by no means eligible for marriage; the recovered pig continues to carry the infecting swine plague bacillus in its air passages. In short, it is the rule that the immunized animal can with safety to itself carry a germ that readily infects its nonimmunized fellows.

In the case of infectious abortion this is one of the most dangerous elements, as the apparently healthy recovered cow receives no attention in the way of separation and disinfection, but is allowed to spread the infection through the bull that serves her in common with other cows and by being sold into new and healthy herds.

Symptoms. Contagious abortion sometimes takes the form of temporary sterility, the animal taking the male at frequent intervals, but failing to conceive. If conception takes place, the abortion is usually deferred until the fœtus has attained a considerable development—in cows till the third or seventh month; in mares till the fourth or ninth month; in ewes or sows till the tenth week.

Often times premonitory symptoms are entirely unobserved. Usually there may be detected some heat and enlargement of the mammæ, with a decrease in the milk yield, or a serous modification of the milk as in colostrum. Still more striking is a muco-purulent discharge from the vulva—opaque, white or yellow—in marked contrast with the perfectly clear, transparent mucus which appears in œstrum. The discharge may be densely white (in mares) or reddish, and may be accompanied by some swelling of the vulva and redness of its mucosa, which is dull, rough and granular, or even the seat of a papillary eruption. There is rarely hyperthermia or other constitutional disturbance, and in some cases the abortion is only discovered by the finding of the fœtus and its membranes in the gutter or pasture. The membranes are, however, not unfrequently retained, becoming offensively putrid. In other cases a muco-purulent discharge persists for a length of time, insuring sterility so long as it lasts, and causing ill health and emaciation. The fœtus is usually born dead.

The lesions are confined to the generative organs. Bang, found an odorless, dirty yellow, flocculent, slimy and more or less watery exudate between the chorion and uterine mucosa involving the connective tissue between the chorion and arachnoid so as to render it thick and friable. These conditions were well marked in the French and English cases, and perhaps somewhat less so in the American, which are habitually slower in reaching the abortion. Bang found the uterine catarrh with the characteristic bacillus in cases in which the calf had been carried to full term, exemplifying the local presence and culture of the bacillus without the usual abortion outcome. The bacilli were occasionally, though not always, found in the body of the fœtus, and in some cases the dead and mummified fœtus was found in the womb, which had not been stimulated to its expulsion. He even found the bacillus in the mummified fœtus, and still virulent, after an apparent seclusion of seven months.

ABORTION IN MARES.

This follows the same general course as does the disease in cows. In certain American outbreaks (Kilborne and Th. Smith) it has been traced to a bacillus like the colon bacillus, propagated in the womb and genital passages, and which produced suppurating vaginal catarrh in cows and mares on which it was inoculated. It is liable to occur, without premonitory symptoms having been observed, and to be followed by no marked sequelæ, so that, as in most cases in the cow, it may be looked on as a purely local infection. In England, Penberthy, found it to occur not earlier than the fourth month of gestation, yet he adduces several cases in which the first case in a breeding stud occurred in four weeks after the introduction of an infected mare from an aborting stud. In America on large breeding farms the introduction of the infection has proved ruinous, as many as 70 or 80 per cent. of the mares having aborted in the same season.

The conclusion is inevitable, that as in the case of cattle, the sire may become the means of transmission, and that the same measures of prevention are demanded. The fact that the affection is less widely spread or injurious, than in cattle, is largely due to the usual presence of but one, two or three breeding mares on a farm, so that there is little opportunity for a rapid extension of the infection. Multiply and encrease our studs of breeding horses, as cows have been in our dairying districts, and abortion, once introduced, would prove equally infective, spreading and injurious.

Therapeutics are useless in contagious abortion as the disease usually runs its course before any danger is suspected. If premonitory symptoms are observed, the abortion may sometimes be warded off for a time by secluding the animal in a quiet place and seeking to obviate labor pains by opiates and ounce doses of viburnum prunifolium.

Prevention. This is to be sought along two principal lines: 1st. The protection of a sound herd against the infection: and 2nd. The extinction of infection in a herd already diseased.

Protection of a sound herd. This requires the greatest possible care, because the infected animal usually presents the general appearance of perfect health, and there is no ready means of testing the presence or absence of the abortion bacillus. In purchasing a cow or mare in a public market the new owner may find her affected with this bacillus, and a serious danger to his whole herd. To protect the latter he must learn that the herd from which she came has had no abortions for several years before, and that the offspring for the different years are present in numbers corresponding to the dams. In the absence of this a certificate, and guarantee against infection of other animals by the one purchased, may well be demanded of the seller. A certificate from the veterinarian attending the herd furnishing the animal, may also be sought as evidence of the absence of abortion from the locality. Imported animals should be safeguarded in the same way but with even greater care, lest the microbian sources of new types of abortion, should be brought into the country. A guarantee of this kind might well be demanded by the Federal Government in the case of all breeding animals imported.

In case of failure to secure the most perfect guarantee with the purchased animal it would be worth the purchaser’s while to seclude it from his valuable herd, and not to breed it with the other animals of his herd until it has been proved to be entirely free from infection. If bought for a sire it should be subjected to a course of disinfection of the sheath and penis: if for a dam and unimpregnated, antiseptic irrigation of the vagina may be made daily for a week, and the external parts, hips and tail daily washed with antiseptics. If very important to have her bred, secure, if possible, a male that is not to be used on other animals. If this is impracticable, let the sheath and penis, and surrounding skin be thoroughly disinfected as soon as the service has been had.

If the newly acquired female is pregnant, keep her by herself until parturition and, even if this takes place at full term, irrigate the womb daily for a week with a disinfectant, delay having her served for a month, and if she must go to the sire of the herd, subject him to thorough disinfection after service. It may be that she still carries the germ but has become tolerant of it.

Extinction of Contagious Abortion in a Herd. 1. Two separate stables, or compartments, not having a common gutter should be provided, one for the sound animals, and one for those that are known to be affected, or that are open to suspicion.

2. The cow or mare that shows symptoms of abortion, or that has aborted, should at once be removed to the quarantine stable, and her stall, including the gutter and drain leading from it thoroughly disinfected. The whole stable should be whitewashed.

3. The aborted fœtus with its membranes, should be at once removed and burned, or boiled, or deeply buried after it has been thickly sprinkled with chloride of lime or other active disinfectant.

4. The manure from the infected stable should be taken into an enclosure into which no animals have access, and freely watered with a solution of sulphate of copper (6:100).

5. All in the quarantined stable and even those left in the general stable, should have the external generative organs, the hips, and the whole length of the tail washed once or twice a day with an antiseptic solution. Carbolic acid or creolin (2 or 3:100) makes a very safe and convenient agent, but copper sulphate (6:100) or mercuric chloride (2:1000) may be substituted. The colorless mercuric solution though effective and inodorous, has an element of danger in it, when left in barns in large quantities.

6. Cows or mares that have just aborted, should have the uterus irrigated daily for a week with a disinfectant solution. Carbolic acid (1:100 with 1 sodium carbonate) or creolin (1 to 2:100) or mercuric chloride (1:1000 with 1 hydrochloric acid) are good examples. Use a long rubber tube and funnel. They should not be bred until all discharge has ceased.

7. It is a good practice to keep a separate sire for the aborting and quarantined suspected animals, but the bull for each herd should, after each service, have his sheath injected with the disinfectant liquid, the orifice being held and the liquid pressed into all parts and finally, the skin around the sheath must be well washed with the same.

8. All cows or mares in an aborting herd, or one from which aborting animals have been removed within a year, should, after delivery, be injected with a disinfectant for one week exactly as if they had just aborted. This will guard against the danger from animals that carry the germ, but have become so tolerant of it that they no longer themselves abort.

9. New born animals brought in from other herds should be sponged all over with one of the above-named disinfectant solutions before being added to the herd.

10. In case the breeding animals go to pasture, separate fields should be furnished for the aborting and suspected ones and those supposed to be sound.

11. Breeding ewes, goats and sows should be excluded from all pastures occupied by suspected herds or those under treatment. The fields should further be cleared of rabbits as being susceptible to the infection and capable of keeping it up and transmitting it.

12. It is important to reserve the herd sires for the exclusive use of the home herds. Where this cannot be done, disinfection of the sheath and penis should be practised immediately after each service.

Attempts have been made at different times to destroy the bacillus by subcutaneous or intermuscular disinfectant injections. Bäuer used in the cow a 2 per cent. solution of carbolic acid, of which he injected two Pravaz syringefuls under the skin of the flank every fortnight from the fifth to the seventh month. It was rather unreasonable to expect much from 10 minims of carbolic acid once a fortnight, even apart from the fact that this agent is converted into the inert sulphophenic acid in the body.

Lignieres followed in the same line by injecting into the bodies of the cervical or other muscles 10cc. (2½ drams) of a mixture of terpinol one part, olive oil nine parts. This was injected during pregnancy every second day for the first three months, every third day for the second three months, and every fourth day for two months. The claim for success is based on the alleged prevention of second and third abortions in the same animals, and this becomes rather shadowy when we consider that the rule with cows is that they do not abort a second or third time. We have met with veterinarians who claimed a splendid success with the single injection of the terpinol. Lignieres claims no such success with his long continued treatment, as he had a percentage of abortions in every herd treated, and from first to last almost every animal in each herd aborted once, or was sold nymphomaniac. It is to be feared that the apparent immunity depended mainly on that tolerance which comes early in nearly every case to the aborting cow.

INFECTIOUS ENTERO-HEPATITIS IN TURKEYS.

Blackhead. Definition: Infectious protozoan disease of cæca and liver and general toxicæmia. Microbiology: Amœba in cæca, liver, etc. Symptoms: Attacks young, dulness, drooping, ruffling, moping, anorexia, greenish diarrhœa, icteric or dusky mucosæ, blackening of gobble, etc. Lesions: Enlarged thickened cæca, epithelial degeneration and desquamation, exudation, mottled liver, with giant and round cells and amœbæ, degeneration, necrosis, caseation, no abscess. Diagnosis from bacteridian typhlitis or diphtheria. Treatment: Intestinal antisepsis. Prevention: Disinfection of buildings, yards, manure, seclude from other flocks, birds, flies, breed new flock on fresh ground from eggs of affected or other flock, set in incubator or under hens.

Synonym: Blackhead.

Definition. An infectious disease of turkeys, especially destructive to the young, due to a protozoön (amœba meleagridis), and characterized by inflammatory thickening of the walls of the cæca, diarrhœa, brownish, yellowish or greenish areas of degeneration of the liver, and congestion with blackish discoloration of those portions of the head which are uncovered by down or feathers.

Microbiology. The microörganism (amœba meleagridis) is found in the thickened walls of the cæca, in the exudate, in the lumen, and in the degenerating patches of the liver. The most common and simple form is that of a rounded body, varying slightly in form, and containing a group of very minute granules situated somewhat eccentrically. They may be enclosed in lymph spaces or less frequently in giant cells, or have portions of broken up cells adherent. Their size varies from 10 to 15μ. They may be stained by the following process: Harden in 95 per cent. alcohol saturated with mercuric chloride, then in the same with an equal amount of a 5 per cent. solution of bichromate of potash, and finally in Hemming’s solution. After a day in these solutions they are washed for a day in running water, then treated with ascending strengths of alcohol, dried by passing through alcohol and chloroform, imbedded in paraffin, sectioned dry, and stained in Delafield’s hæmatoxylin and eosin. The spherical or slightly oval amœbæ have a homogeneous, bluish red tint, feebler and therefore distinct from the tissue nuclei. Near the centre in most a blue circular line shows the outlines of the nucleus.

Th. Smith compares this affection with the amœbic dysentery affecting the large intestine and liver of man, and notes these differences, that amœbic movements have not been observed in amœba meleagridis, and that hepatic abscess does not occur in the turkey. The indisposition of the bird to suppuration may perhaps account for the latter distinction. Smith found rounded organisms in the tubules of the cæca and flagellates in the lumen of the gut, but did not attach any importance to their presence. Bacteria were only found in the lesions in the solid tissues where the subject had not been killed and immediately examined, but left over night for examination in the morning. There was no constancy in their species as in the case of the amœbæ, all indicating that their invasion was post mortem.

Symptoms. The disease is most frequent and fatal in the young (1 to 4 months, exceptionally 6 to 10 months), and the symptoms vary much in different cases, according to the intensity of the disease and the relatively extensive implication of the different organs. Among the general symptoms are those of general suffering and ill health, dulness, spiritlessness, drooping of the head between the wings, a pendent condition of wings and tail, erection of down or feathers, separation from the flock, the bird moping alone and sitting much of the time. The more characteristic phenomena which are rarely sufficient to identify the disease unless it is known to be prevalent, are loss of appetite, a greenish diarrhœa, yellowish or brownish discoloration of mucosæ, emaciation which becomes extreme if the subject survives long enough, and more or less blackish discoloration of the gobble and bare portions of the skin covering the head.

Lesions. These are characteristic, the cæca being greatly enlarged, the walls thickened by a yellowish submucous exudate, the epithelium disintegrated and desquamating, and the mucosa covered by a solid yellowish gelatinoid exudate arranged in superposed layers, while the contents are soft, pasty or of a greenish liquid appearance. The comparative stagnation of the contents as in the appendix of man appears to favor microbian infection. Amœbæ are especially abundant in the exudate into the submucosa and in the lymph spaces. The liver changes show infective inflammation in the spots of mottling, followed by degeneration, and necrosis, the liver cells disappearing under the compression of the giant and round cells and the amœbæ, the surface over the affected parts is depressed, and the mottling may show a variety of colors, as brown, brownish red, or yellow, pale yellow, grayish or dirty white. The degenerating tissue may become caseated, but abscess appears to be unknown, though so common in amœbic dysentery of man. In the skin of the head the blackish color predominates; there is more or less congestion, capillary embolism, and tissue degeneration.

Diagnosis. Th. Smith notes three cases of diseased cæcæ without great thickening of their walls, and an exudate in the lumen having the general appearance of that seen in the amœba disease but with no amœbæ, only the bacillus coli communis. The odor was strongly feculent. In all three cases the liver was healthy. In one there was an abundance of tapeworms in the bowels. Manifestly the absence of liver lesions may be held to indicate the absence of the protozoan disease. VonRatz (Budapest) gives two similar cases, with many nematodes, those in the exudate being 8 to 14 mm. long.

Zurn describes the presence of the diphtheria of fowls in the intestines of hens, turkeys and palmipeds and sometimes confined to the cæca. It is characterized by great prostration and debility, and an offensively smelling diarrhœa at first pultaceous and mucous, later bloody, and followed by constipation, in which case the cæca and rectum are ulcerated and blocked with the yellow croupous exudate. It lasts 2 to 3 weeks or even months, is subject to relapse, and sometimes occurs as a sequel to the diphtheritic affection of the head and throat. The absence of marked thickening of the cæcal wall, and of the protozoön, the presence of the diphtheritic exudate in the lumen, and the croupous condition or congested appearance of the head and throat are distinctive. Th. Smith, however, refers to two cases, supposed to be of this kind, in which the walls of the cæca were greatly thickened, the result of reparatory inflammation following a slough of the mucosa. Siedamgrotzky also describes thickening of the walls of both cæca in a hen, the mucosa being covered with a thin pseudo-membranous exudation, without ulceration.

It would seem that the cæca of birds, like the vermiform appendix of man is very subject to invasion microbes, bacterian and protozoan, and should always be carefully examined in case of intestinal or hepatic disorder.

Treatment would be in the line of intestinal antisepsis with carbolic acid, salol, sulphurous acid, or the sulphites, with a laxative of castor oil, to carry these agents unchanged to the cæca, but no success has attended attempts in this direction, and the danger that comes from preservation of the infected animal, and consequent multiplication of the microbe would as a rule far more than counterbalance any probable recoveries.

Prevention. Moore has shown that the amœbæ, passed with the fæces, contaminate the food and water and thus actively propagate the disease, so that preventive measures must be mainly directed toward the purification of these infecting media. To be thorough new ground must be secured on which no diseased turkeys have been, and through which no water from contaminated or suspected land can flow; if necessary this must be closely fenced to prevent all ingress or egress, and on this ground we can place, as soon as they leave the shell, young turkeys hatched from eggs obtained in noninfected localities, or the eggs carefully washed of the turkeys living on infected ground. In this way the heredity and quality of the flock can be preserved without risk of contamination from the parents. The amœba is not known as a parasite of other birds, but if it should eventually be found to be so or to occupy any other animal body as an intermediate host, the local extermination of such host will become a necessary precaution.

When a new flock has been started in this way, the birds of the old flock may be fattened, killed and marketed, and as suggested by Cooper Curtice the grounds they have occupied may be secluded by fencing for one or two years, in the hope that the amœba will perish by this break in the chain of its life history. If this should prove successful with the land, the infection might be easily exterminated in the whole infected district or state.

The poultry buildings will require thorough disinfection. All manure and droppings must be carefully removed and the building whitewashed, using freshly burned quicklime and ¼ lb. of chloride of lime to the gallon of the mixture. The litter should be burned, and all nests, roosts, drinking vessels and troughs soaked with a mixture of sulphuric acid ½ gallon, carbolic acid ½ gallon, and water 20 gallons, (Th. Smith). The agents are mixed slowly in a vessel set in cold water. The same may be liberally applied on the surface, fences, etc., of the yards. Or quicklime, freshly burned, may be used freely on the yards holding the infected flocks (Moore). Mercuric chloride is dangerous. When the infected flock has been finally disposed of, the buildings and yards should be again thoroughly disinfected, and together with the field runs, abandoned for at least one year.

ASTHENIA IN CHICKENS.

Microbiology: bacillus of colon group. Pathogenesis to Guinea pigs: rabbits, pigeons and chickens refractory to artificial cultures. Treatment.

Synonym. “Going Light,” Bacterial Infection of the Duodenum.

C. F. Dawson, in investigating a wasting disease of well fed Brahma fowls in Maryland in which there was no appreciable symptom except the gradual and extreme loss of flesh and weight found in all cases a catarrhal duodenitis, with the presence in the contents of a bacterium in pure cultures, and apparently allied to bacillus coli communis.

Bacteriology. The bacterium is 1 to 1.3μ long, by .5μ wide, with rounded ends, often in pairs. It does not stain in acid nor alkaline methylene blue, carbol fuchsin, nor alcoholic dyes, but stains easily in aqueous solutions of the same stains and by Gram’s method. It is ærobic, facultative anærobic, grows at 50° to 120° F. in acid or alkaline beef bouillon, with fœtor; in glucose, saccharose, or lactose bouillon with the production of acid; in milk causing coagulation; on gelatine, agar and potato. Growth in Bouillon ceased at 131° F. and sterilization took place at 135° to 140° F. Vitality was not lost under freezing nor drying. It was killed by a 1 per cent. solution of carbolic acid in five minutes, or by formaldehyde gas, but not by lime water.

Pathogenesis. Inoculated subcutem, in a Guinea pig caused death in 24 hours, with a necrotic œdematous condition of the adjacent tissues like malignant œdema, and containing the microbe. It was further found in the liver, spleen, abdominal exudate, heart, blood and lungs, but not in the kidneys.

It proved harmless to rabbits when injected subcutem, but fatal in 24 hours when thrown into the peritoneum. The lesions were severe duodenitis and omental inflammation, and the bacterium was found in the liver and duodenal wall.

Pigeons, rats and mice proved refractory to the artificial cultures, also chickens. The latter were injected subcutem, intraabdominally and intravenously. Yet in view of the constancy of the lesion in hens with the microbe in pure cultures and the absence of all other morbid conditions, Dawson felt justified in attributing the disease to this microörganism. It is possible that his experimental hens had become immune from a previous attack, or failed in some condition of food or environment which is essential to pathogenesis, or finally there may possibly be some other infinitesimal microbe present which escaped observation, but which furnished the occasion for the coincident development of the colon bacterium.

Treatment. The indications are: the expulsion of the offending bacterium to be followed by nutritious, easily digested food, pure water and tonics. Dawson advises castor oil in dose of two teaspoonfuls, or calomel ¼ grain repeated till purgation occurs; and to be followed by powdered fennel, anise, coriander, cinchona of each 30 grains; powdered gentian and ginger of each ½ dram; powdered copperas 15 grains. The addition of bismuth, pepsin, or orexin may be suggested.

APOPLECTIFORM SEPTICÆMIA IN CHICKENS.

Streptococcic infection in hens. Most violent in pullets and hens; less so in capons and cockerels. Found dead, or sick 24 hours, ruffled, prostrate, neck limp, head drooped, indisposed or unable to rise, liquid icteric fæces, blood-stained skin of neck and breast, death without agony. Lesions: Soiled anal feathers, plump carcass, skin pallor save neck and breast, extravasation of blood subcutem and intramuscular, mucosæ anæmic, peritoneal engorgement and effusion, enlarged, engorged liver, cell proliferation, degeneration, coagulation necrosis, gall bladder full. Enlarged congested spleen, degeneration. Congested swollen kidneys, epithelial degeneration, casts, streptococcus. Congested, consolidated bronchioles, alveoli, lungs, with microbe. Meningeal congestion, exudate. Bacteriology: Streptococcus, pure cultures in lesions, size, chains, tetrads, staining qualities, culture media, colonies, action on sugars, acid, no gas, on milk no coagulation, on gelatine no liquefaction. History: Stagnant water; no evident source of infection, buzzards, etc. Pathogenesis: Inoculation, intravenous or intramuscular, feeding. On duck, pigeon, rabbits, mice, dogs. Guinea pigs and sheep immune. Immunization by injection of sterilized cultures.

Under this name Norgaard describes a hæmorrhagic streptococcic infection which prevailed in 1901 in a flock of 200 to 250 Plymouth Rocks in Loudon County, Va. Forty birds died within six weeks, and later the mortality reached 200, death often occurring suddenly while feeding, or the birds would drop from their roosts in the night and be found dead in the morning.

Symptoms. In the majority, the pullets which died suddenly, no symptoms whatever were observed, yet a certain number of the capons and cockerels were noticeably ill for 12 to 24 hours. In these the feathers were ruffled, the prostration extreme, the head drooped between the wings, the neck was weak and wobbling (limber neck), the wings and tail drooped, and the animal lay on its breast often unable to rise. Sometimes there was a passage per anum of liquid bile-stained mucus. Close examination of the neck and breast might detect hæmorrhagic discoloration of the skin, though the skin elsewhere was pale and smooth. Death takes place without a struggle.

Lesions. The anal feathers were usually stained, indicating diarrhœa; the picked carcass was plump and fat, with pale, healthy looking skin, except on the neck and breast, where it was discolored by extravasated blood; at such points the connective tissue and muscles were infiltrated with blood in areas of an inch in diameter, more or less, and with irregular outlines. The buccal mucosa was clear, pale and bloodless. The cavity of the body contained an abundance of sero-sanguinolent exudate, and the mesenteric veins were engorged. The liver was greatly enlarged and congested, the greater part of its substance being apparently composed of the distended blood vessels. The hepatic cells were granular and fatty, and if death had been delayed over twenty-four hours their outline became indistinct and the nucleus stained only faintly. In the foci of disease were clumps of round cells and leucocytes in and between the acini, and in still more tardy cases points of coagulation necrosis. The streptococcus was abundant in the necrotic centres, among the clumps of leucocytes, in the parenchyma and capillaries. The gall bladder was usually distended with bile. The spleen had the large size and well developed Malpighian bodies that characterize the well-fed bird, but it showed still greater enlargement, combined with sanguineous congestion and circumscribed blood extravasations. With a hand lens were seen numerous round, semi-transparent points, the size of pin holes, which the microscope revealed to be centres of coagulation necrosis, surrounded by embryonic tissue. The centres consisted of a granular debris with abundance of the streptococcus. The kidneys were congested and swollen, and in cases that had survived two or three days there was granular degeneration of the epithelium of the tubules, and the lumen of the tubes contained casts with leucocytes and streptococci. The organism was also present in the capillaries. The lungs presented areas of congestion and consolidation, exudation into the walls of the bronchioles and the alveoli, and an abundance of streptococci in the lesions. In the cranium were a subdural exudate and meningeal congestion. For examination of the tissues they were hardened in specimens of alcohol of encreasing strengths, embedded in paraffin and stained with carbol fuchsin with a counterstain of methylene blue.

Bacteriology. The streptococcus was found in pure cultures in all the diseased centres except in the intestinal contents. Smear preparations were made from the blood, the abdominal exudate, the intestinal contents, the bone marrow, the cerebral exudate and the sanguineous effusions into the muscles.

The coccus is .6 to .8μ in diameter, in short chains of 2 to 8 cells, or in some media much longer. Involution forms are common, and Norgaard claims to have seen indications of fission in two directions to form tetrads. The organism stains in the usual aniline dyes, as well as by Gram’s and Gram-Weigert’s method. It is nonmotile, ærobic, facultative anærobic, grows in solid and liquid media that is neutral, or slightly acid or alkaline (not if strongly acid), best at 98.6° F., and slower at the room temperature. In alkaline peptonized beef bouillon in 24 hours it forms threads and balls on the sides and bottom of the tube, leaving the liquid clear. On agar there are formed small shining, grayish colonies 1.5 mm. in diameter with brownish centre and bluish periphery. With all the sugars it produces acid, but no gas. It does not coagulate milk. On gelatine colonies are formed in four days, and there is no liquefaction.

History of the Outbreak. The outbreak commenced early in January, without any obvious occasion for the introduction of infection. There had been no chicken disease on the place for 25 years, and no chickens had been purchased except from a neighboring farm where the stock remained healthy. They had been fed on corn meal, wheat bran, wheat tailings and whole corn, together with scorched wheat from a burned barn. The poultry houses were clean and well aired, and after they had been closed there was no abatement of the disease. The water was from a stagnant pool receiving drainage from the stable, but this was no new condition and January is not the driest month with the foulest water. The suggestion may be hazarded that the infection may have been introduced by the usual infection bearer, the buzzard, or by some other wild bird, or mammal.

Pathogenesis. Among the chickens the most rapid and fatal cases were in pullets, then among the laying hens, while the capons and cockerels were less severely affected, and some survived from three to seven days.

Those inoculated intravenously as a rule sickened on the second or third day with a temperature of 110.7° F., and were found dead the following morning.

Some took injections of .25 to 1cc. in the pectoral muscles with impunity.

Chickens that had fasted 24 hours, took each daily for 3 days, a few cubes of bread soaked in a fresh bouillon culture. Death followed in four out of six, in from four to thirteen days from the beginning of the experiment. The birds gradually became listless, refused to eat, and remained quiet in a corner of the cage, with closed eyes and head drooping until it rested on the ground. Diarrhœa was frequent but not invariably present.

Chickens fed on the chopped up viscera of rabbits that had died of the disease perished in 3 to 10 days.

A white duck inoculated intravenously with .5cc. of peptonized beef bouillon culture, took ill on the 8th day, and died on the 12th. There was loss of coördination and use of the wings, temperature 109° F., and necropsy showed valvular endocarditis containing the streptococcus. A second duck sickened on the 11th day, but recovered after three days’ illness. Killed on 21st day, all cultures from heart, spleen and kidney remained sterile. Subcutaneous, intramuscular and feeding experiments failed to produce the disease in ducks.

A pigeon injected with .5cc. bouillon culture intravenously died on the fourth day with the internal lesions of chickens, and blood extravasations on head and neck. Intra-muscular injections and feeding experiments were fruitless.

In rabbits, intravenous injections of 1 to 1.5cc. led in 24 hours, to temperature of 105.3° F., without impairment of appetite, or other marked sign of illness, and as a rule the subject is found dead next morning. Intra-abdominal and intrapleural injections kill in two to four days, and subcutaneous ones in three days. In addition to the lesions found in chickens, there is often bloody urine, a sanguineous lymph on and beneath the cerebral meninges and in the fourth ventricle, and deep congestion of the cancellated tissue of the vertebræ. Streptococci are abundant in the lesions.

In mice intraabdominal injection of .01cc. killed in 48 hours, and subcutaneous injections in 2 to 5 days. The lesions were like those seen in birds, and streptococci were abundant.

In dogs after intravenous injection there was hyperthermia (103.6° and 104.1° F.) and lameness of the right fore shoulder joint, followed in 5 to 8 days by recovery. Feeding on the viscera of the diseased chickens, was followed by anorexia, and vomiting only.

Guinea pigs and sheep proved refractory.

Immunization. The injection into the wing vein of .5 to 2.5cc. of bouillon culture, sterilized by heat proved protective to the chickens against inoculations of the virus while the check animals invariably died.

TUBERCULOSIS.

Synonyms. Definition: infectious disease caused by bacillus, attended by productive inflammation, tubercles, necrotic degeneration, caseation, fibroid change, calcification or ulceration. Animals susceptible: python, salamander, carp, fish, birds, rodents, sheep, goats, solipeds, cattle, dogs, cats, apes, swine, wild ruminants, kangaroo, carnivora, cage birds, civilized (housed) man. Geographical distribution: with dense population, Central Europe, Britain, Eastern States; little in absence of cattle products—Scottish Western Isles, Iceland, Newfoundland, Greenland Highlands, Arctic North America, Northern Norway, Sweden, Lapland: open air life protects. Virulence: ancient records, modern, early antituberculous legislation, decimation of herds, researches of Vilemin, Gerlach, Chauveau, Semmer, Parrot, Tappeiner, etc. Bacillus tuberculosis: evolutionary changes, relation to actinomyces, 1.5 to 3.5μ by 0.2μ shorter and thicker in ox, solitary, exceptionally short chains, on blood serum may be filamentous, staining slow, carbolated fuchsin, technique, sections; biology, adaptation to environment, to genera, variation in same genus, experiments showing real identity of variant forms; vitality: in water human bacillus 50 to 70 days, bovine bacillus indefinitely, avian 117 days, dried sputa 9 months, cow’s lung 102 days, putrid material 43 days to years, survives gastric juice, sunlight kills in some hours, if in thin layer, day light 7 to 18 days, dry heat (212° F.) for an hour left living bacilli, moist heat 140° F. for 1 hour kills, low temperatures (−25° F.) fail, after 15 days in salt failed in rabbit, after 30 in Guinea pig. Chemical disinfectants. Accessory causes: racial vulnerability, close buildings, dark, foul, damp stables, poor scanty food, heavy milking, conformation, early breeding, inbreeding, age, predisposing diseases, traffic in animals, dairy extension, admission of tuberculous animals from other states, assorting tuberculous for sale in a given State, sale of sound from tuberculous herd, lack of indemnity for animals killed, private testing of herds and sale of tuberculous, accustoming to tuberculin test, antipyretics during tuberculin test, false certificates of tuberculin tests, feeding hogs on tuberculous offal, feeding calves and hogs on tuberculous milk, feeding hogs after tuberculous cattle, feeding from a common trough, dry, dusty stables, extension through vermin, flies and other insects carry virus. The tubercle: miliary, pinhead, conglomerate, proliferation of cells—tissue and leucocytes, in nests in stroma, giant cells in center, then epithelioid, then lymphoid, caseation, calcification, fibrosis, pearl disease. Localization: Cattle: pulmonary: miliary tuberculosis, aggregation into larger tubercles, caseated centres, fibroid, cretified, abscesses, vomicæ, complex infections, infiltrations, difference from broncho-pneumonia, lesions of different ages; pleural lesions; congestion, exudation, fringes, nodules, grapes, adhesions, caseations: bronchial and mediastinal glands, congestion, swelling, softening, induration, caseation, cretefaction: cardiac lesions: lesions of mouth and throat, pharyngeal glands: gastro-intestinal, peritoneal, mesenteric glandular; œsophagastoma; liver tubercle; splenic; pancreatic; genito-urinary; mammary; cerebral; spinal; orbital; skeletal; cutaneous; muscular; glandular; table of distribution. Swine: lesions: pharyngeal, intestinal, mesenteric, muscular, hepatic, splenic, glandular, pulmonary, skeletal, caseation, liquefaction. Horse: lesions: thoracic, abdominal, glandular, of serosæ, vertebræ, etc. Sheep and goat: lesions: thoracic, abdominal, glandular, hepatic, pharyngeal, facial, etc., verminous affections. Dog and Cat: lesions: respiratory, abdominal, pharyngeal, tonsillar, hepatic, pancreatic, splenic, skeletal, arthritic, cutaneous. Apes and Menagerie Animals: lesions. Chickens: lesions: intestines, liver, spleen, peritoneum: lungs and kidneys often escape. Pheasant: lesions: as in hens, centre zone has epithelioid cells, fibroid, cretefaction, amyloid degeneration. Parrot: lesions: eye, beak, tongue, palate, larynx, bones, joints, lungs, liver, intestines, muscles, skin. Primary and secondary infection, extension by lymphatics, blood channels, tonsils, inhalation, deglutition.

Synonyms. Consumption; Tabes; Scrofula; Pining; Grapes; Great White Plague, etc.

Definition. An infectious disease common to man and a large number of animals, caused by the bacillus tuberculosis, and characterized by a productive inflammation giving rise to small, rounded bodies (tubercles), or diffuse infiltration, with a tendency to necrotic degeneration, and caseation, or to fibroid degeneration (sclerosis), calcification or ulceration.

Animals susceptible. Tuberculosis comes near to being a panzoötic, since although reptiles, fishes, birds and some mammals do not readily contract it under normal conditions, yet under abnormal and debilitating conditions nearly all will succumb to it.

Reptiles. Sutton found tuberculosis in a python which was kept so warm in the London Zoological Gardens that a thermometer between its folds registered 85° F. Kráhl, Battaillon and Ferre cultivated the bacillus in frogs, Kráhl in snakes. Blauvelt found tuberculosis in a salamander. Lechner found it in amphibia.

Fishes. Broussais records the prevalence of tuberculosis in carp in a pond which received the sputa of a consumptive man. Under the skin were found rounded tumors, containing abundance of bacilli, that infected rabbits and Guinea pigs on which they were inoculated.

Birds. In birds of the farmyard—hens, pheasants, turkeys, ducks and pigeons—it is very frequent and often occurs as an epizoötic. While the tuberculosis of barnyard fowl is a manifest variety and not readily interchangeable with the varieties affecting the mammal, yet, with a special predisposition, it can be transferred and can then be conveyed from animal to animal in the new genus in which it has been implanted. That of cage birds is interchangeable with that of man.

Rodents. Guinea pigs have a strong susceptibility to tuberculosis, whether from human or bovine source, and rabbits for that of birds, and by continuous transmission through the body of the rodent, all alike seem to tend toward acquiring common characters. The Guinea-pig, therefore, has been especially availed of for the experimental transmission of tuberculosis, and, as the disease in them becomes acute and rapid in its progress, these subjects permit the multiplying of experiments in a short period. Rabbits are less vulnerable to the bovine or human form.

Sheep and goats, kept under usual conditions, show a remarkable immunity from tuberculosis, yet if directly inoculated an inherent susceptibility is easily shown. Habitual immunity may be in some degree due to their open air life, to the heavy winter fleece protecting them against chills, to the comparative absence of the heavy and continuous milk yield demanded of cows, to the more restricted development of the lymph plexuses in the lungs and elsewhere, and to the limited opportunity offered by the small tonsils for infection entrance.

The horse, ass and mule rarely contract tuberculosis casually, the more spacious stall, outdoor life, hard muscular condition, the very small tonsils, the exclusive nasal respiration, the paucity of connective tissue lymph plexuses, and the abundance of red globules, probably favor immunity. Yet on inoculation by Chauveau, Nocard and others, the horse readily succumbed to infection, generalization taking place more certainly than in the ox.

Cattle. The bovine races are remarkably subject to tuberculosis. This is probably due in part to the great amount of connective tissue lymph plexus in the lungs and elsewhere, the habit of using the mouth in hurried breathing, the deep, sudden inspiration through the mouth and over the tonsils that follows a cough, the habitual restricted size of the cow stables, the absence of individual separated stalls, the habit of feeding from the same trough with the cattle adjacent, the great drain of yearly breeding and heavy milking, the retention in the herd of old, failing cows for their milk product and high priced offspring, and the bovine habit of licking each other with the infected tongue. In many European cities and even in country districts the disease is very prevalent. In Copenhagen a few years ago 17.7 per cent. of all oxen and cows killed in the abattoirs were tuberculous; in Berlin 15 per cent.; in Holland 20 per cent.; in Pomerania and Bomberg 50 per cent.; in Hildesheim, Hanover, 50 per cent.; in Berlin dairies 75 per cent. (Ostertag): in Leipsic and Edinburgh 20 per cent. The great variation in the data for the different cities is suggestive of different inspection standards. American figures as given by the Bureau of Animal Industry are for Baltimore (mostly cows recently from the country) 2.5 to 3.5 per cent.; and for the packing centers (among 2,273,547 mostly fat steers, and therefore selected) 0.02 per cent. It is here largely a matter of locality and infection, I have seen large herds with 100 per cent. tuberculous, and extensive districts, in the north and especially in the south entirely free from the disease.

Dogs and cats in their natural condition rarely show the disease, but contract it readily on inoculation. Cadiot found 40 cases in 9,000 post mortems of dogs. The young are apparently more susceptible than the old, and primary lesions in the abdomen are common and suggest infection through the food. The majority belonged to consumptive persons, and gnawed the bones that had been first picked by the owner, and ate from his plate what he left. Jacobi records the case of a dog, with general tuberculosis, which habitually licked up the expectorations of his phthisical master.

Apes and Monkeys, in confinement, almost all die of tuberculosis.

Swine contract tuberculosis readily, the large tonsils, the habit of breathing through the mouth, and the abundance of connective tissue and lymph plexuses in the lungs and elsewhere contributing to this. Yet in them the affection is mainly a dietetic disease. Swine kept in the country and fed on vegetable food are rarely affected. In Saxony, where 17 per cent. of the cattle are tuberculous only a shade over one per cent. of swine were so, and in Baden only 0.02 per cent. In hogs raised on our western farms and corn-fed the proportion is much less. Yet in those fed on uncooked skim milk, kitchen scraps and the refuse of slaughterhouses in a raw state, tuberculosis becomes very common. In one case, in a large public institution, where the dairy herd was universally affected, and where, on their slaughter, their raw offal had been thrown to the hogs, I found that the latter were almost all tuberculous. Similarly, in feeding experiments, from the time of Gerlach, pigs and especially young pigs, have shown themselves to be very susceptible.

Among the less domesticated animals that contract tuberculosis may be named deer, elk, gazelle, antelope, camel, dromedary, giraffe, kangaroo, lion, tiger, jackal, jaguar, bear, arctic fox, rat, mouse and the common cage birds, etc. Fröhner found 36 per cent. of parrots affected in Berlin.

Man has long been recognized as standing in the front rank of susceptibility to tuberculosis. Yet even in his case the prevalence of the affection bears an intimate relation to his indoor life. In large cities post mortems often show that one-third have suffered, and that one-seventh and upward of the whole population die of tuberculosis. Natives of tropical islands and countries, living in the open air and apart from close association with civilized man, often escape entirely. In South Africa the herdsmen living in close buildings suffer encreasingly, while their cattle, kept constantly in the open pasture, escape.

Geographical Distribution. The prevalence of tuberculosis shows a direct relation to the opportunity for infection rather than to climate, latitude or altitude. It is the prevailing disease of civilized communities with dense populations, and especially in large cities where the general vitality is lowered and the crowded buildings give every opportunity for infection. It is preëminently the disease of Central Europe, of Great Britain and of our Eastern States, where there is the greatest activity in business, manufacture and commerce. Yet in the Scottish Hebrides, Iceland, Newfoundland, the Greenland Highlands, Arctic North America, the northern parts of Norway and Sweden, Lapland and Finland it is hardly known. The absence of commerce and cattle and the sparse population have much to do with this. The coasts of Greenland with their Danish stations have two-thirds of the population tuberculous (Cook); the Indians of Barrow’s Straits, when infected in 1899 by the frozen-in whalers, suffered from it as from a plague; in Christiana, Stockholm and St. Petersburg it is as prevalent as in the large cities of Central Europe. Elevated and dry climates have often been found to be free from the affection, yet it prevails inside the double windows of houses in the higher Alps, and has, within a generation established a notorious prevalence in Minnesota, Dakota and westward, as it has in Australia, mainly owing to the advent of consumptives who sought for health in the dry atmosphere. The hills and dry tablelands in North and South America, Africa and Asia which have acquired a reputation for salubrity, owe this largely to the sparse population and the absence of facilities for infection. In South Africa, in spite of the dry and genial climate, the disease is constantly encreasing in the human (housed) population. The sea-coasts, which are the seats of large cities and the centres of population and trade, are also the most extensively affected with tuberculosis—in the West Indian Islands, Panama, Nicaragua, Mexico, Yucatan, Columbia, Equador, Peru, Chili, Ceylon, Guinea coast—while the sparsely peopled highlands of the same countries are practically free.

What is true of man is equally so of cattle. In the Gulf states of this country, herds living in the open air are practically free from tuberculosis, while in New Orleans and other large cities, the cows shut up in the confined stables and yards, are as tuberculous as those of the great cities of the north. So in many districts in the northern states we find no bovine tuberculosis, while in others, differing in no essential particular as regards geological formation, altitude, exposure, and industrial use of the animal, a large proportion are affected.

Virulence. Tuberculosis has long been recognized as virulent. “It is indicated in the Mishna and other Jewish works as rendering the meat unfit for consumption, but to come to more modern times, we find that throughout the seventeenth and eighteenth centuries the flesh of tuberculous animals was excluded from human food, alike by the civil and ecclesiastical laws of Europe. Tuberculosis in cattle was erroneously identified with syphilis of man, which made a frightful extension in the end of the fifteenth century, spreading from the army of Charles VIII which had been engaged in the siege of Naples. This conviction lasted until it was disproved about 1782. Though mistaken in the identity of the two diseases, the fact that for centuries the common people and physicians both associated tuberculosis with a malady so notoriously contagious as syphilis, speaks strongly for the forcible evidence of contagion manifested at that time. Morgagni, who must have begun practice about 1700 A. D., testifies to the strong conviction of the contagious element in tuberculosis. Indeed it became a common practice to isolate the consumptive person from the public, and after his death to burn his clothes and sometimes even the house, or at least to subject them to a careful disinfection. It is recorded that in 1750, in Nancy, the magistrates ordered the burning, in the public square, of the personal property of a woman who had died of phthisis, from sleeping in the bed of another consumptive person.

“At Naples, a royal edict of September 20, 1782, prescribed the sequestration of the phthisical, the disinfection of the rooms, chattels, movables, books, etc., with vinegar, eau-de-vie, lemon juice, sea-water, fumigations, etc., under a penalty of three years at the galleys, or in the case of nobles, of three years imprisonment and a fine of 300 ducats. A physician who failed to report a case of consumption was fined 300 ducats for the first offense, and banishment for ten years in case of a second. Any one assisting in such evasion of the law was sent to prison for six months.

“Chateaubriand found that, in 1803, he could not sell his carriages in Rome, because Mme. Beaumont, who had died of consumption, had ridden in them three or four times. George Sand, who was with the phthisical Chopin in Minorca in 1839, was refused a lease of the house for the second month, and the price of repainting and purifying was demanded. Later, in Barcelona, they were assessed for the bed on which Chopin had slept, as the police regulations prescribed it should be burned.

“This was not a mere survival of vulgar prejudice. Jacobi tells us of a dog which died of consumption from eating the sputa of his phthisical master. Laennec, the discoverer of auscultation, and the great authority on pulmonary consumption, records that he himself contracted a tuberculous nodule, through a wound with a saw, while making a necropsy in a case of phthisis. Laennec died of tuberculosis later, although he seemed to have checked this lesion by caustics. Andral joins Laennec in enjoining the greatest caution and cleanliness in taking care of, or associating with persons having advanced tuberculosis.

“Cullen, who started with a strong prejudice against the doctrine of contagion, leaves us the following instance of its occurrence: ‘A young man predisposed to phthisis married a Dutch girl of a sanguine temperament and good constitution. Some days after the marriage the woman lost her fresh color and was attacked by a bad cough; a month later she commenced spitting blood. The physician advised her not to sleep in the same bed with her husband, but she refused to follow his advice, and six months later she died of phthisis. The servant who took care of her and the domestic, who avoided, as far as possible, staying in the sick chamber, both died of consumption.’

“Wickmann, court physician in Hanover, in 1780, pronounces emphatically for contagion. In Zurich, at that time, one death in every six was from phthisis. The contagion of phthisis was slow in its operation, and was, therefore, less evident than that of plague, smallpox, scarlatina and other affections attended by a skin eruption, but it was no less real and deadly. It was also less frequently indirect, or carried from victim to victim by intermediate agents. He cited instances of the transmission of consumption from husband to wife and vice versa, and claimed that the marriage of a phthisical person should be legally prevented. As a means of preventing the disease, he proposed a strict surveillance of establishments for the sale of old clothes, and the avoidance of leaving infants with consumptives.

“Valsalvi and Sarconi refused to make necropsies of persons who had died of phthisis.

“Dr. Ruhling, of Gottingen, writing in 1774, of the disease in animals, says: ‘The malady is transmitted to sound animals by direct contact of animals standing side by side in the stall, and licking each other, and breathing the expired air direct from the diseased lungs; the frequenting of the same pastures will also serve to propagate it.’ In Krunitz’s encyclopedia, published in Berlin, in 1787, is the following: ‘The heifers show an ardent desire for the male, and remarkably enough, do not become pregnant, but part with the fruit of conception. When opened these animals show the first stomach, kidneys and surface of the lungs, covered with pustules like dried mulberries or in suppuration. The affection is contagious, and communicates itself from one animal to another by contact.’

“Fromage, in the Dictionaire de Rozier, Article Phthisis, says: ‘Men of art are very much in accord that this malady is not contagious, but some stock owners think differently.’

“Huzard, who saw much of tuberculosis in the Parisian dairies in the concluding decade of the last century, said that most of the veterinarians looked upon the disease as contagious, and that some of the physicians believed the same of the phthisis of man.

“Dewar, speaking of his experience in Scotland in 1839, and succeeding years, in a particular herd, says: ‘The proprietor agreed to remove partition walls, and to make openings opposite one another in the outside walls, so that there might be a current of fresh air passing through. These alterations combined with cod liver oil, tonics and stimulants, may have prolonged life but yet no cure was effected, and that herd died out. I resorted to every precaution when new cattle were purchased to prevent infection; as I had an idea, even at that time, that the disease might be communicated from one to another when in immediate contact. The precautions adopted when fresh cattle were purchased had the desired effect, for in a few years afterward, they were as good a lot of cattle as any in the district. That herd left an impression on my mind that never can be effaced, and made me always dread the evil consequences of tuberculosis. Having practiced in the same locality, which is an extensive breeding and rearing district, I have seen several herds decimated. Though I have sometimes foretold the owner what he might expect, yet he did not believe me until so many were infected that the byres were infested with the fearful malady, and your remarks in regard to nose contamination are so true that I do not think it possible any can escape that are so exposed. I have also seen, as Grad has, the same stall infecting beast after beast until a thorough cleaning and disinfecting, with plenty of fresh air had removed all infection.’

“Spinola, writing in 1858, of bovine tuberculosis, gives contagion as a possible cause, and Lafosse, in 1867, says: ‘Physicians begin in imitation of Morgagni to believe in the contagion of phthisis. The facts published by Villemin appear to support this opinion, which has been held by our colleague, Dupont, of Bordeaux, for several years.’

“Cruzel in his work of date, 1868, is much more positive; he says: ‘This fœtid expired air, inhaled immediately by another cow upon a sound lung, gives the latter tuberculous infection. It is a matter of every day experience to the veterinarian. Two oxen or cows are kept in the same stable, take their food from a common rack or manger, lie in the same stall, and respire nose to nose. The one is, to all appearances, perfectly sound, the other is in as good a condition, and is vigorous, but it coughs from time to time, and its breath is foul. Soon we notice that the animal that does not cough, eats with less appetite, he loses flesh and soon he is unequivocally affected with the same malady as the first.’ The foregoing quotations show clearly that in spite of the misleading teachings of Broussais and others, the doctrine of contagion in tuberculosis could not be overcome, and that up to the time of the remarkable experiments of Villemin, in 1865, it maintained its hold upon the minds of extensive and careful observers. In animals, especially, the evidence was so frequent and clear, animal following animal in the same stall, and eating from the same infected manger, only to be infected in turn, and two animals stalled together, and licking the same manger with their prehensile tongues, transmitting the infection with certainty the one to the other, were facts that could not possibly be ignored. Other cattle in the same building might escape for a length of time, but the eating in common from the same fatal manger, by a tuberculous and a healthy animal, quickly sealed the fate of the latter.

“Physicians, too, who were compelled to investigate the causes of the extraordinary fatality from tuberculosis in the armies and navies, could not shut their eyes to the fact notwithstanding that they came to the task strongly prejudiced through education against the acceptance of contagion. Thus, Dr. Bryson, in his report to the Epidemiological Society, in 1860, on consumption in the several ships of the English navy on the Mediterranean station, says distinctly that the disease appeared to be propagated by contagion. Dr. Parkes, quoting this in his Practical Hygiene, says: ‘It may be inferred that pus cells were largely thrown off during coughing, and floating through the air, were received into the lungs of other persons. The production of phthisis in animals confirms this view. The case of monkeys in the zoological gardens, narrated by Dr. Arnot, is a striking instance. Cows in close stables frequently die of phthisis. But not only phthisis may reasonably be considered to have one of its modes of origin in the breathing of an atmosphere contaminated by respiration, but other lung diseases, bronchitis and pneumonia, appear also to be more common under such circumstances.’

Villemin in 1865, published his investigations in which he had produced tuberculosis in a great number of animals, by inserting particles of fresh tubercle or injecting the tuberculous sputa of man into the subcutaneous connective tissues, the peritoneum and the trachea. There resulted in nearly every case a chronic disease, the marked phenomena of which were caseated centers devolving from firm inflammatory nodules in the seat of inoculation, in the adjacent lymphatic glands, in the lungs, serous membrane, liver, spleen and kidneys. The centers of such nodules were at first transparent and grayish, but soon the center underwent necrobiosis, forming a soft cheesy mass the size of a pin’s head, and gradually enlarging to that of a pea, a bean, a hazel nut or larger. After a period of about 14 days the lymphatic gland nearest the seat of injection could be felt as a firm pea-like nodule, and in two weeks more a second gland on the line of the lymph circulation, had become enlarged and nodular, while the first, now the size of a large bean, had probably undergone distinct softening. This became adherent to the skin, burst and discharged continuously or at intervals with little or no tendency to heal. If killed at this date, the animal showed only the open sore and a chain of nodular pea-like caseated lymphatic glands leading up from it. The lungs might be apparently sound, but the spleen and liver usually showed miliary elevations on the surface, with clear grayish centers, as viewed under a magnifying glass, opaque patches were found on the omentum, and the lymphatic glands of the mesentery, of the portal fissures of the liver and of the Hilus of the spleen were distinctly enlarged and resistant. If not killed, the subject usually died 100 to 120 days after inoculation, and then the lungs were found studded with tubercles miliary or larger and more or less caseated; the bronchial mediastinal, subdorsal, pectoral, prepectoral, phrenic, mesenteric, hepatic, and splenic lymphatic glands were more or less enlarged and caseated, while the liver and spleen were enlarged and studded with multiple tubercles. Guinea pigs give the most extensive and intensive lesions, rabbits much less so, but in both emaciation and wasting are very marked. In short the lesions are essentially and unmistakably those of generalized tuberculosis.

“At first, however, incredulity prevailed and experiments on a large scale were inaugurated all over Europe and America to put the question to crucial test. Martin, Conheim, Burdon-Sanderson, Simon, Wilson, Fox, Lebert and Wyss, Fraënkel, Waldenbourg, and others inoculated with all sorts of non-tuberculous organic materials (bronchial mucus, foul pus, cancer juice, diseased liver, simple cotton setons, etc.) and from these in Guinea pigs there resulted local caseated foci, and implication of the adjacent lymphatic glands. It was found that the liquids from low types of pneumonia produced these apparently tubercular deposits, while that from acute sthenic pneumonia did not; that the cotton thread seton failed to produce the disease if it were first steeped in carbolic acid, and that the lesion caused by breaking a bone without injury to the skin failed to produce the characteristic lesions even in the very susceptible Guinea pig. It became evident, therefore, that the morbid results in these cases, were due to accidental inoculations with the poison of the tubercle, which is widely distributed, or with some pyæmic or other germs.

“Gradually the truth triumphed, and those who had at first been loudest in their opposition were led by their own experiments to become the firmest supporters of the new truth.

“As early as 1874, Gerlach had experimented largely in feeding the milk of tuberculous cows, and had infected calves, pigs, sheep and rabbits in this way. Chauveau in (1874), Klebs (1873), Semmer (1880) and Parrot (1870) fed calves, cats, Guinea pigs, pigs, sheep and a variety of other species of animals with tuberculous flesh or lungs, or saliva, producing tuberculosis in a large proportion of cases. In this manner they escaped the charge of the operation of a wound and of ærial bacteria, and yet succeeded in producing infection. The lesions in this case began in the intestinal mucous membranes and mesenteric glands.

“Another essay in the same direction was made by Tappeiner (1878), who infected rabbits, Guinea pigs and dogs, by enclosing them in boxes and compelling them to breathe tuberculous liquids intimately mixed with the air atomization. In these cases lesions began in the lungs and bronchial and mediastinal glands.[1]”

Footnote 1:

(From Report to the N. Y. Legislature, 1895. James Law.)

Bacteriology. The bacillus tuberculosis, the essential cause of tubercle, was demonstrated by Koch in 1882. It was at first supposed to be peculiar in its indisposition and tardiness to take a stain, and in its retention of the stain once imparted, even when it is treated with acids. Later observations have shown that these characteristics are common to certain other bacilli, notably to those of leprosy, smegma, and to specimens found in timothy hay and other grasses, cow dung, milk and butter. These furnish sources of fallacy in the milk and butter especially, but when the specimens examined are taken from the interior of a tubercle, lymph gland or serous cavity the danger of error may be practically ignored. What is quite as important is the fact that the tubercle bacillus is subject to evolutionary changes in adapting itself to a habitat in different genera of animals, and to a lesser extent in different parts of the same animal, by which its pathogenesis is modified, but these variations do not materially affect the staining qualities. Still more striking variations have been found in old cultures, ovoid forms (Metchinkoff), club-shaped microbes and filaments (Metchinkoff, Klein, etc.), branching filaments (Fischl, Coppen Jones), divergent club-shaped groups, like actinomyces (Babes and Levaditi). The last named, seen in inoculated rabbits, have been held to establish a relationship between the microbes of tuberculosis and actinomycosis, as the club-shaped cells do not take the usual Ziehl-Neelsen stain for tubercle bacilli, but the Birsch-Hirshfeld’s actinomyces stain. Apart from the rabbit such variations are not likely to prove sources of fallacy in identification of the microbe.

Morphology. As met with in the tubercle of man or ox the bacillus is a minute rod with rounded ends, 1.5 to 3.5μ long, by 0.2μ in thickness. In the ox it is shorter and thicker on an average than in man. They are usually solitary, but two and exceptionally even three or four elements may be united. In stained specimens unstained portions are frequently seen (spores?). When cultivated on blood serum there is a tendency to form elongated rope-like colonies having a waving outline. Other evolution forms have been already noted.

Staining. The resistance to staining is overcome by a heated alkaline watery solution of methylene blue (Koch), or better by a carbolated solution of fuchsin (Ziehl-Neelsen). To a 5 per cent. watery solution of carbolic acid add one tenth of its volume of saturated alcoholic solution of fuchsin. The suspected sputum or scraping from a section of a lesion is spread in a thin layer on a cover glass by drawing over it the straight edge of a second cover glass, dried in the air, and passed three times through an alcohol flame with the smeared side up. It may then be floated on the surface of the staining fluid with the specimen side down, then gently heated for three or four minutes almost to ebulition, drying being prevented by the addition of more of the carbol-fuchsin solution as required. It is then washed in water to remove excess of the staining fluid and treated with a bleaching acid solution (sulphuric acid 5 per cent. or nitric acid 15 per cent.) When decolorized it is well rinsed in two or more portions of a 60 or 70 per cent. alcohol and then in water. Next stain with a 1 or 2 per cent. aqueous solution of methylene blue for one minute and wash off the excess with water. The tubercle bacilli will appear of a deep red and other bacteria blue.

Gabbett’s counter-staining and decolorizing solution is especially useful in economizing time. After staining, as above directed, in the carbol-fuchsin solution for one minute, wash in water, then cover with a solution of 2 grams methylene blue (powder) in 100cc. of 10 per cent. sulphuric acid, until the film has a faintly bluish tint: then wash thoroughly in water and examine. Tubercle bacilli come out red, others blue.

In examination of tissues the microscopic sections are steeped for twenty-four hours in the carbol-fuchsin solution (or 1 hour at a temperature of 45° to 50° C.), then decolorized in a 5 per cent. sulphuric acid for a few seconds, then in a 70 per cent. alcohol: they are then counter-stained in an aqueous solution of methylene blue, washed in water dehydrated with absolute alcohol, cleared up in xyol or oil of cedar, and mounted in Canada balsam.

Biology. The bacillus tuberculosis is notorious for its variant forms, assumed in adapting itself to given environments, and which it retains with considerable tenacity for a time, even when placed in a new and different medium. It is largely held to be an obligatory parasite, and incapable of survival as a saprophyte, yet Straus, Nocard and others, have shown that the form obtained from the tuberculosis of birds can easily be made to live in suitable dead mixtures of organic matter. It is also notorious that the bacillus taken direct from the tubercle of the mammal, and which, as a rule, fails to grow at once in glycerined bouillon, yet, after a first successful culture in the new medium, often adapts itself completely, and thereafter it can in many cases be transferred from bouillon to bouillon, with as great certainty as it could formerly be inoculated from ox to ox. The difference is one of habit and adaptability, rather than any primary and permanent distinction of species. There is every reason to believe that the microbe has lived, and under given conditions can still be made to live as a saprophyte, with a greatly reduced adaptability to parasitic life in the animal, just as we see to-day that it is only with great difficulty transferred from certain genera of animals to certain other genera (from bird to ox and vice versa). Trudeau tells us of a culture of a bacillus tuberculosis from man, inoculated on the rabbit and then cultivated in vitro in successive generations for six years, that was in this way robbed of its pathogenesis for Guinea pigs, which, after inoculation, lived for many months, some two and a half years, and some even recovered. The average duration of life in the Guinea pig, after tuberculosis inoculation from man, rabbit, Guinea pig or recent culture is but seventeen days. The bacillus of human sputum often produces only localized tuberculosis in the ox. Even in the same species and individual the pathogenesis often varies materially. Nothing is more familiar than the slow progress of tuberculosis in the bones and lymph glands of man, on the one hand, and its frequently rapid progress in the lungs, liver and brain, on the other. As inoculated on the lower animals bacilli from the lungs of man are usually more virulent than those from the lymph glands (Creighton, Arloing, F. Craven Moore, Courmont and Denis). Among seven specimens of human sputum, the bacilli in six cases showed a fair average vitality, whereas those of the seventh failed to grow on blood serum of the dog (Theobald Smith). In both man and cow a large proportion of cases of tuberculosis remain localized, the disease lasting for years with little or no appreciable advancement, and not a few subjects appear to make a permanent recovery.

On every hand this evolutionary tendency of the bacillus tuberculosis places itself in evidence, demanding a recognition of the fact, that more or less transient or lasting variations in accordance with previous or existing environment, control to a large extent the transmissibility of the disease among different genera and even among individuals of the same genera and species, and also the fatal progress, or the mild and evanescent issue of the infection.

Even the most widely divergent of these evolutionary forms can often be made to approach each other and apparently merge into one type. Profiting by the example of Metchnikoff, Nocard enclosed in collodion capsules the bacilli of the human sputum and inserted the capsules into the peritoneal cavity of chickens which had proved refractory to their direct inoculation. This excluded the direct action of the leucocytes from the encapsuled bacilli, but allowed the endosmosis of the serum of the fowl for their nourishment. After a sojourn of four months or more they were transferred to other capsules and again enclosed in the peritoneum and after a second and third transference of this kind it was found that the bacillus had become actively pathogenic for the chicken, having acquired the infecting potencies of the bacillus of avian tuberculosis.

In keeping with the above is the fact that both rabbit and horse are easily infected by the bacillus obtained from birds, and that after a certain number of transmissions through the rabbit the issue of the bacilli of bird and mammal appear to become identical. No less instructive are the cases of the infection of carp by human sputa and the conveyance of tuberculosis to rabbits and Guinea pigs by inoculation with the nodules of the infected carp.

The vitality of bacillus tuberculosis is strong but variable. In sterilized water at 46° to 64° F. the human bacillus survived for fifty to seventy days (Chantemesse and Vidal), the bovine indefinitely (Galtier) and the avian bacillus at a higher temperature one hundred and seventeen days (Straus and DeBarry). In dried expectoration the bacillus of man still infects after nine or ten months (Koch, Schill, Fischer, De Thoma). In infected cow’s lung, dried and pulverized, it infected Guinea pigs at 102 days (Cadeac and Malet). In putrid matter it infected after 43 days (Schill, Fischer), 167 days (Cadeac and Malet), several years in a grave (Schottelius).

It is not destroyed by gastric juice (Fischer, Falk). The bacillus from tubercle of birds has a much greater vitality than that of mammals. Marfucci successfully seeded new media from a culture of two years old, and cultures in artificial media can be started more successfully.

Full sunlight renders sputum on a solid nonabsorbent surface noninfecting in several hours, varying according to the thickness of the layer (Koch, Straus). When sputum is mixed in soil it may survive until the 137th day (Feltz). On woolen cloth it may live five hours (Migneco).

Diffuse daylight, with shading from the sun, killed in seven days (Koch), to eighteen days (Lucibelli).

X-Rays do not arrest the growth of cultures (Blaikie, Pott, Ausset).

A dry temperature of 212° F. for an hour left some of the bacilli still infecting to Guinea pigs (Lartigan).

A moist heat of 140° F. for one hour sterilizes (De Man, Th. Smith, etc.). The scum formed on the milk may still prove infecting (Th. Smith). Half an hour of a moist temperature of 212° F. is sterilizing. Yet in the case of steaks, roasts and boiled meats the size of the piece often prevents the reaching of this temperature throughout, and it becomes unsafe to use any meat in which the redness of the juice shows, that the albumen has not all been fully coagulated (162° F.).

A freezing temperature, −16° to −26° F., does not devitalize the bacilli, even when alternated with thawing at intervals for several weeks (Galtier, Cadeac and Malet).

Heavy salting of meats has been thought to kill the bacillus in a month. After 15 days in salt the microbe failed to kill rabbits, but still killed the Guinea pig, whereas after 30 days it killed neither (Galtier). The fact that salted meats are always unequally impregnated in different parts, renders this extremely unreliable and more of a snare than a guide.

The action of chemical disinfectants varies not only with the agent but also with the medium in which the bacillus is found. In simple liquid media (bouillon) the following results were obtained:

Parts per 1000. Killed in. Carbolic Acid 50:1000 30″ (Yersin) „ „ 10:1000 1′ „ Alcohol (absolute) 1000:1000 5′ „ Ether 1000:1000 10′ „ Iodoform ether 10:1000 5′ „ Mercuric chloride 1:1000 10′ „ Salicylic acid 2.5:1000 6 hrs. „ Anilin water Saturated ———————— ——————— ———————— Thymol 3:1000 3 hrs. (Yersin) Formalin vapor 60:1000 40 hrs. (Murray) Sulphurous Acid (Sulphur 1 oz. to cubic metre) ————————— 14 hrs. (Vallin).

The following agents proved ineffective: Saturated aqueous solution of creosote, or of B-naphthol, of naphthalin, of potassium iodide, of potassium bromide:—bromine water, iodine water (1:500), iodoform solution or vapor, vapor of oil of turpentine.

ACCESSORY CAUSES OF TUBERCULOSIS IN ANIMALS.

While recognizing that in the absence of the tubercle bacillus there can be no tuberculosis yet we must not ignore the fact that many conditions of the animal system and its environment contribute largely to the propagation of the disease on the one hand, or to hinder its progress on the other. None of these conditions can call the germ into being de novo, but in its presence, they greatly favor its diffusion or even its malignancy. Like any other seed, this bacillus requires a suitable soil and favorable climate, to bring out its most destructive development. In striking the balance, we have to guard against the error of so many, who would attribute to the germ alone the deadly results and who assume that these should be the same under all conditions, and the opposite error no less prevalent, that ascribes the evil to the conditions, and holds that without these the germ would be harmless.

Hereditary Predisposition. Racial Vulnerability. Before the discovery of the specific bacillus, when as yet tuberculosis was held to result from a constitutional weakness, or cachexia in which deterioration of cells was held to be the main factor, the disease was held to be mainly hereditary, and its every day transmission in the line of descent, and the increasing mortality to extinction of given families were confidently appealed to in support of the doctrine. Now, however, we recognize that congenital tuberculosis in man or beast is very exceptional, and that the morbid process almost invariably takes its start from the germ implanted after birth. In Saxony when the tuberculous cows were 16.5 per cent. tuberculous calves were but .2 per cent., though the latter had been fattened on the milk of the former. In Munich but two calves were found tuberculous in 400,000 killed, and in Lyons but five in a similar number. Up to the present the number of calves recorded as tuberculous at birth does not exceed seventy.

That the young almost always contracted the disease, only after birth, virtually disposes of the alleged heredity of the tuberculosis but it by no means antagonizes the heredity of the racial vulnerability. As man, cattle, swine and Guinea pigs show a much greater vulnerability than the carnivora in general, so certain families in each of these genera show a more decided susceptibility to tuberculosis under similar conditions than do certain other families. This goes far to explain the appearance of tuberculosis, in certain lines of blood, and its advance to the extinction of the family, while under no better environment, other families can count on a practical immunity. In the Burden herd of Jerseys in 1877, I condemned eleven animals, verifying my diagnosis by necropsies, and found to my surprise that I had taken every representative, even the grades, of a given family, and left all the pure bred members of a second family untouched. Both families had mingled freely in the pastures and yards, yet the second family furnished no cases of tuberculosis then nor for many years afterward. The case is all the more striking that the non-tuberculous family gave the largest yield of milk and might have been expected to run down rather than the other on account of this drain.

Close Buildings. Lack of Ventilation. Air rendered impure by being breathed again and again, predisposes strongly to tuberculosis, and has been even looked upon as the sole cause (Macormac). Everywhere city dairy cows, kept in confined, close buildings, suffer severely (6 to 20 per cent. and upward); in Berlin 75 per cent. (Ostertag); in Denmark 61 per cent. (Bang), while in the same districts country cows are comparatively immune (often 1 to 2 per cent.), and steers raised in the open air still less (0.02 per cent. for our Plains cattle). For the slighter cases of tuberculosis in man and beast, life in a pure open air, day and night, in a genial climate, gives the best hope of improvement or recovery. In the Burden Jersey herd above referred to, animals condemned in spring as tuberculous, were turned out to pasture during the summer where they maintained an appearance of robust health, yet when returned to the barns in fall they fell off rapidly, so that some had to be helped to rise in the stall. “The stabled cow, the tame rabbit, the monkey, the caged lion, tiger or elephant are almost invariably cut off by scrofulous affection” (Aitken). It has long been noticed that sailors sleeping in close spaces (Bryson, Parkes), soldiers confined to close stone barracks even in the tropics (Parkes), suffer much more than the officers in more spacious rooms (Clark). Monks and nuns (two-thirds of the deaths, Leudet) occupying confined cells, and the inmates of prisons (four times the average outside, Baer) have shown an extraordinary prevalence of tuberculosis and attendant mortality. While this can be attributed mainly to the preservation and concentration of the bacillus in such places, a considerable allowance must be made for the impure and rebreathed air.

Dark, Foul, Damp Stables. Dark stables are usually close, dirty and damp as well, and all these conditions alike conduce to tuberculosis. Darkness hinders the development of organic coloring matter in living bodies, whether chlorophyll in plants or hæmoglobin in the blood of animals. Hæmoglobin is the main oxygen carrier in the blood, and in case of its deficiency the tissues are not properly ærated. The result is as if the inhaled air contained little oxygen, so that darkness further intensifies the evil of rebreathed, deoxygenated air. The extraordinary mortality from tubercle among prisoners, monks, nuns and miners serves to further accentuate this conclusion.

Trudeau’s experiment with rabbits is instructive in this connection. Of a number inoculated with the same number of tubercle bacilli, one half were kept in the open air and the rest in a dark, damp, underground place deprived of sunlight. When killed on the same day, it was found that the open air rabbits showed only slight lesions or none, while the underground lot had extensive tuberculosis.

The impure stable air lowers the vital tone of the animal, especially if the impurity has come from animal exhalations.

The same is true of damp air, “a damp ship is an unhealthy one,” and Bowditch and Buchanan pointed out the especial prevalence of tubercle in cold, damp, undrained, foggy localities. This does not hold for all damp lands, yet damp, fog, and cold are especially hurtful in presence of the germ.

INSUFFICIENT OR UNWHOLESOME FOOD.

Starvation and indigestible or innutritious food contribute to debility, and lessen the power of resistance. Hence in the poor, half starved denizens of city slums, and among neglected herds of cattle, tuberculosis, once introduced, makes rapid and extensive ravages. Conversely overfeeding often acts in the same way, developing indigestion and thereby robbing the tissues of their proper nourishment.

HEAVY MILKING.

In dairy cows, of milking breeds, the drain on the system is liable to prove too great, under a ration-for-milk, warm sloppy mashes of grains, bran, middlings, roots, distillery swill, exclusive diet of silage, saccharine roots, or marc, warm drinking water, a warm atmosphere, liberal salting, and enforced idleness in the stall, with careful stripping of the bag. The butter cows, (Jerseys, Guernseys, Alderneys, etc.) are especially liable to suffer, as the greater the yield the more the system is robbed of the adipose material which is so needful to a vigorous health. When the cow has been reduced to a high-pressure milk factory her physical size reduced to obviate the need of a large sustaining ration, and her milking capacity stimulated to the highest degree, the presence of the tubercle bacillus is especially dangerous.

CONFORMATION.

It was formerly held that cows with heads narrow between the horns, small thin necks, narrow chests defective also in depth and length, loose projecting shoulders and elbows, pendent, pot bellies, with hollow flanks, and a general laxity of the frame were especially predisposed to tubercle. In many such cases the suspected animal was already the victim of the affection, which had brought out these characteristic features of weakness and emaciation. In other cases the unthrifty appearance was due to poor feeding and care or to chronic disease, which in robbing the system of vigor and hardihood laid it open to the attack of the tubercle bacillus whenever it was introduced. Even when there was no such depressing influence affecting the individual, the inheritance of such a frame, betokened a constitution lacking in vigor, and with little power of resistance to the invading microbe. Some milking breeds which tend to the above conformation, show an unusual development of the lymph glands and plexuses, and as tuberculosis attacks the lymphatic system preëminently, the bacillus finds an especially favorable field for development in such systems. It would, however, be an error to assume that the compact, rounded frame, with circular chest and abdomen, and full, firm neck and shoulders, with a great disposition to fat and little to milk, is in any degree immune. Under the presence of the tubercle bacillus, and close stabling, they often succumb quite as rapidly as the most susceptible milking breeds. The meat producing breeds with a strong propensity to fatten, have an extraordinary development of lymph spaces and plexus in the intermuscular and subcutaneous connective tissue, and the microbe finds a welcome home in their sluggish, inactive and atonic systems as well as in the typical dairy cows.

BREEDING TOO YOUNG.

Breeding from immature animals undermines the vitality as the system is overtaxed to sustain at once the demands for further growth, for the nourishment of the unborn offspring, and for the yield of milk. Some families of Jerseys have been undoubtedly injured in this way, through the desire to diminish the size of the cow, and yet retain the highest milk and butter yield.

CLOSE BREEDING.

Inbred families are proverbially subject to tuberculosis. By pairing individuals that show in a marked degree the desired qualities of early maturity, heavy milking, or fattening, the greatest stimulus is given to the enhancement of such qualities, and with this there is the correspondingly ready receptiveness to the tubercle bacillus. To this is added a degree of constitutional delicacy which comes from too close breeding, and which otherwise shows itself in an encreasing infertility, when bred with an animal that is nearly related. In addition, the high bred animal is kept much indoors, where the bacillus, once introduced, is easily preserved and propagated, and is denied the free outdoor life and exercise which might develop muscle and vigor. This is no valid argument for introducing inferior blood to the deterioration of the economic value of a race, but rather for the complete exclusion of the bacillus which may find in our treasured herd an especially inviting field for its ravages.

AGE.

In both man and beast, age appears to have a predisposing effect, but apart from debility or trauma, this may be fully explained on the ground of often repeated infection, an indoor life, and, in dairy cows, the excessive drain upon the system. In thoroughbred herds of cattle, in which the cows are preserved as long as they will breed, and in dairies where they are kept as long as the milk yield is satisfactory, the oldest show by far the largest percentage tuberculous. In secluded individual dairies we have found 100 per cent. affected, Ostertag gives the average for Berlin at 75 per cent., and Bang for Denmark at 69 per cent.

PREDISPONENT DISEASES.

As already noted all diseases which undermine the health tend to diminish the powers of resistance to the tubercle bacillus. To be especially dreaded, are long standing diseases which produce emaciation and debility, fevers that for a length of time impair sanguification, metabolism and nutrition, diseases of the digestive organs which cut off the requisite supply of nutritive material, and, above all, diseases of the lungs and air passages that impair the tone of the tissues and invite the attack of the invading microbe. Bronchitis, laryngitis, pharyngitis and tonsilitis in all their varied forms are to be particularly noted. Even in man it is believed that one of the most common channels of infection entrance is through the open tonsillar crypts, and the same doubtless is true of animals. Pigs, with their large tonsils and frequent infection through feeding, are probable examples of this, and when, in addition to the detention of the microbe in the cavities, there is an inflammation and debility of the tissues, the opportunity for infection is greatly enhanced.

ENCREASED TRAFFIC IN (TUBERCULOUS) ANIMALS. DAIRY EXTENSION.

In common with all infectious diseases, tuberculosis owes its great extensions to the sale and purchase of animals. Where an indigenous race of cattle is raised and sold, without any additions from without, tuberculosis is usually rare and confined to the one herd, or to those having intimate intercommunication with it. Where, on the other hand, a large stock is kept up, as in milk dairies, and few or no calves are raised, but the bulk of the cows are sold off yearly and replaced by new purchases, tuberculosis, sooner or later, finds admittance through the body of an infected animal, and once implanted in the herd, it goes on encreasing, without limitation, except by the sale or death of the more seriously affected. The larger the herd and the greater the number of yearly changes, the greater the number of opportunities for the introduction of an infecting animal. Where a great part of the herd is turned off yearly, and the new animals are drawn from any or every source indiscriminately, it would border on the miraculous if such a herd were to remain free from the infection for any great length of time. The recent extension of tuberculosis in herds has been coincident with the great development of commerce in live stock, and the rapid transit on land and water by steam. Before the days of the steam engine, animal plagues advanced slowly and uncertainly, excepting in the presence of a great European war, which drew animals from all available sources, congregating them in large mutually infecting droves in commisariat parks, and marching them in the wake of the army for its daily supply. Inevitably every country invaded was infected, and the plagues spread from the line of march in all directions. The more deadly plagues, like rinderpest and lung plague, were the first to appear, and in this lay a certain measure of palliation of the evil, as the exposed and often weaker animals were killed off, so that the slower contagion like that of tuberculosis had not time to develop. This mitigating influence held good so long as the deadly plagues were not placed under effective control. When, however, a nation successfully extirpated and excluded lung plague and rinderpest, the way was opened for a freer extension of tardily developing plagues like tuberculosis. The great development of beet sugar factories and the accumulation of herds to consume the marc; the extraordinary extension of manufactures which have made England and certain countries of Western Europe consuming rather than agricultural lands, and the wonderful modern expansion of dairy husbandry have combined to encrease and concentrate the cattle industry in ratio with the manufacturing and commercial progress of the nations, and as the live stock are kept under a milk-stimulating regimen and a life passed largely indoors, the way has been open for an ever-advancing encrease of tuberculosis. In the United States the centralization of population in the Eastern States and in all great centres of industry and the concentration of cows for the milk supply, and in certain districts in connection with butter and cheese factories, have contributed to wide local extensions of consumption. Hence it has been no uncommon thing to find herds in the vicinity of cities with 20 to 100 per cent. affected, in striking contrast with the 0.02 per cent. found in the fat cattle from the plains.

The modern railway traffic brings to all these swarming centres of animal industry, live cattle from long distances to supply the constant depletion through deaths and the disposal of dry cows, and thus the whole Atlantic slope is drawn upon to fill the eastern stalls. Infected animals thus shipped from Ohio, Indiana, Illinois, Wisconsin and Michigan for the good of the herds in those states find new homes in New York, or New England, where they have four to twelve mouths to propagate the infection before they are themselves disposed of. As in the days of the lung plague in America, the eastward trend of bovine traffic, becomes to a certain extent a protection and benefit to the herds of the west, but in equal ratio it operates to the detriment of our eastern stock. What is true of the planting of new centres of infection in the busy dairy districts of the east, and of the steady increase of disease in already infected herds, through the constant addition of new cases purchased, is no less true of the corresponding districts devoted to dairying interests in the west. It is the natural order of things, that, everywhere, the new accessions of infection, coming in the lines of trade, into large dairy herds, kept to a great extent indoors for months at a time, must hasten the general infection of such herds. When, therefore, no intelligent measures are interposed to check the evil, we must expect that the marked increase in the prevalence of tuberculosis, which we have witnessed of late years, shall become more and more evident year by year. Journals have claimed credit for befriending the stockman, in opposing all control of the cattle traffic, dealers have denounced all control as ruinously oppressive and injurious, and legislators have turned a deaf ear to the warnings of science and experience, but time, in this as in all other plagues, will justify the demand for an intelligent control, and the increasing losses will one day open the eyes of the stockowners to the fact that their truest friends are those that would exclude the baneful seed, and kill it ere it has had time to germinate and bring forth its ever increasing harvests.

In the absence of any systematic and efficient government protection in this line, the stock owner can only protect his sound herd by the rigid exclusion of all animals that are not of his own breeding, or in case of purchase, by an exhaustive inquiry as to the occurrence of sickness or deaths in the herd from which he buys, and by the professional examination and test of every animal to be bought. Even then he must promptly separate, test, and, if necessary destroy any animal that proves unthrifty, or which by cough, diarrhœa, wheezing or other sign gives evidence of probable tuberculosis.

Unregulated Traffic in Tuberculous Animals from Other States. The danger of buying animals untested is in no degree lessened when they are sent in from other states. While some make a business of supplying the store market with what they believe to be good stock, there is always the temptation to turn off animals that are unthrifty or poor milkers and which have proved less profitable than the others. Some even have the herd tested and sell off those that show evidence of tuberculosis. Unless, therefore, it is held in check by the tuberculin test, the traffic is made to the extent of such sales a direct means of disseminating tuberculosis.

ASSORTING THE TUBERCULOUS ANIMALS FOR SALE IN A GIVEN STATE.

A still more injurious result comes from the order of given States, that the admission of store cattle shall be guarded by the tuberculin test of each animal, and the supineness or worse, of adjacent states in establishing no effective safe guard against the disposal of the tuberculous culls in the unprotected State. Cattle from the west or elsewhere in the United States, arrive in a great public market as, for example, New York, they are here tested, those that stand the test are shipped into one of the States requiring the test (Massachusetts, Pennsylvania, New Jersey, Canada), and those that have shown the reaction of tuberculosis are sold into the herds of the State in which they were tested. The most malicious enemy of the New York stock owners, could not devise a surer means of stocking the herds of the State with tuberculosis than this atrocious system. Yet when the present writer had a bill introduced into the legislature to correct the evil the opposing interest proved strong enough to prevent it from coming to a vote. The legislative committee on tuberculosis which sat later, and upon whose attention the subject was pressed, also practically ignored it and the statute which this commission inspired leaves the matter as bad as before. Under the present law the New York purchaser must secure his own interests by having every animal he buys tested by a trustworthy veterinarian.

Sale of Sound Animals Concentrates the Tuberculosis. The action of one or more States in admitting store cattle only after a tuberculin test, acts directly in encreasing the relative number of tuberculous animals in adjacent States. The purchaser from Pennsylvania for instance, goes into a New York herd and purchases all the best animals on the condition that they pass the tuberculin test uncondemned. It follows that the New York herd is left with the tuberculous cattle only, and those that, aside from tuberculosis, are of low value or profitless to keep. Further as the advance of tuberculosis is proportionate to the relative number of tuberculous subjects in the herd or building, and the concentration of the poison, the depreciated herd is almost certain to become rapidly and generally affected by the disease.

The Denial of Indemnity for Tuberculous Animals Killed. Several American States (and notoriously New York in the recently enacted statute) forbid compensation to the owner for any animal killed because it is affected with a contagious disease, and to prevent the extension of such contagion. All history attests, and any consideration of human nature might teach, that such a measure is only calculated to spread the infection. The owner of an animal, affected with a contagious disease, who can get little salvage by turning it into beef, and none at all if he hands it over to the State for slaughter, will naturally think of putting it on the market, where he can secure a good price. How much more is he tempted to do this when the disease is an occult one, and the animal shows the outward appearance of health, as is the case in nine-tenths of many tuberculous herds! Crime cannot be fixed on the seller, for he is not an expert, and cannot be expected to diagnose the disease. If the infected cow is of little value for the dairy, she is passed on, from hand to hand, leaving infection in every herd she has entered. The ultimate owner (in whose hands the State finds her and diagnoses her disease), though he may have bought her in good faith as a sound animal and paid a correspondingly high market price, is made to lose the whole value of the cow. The real offender who knew her to be a tuberculous animal, and sold her in consequence at the price of a sound cow is shrewd enough to keep himself out of the clutches of the law, while the honest purchaser who has been already swindled, has his income and property cut off without compensation. Such a law is self-evidently unjust; it plays into the hands of the swindler at the expense of the just man; with the object of protecting the community against infection, it refuses to call on the public for any contribution toward its own protection. The system is a direct bid for extensive and encreasing violation of the law and diffusion of the infection and must be accorded a prominent place in the list of causes. It would be surprising to find that any country ever extirpated an animal plague by working on such a system. As a matter of fact no country ever did; all such sanitary successes from the extinction of sheeppox or rinderpest in Western Europe, to the recent stamping out of lung plague in the United States, were based on a just compensation to the owners of the stock. When, therefore, veterinary sanitary principles and experience have been so far ignored as to allow the passage of a law, which at once favors the diffusion of infection by the crafty sale of the infected, the expatriation of the healthy animals from the home herds, leaving only the diseased, and finally the selection from herds in transit of the tuberculous ones to be scattered widely among the herds of the State, we must not wonder at the continuance or encrease of tuberculosis in the commonwealth. Until a more rational and common sense legislation can be secured, the unfortunate stock owner must defend himself by the expensive alternative of testing every animal he buys.

Private Testing of Herds and Sale of the Tuberculous. A most reprehensible practice is the private testing of herds and the sale as store animals of those that react. In this way a herd may be cleared of infection, but at tenfold expense to the public at large, as every animal sold may convey the infection into a separate herd. It is, however, a natural outcome of the unwise system of refusing indemnity for the infected.

Habituating to Tuberculin Testing and then Selling under Test. Many (not all) cattle, when injected with tuberculin repeatedly at short intervals, acquire a tolerance of the agent and fail to react as at the first test. We have in such cases examined the animals post mortem and found active tuberculosis. Unscrupulous owners, aware of the fact, have their diseased cattle injected repeatedly every few weeks, and as soon as they fail to respond, sell them under the guarantee of the tuberculin test. The cattle, of course, carry the infection into other herds. This swindle could be obviated if it could be made a misdemeanor to have or use tuberculin except as a State or Federal official acting for the government. This would imply the corollary that the State should test the herds when called upon.

Antipyretics During Tuberculin Test. Another method of undoing the tuberculin test is to feed large doses of antithermic agents to depress the temperature at the time the rise from tuberculin would take place. Tuberculous cattle may thus be sold as sound animals, with a certificate of having successfully passed the tuberculin test, the operator having given such certificate in perfect good faith. It suggests the importance of withholding tuberculin from public use, or of securing an absolute control of the feeding and watering of the animals during the test.

False Certificates of Tuberculin Tests. Stock owners have reported to the writer alleged tuberculin tests of their herds which were completed in three hours, and others have named instances of marking animals for shipment and giving certificates of testing where no tuberculin had been used and no examination beyond the most cursory glance had been made. This might be expected of some non-graduates, registered on a basis of alleged practice, shamefully ignorant of veterinary medicine and conscious of their false position, and some educated veterinarians thus placed at a disadvantage may have been tempted to follow suit, but it can only end in personal disgrace and an inevitable extension of tuberculosis. Begotten in a legislative wrong and nourished by moral weakness, it can only grow into greater evil. Unfortunately such unworthy actions throw discredit on the very name of sanitary police. To avoid the evil every one aspiring to the responsible work of testing cattle should be thoroughly examined as to fitness and licensed to practice under a heavy penalty for neglect or malpractice.

Feeding Hogs on Fresh Offal from Abattoirs. It has been a common practice, especially in country districts, to turn the raw offal of slaughterhouses to pigs, and as the tubercle is usually concentrated in internal organs, the hogs become infected in large numbers. In public institutions which slaughtered their own meat I have found the hogs all but universally tuberculous. The danger is only slightly lessened when the hogs are fed raw butcher and kitchen scraps in swill. It suggests the compulsory boiling of all swill or garbage containing raw meat.

Feeding Calves and Hogs on infected Milk. Though it has been repeatedly shown that the majority of moderately tuberculous cows do not yield infected milk, yet in every tuberculous herd, at irregular intervals, one or more are attacked with tuberculosis of the mammæ, and the drinkers of the milk take in the tubercle bacilli. This will happen in the most strictly supervised tuberculous herds, while in those that are less carefully managed, the milk that is considered unfit for human consumption is fed to pigs or calves. In one dairy, I found that the calves, all fed in this way afterward reacted under the tuberculin test, while the following year the crop of calves, though fed on the milk of the same diseased cows, with this difference that the milk had been first heated to 180° F., without exception grew up healthy, and not one reacted under the tuberculin test.

Feeding hogs after Tuberculous Cattle. Where cattle and hogs are kept on the same place, it is a common practice to let the swine clean up all food left by the satiated cattle. If there are tuberculous cattle, affected either in the air passages or alimentary tract, the pigs become infected by taking in the expectoration by which the food is soiled, or by rooting around where the cow manure has fallen.

Feeding from a Common Trough. In an infected herd, a common cause of extension is found in the use by the whole herd of a common feeding trough, in which the food soiled by virulent discharges, is taken by healthy animals. The habit of tying a cow in different stalls in succession as she happens to strike one, in place of keeping each cow by its own stall is a fruitful source of infection. Even when each cow is kept by its own stall, she often becomes infected by reaching into the feeding trough in front of the next cow on the left or right and taking in soiled and infected fodder. In swill stables the evil reaches its maximum, as the feeding trough for 50 or 60 animals is slightly inclined so that the liquid food runs from the supply end to the other, and infecting expectorations are carried in front of all in turn.

Dry, Dusty Stables. Tubercle bacilli are not carried out on the expired air, unless there is forced expulsion as in coughing, snorting or sniffing. In such cases the solid particles are thrown off in masses or fine spray and lodged on surrounding objects. These, together with infecting discharges from bowels, urinary or generative organs, open sores, etc., dry up, and rise on the dust, and, as sterilization occurs slowly indoors, they cause more or less infection of the animal inmates. Cornet, Tappenier and others have thoroughly established this as a common form of transmission, and shown the great importance of cleanliness, disinfection and the removal of infecting materials without raising dust. In an establishment in Paris, a consumptive had served for 3 years. In the following 10 years, 15 of the 20 employés died of phthisis.

Extension through Vermin. As rats and mice (and other rodents) are susceptible to tuberculosis by ingestion (Galtier) it follows that they may become the media for extension of the infection through fodder in which their droppings are scattered, or from their feeding in the same troughs as the cattle or swine. For swine in particular the danger is greater because of their carnivorous habits; the rat acquires tuberculosis through eating the offal of the abattoir, or the scraps of the butcher’s stall, or kitchen, and the sick rat is thereafter easily caught and devoured by the pig to its own undoing. To block this channel of infection the destruction of vermin about slaughter houses, stables and pig pens is a most important consideration.

Flies and Other Insects as Carriers of Tuberculosis. These congregating on tubercular sores, around the nares or lips, on the skin contaminated by the virulent bowel discharges, on dishes holding infecting milk, on objects soiled by infecting discharges, on diseased carcasses at abattoirs, rendering works and elsewhere, (Spillman, Hoffmann, Lartigan, etc.,) and on graves where the earth worms have brought the bacillus to the surface, (Lortet, etc.) become more or less active agents in disseminating the virus. In this way food and water are contaminated, and exceptionally, infection may even be implanted on sores. As the excreta of the flies contain the virulent bacilli, the latter are deposited on windows, walls, furniture, etc., and may be later disseminated in the dust of the apartment.

Dewevre found tubercle bacilli in the bedbugs infesting a bed in which successive cases of consumption had developed, showing that other parasitic or rapacious insects besides flies must be looked on as possible propagators of the bacilli. There is reason to suspect, lice, fleas, ticks and acari especially. The same is true of leeches and other rapacious invertebrates.

LESIONS. THE TUBERCLE.

The characteristic lesion in tuberculosis is the tubercle, taking its name from the small rounded nodule which, at first virtually invisible, encreases often to the size of a millet seed, or a pinhead or even larger, and which by confluence with others, forms conglomerate masses of all sizes to which the term tubercle is still applied. Where the bacillus tuberculosis is implanted, the fixed tissue cells are stimulated to an undue proliferation, and a diapedesis of leucocytes takes place from the neighboring capillary blood vessels, the whole eventuating in the formation of a rounded cluster or nest of epithelioid and giant and later small rounded lymphoid cells in a fine fibrous stroma. Baumgarten and his followers claim that the larger epithelioid and giant cells result from the karyokinesis and proliferation of the fixed tissue cells, epithelial and endothelial cells, and that the lymphoid cells which later (often after the eighth day in experimental cases) invade the lesions, are alone the product of the migrating leucocytes. Metchnikoff, Yersin and others contend, on the other hand, that epithelioid and giant cells are directly derived from the leucocytes and endothelial cells and like these are possessed of actively phagocytic qualities. As the final outcome before caseous degeneration, is the great predominance of the small lymphoid cell, it may well be questioned whether this is not the result of active encrease in both kinds of cells, as appears to happen in many other inflammations. For our present purpose it is well to note the early characters: Centrally often a large (giant) cell with a number of peripheral nuclei and at times, branching processes; around this as a second zone epithelioid cells of large size, with round or oval nuclei, and sometimes giant cells; outside this a third zone of small rounded lymphoid cells with large nuclei. There is a delicate fibrous network between the cells, but no indication of capillary blood vessels, the absence of which may partly explain the constant tendency to degeneration, necrosis, and caseation. The tissue around the miliary tubercle is red and congested.

Caseation. A striking characteristic of tubercle is the occurrence of coagulation necrosis, beginning in the centre of the specific nodule as a whitish or pale softening and degeneration of the cell elements and gradually extending toward the circumference. The cells, and even the proximate tissue elements, die and disintegrate passing into a structureless, granular or hyaline debris, which has been named from its supposed resemblance to old, ripe, soft cheese. Baumgarten has observed that the small lymphoid cells are the first to degenerate, followed by the epithelioid and giant ones.

While the formation of tubercle is at first a productive inflammation of which the cell clusters and nodules are the result, yet the tendency to necrosis, and caseation is so great that it must be looked upon as one of its most prominent features, and is rarely absent, whether the lesion exists in the connective tissue of the lungs, liver or other organ, in the lymph glands, in the respiratory or intestinal mucosa or submucosa, in the osseous cancelli, brain or skin. It is, therefore, largely pathognomonic, yet it is not peculiar to tubercle, being common in glanders, and other infective inflammations. Its presence should always lead to a search for the primary tubercle nodule, with its nonvascular cluster of lymphoid and giant cells and above all for the specific bacillus resistant to staining.

The tendency to extensive degeneration and caseation is especially marked in swine, in which the resulting debris is often so liquid that the tubercles bear a strong resemblance to abscesses.

Calcification. The deposition of lime salts (mainly phosphates) in the tubercle is a common feature of advanced cases in man and pig, but especially in cattle. It is unknown in rabbits and Guinea pigs. The tubercle assumes a hard cretaceous aspect and feeling, grates under the knife and crepitates when pressed. This is always an evidence of chronicity, but it has been observed in swine in 3½ months.

Fibroid Degeneration. Fibrosis. In this case a productive fibroid inflammation takes place in the tissue of the tubercle, and it is resolved more or less extensively into a hard, white, resistant body. This is the pearly mass which has given rise to the name of the pearl disease (perl-zucht) in Germany. It may be fibrous throughout, but usually a number of the nodules show a caseated centre while the external zone, that nearest to healthy tissue, has alone taken on the conservative fibroid development. Like cretifaction, fibrosis is an indication of chronicity in the lesion. It is often seen in man, but still more so in cattle, in which it affects particularly the abdominal cavity, but also to a lesser extent the chest and other parts. It is remarkable for the paucity of bacilli to be found in its substance, often requiring many sections and infinite patience to reveal the presence of the microbe. This comparative lack of actively multiplying bacilli is doubtless one factor, operating in the direction of conservative processes, chronicity and even partial recovery. In experimental tuberculosis the extent and rapidity of development of tubercle, as also of the degeneration are found to be closely allied to the number of bacilli introduced.

Cattle: Pulmonary Tuberculosis. One of the most frequent seats of tuberculosis, the lung, may in acute cases show a diffuse miliary tuberculosis, a considerable part of a lobe or of several lobes being congested, infiltrated, and filled with small individual tubercles, grayish or transparent in the midst of the general redness. A second form, often of old standing, is in the shape of hard masses, often circumscribed or isolated, and easily felt when the soft lung tissue is manipulated. They are respectively formed by the local aggregation, and confluence of the small miliary nodules and may vary in size from a pea to a mass of ten or twelve inches in diameter. On section the miliary tubercle may not yet show central caseation, but the larger ones do so as a rule. The caseated nucleus may be soft, cheesy and somewhat homogeneous; it may be dry, granular and yellow, resembling damp farina of maize; it may be calcified in its outer portion and invested by a firm fibrous envelope. The tubercle may be the seat of general fibroid degeneration, constituting the pearl nodules (perl-knoten) dense as cartilage and either with or without a soft caseated centre; it may show an agglomeration of nodules in all stages from the early congested nodule to advanced caseation or cretefaction, the whole embedded in a solid congested and infiltrated tissue, largely fibroid. There may be extensive abscesses, the seats of complex infections, having thick uneven walls, often showing grape like tuberculous outgrowths, and containing thick, caseopurulent, viscous, granular, yellowish or greenish and comparatively odorless contents; in other cases the abscesses have burst into the bronchia, leaving vomicæ and with the new resultant infections the contents have acquired an offensive putrid odor; finally, there may be extensive inflammatory infiltrations, affecting lobules or lobes, and interspersed with tubercles in the form of the early grayish or transparent nodule, or even more advanced caseous or cretaceous centres. These latter serve to distinguish the condition from broncho-pneumonia, the grayish centres of which might suggest miliary tubercle. The broncho-pneumonia, however, has the whitish centres confined to the bronchioles and their terminal air sacs, and represent their thickened walls and muco-fibrinous contents; they do not show the same tendency to caseation, nor necrosis of the tissue, nor to caseation of the dependent lymph glands, and, above all, they do not contain the bacillus tuberculosis.

A noticeable feature in the tuberculous lung is the great frequency of tubercles of all different ages from the initial transparent nodule to the caseated or calcified mass side by side. A tuberculous bronchitis is a familiar accompaniment, with lines of miliary tubercles, ulcers and a flocculent (sometimes gritty) muco-purulent discharge, containing elements of the necrotic tissue and bacilli. Emphysema and interlobular œdema are also met with.

The Pleuræ often suffer by continuity of tissue from the diseased lung, but they may be affected primarily through infection of the circulating blood. The earliest pleural lesions may be congestion, exudation and the formation of false membranes in fringes, but soon these become the seats of minute nodules or forming tubercles which steadily encrease to form pale red cauliflower-like growths—which have been spoken of as grapes, from their supposed resemblance to bunches of that fruit. Extensive areas of the mediastinal, costal or pulmonic pleuræ are often completely covered by these productions. Dense, and thick adhesions sometimes form, holding in their substance characteristic tubercles.

The bronchial and mediastinal lymph glands receiving as they do the afferent trunks from the lungs and the great lymph sac of the pleura, offer in their sluggish currents the most favorable culture vessels, and almost always become affected in consequence. Not unfrequently they are found to be tuberculous when the tissues which they drain appear to be sound, and we must therefore, conclude that the primary slight lesions in the latter have recovered, or that the bacilli have passed through the tissues and lymph channels without establishing any centre of disease. The glandular lesions are primarily congestion and redness, with more or less infiltration and swelling, followed by a nodular induration, with enlargement or exceptionally shrinking. When bisected they may show all stages of the tubercle from the miliary granule to the caseous, dry, yellow, granular or cretaceous necrosis. By aggregation these often grow to a large size, a long diameter of 6 to 12 inches being not uncommon.

Pericardial and Cardiac Lesions. The pericardium may be implicated from the pleuræ or independently, and though tuberculosis of the heart is rare, it may be the seat of primary tuberculosis or of extension from the pericardium or endocardium. In the N. Y. State Veterinary College Museum is a cow’s heart, greatly enlarged, and completely invested and invaded by tubercle several inches thick.

Tuberculosis of the Mouth and Throat. Tubercles sometimes form in the tongue causing nodular swelling, with a caseated centre. Much more frequently they attack the pharynx or larynx with the formation of nodular necrotic swellings, followed by ulcers and the implication of the adjacent lymph glands. The glands are liable to be invaded through the tonsillar and other follicles of the faucial and pharyngeal regions, which like the solitary and agminated glands of the intestines form excellent culture vessels. The glands most frequently attacked are the retro-pharyngeal, but the lateral pharyngeal, the intra-parotidean and submaxillary lymph glands occasionally suffer. They often become indurated, yet the formation of abscess-like sacs is not uncommon especially in the retro-pharyngeal.

Gastro-Intestinal, Peritoneal and Mesenteric Tubercles. Tubercles of the interior of the stomachs are rare, though they are frequent on the peritoneal surface of the first three stomachs, as rounded, subserous nodules varying in size from a pea upward. The mucosa of the small and large intestines may suffer, by preference in the seats of the solitary or agminated glands, and the resulting ulcers may extend in the lines of the lymph vessels from the convex to the attached border of the gut. The small greenish caseated and calcified nodules on the intestines, which are so often mistaken for tubercles, are the degenerated cysts of the œsophagastoma. Tuberculosis of the mesenteric lymph glands is much more common, the successive stages being essentially like that seen in the bronchial glands. Beside these the surface of the mesentery, omentum and abdominal parietes often becomes the seat of congestion, exudation and cauliflower-like neoplasms or grapes, as already stated of the pleuræ. In a certain number caseation or cretefaction may be detected.

Liver Tuberculosis. The liver is greatly exposed to tuberculosis as the single destination of all the blood from the gastro-intestinal tract. Tubercles also form on its surface by direct infection from the peritoneum. The hepatic tubercles are often very large and numerous, adding greatly to the bulk and weight of the viscus. There is usually coincident tuberculosis of the lymph glands of the porta.

Tubercle of the Spleen. This is also a favorite seat of the morbid process, exposed as it is to the reflux of infected blood in the portal vein, and to access of the bacillus from the peritoneum and omental lymphatics.

The pancreas is less exposed to the channels of the circulation and is less frequently affected.

Genito-Urinary Tubercles. The kidneys are always liable to suffer in generalized tuberculosis, in accordance with their function of elimination and the great quantity of blood that passes through them. The tubercles may be numerous, encroaching upon and destroying the glandular tissue, and determining congestion, nephritis and hæmorrhage (Schütz). The ovaries, when tuberculous, lead to nymphomania and sterility; they become swollen, with rounded projections, indurated, and on section show all stages of infiltration, caseation and calcification. They may encrease to a great size. Tubercles are found on the Fallopian tubes, the serous and mucous surfaces of the womb, and in the broad ligaments, in all their characteristic forms. The bladder and vagina are less frequently involved. In the male the testicle, epididymus, tunica vaginalis and prostate vesicles are sometimes affected. The swelling and induration of the affected organ, or the existence of hydrocele, may be noted.

Tubercle of the Udder. From the mass of blood passed through the udder it is specially exposed to infection whenever the bacilli enter the circulation. It may also be directly infected by the entrance through the teat, or a trauma, of the bacillus of the stable dust. There may be for a time only a slight general swelling which leads to no suspicion on the part of the milker, and as the secretion is not arrested, a dangerous product may be distributed. At this stage the lobules on section appear swollen, gray, with paler or yellowish points and minute hæmorrhages. The milk ducts contain coagula and bacilli (Bang). In other cases, usually more advanced, the gland is hard, nodular, enlarged, and shows a marked thickening of the walls of the smaller milk ducts and secreting follicles, with yellowish and even caseous and calcified centres. The gland is often greatly enlarged, the milk suppressed or completely altered, and tubercular neoplasms or ulcers exist in the larger ducts.

Tuberculosis of the Brain and Spinal Cord. As noted in Volume III. this occurs in young cattle especially in the form of tubercles of all ages attached to the pia or arachnoid, on the brain, or cerebellum, or in the ventricles, also in the cerebral matter, in or on the lumbar enlargement of the cord or on its pia. Several cases have come under my notice in the mature cow.

Tuberculosis of the Eye. This has been seen mainly as a result of experimental inoculation, yet casual cases also occur in the cornea, sclerotic, iris or choroid, the product undergoing early necrosis and softening into a yellow mass filling the different chambers.

Tuberculosis of the Bones. Though less frequent than that of internal organs this is not rare. It usually attacks the spongy tissue, near the articular extremities, or the vascular line between epiphysis and diaphysis, giving rise to considerable exudate, thickening of the bone and arthritis. The vertebræ, ribs, sternum, petrous temporal, frontal and occipital also suffer. Sections of the bone show dilatations of the cancelli, filled with the characteristic nonvascular groups of giant, epithelioid and lymphoid cells with, at times, softened and caseated centres. The adjacent bone is congested and softened, so that the detachment of epiphysis and apophyses is not uncommon. In case of invasion of the joints the cartilages and ligaments are the seat of tubercular deposits, softening, fibroid change and caseation, and there is general synovitis. The cartilages of the ear (concha) and nose (septum) may also be invaded.

Tubercles of the Skin. These are not very uncommon in cattle being the counterpart of the tuberculous warts and ulcers of the hands of butchers, tanners and others that handle the products of diseased animals. They may show as little pea-like nodules in the substance of the skin, or immediately beneath, very commonly on the side of the abdomen, where their presence in life furnishes a useful suggestion, as enlarged masses forming raw, warty projections with centres of caseation, or as clusters of warty-like growths of this kind (grapes).

Tuberculosis of the Muscles. This is comparatively rare in cattle, though by no means unknown, appearing as tubercles of the size of a pea and upward, in or between the muscular masses, often showing a caseated centre.

Tubercle of Lymph Glands. No organs in the body suffer more than the lymph glands as they receive through their afferent trunks and develop the bacilli coming from any adjacent tissue to which they are subsidiary. There is also evidence to show that bacilli entering from the lungs or bowels may pass through these without apparent effect to develop in the connected lymph glands. The frequent infection of the pharyngeal, bronchial, mediastinal and mesenteric lymph glands has been already sufficiently noticed, and if the other groups suffer less it is mainly because the tissues from which they derive their lymph are less frequently infected. An intimate knowledge of the different groups of lymph glands is a most essential prerequisite to the diagnosis of tuberculosis in life, and no less to a satisfactory post mortem examination. The order of relative susceptibility and importance is somewhat as follows: Bronchial, mediastinal, mesenteric, hepatic, sublumbar, mammary inguinal, subdorsal, phrenic, intercostal (especially the first and second), pharyngeal, parotid, submaxillary, prescapular, prefemoral (stifle), prepectoral, axillary, cubital and popliteal.

Relative Frequency of Tubercle in Different Parts in Cattle. The following table gives the seat of tubercle as noted by a number of observers. It is open to the objection that it is the result of examination for diagnosis, and therefore gives the most obvious rather than the complete list of lesions. Examination of the brain, bones, deep muscles and intermuscular glands, etc., was usually omitted. Again, as the animals were often steers, the indications as regards the generative organs are unreliable. The œsophagostoma nodules on the bowels have been so often mistaken for tubercles that I have omitted all reference to intestinal tubercle.

DISTRIBUTION OF TUBERCLES IN DIFFERENT ORGANS OF CATTLE: PER CENT OF AFFECTED CATTLE.

────────────┬─────┬───────────┬────────┬──────────┬──────┬─────── │ % │ │ │ │ │ │Right│ % │% Costal│ │ │ │Lung.│Mediastinal│Pleura. │ │ │ │ % │ Glands. │ % │ % │ │ │Left │% Bronchial│Visceral│Mesenteric│ % │ % │Lung.│ Glands. │Pleura. │ Glands. │Liver.│Spleen. ────────────┼─────┼───────────┼────────┼──────────┼──────┼─────── German │ │ │ │ │ │ Abattoirs,│ 75 │ 29 │ 47–55 │ │ 28 │ 19 Pearson, │ │ │ │ │ │ (Penna), │63–57│ 60.7–33.8 │ 22 │ 23.25 │ 20.7 │ 5.7 Bryce │ │ │ │ │ │ (Canada), │77.27│ 56.8 │ 11.36 │ 11.36 │ 40.9 │ Reynolds │ │ │ │ │ │ (Minn. │ │ │ │ │ │ Agr. Ex. │ │ │ │ │ │ Station), │89.4 │ 33.3–64.9 │ 79 │ 12.5 │ 35.4 │ 27 Law (N.Y. │ │ │ │ │ │ Grade │ │ │ │ │ │ Herds), │34.8 │ 64 │ 6.4 │ 9.6 │ 1.6 │ Nelson (N. │ │ │ │ │ │ J. Exp. │ │ │ │ │ │ Station │ │ │ │ │ │ Cows), │33.9 │ │ │ │ 28 │ Russell │ │ │ │ │ │ (Wis. Exp.│ │ │ │ │ │ Station), │ 55 │ 72.4 │ │ 24 │ 10 │ Stalker & │ │ │ │ │ │ Niles (Ia.│ │ │ │ │ │ Exp. │ │ │ │ │ │ Sta.), │ 36 │ 61 │ │ │ 8.3 │ Reick │ │ │ │ │ │ (Leipsic),│ 100 │ │ [2]57 │ │ 83 │ 18 ────────────┴─────┴───────────┴────────┴──────────┴──────┴───────

────────────┬───────┬───────┬───────┬───────────┬──────────┬────────── │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ % │% Liver│ │ % │ │ % │Lumbar │ Lymph │ % │Pharyngeal│ % │Uterus.│Glands.│Glands.│Peritoneum.│ Glands. │Diaphragm. ────────────┼───────┼───────┼───────┼───────────┼──────────┼────────── German │ │ │ │ │ │ Abattoirs,│ 10 │ 5 │ 1 │ │ 4 │ 0.2 Pearson, │ │ │ │ │ │ (Penna), │ 5.5 │ │ 10.3 │ 14 │ 15.15 │ 11.4 Bryce │ │ │ │ │ │ (Canada), │ │ │ │ 45 │ │ 2.27 Reynolds │ │ │ │ │ │ (Minn. │ │ │ │ │ │ Agr. Ex. │ │ │ │ │ │ Station), │ │ │ 8.3 │ │ 18.7 │ Law (N.Y. │ │ │ │ │ │ Grade │ │ │ │ │ │ Herds), │ │ │ │ 17.7 │ 6.4 │ Nelson (N. │ │ │ │ │ │ J. Exp. │ │ │ │ │ │ Station │ │ │ │ │ │ Cows), │ │ │ │ │ │ Russell │ │ │ │ │ │ (Wis. Exp.│ │ │ │ │ │ Station), │ │ │ │ │ 31 │ Stalker & │ │ │ │ │ │ Niles (Ia.│ │ │ │ │ │ Exp. │ │ │ │ │ │ Sta.), │ │ │ │ │ 5 │ Reick │ │ │ │ │ │ (Leipsic),│ │ │ │ [2]57 │ │ ────────────┴───────┴───────┴───────┴───────────┴──────────┴──────────

────────────┬────────┬──────┬────────┬──────┬──────┬───────── │ │ │ │ │ │ │ │ │ │ % │ % │ │ │ │% Iliac │Lymph │Lymph │ │ │ │ and │Glands│Glands│ % Lymph │ % │ % │Inguinal│ of │ of │Glands of │Stomach.│Udder.│Glands. │Udder.│Flank.│Shoulder. ────────────┼────────┼──────┼────────┼──────┼──────┼───────── German │ │ │ │ │ │ Abattoirs,│ 0.16 │ 1 │ 0.06 │ │ │ Pearson, │ │ │ │ │ │ (Penna), │ 7.2 │ 8.75 │ │ 13.5 │ 9 │ 7.75 Bryce │ │ │ │ │ │ (Canada), │ │ │ │ │ │ Reynolds │ │ │ │ │ │ (Minn. │ │ │ │ │ │ Agr. Ex. │ │ │ │ │ │ Station), │ │ 16.6 │ │ │ │ Law (N.Y. │ │ │ │ │ │ Grade │ │ │ │ │ │ Herds), │ │ 6.4 │ │ │ │ Nelson (N. │ │ │ │ │ │ J. Exp. │ │ │ │ │ │ Station │ │ │ │ │ │ Cows), │ │ │ │ │ │ Russell │ │ │ │ │ │ (Wis. Exp.│ │ │ │ │ │ Station), │ │ 6.9 │ │ │ │ Stalker & │ │ │ │ │ │ Niles (Ia.│ │ │ │ │ │ Exp. │ │ │ │ │ │ Sta.), │ │ │ │ │ │ Reick │ │ │ │ │ │ (Leipsic),│ │ 17 │ │ │ │ ────────────┴────────┴──────┴────────┴──────┴──────┴─────────

────────────┬────────────┬──────┬────────┬──────┬────────┬─────── │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ % │ % │ % │ % │ % │ % │Pericardium.│Heart.│Kidneys.│Bones.│Muscles.│Larynx. ────────────┼────────────┼──────┼────────┼──────┼────────┼─────── German │ │ │ │ │ │ Abattoirs,│ 0.9 │ │ 0.7 │ │ 0.1 │ 0.13 Pearson, │ │ │ │ │ │ (Penna), │ 8.2 │ │ 2.1 │ 0.4 │ │ Bryce │ │ │ │ │ │ (Canada), │ │ │ │ │ │ Reynolds │ │ │ │ │ │ (Minn. │ │ │ │ │ │ Agr. Ex. │ │ │ │ │ │ Station), │ │ │ 2 │ │ │ Law (N.Y. │ │ │ │ │ │ Grade │ │ │ │ │ │ Herds), │ │ │ │ │ │ Nelson (N. │ │ │ │ │ │ J. Exp. │ │ │ │ │ │ Station │ │ │ │ │ │ Cows), │ │ │ │ │ │ Russell │ │ │ │ │ │ (Wis. Exp.│ │ │ │ │ │ Station), │ │ │ │ │ │ Stalker & │ │ │ │ │ │ Niles (Ia.│ │ │ │ │ │ Exp. │ │ │ │ │ │ Sta.), │ │ │ │ │ │ Reick │ │ │ │ │ │ (Leipsic),│ │ │ 52 │ 9 │ 49 │ ────────────┴────────────┴──────┴────────┴──────┴────────┴─────── Footnote 2:

All serosæ.

Swine. The lesions in swine, though essentially like those in cattle, differ in some particulars. The primary tubercles are more commonly pharyngeal or intestinal and mesenteric, in keeping with infection by ingestion; caseation will often proceed to liquefaction, so that the tubercles appear like grumous abscesses with irregular outlines and vascular growths on their walls; there is less tendency to cretefaction than in cattle; the muscular and intermuscular tissues and the lymph glands are far more frequently affected; ulceration of the pharyngeal and intestinal mucosæ is more common. The lungs, liver, spleen and visceral lymph glands are very subject to tubercle, the kidneys, uterus and testicles somewhat less so, and the nerve centres least of all. The serosæ are often involved and the seat of clusters of vascular or caseated neoplasms (grapes). The bones and joints also suffer, particularly in young growing animals.

Horse. The horse suffers much less frequently than cattle or swine, probably largely because of his outdoor life, his better tone as the result of muscular work, and the absence of the excessive milk secretion which is secured from cows and of the dangers from ingestion that attend on swine. Yet, according to Nocard, it is even more susceptible, and the disease once established is liable to advance more rapidly to a diffuse generalization. The lesions in the lungs and abdominal cavity resemble those of cattle, both in nature and abundance; tuberculous polypi and ulcers are more common; the visceral lymph glands (bronchial and mesenteric) are early and severely attacked; the liver and spleen suffer extensively, the serosæ somewhat less so; lesions have been noted in the vertebræ, skin and muscles (Cadiot). In rare instances tubercles have been seen in the heart, and the aorta has been atheromatous (Cadiot). Necrotic degeneration, caseation and cretefaction occur as in cattle.

Sheep and Goat. Tuberculosis is infrequent in the goat and especially so in the sheep, owing perhaps largely to open air life and their predilection for high, airy pastures. When inoculated they show a marked susceptibility, and under favorable conditions they contract the infection casually. The tubercles may be found in all parts of the body,—lungs, thoracic lymph glands, intestines, mesenteric and sublumbar glands liver, spleen, serosæ, lymph glands at large, vertebræ, etc. There is less tendency to calcification than in the ox, the older tubercles remaining in the caseated condition or bursting and forming vomicæ. A common seat of casual tubercle in sheep is around the throat or on the sides of the cranium or face.

More frequently than in cattle, verminous affections (œsophagostoma columbiana, and venulosum in the bowels, stongylus filaria and rufescens in the lungs, linguatula denticula in the mesenteric glands) are mistaken for tuberculosis, hence the necessity for a careful investigation into the nature of the neoplasm, the presence of the tubercle bacillus, and the absence of the worms and their eggs. Except in the case of the linguatula the lymph glands are little affected by the worms.

Dog and Cat. The lesions are often concentrated on the respiratory or alimentary tract, but they have been noted also in the pharyngeal glands, tonsils, posterior nares, serosæ, liver, pancreas, spleen, nerve centres, ovary, uterus, testicle, epididymus, tunica vaginalis, prostate, heart, aorta, bones and joints. They follow the regular development of bovine tubercle, and caseation and cretefaction are prominent features. These animals are especially liable to infection by eating the left victuals from the plate of a consumptive owner, as well as by devouring consumptive prey, and the primary lesions are to be looked for along the line of the throat, bowels, liver and lungs. For the dog Cadiot records caseating polypi and ulcers on the mucosa of the larynx, trachea and bronchia, and Müller and Cadiot several cases of pharyngeal caseating adenitis in the dog bursting externally and developing intractable fistulæ, having abundance of bacilli in the discharge. These he attributes to expectorated virus from old standing tubercles in the chest infecting the pharyngeal mucosa and indirectly the lymph glands. The infection entering with the food and lodging in the follicles of the tonsils would act in the same way, and infected wounds received in fighting must also be quoted. Cats suffer from similar intractable sores, some of which may be traced to a tuberculous origin. The lungs are often extensively hepatized and of a general pale grayish color, but the early miliary lesions, the caseating and cutaneous centres, the vomicæ often intercommunicating, the tuberculous bronchial and mediastinal glands and the bacilli show the true nature. Intestinal ulcers are common, especially on the agminated glands, and small tubercles, in all stages of degeneration are met with in the enlarged liver, the spleen, pancreas, kidney, etc.

Apes and Menagerie Animals. In these tuberculosis is common alike in the thoracic and abdominal forms, and the lesions in the main are those of domestic cattle.

Chickens. The lesions are common in the abdominal cavity, the intestines, liver and spleen being the most frequently attacked, while the subcutaneous connective tissue, bones and joints also suffer. The lungs and kidneys usually escape. The intestinal mucosa shows small nodules, often caseated, or ulcers; the enlarged and friable liver is studded with tubercles from the size of a hemp seed upward, gray or translucid, homogeneous or with central necrosis, simply or in conglomerate masses, with congested or hæmorrhagic periphery; the spleen is swollen and permeated by similar deposits; fibrinous ascitis is not uncommon; the abdominal lymph glands are enlarged and congested.

The early tubercle shows a central, necrotic, hyaline area, consisting of the debris of disintegrated cells, which is colored brown by picro carmine, unlike the nucleus of the pheasant tubercle (Cadiot). Around the hyaline centre is a zone of large epithelioid cells, the nuclei of which stain strongly in carmine. Outside this is the usual zone of small, round, lymphoid cells. In the whole the tubercle bacilli can be made manifest by the carbol-fuchsin (Ziehl-Neelsen) stain. In the older and larger tubercles the central necrotic mass has encroached in part or in whole on the epithelio-lymphoid zone.

Pheasant. The lesions have the same seats and naked-eye aspect as the chicken tubercle, but under the microscope the smallest and most recent tubercles show epithelioid cells to the centre, or later, the central zone presents a dense fibrous network enclosing open spaces and giving a mahogany stain with Lugol’s solution (iodine and potassium iodide). (Cadiot). There has been an organisation of connective tissue which has submitted to amyloid degeneration, making a clear distinction from the tubercle of chicken.

Parrot. The lesions were thus located by Eberlein and Cadiot:

│ Cadiot.│Eberlein. Eye and periocular region, │ 12│ 14 Commissure of the beak, │ 7│ 11 Tongue, │ 8│ 9 Palate, │ 4│ — Larynx, │ —│ 2 ──────────────────────────────┼──────────────────────────────┼───────── Bones and Articulations, │Upper limbs (wings), 7│ 14 „ │Claws, 3│ — „ │Cervical, Dorsal and 5│ — │ Caudal, │ ──────────────────────────────┼──────────────────────────────┼───────── Lungs, │ │ 7 Liver, │ │ 4 Intestine, │ │ 3 Muscles, │ │ 1 Heart, │ │ 1

The skin lesions are vascular neoplasms containing bacilli and usually invested with a covering of horn, but sometimes, on the legs and feet raw. The morbid growth may be rounded or conical, narrowing to a point. The lesions of the buccal mucosa begin as small, grayish swellings on the angle of the mouth, palate, tongue or larynx which grow out into more or less rounded vegetations. The lesions of the liver and lungs are mostly miliary with the usual tubercular features, but they may grow to larger size, as a pea or bean. In the cancelli of bones and on their surface, the lesions resemble those of the mammal.

The cutaneous form has been held to be the counterpart of warty lupus of man, the more plausibly that the disease is developed by inoculation from tuberculous men. The arthritic type represents what is described as gout in parrots.

In any case the recent miliary lesion presents the true tubercular type of a central giant cell or cells with bacilli, surrounded by epithelioid cells, and they in turn by small, rounded lymphoid globules.

PRIMARY AND SECONDARY INFECTION.

The estimate of the relative, early or late infection of two organs or tissues may often be made with reasonable accuracy from the fact that the lesions in one organ are old, caseated, calcified or sclerosed, while those in the other organ are all recent, with vascular environment and almost devoid of caseation or other degenerative process. We cannot safely predicate our decision on the greater number of old lesions in one organ rather than another, as the disease may have advanced much more rapidly in the one tissue. Still less can we state with certainty that the disease has not entered by a given channel because no lesions are left to show the transit of the bacillus along its supposed course. We frequently find tuberculosis of the bronchial or mesenteric glands, when we can detect no lesion in the lung, nor intestine. The bacillus has been passed on without establishing any lasting lesion in transit.

It is often too confidently asserted that the infected dust inhaled, falls directly on the air cells and determines the extensive pulmonary tuberculosis that ensues. So, on the other hand, it is often too arrogantly assumed that tubercle bacilli ingested with food, must necessarily show their results mainly in the intestines, mesenteric glands and liver. That solid particles can find their way directly into the lungs, has long been demonstrated by the pulmonary anthracosis of the miner, and the deadly phthisis of the stone hewer and cutler. The experiments of Cornet, Tappeiner and others in producing pulmonary tuberculosis, by compelling the inhalation of infected spray, corroborate this experience very satisfactorily. Yet it does not follow that all of the offensive matter penetrated the air cells at once on the air inhaled. The heavy particles of steel, quartz and even of coal dust must be mainly arrested on the surface of the moist air passages, yet, under the irritation caused by their presence and the consequent arrest of the ciliary motion, they would slowly gravitate downward to the pulmonary cells. In the case of the inspired tubercular spray or dust, we must recognize the possibility of the approach of the bacillus to the lungs through the lymph and blood channels as well. The bacilli lodged in the pharynx, and, above all, in the tonsillar follicles, can readily enter the lymph vessels, and are finally poured into the lower end of the jugular vein, but a few inches from the right heart, by which they are instantly propelled into the lungs. If then the lung is the most receptive and least resistant organ, it may easily be that this is the first point where the bacillus can establish a strong and effective colony. Apart from this the colonization of the tonsillar follicles may determine a constant supply of fresh bacilli, which may gravitate down with the abundant mucus toward the lungs.

This tuberculous colonization of the tonsillar follicles is doubtless the main source of the infection of the pharyngeal lymph glands, which is so common in ox, pig and dog. It tends further to intestinal tuberculosis through the frequent swallowing of the products of the infected follicles. Then the infection of the pharynx and tonsils, whether established by inhalation or deglutition, may be the first step toward a secondary infection of the intestines.

Again the bowels can be infected by the frequent swallowing of the expectorations brought up from the diseased lungs or bronchia.

Conversely the lungs may be easily infected secondarily from preëxisting disease of the abdominal organs, and again primarily through the lymph channels. With tuberculosis of the cardia or liver the bacilli can follow the lymph vessels of the œsophagus or vena cava so as to reach the mediastinal glands, and from these glands in a state of disease they can easily pass into the adjacent pleural cavity and reach the lung. Or by following the mesenteric lymphatics they reach the thoracic duct and enjoy what is virtually for them a culture fluid, until discharged into the jugular, which, as already stated, is but a few inches from the right heart and lung.

Extension through the general blood stream usually takes place only when tubercles have already become numerous and extensive in a given region of the body, and its occurrence is the signal for a generalized tuberculosis.

The extension from the gastro-intestinal organs, pancreas and spleen may be considered as a partial exception. Here the infecting blood is not the general blood stream, but has to run the gauntlet of the liver capillaries by which the bacilli may be sifted out and delayed. This arrest subjects the liver to secondary tuberculosis in almost all cases of abdominal tuberculosis, and goes far to explain the extraordinary frequency of the disease in this organ. Ingestion tuberculosis almost necessarily leads to hepatic tuberculosis, and this notwithstanding that the primary lesion may have been very circumscribed.

The tuberculization of such a large vascular organ as the liver, however, paves the way for further extension, and if once extensively diseased, the early generalization of the infection is to be dreaded.

TUBERCULOSIS CONTINUED.

SYMPTOMS OF TUBERCULOSIS IN CATTLE.

Microscope and staining; by centrifuge; by agglutination test; by inoculation; by tuberculin test; tuberculin; reaction; precautions, temperature before injection, exclusive of other illness, of parturition, abortion, heat, isolation, of hot building, of cold draughts, of hard floor, of faulty milking, privation of water, of change of food, of journey, of rude handling, of previous recent tests, of antipyretics, make special examination in unthrifty, test excluded animals later, danger of infecting through thermometer; technique; dose; time of injecting; identification and record of subjects; seat of injection; sterilization of syringe and skin; temperatures hourly or every second hour from 8th to 16th or later; typical reaction; accurate record of feeding, watering, milking or other occasion of hyperthermia or hypothermia; passing on the value of a rise; local swellings; chills; tremors; effect of test on general health of reacting and nonreacting animal; action on parturient cows; reliability of test. Relation of human to bovine bacillus; varying character of microbes generally, of tubercle bacillus in man; bacillus of man and bird interchangeable; tuberculosis in man and ox, similarity, coextensive, apparent exceptions, direct infection—man to cattle—cattle to man; encrease of tabes; experiments of Adami, Ravenel and Garnault; experiments on cold blooded animals; bearing of variations of susceptibility on sanitary work. Treatment: When admissible; hygiene; rich feeding; oleaginous seeds: cod liver oil; pneumatic cabinet; grooming; warm bath; medicated inhalations; sulphurous acid; chlorine; formaline; calmatives; carbonate of creosote; derivatives; streptococcic serum; air or oxygen in peritoneum; excision of tubercle; Prevention; Extinction in cattle; expense, supply of tuberculin and efficient veterinarians; appraisment; indemnities; vermin; disinfection; scheduling; control of purchases. Breeding healthy stock from infected; raising healthy offspring without sterilizing the milk. Removal of unthrifty and suspicious animals. Removal of animals showing objective symptoms, or, tuberculin reaction. Generally applicable measures. Hygiene of milk, butter, cheese, whey, oleomargarine. Hygiene of meat.

Tuberculosis may be acute or chronic, yet as seen in cattle, from casual infection, it usually comes on very slowly and insidiously and follows a chronic course. As the symptoms vary according to the organs involved it will be convenient to consider these in turn beginning with such as show the most diagnostic phenomena.

Pulmonary Tuberculosis. Though one of the most common and dangerous forms of the disease this may last for months or years without any suspicion on the part of the owner or caretaker of anything amiss. There may be an occasional cough, short, weak, dry, wheezing, perhaps repeated and roused by opening the stable door in cold weather, by leaving the stable for the cold outer air, by rising suddenly in the stall, by being driven on a run for a short distance, by drinking cold water or by eating dusty food. If driven for some distance, or put to draught work (ox) the subject blows more than the others. Sometimes even at rest, breathing is slightly accelerated. Yet the spirits may be as good, the eye as clear and full, the coat as smooth and sleek and the skin as soft and mellow as in health. Some such animals give as much milk, of as rich a quality, or, when put up to fatten, lay on flesh apparently as well as their healthy fellows. In favorable cases percussion may elicit circumscribed areas of dulness, and wincing or other sign of tenderness, and auscultation may detect crepitation or wheezing over the same points. By covering the nose and mouth with a sac or blanket the breathing is rendered more labored and the morbid sounds become clearer and more definite. The use of a stethoscope or phonendoscope may also render them more distinct. The morbid râles are more significant of tuberculosis if found in a number of isolated and circumscribed spots, with healthy respiratory murmur between, than if simply surrounding a single extended area of flatness as is usual in pneumonia. Much, however, stands in the way of success at this early stage. The heavy muscular and bony mass of the shoulder covers the anterior lobe and partially muffles the auscultation sound, while it renders percussion useless. The thick covering of the ribs in fat animals proves a serious barrier to successful auscultation and percussion. The varying plenitude of the abdominal viscera, and the rumbling, trickling, gurgling, and in the case of the rumen the crepitation of the contents, tend to complicate, obscure or cover up the pulmonary sounds. There is usually no appreciable elevation of temperature, or a slight rise of about one degree takes place at distant and uncertain intervals so as to render it useless for purposes of diagnosis.

When the disease is more advanced and the pulmonary lesions more extensive, the animals usually appear less thrifty on the same feeding, yet fat animals are habitually killed for food that show quite extensive pulmonary tuberculosis. With loss of condition, the coat loses its lustre somewhat, the hair becomes dry and stares in patches, and the skin loses its mobility and mellowness. The cough may be more frequent, perhaps paroxysmal under excitement, harsher, more short and broken, and either dry and husky or moist and gurgling, with a succeeding deep inspiration perhaps a moist râle. When the skin on the last ribs is pinched up between the fingers and thumb it is slower in flattening down to its normal smoothness, pinching of the spine at the shoulder or back, or it may be of the sternum, may cause wincing and even moaning, and the same may come of percussing the ribs smartly with the closed fist. There is now more decided evidence of flatness on percussion on the various affected points, and of abolition or lessening of the respiratory murmur, which is replaced by wheezing, or by bronchial blowing sound, heart beats and abdominal crepitation or gurgling, conveyed to the ear more clearly through the intervening consolidated tissue. The breathing may be slightly accelerated even at rest, and becomes distinctly so on exertion. The appetite fails somewhat and the secretion of milk lessens, or it may become more pale and watery. Chronic tympany occurring after meals occasionally appears, usually indicating tuberculosis of the glands along the œsophagus with pressure on that organ impairing eructation, and on the vagus nerve so as to impair nervous control. In connection with this there come on signs of generalization of the tubercle, as irregularity of the bowels, or enlargement or nodular induration of some of the superficial lymph glands, as the pharyngeal, prescapular, prepectoral, axillary, prefemoral, inguinal or mammary. Expectoration is usually abundant but it is difficult to secure it for diagnostic purposes since the moment it reaches the pharynx it is instantly swallowed, while any that may have been projected into the anterior nares is licked out by the pointed tongue. Nocard tried to secure this through a cannula passed in between the tracheal rings but with very little success. Others have introduced the hand into the pharynx, rousing the cough by tickling the larynx, and attempting to bring out the expectoration in the hand. When it can be secured its solid and opaque flocculi may be stained and examined for the bacillus, or it may be inoculated on a Guinea pig, intraperitoneally, to test its virulence. If there are open vomicæ or complex infection the breath is usually heavy and mawkish.

In the most advanced stages the symptoms are very characteristic. The subject is miserably thin and wastes visibly from day to day, the hair is dry and erect, most marked along the spine, the skin is scurfy, rigid, lousy, and clings firmly to the bones, the eyes are pale, deeply sunken in their sockets and bleary, the tears running over the cheeks, while a yellowish, granular, fœtid, and often gritty discharge flows from the nose, and dries in masses around the alæ. The cough is weak, painful, paroxysmal, and easily roused by pinching the back or breast or percussing the ribs. The breathing is liable to be hurried, even panting, and the animal may stand most of its time with nose extended to obviate the oppression that comes of recumbency. All the visible mucosæ are pale and blanched, and the pulse weak and rapid with every indication of anæmia. The temperature is usually raised to 104° or 105° F. and the milk secretion is completely arrested. Indications of generalized tuberculosis become more marked in the enlarged glands, diarrhœa, and clouded (purulent), or blood stained urine with microscopic casts, and even anasarca. The morbid sounds in the lungs have become a complex variety according to the nature of the lesion, blowing, wheezing, amphoric, friction, creaking, mucous, with the other bruits conveyed from adjacent organs. Death usually occurs in a state of complete marasmus, after months or years of illness.

Tuberculosis of the Abdomen. This usually affects the intestines, mesenteric glands, peritoneum, liver, spleen and pancreas, and has been known as tabes mesenterica. The generative organs also occasionally suffer, in which case, an early and rather persistent symptom is sterility, with a too frequent or it may be persistent desire for the bull (nymphomania). There is usually a steady loss of condition in spite of good feeding, the impaired functions of the intestinal mucosa, but especially of the mesenteric glands, liver and pancreas, interfering seriously with absorption and assimilation. The victims are therefore known as piners. While there may be more or less fever, highest in the evening, this is by no means marked, and cough and respiratory trouble may be entirely absent. Indications are not lacking, however, of digestive trouble. Slight tympany may follow meals, and the bowels are irregular, costiveness alternating with diarrhœa. If heavy feeding is resorted to, diarrhœa is the usual result, accompanied, it may be, by colic and tympany. There is a tendency to formation of pea or nut-like nodes under the skin of the flank, and Kleinpaul claims that the tubercles or vegetations on the rumen can be felt by manipulation of the left flank. Clearer evidence can often be had by rectal exploration, the tubercles and enlarged glands being felt on the rumen, in the knotted mesentery and in the sublumbar and subsacral region.

In case of uterine tuberculosis, the nymphomania may be supplemented by a purulent discharge, and rectal exploration may detect the tubercles on its surface, in the broad ligaments or even in the enlarged ovaries.

Great fœtor of the fæces may indicate ulceration of the mucosa, indigestion or impaired hepatic function.

For a great length of time the disease may be virtually confined to the mesenteric or portal glands, or even to the spleen, while the animal enjoys fairly good health. Again, in some instances, the subject may be fat and sleek, though the rumen, omentum or mesentery is to a large extent literally covered with tuberculous vegetations. The tuberculization of the intestines, mesenteric glands, liver or pancreas interferes far more with the general health than does even extensive peritoneal tuberculosis.

As the case advances it tends to generalization and winds up with the general symptoms predicated above of pulmonary tuberculosis.

Genital Tuberculosis in the bull is associated with nodular swelling of the testicle, epididymus or cord, hydrocele, and exceptionally tubercle on the penis, or in the prostatic sac.

Mammary Tuberculosis. This may be primary and circumscribed under direct infection through a trauma or by the milk ducts, but more commonly it is secondary to generalized tuberculosis. It may be a rather firm, uniform, painless swelling of one or two quarters (usually hind ones) without at first serious interference with milk secretion. As the disease advances, the follicles and ducts being invaded, an irregular knotted condition is developed, the milk becomes pale, watery, semi-coagulated and filled with bacilli, and the climax is reached in a densely indurated condition of the gland. From the first the mammary lymph glands, behind and it may be in front of the organ, become swollen, and they are finally indurated as caseation or calcification ensues. The superficial inguinal glands often participate.

Pharyngeal Tuberculosis. In this rather common localisation the retro-pharyngeal glands and those on the side of the pharynx especially suffer, though the parotidean lymphatic gland and the submaxillary often participate. Enlargement and induration of the tonsils and ulceration of the mucosa may be present. There is distinct swelling of the throat or displacement downward of the larynx, and the enlarged or hard nodular, perhaps even shrunken, glands may often be detected by manipulation. The nose is carried slightly protruded and a stertor or wheeze accompanies the breathing. A glairy liquid may run from the mouth or nose, and in this, bacilli may often be detected under the microscope. The retro-pharyngeal glands are very subject to softening and liquefaction, and in such a case an obscurely fluctuating swelling may be detected above the pharynx when the hand is introduced through the mouth.

This usually terminates in generalized tuberculosis, though it will often remain for a length of time the one appreciable localization.

Cutaneous Tuberculosis. The counterpart of tuberculosis verrucosa of man, this probably usually occurs by direct inoculation in a sore, yet the infection may reach the seat of lesion through the blood. It is usually represented by an irregular clustering warty growth, hanging more or less loosely from the skin and showing at points caseating centres. Bacilli may be recognized under the microscope.

Glandular Tuberculosis. Aside from the tuberculosis of the internal lymph glands already referred to, tubercles may form in any group of lymph glands, causing swelling, induration, fibroid degeneration or tuberculous abscess. Among these may be named the glands in front of the stifle or shoulder, at the root of the ear, beneath the zigoma, in the jugular furrow, the prepectoral, axillary, inguinal, etc.

Tuberculosis of the Brain and Meninges. Disorder of the cerebral functions occurring in generalized tuberculosis may be held to point to this disease. The earlier meningeal symptoms are often those of excitability, timidity, spasms, visual troubles, etc., merging later into vertigo, hebetude, paresis, unsteady gait, local paralysis and coma.

Tuberculosis of the Eye. This has been seen mostly as the result of experimental inoculation, with conjunctival and sclerotic congestion, corneal opacity, and the development of yellowish centres in the iris and choroid, from which the tubercle extends into the chambers.

Tuberculosis of the Heart, Pericardium or Pleura. Tuberculosis of the pleura is usually a concomitant of pulmonary phthisis, yet it may exist for a time independently, and its diagnosis presents serious difficulties. There may be tenderness of the intercostal spaces, a friction sound in case of raw granular surface or vegetations, creaking from false membranes or even flatness low down on percussion. If these escape notice, a short painful cough and slightly hurried breathing under exertion, in the absence of objective symptoms of lung disease, may lead to suspicion, but the true nature of the affection must remain in suspense. It usually leads to pulmonary or glandular (bronchial), and finally generalized tuberculosis.

Pericardial or Cardiac Tuberculosis is usually secondary and may be suspected when friction is synchronous with the heart sounds, when the heart beats or sounds are irregular or intermittent, or when the area of cardiac dulness is greatly encreased.

Tuberculosis of Bones and Joints. This is more common in calves and growing cattle, but may be present at any age. As affecting the vertebræ it causes stiffness and unsteady gait, perhaps what was looked on as a simple sprain causes persistent lameness in spite of treatment, and a point or area of tenderness on pinching is manifest. In the large bones and joints of the limbs, the cancellated extremities, or it may be a simple process with its inserted tendon or ligament, shows a firm, persistent swelling, and there is acute synovitis of the joint. In acute cases in calves the epiphysis may become detached from the diaphysis so as to make the limb useless. In the mature animal the enlargement and lameness may last for years without material change. The condition may be difficult to diagnose, in the absence of signs of tuberculosis elsewhere in the body, or unless the synovia, withdrawn through a sterilized nozzle, with antiseptic precautions, should show the presence of bacilli.

SYMPTOMS OF TUBERCULOSIS IN SWINE.

In young pigs, infected by the milk of the dam, there are general unthriftiness, stunted growth, emaciation and unhealthy skin, encrusted with a dark unctuous matter or scurf, as in chronic hog cholera. Temperature is variable on successive days, or times of the same day. Digestive disorder is manifested by slight colics, diarrhœa, vomiting, tympany and abdominal tenderness. The pig becomes pot bellied, with hollowness of the flanks in front of the iliac bones, and manipulation may detect the tuberculous bowels and mesentery in the form of a knotted mass.

Roloff describes a caseous colitis with ulceration of the mucosa, which is probably tuberculous.

Enlargement of the superficial lymph glands (pharyngeal, inguinal, prescapular) may be present. Traumatic infection of the castration sore and inguinal glands has been noted. As the disease becomes generalized, implicating the lungs, there is a dry paroxysmal cough and hurried breathing, becoming more oppressed on the slightest exertion. If quiet and thin enough for auscultation and percussion the usual morbid lung sounds can be heard. Unlike cattle, pigs are very subject to muscular and intermuscular tubercles, and as there is a general tendency to caseation, these are usually to be found as saccular cavities with soft, sometimes liquid, caseated contents. The bones and joints may suffer, as in cattle. The tonsils are usually enlarged and even caseous. The outer auditory meatus and the interior of the eye have been found affected. Cases affecting the brain were manifested by nervous disorder, rearing up on the fence, turning in a circle, spasms, rolling of the eyes, paresis and paralysis, often hemiplegic. When one or other of these indications of local disease is found associated with the general disorder of the lungs or bowels, in a herd fed on raw meat scraps, milk, or the soiled food of tuberculous animals, the evidence is strongly in favor of the local tubercle corresponding to the symptoms. It is noticeable that diagnosis by microscopic examination is difficult and uncertain because of the relatively very small number of the bacilli. In the mature pig the disease may be difficult of diagnosis without tuberculin, and a post mortem examination may be necessary to identify the disease in the herd.

SYMPTOMS OF TUBERCULOSIS IN THE HORSE.

Though not a common disease in the horse yet a large number of cases are on record, and accidental and experimental cases alike show that this animal is peculiarly receptive to the disease. The early symptoms depend on the location of the primary lesions, yet the general phenomena of debility, languor, early fatigue, unfitness for violent efforts, perspiration on slight exertion, irregular appetite, occasional rises of temperature and emaciation may usually be noted. The advance is usually slow, almost imperceptible, with periods of improvement and aggravation.

Some cases have appeared in the submaxillary and pharyngeal lymph glands with sore throat and were for a time mistaken for glanders (Ehrhardt, McFadyean). Others show a swelling of the appearance of cold abscess in the seat of the prepectoral glands (Johne, Röbert). One showed widely distributed lymph nodes and enlarged and indurated lymph glands (prepectoral, inguinal, etc.) with thickening of the intervening lymph vessels (Cadiot). This last suffered from bronchitis two months before. A number of cases reported by McFadyean showed special stiffness of the neck, with swelling and distortion of the vertebral joints, due to a tubercular osteitis and periostitis, and associated as necropsy showed with internal tuberculosis. Cases of this kind occurred in the practice of McConnell, Dawes, Insall, Malcolm and Hill, so that tuberculosis may well be suspected in cases of disease of the cervical vertebræ. In all of these cases post mortem examination, performed at once, or after a long delay, showed generalized internal tuberculosis.

When the chest is extensively affected, the symptoms are those of broncho-pneumonia or heaves (broken wind), there is hurried breathing with paroxysmal cough sometimes dry and wheezy, at others moist or mucous, a double lift of the flank in expiration, and a muco-purulent discharge from the nose, sometimes streaked with blood. Auscultation detects a varying force of the respiratory murmur at different points, with more or less wheezing. Blowing and other sounds conveyed to the ear through the solidified lung tissues are more rare or less marked. Percussion may show general resonance, encreased at emphysematous points, and diminished in small circumscribed areas, the seats of tubercle or consolidation. There are of course the attendant debility, inappetence, fever and steadily advancing emaciation. In some cases the enlarged tracheo-bronchial glands are seen to bulge forward between the two first ribs, and by the sides of the trachea. Stocking of the limbs is frequent.

Abdominal tuberculosis is most common in the young foal and when not secondary, may be due to feeding on tuberculous milk, especially in those brought up by hand on cow’s milk. There is debility, emaciation, anæmia, irregular appetite, digestive disorder, constipation alternating with diarrhœa, colics, pot-belly, falling in beneath the lumbar transverse processes, dry, harsh, scurfy skin and advancing marasmus. Rectal exploration will usually detect the enlarged sublumbar and mesenteric glands, and the simultaneous manifestations of disease of the lungs, superficial lymph glands, throat, or bones serve to identify the disease.

In the advanced stages of tuberculosis in solipeds polyuria is a frequent phenomenon (Nocard) tending to hasten the general anæmia and marasmus.

The patient often works for months or years but with gradually encreasing debility, which is soon fatal after the occurrence of generalized tuberculosis.

In estimating the nature of the disease, indications may often be drawn from the environment, feeding, etc. Nocard as the result of a careful study of the morphology and habits of the bacilli has shown that the more purely abdominal form of equine tuberculosis is near akin to that of the chicken, while the pronouncedly pulmonary form resembles the human type. McFadyean on his part adduces a number of cases of tuberculosis in horses that had been fed largely on cows’ milk, a most significant fact considering that such a ration is rare for this animal, and that few horses contract tuberculosis casually. Exposure therefore to the sputa of man, of the nasal or bowel products of birds or to the milk of cows, may suggest the probability of tuberculosis in a horse with chronic anæmia, debility and wasting.

The discharges from the nose of the affected horse are more available than those of cattle for examination and experimental inoculation, yet in many occult cases the diagnosis by tuberculin is the only reliable resort.

SYMPTOMS OF TUBERCULOSIS IN SHEEP AND GOATS.

The tubercles have been usually found post mortem in these animals or as the result of experimental inoculation, and symptoms have not been well recorded. They follow the same order as in the ox, weak husky cough, wheezing and other râles in the lungs, disorders of the digestive organs, swollen lymph nodes and glands, and caseated products in those that were of some standing. I have found these latter especially, in the region of the throat in high bred rams kept in confined buildings or yards and highly fed to prepare for letting or sale. These lose in vigor and activity and scrofulous swellings form on the neck, head or elsewhere and become rapidly caseated. In German abattoirs tuberculous sheep proved 0.1 to 0.15 per cent. In Saxon goats the percentage was 0.6.

SYMPTOMS OF TUBERCULOSIS IN DOGS AND CATS.

These follow in the main those of consumptive cattle. As the infection generally enters with food, the early symptoms often point to disease of the throat and alimentary tract, while the later ones involve those of the respiratory organs as well. Impaired and capricious appetite, debility, early exhaustion under exertion, emaciation, sunken pallid eyes, apathetic expression of the face, lack of life and gaiety, a knotted feeling of the abdomen if the region is flaccid, and a tense fluctuating sensation if ascitic, with usually enlargement of the superficial lymph glands are noticeable.

When the chest becomes affected there is the hurried breathing, quickly encreased by exertion, panting, paroxysmal cough, wheezing, and the various morbid râles in the chest, crepitant, friction, creaking, blowing, cavernous, mucous, etc. On percussion, flatness is detected in limited areas in a number of centres. Expectoration is usually promptly swallowed and can only be secured with difficulty for examination.

When tuberculous sores and fistulæ occur in the region of the throat or elsewhere, the evidence is patent and the bacilli can easily be found in the discharges.

In cats the course and symptoms do not materially differ. In both animals the history usually shows the connection of house life and the habit of eating after tuberculous persons.

SYMPTOMS OF TUBERCULOSIS IN BIRDS.

In the gallinaceæ there may be inappetence, vomiting, diarrhœa, with hurried breathing, sneezing, and the general phenomena of debility, weakness, advancing emaciation and anæmia, the comb and wattles becoming pale and flaccid and the visible mucosæ bloodless. The eyes are sunken and lack lustre, the head sinks, the wings and tail droop, and weight is steadily lost. When the bones and joints of the legs and wings are involved the local swellings and distortions are visible indications of the trouble.

In parrots these local swellings and particularly the horn-covered vegetations on the face and around the beak are characteristic.

Canary. Tuberculosis is common in the canary, contracted, as in the parrot, from man, with whom alone the caged bird comes into dangerous contact. The interchange of the disease between pet birds and their owners would demand the exclusion of such from the rooms of consumptives, and a careful watch for indications of disease of the air passages with marasmus, that the bird may be disposed of before it has become a source of danger.

DIAGNOSIS OF TUBERCULOSIS.

It is needless to repeat the various symptoms of tuberculosis according to its different seats and the degree of its extension in the animal body. In cases in which the indications are slight, greater importance may be given to them through the knowledge of the existence of more advanced or decided cases in the same herd, or the necropsies of animals taken from it. Yet in the average herd it is safely within bounds to say that three fourths of the affected cattle will escape condemnation if we employ objective symptoms alone. In one herd of seventy head, in which the tuberculin test condemned twenty-four head (being 50 per cent. of the mature animals), I left the examination after slaughter to the veterinarian of the A. J. C. C. who was at the time skeptical as to the value of the tuberculin test. He wrote me afterward of his surprise at finding every one of the twenty-four condemned animals tuberculous, when not one of them had shown symptoms by which he could recognize the disease in life. This is no exceptional case, and may be advanced rather as a typical example of the ordinary infected country herd.

Microscopic detection of the bacillus in the expectoration may be successful in the horse with pharyngeal or pulmonary tuberculosis, but fails in those forms that affect the other internal organs. It is all but useless for the expectoration of cattle and dogs. When there is cutaneous tuberculosis or a tuberculous fistula this is much more valuable, and it is especially useful in dogs and parrots.

The precipitate in the centrifuge will often show the bacilli that are present in milk, but in very many cases of tuberculosis the bacilli are not present in the milk.

The centrifuge used on the urine may also succeed when kidneys, bladder or prostate are affected, but the bacilli are rarely found in the absence of disease of these organs. The smegma bacillus is a source of fallacy.

The serous effusions in the affected serosæ (pleura, peritoneum, pericardium, synovial cavities) may also be centrifuged and the presence of the bacilli revealed.

The agglutination test of Arloing and Courmont though often giving positive results, (95.5 per cent. in pulmonary tuberculosis, 50 per cent. in surgical, Arloing and Courmont; 40 per cent., Knopf; 25 to 50 per cent., Lartigan); yet proved too unreliable, and frequently gave positive results when tuberculosis was absent. The best medium for cultures to be so used is 6 per cent. glycerine bouillon, and the age of the tuberculosis culture 8 to 12 days. One part of fresh blood serum of the suspected animal in a sterilized capillary tube is added to ten parts of the bacillus culture, and the tube placed in an oblique position. In 2 to 24 hours a fine sand-like material precipitates along the sides of the tube, and the microscope shows the bacilli in clumps, absolutely still without even Brownian movements. Gallemaerts found that it proved very satisfactory with the serum of Guinea pigs after three days from intraperitoneal inoculation, was less marked after inoculations subcutem, and that in man the agglutination appeared in influenza and pneumonia in the entire absence of tuberculosis. Such an uncertain test cannot be utilized in veterinary sanitary work.

Experimental inoculation with milk, expectoration, morbid discharges, the scraping of nodules, etc., is much more searching, and will detect more cases than the microscopic examination. But it fails entirely in cases in which the milk of unquestionably tuberculous animals is free from bacilli, or in which the local nodule or discharge tested is itself free from tubercle. It is a test of the local lesion and not of the entire animal system.

In choosing a subject for inoculation, the first consideration is that it must come from a healthy stock and be itself free from tuberculosis. Next, it must be of a species actively susceptible to the habitual tuberculosis of the animal from which the inoculated matter is taken. Thus for man, ox, dog and parrot, the Guinea pig is especially appropriate, while for gallinaceæ and horses, the rabbit is to be preferred. Inoculation is usually made into the peritoneal cavity.

As a period of two or three weeks is usually necessary to allow of an extensive development of tuberculosis, the method must be too often discarded on account of the delay in obtaining results.

Tuberculin test. Many stock owners still entertain an ignorant and unwarranted dread of the tuberculin test. It is quite true that, when recklessly used by ignorant or careless people it may be made a root of evil, yet as employed by the intelligent and careful expert it is not only perfectly safe, but it is the only known means of ascertaining approximately the actual number affected in a given herd. In most infected herds, living under what are in other respects, good hygienic conditions, ⅔ or ¾ are not to be detected without its aid, so that in clearing a herd from tuberculosis and placing both herd and products above suspicion the test becomes essential.

Tuberculin is the bouillon in which the tubercle bacillus has been grown, charged with the toxic products of its growth, but which has been raised to a boiling temperature to destroy all germ life, and from which the dead germs have been removed by passing it through a porcelain filter. When a physiological dose of this has been injected, subcutem, into the suspected animal, it has no effect on the non-tuberculous, while in the tuberculous it produces, in the course of the next 24 hours (usually from the 8th to the 16th), a steady rise of temperature by 2° F. or more, followed by a slow subsidence to the normal. This may last for from three to ten hours in different cases.

Among the precautions may be named:

1. The temperature of the animal is best taken at intervals, or at least, morning, noon and night, on the day preceding the injection to see that the animal shows no habitual rise at any time of the day. Yet in busy field work the one night temperature taken just before injecting will rarely fail to give a satisfactory normal as a standard for the animal. Any quotidian rise almost invariably reaches its climax at night.

2. The subject must be in good general health. If there is present in the system any concurrent disease it may undergo an aggravation within twenty-four hours and give a rise of temperature that will be mistakenly set down for tuberculosis. At the very start, therefore, it is important that the general health of the subject should be first assured by a critical professional examination. If some other disease is present the tuberculin test had best, as a rule, be delayed until that has subsided, while if tuberculosis is found the test will be superfluous.

3. The subject must not be within three weeks of parturition, nor about to abort. In many cases, though not in all, as preparations are made for calving, the system becomes unduly susceptible to the presence of tuberculin and that agent will cause a rise of temperature, though no tuberculosis is present. Unless this source of error is carefully guarded against the most valuable cows in the herd may be condemned unjustly.

4. The cow must not be within three days of the period at which “heat” would naturally occur. Under the excitement of œstrum the body temperature usually rises two or three degrees, and if tuberculin has been used this rise may be attributed to tuberculosis and a sound animal may be condemned. Nor is it always enough that the animal is supposed to be pregnant. Abortions sometimes take place unexpectedly and unknown to the owner. If, therefore, a cow under the test and which is not well advanced in pregnancy should show a rise of temperature it should be at once ascertained whether the animal is not in “heat.” If symptoms of “heat” are found she should be set aside along with any calving cows to be tested again when such a source of error is no longer present.

5. The tested animal must not be exposed to a hot sun in a closed area. In excess this will cause heat apoplexy, and the fever heat which ushers this in, may easily be mistaken for the indications of tuberculosis.

6. Cattle taken from pastures must not be enclosed in a hot, stuffy stable. While they must be tied up to allow of the temperature being taken at short intervals, coolness and ventilation should be secured in summer by a sufficient air space and the requisite ventilating openings.

7. Exposure to cold draughts between open doors and windows, or to wet or chilly blasts out of doors should be carefully guarded against. A chill proceeding from any source and alike in the presence or absence of tuberculin causes a rise of the internal body temperature.

8. Heavy cows unaccustomed to stand on hard boards may have a rise of temperature in connection with resulting tenderness of the feet. One must avoid hard floors on the day of the test or make examination of feet and allow for attendant fever.

9. Omission of the previous milking or a change of milker and consequent retention of part of the milk will raise the temperature of a nervous cow, and in careless hands secure an erroneous condemnation.

10. Privation of water at the regular time will often cause rise of temperature especially when on the dry feeding of winter. I have seen a general rise of two degrees and upward from the delay of watering for a single hour, while after watering the temperature went down to the normal and remained so. Water always tends to a temporary lowering of temperature but in the presence of tuberculosis it soon rises again.

11. Change of food is liable to produce a slight indigestion and rise of temperature. This should be avoided as far as possible, and when a herd is taken up from pasture for the test, it should have grass, ensilage or other succulent food.

12. Cattle just from a long journey by road or rail, or other cause of violent exertion are liable to have an elevated temperature from the leucomain poisoning. Such should be left at rest until the transient fever shall have subsided.

13. Violent handling of nervous cows in taking the temperature must be carefully avoided. The operator who cannot handle them gently is not fit for this work.

14. There must be evidence that the animals have not been repeatedly tested at short intervals shortly before. In a number of instances I have found a proportion of the cattle irresponsive to tuberculin, though a post mortem proved the presence of tuberculosis. Unscrupulous men, wishing to sell on a guarantee, can avail of this in animals so unaffected by the test.

15. The operator must have absolute control, even of the feeding and watering of the animals on the day of testing. Otherwise the rise of temperature may be prevented by a liberal use of antipyretics and a false guarantee may be secured.

16. An unthrifty animal, having general symptoms suggesting tuberculosis, must be subjected to the most critical examination in addition to the tuberculin which in such animals often fails to cause hyperthermia. Fortunately in such animals the tubercles are usually numerous and extensive enough to be discovered through objective symptoms.

17. Animals excluded from the test by reason of some individual unfitness at the time (parturition, œstrum, abortion or any other disease) must be marked and held for the test later after such disqualification shall have passed.

18. The operator must bear in mind the possibility of transferring other diseases from animal to animal, by contact, by the use of the same hypodermic needle on two in succession, and above all by the clinical thermometer. Diseases like contagious abortion, which present no obvious symptoms in the intervals, are especially liable to be carried in this way, and instances of the active extension of this after a test, have come under my notice. The operator should always enquire carefully as to the existence of abortions and sterility in the herd, put the aborting animals by themselves, using a special thermometer upon them, and carefully washing the hands before going to other cattle. It is well further to clean the thermometer after each animal and disinfect it with carbolic acid solution (5:100).

Dose of Tuberculin. Of the usual American preparation 2cc. (30 drops) is adapted to a cow or ox of 1,000 to 1,200 pounds. For larger and smaller animals a moderate encrease or reduction must be made, yet a considerable latitude is allowable. The new-born calf will take five drops and the animal of 700 pounds 25 drops.

Technique of the Operation. Lapses are so easily made when dealing with a large herd and are so dangerous that a regular plan should be systematically followed. The following will be found simple and convenient:

1. Inject the herd at 10 or 11 P. M. to secure a good rest and be fresh for the rise of temperature early next morning.

2. Before injecting have the subjects arranged in order and record them by name or other means of identification, with age, sex, breed, weight, pregnant or not, past or prospective date of calving, abortion, indications of disease, temperature taken just before injection and appropriate dose.

3. Inject into the loose connective tissue on the side of the neck, the animal being held by the nose, if necessary, by an assistant.

4. Use a syringe which has not been employed for any infectious products, and see that it is thoroughly cleansed and disinfected by boiling or by filling it with a carbolic acid solution (5:100).

5. After drawing the appropriate dose into the syringe, wipe the nozzle and dip it in strong carbolic acid before inserting it into the skin. This safely disinfects any virulent matter that may be lodged on the surface of the skin, and obviates those infected swellings and abscesses that have been a cause of complaint by stock owners.

6. When the nozzle is withdrawn from the skin, wipe it and dip it again into the strong carbolic acid to prevent any risk of infecting the tuberculin into which it is to be plunged.

7. The nozzle is much more easily inserted in the skin if the latter is pinched up so that the needle will transfix it at a right angle, instead of passing through a greater amount of the dense tissue because of the oblique direction. An excited animal with a thick, tense hide and a contracted panniculus muscle will offer serious obstruction which lessens greatly as the subject gets over its excitement and the muscle relaxes.

8. Temperature should be taken at 6 or 7 A. M., eight hours after injection of tuberculin, and every two hours thereafter, until the sixteenth hour.

9. If any subject shows no rise of temperature until the 16th hour after injection, its examination may be discontinued, but if it shows a slight rise toward the 16th hour it should be continued until it has shown a distinct reaction with steady rise and fall, or until, without such distinct reaction, the temperature descends to the normal.

10. If one has shown a distinct reaction but is still rising at the 16th hour, it should be continued till it begins to fall. The typical reaction is one in which the rise and fall are both gradual, and extend over a number of hours.

11. In recording the temperatures, there should be noted the exact time of each feeding, watering and milking, or any other condition (change of weather), which may in any way affect the heat production or radiation.

12. In old, emaciated animals and in second or third tests, Pearson uses twice the usual dose of tuberculin or more.

Tuberculosis Reaction. With slight variations different operators make their estimate of tuberculosis reaction on nearly the same general basis. A rise of 2° F. over the highest temperature of the day or days before, in the absence of any other appreciable cause, and provided that the elevation has followed the tuberculosis type of gradual rise and fall, is held to condemn. If, however, this rise does not exceed the normal average, if the temperature before injection did not exceed 100° and that after injection 102°, the case may well be held in doubt and reserved for re-testing. If, on the contrary, the initial temperature of the animal was 103°, and there was, between the 8th and 16th hours, a gradual typical rise and fall, reaching 104° or a little over, in the absence of any other cause for this, the subject would be condemned. Cattle having an initial temperature of 103° or above are not favorable subjects for the test, except in the case of calves in which the temperature is normally higher and the reaction must reach a higher point. In all cases of doubt it is well to hold for a second test, unless urgent sanitary considerations demand that a herd should be freed from the infection in short order. Then it may be better to risk a single error, with the concurrence of the owner, than to leave a possible centre of infection in the herd.

Local swelling in the seat of injection may be charged to lack of antiseptic care, or the presence of septic germs in the system of the animal prior to injection.

A chill during the period of reaction is not uncommon, especially in cold weather, or in a draught of cold air. The coat may stare along the spine in patches, or generally, tremors may be seen on the body or limbs, and a clammy coldness invades the ears and horns, and especially the points of the hocks and ischia. The back is sometimes arched and the feet drawn together somewhat.

In the absence of any source of excitement the head may be less elevated, the ears lopped forward or drawn back, and even the eyelids may droop somewhat. These phenomena may last for a few minutes or for an hour or two.

In testing other genera consideration must be had of the different normal temperature (horse 99.5°, dog 98.5°, sheep or pig 103°, bird 106°), and the varying susceptibility to tuberculin, the Guinea pig requiring a maximum dose relatively to its size and man or horse a minimum.

Effect of Tuberculin Test on the Later Average Health of the Animal Reacting. The transient fever and reaction on the day after injection modifies the milk secretion temporarily to a certain extent in ratio with the hyperthermia. The consensus of veterinarians of the largest experience, and the voice of the International Veterinary Congress at Berne in 1895, oppose the doctrine of any continuous effect on the health even of the tuberculous. Yet in the case of Governor Morton’s large herd of Guernseys a careful record of temperatures showed that for weeks after the test the reacting animals presented oscillations which were not shown before, and which were not found to occur in the sound animals. In the activities of sanitary work such indications are easily missed.

Effect of Tuberculin Test on Sound Animals. In 1894 I tested this on a number of thoroughbred Jersey and grade cows, injecting them six times at intervals of from five to fourteen days. It led to no appreciable change of the general health as shown by the temperature, breathing, pulse, yield of milk or its quality. Careful analysis was made of the milk at each milking, and in two animals soundness was attested by post mortem examination. Similar tests made by the Bureau of Animal Industry and others led to the same results. Cows in which the yield of milk was on the gain continued to encrease in the same ratio as those that had not been injected, and those in which it was on the wane showed no more rapid decrease. The butter fats and total solids showed no variation more than appeared in the healthy.

Action of Tuberculin on Parturient Cows. The testimony of Bang, Eber and Pearson, based on a very extensive experience, would indicate that the tuberculin test is not forbidden by the parturient condition. Eber concludes that unless the initial temperature materially exceeds 39.5° C. (103° F.) the parturient state is no barrier to successful testing. My own experience, on the contrary, is that a considerable proportion of parturient cows give a reaction when the initial temperature did not exceed 103° F., and when no sign of tuberculosis could be found. As an example, a cow in high condition, with an initial temperature of 102.8° F., rose gradually from the eleventh hour after injection and reached 106.3° by the eighteenth, a rise of 3.5°. From the record she was not due to calve for three months, but a fortnight later, when already killed and laid open, she showed all the signs of parturition, a fully matured calf, and not a trace of tubercle. This is far from unusual, and I am convinced that many errors will be avoided by refusing to condemn parturient animals or those within a couple of weeks before or after parturition on the tuberculin test alone.

Reliability of the Tuberculin Test. Even in the most careful hands the tuberculin test cannot be held to be infallible. A certain very small proportion of cows react without the recognition of any tubercle post mortem, some because of other bodily conditions, like parturition or abortion, but in skilled hands these may be ignored in ordinary sanitary work. Pearson claims to have had but 8 such cases in 4400 cows that gave a typical reaction. He suspects that some of these even had undiscovered tubercle, and Nocard thinks that all such cases are to be explained in this way. On the other hand a very few really tuberculous animals fail to react, some in connection with advanced disease, some because of repeated previous testing, and some because of the introduction of antipyretic agents into the system, but such cases can either be detected and controlled or are so infinitesimal in numbers, that they can be safely ignored in sanitary work. In skilled hands, the tuberculin test will show at least ⁹⁄₁₀ths of all cases of tuberculosis, when other methods of diagnosis will not detect ⅒th. See above case of herd where objective symptoms showed nothing, yet tuberculin condemned half the mature cattle, and post mortem confirmed this, the skeptical veterinarian being judge.

The Relation of the Bacillus Tuberculosis of Man to that of Cattle. On the discovery of the bacillus tuberculosis it was largely assumed that it was the same in all tuberculous animals, in all organs and in all circumstances. But it was soon found that the bacillus of chicken tuberculosis differed materially from that of the mammalian, that it could be inoculated only with difficulty on cattle or Guinea pig, as could that of the latter on the bird. The bacillus of the chicken found a most receptive home in the rabbit and horse, and was more easily started in artificial culture in glycerine bouillon, than was that of man or ox. But presently it appeared that the affinities and disparities did not end here. The bacillus from man or ox led to much more pronounced lesions in Guinea pigs than in rabbits, and the abdominal bacillus of the horse was inoculable on the chicken. Both horse and parrot proved receptive to the bacillus from man. Swine, like Guinea pigs showed a receptiveness to the bacillus of man or ox. The bacilli from the sputum, open tuberculous sore, or bones of man showed less virulence for Guinea pigs and rabbits than did those from tubercles in the human lungs and liver. The bacillus from the ox showed a greater virulence toward rodents and other small animals than did the bacillus from man. The bacillus of human sputum inoculated on the ox did not habitually cause generalized tuberculosis, but oftentimes a local tubercle or group of tubercles, and sometimes the inoculation wound healed without permanent lesion. These last points were seized upon to sustain a doctrine of probable duality for the microbe of tuberculosis, but if duality it was quite evident it could not end there, but must be extended to multiplicity, each small group of genera having a tubercle bacillus peculiar to itself. Those who thought their interest lay in arresting all sanitary control of tuberculous cattle and their products, became urgent in opposition to active government measures, demanding mathematical proof of the infection of man from cattle, under conditions that would exclude the remotest possibility of the introduction of infection from another source. The clearest and most abundant circumstantial evidence would not suffice, they must have direct experimental inoculation under conditions of precaution against outside germs, which were practically impossible in any community, conveniently ignoring that such inoculation, if successful, would have amounted to manslaughter, and that no such experimental evidence has been had, or can be had, of any of the deadly diseases of man. Infection by exposure and accidental inoculations can be had in abundance, just as they can in tuberculosis, but never under the rigid precautions which would exclude the possibility of extraneous infection.

The subject has assumed such importance that I may be excused for introducing a portion of my paper read before the New York State Medical Society in 1900.

1. This Variability is Common to Microbes Generally. Certain bacilli, like those of anthrax, grow in the living body as rods only, but become long filaments in given artificial media. They produce no spores in the living tissue, but do so readily in the carcass or soil. Transferred from ox to ox they are generally fatal, but if grown for several generations in Guinea pigs, and then transferred to cattle, the resulting disease is slight (Burdon-Sanderson, Duguid, Greenfield). Rabies passed from dog to dog is almost constantly fatal, but if passed through the ape and then back to the dog it is comparatively harmless (Pasteur). In both these cases the inoculated animals become immune from the more virulent germs, showing that they have passed through the actual disease in an unusually mild form. The later system of Pasteur is founded on this same general truth, as are also the methods of lessening the pathogenesis of germs by subjecting them to compressed oxygen, to graduated heating, to an altered chemical condition of the culture medium, to antisepsis, etc. For a time such weakened cultures often retain their lessened pathogenesis, even through a succession of cultures in a susceptible animal body, acting as if the germ were indeed a distinct species. But it might well have been considered that a microbe which had changed its aptitudes in a given environment could presumably revert to its original habits under the incentive of a suitable medium. And this is precisely what does take place. Pasteur has shown that the less potent rabic virus becomes more potent when passed several times through the body of a rabbit, and that the weakened anthrax germ acquires greater force when passed through a series of small birds or newly-born mammals.

To come to tuberculosis, Trudeau tells us that a culture of bacillus tuberculosis from man inoculated on the rabbit, and then cultivated for two years in vitro, becomes much less destructive to Guinea pigs, and that after six years of such artificial culture all the Guinea pigs inoculated with it live for many months, some for two and a half years, and some even recover. The usual life of the Guinea-pig after inoculation is seventeen days.[3] All of our zymotic diseases have in a similar way cycles of malignancy and benignancy. For a series of years measles, scarlatina, diphtheria, smallpox, or grippe have an unwonted mildness, and, again, one or another merges into a cycle of extreme and fatal malignancy. Rinderpest on the steppes of Asia is comparatively harmless to the native stock, but among outside cattle imported into the steppes or attacked in their native lands it is habitually fatal. Texas fever is mild among the indigenous cattle in the Gulf States, but very deadly to Northern stock. Glanders is not at all fatal to horses of the plains, the Rockies, or the Sierras; but it becomes redoubtable when these horses carry it to the Eastern seaboard, and still more so in Western Europe. It is a common experience to see a malady transformed through the effects of heredity or acquired immunity, through environment or the temporary mitigation of virulence in the germ; and again we see the same disease, no longer restrained by such inhibitory conditions, bursting forth as a malignant and deadly plague. We have, therefore, no warrant for the hypothesis that a pathogenic germ which, under given conditions of life, has lost in pathogenesis, but not in vitality, should continue forever to exist as a harmless microbe.

Footnote 3:

Johns Hopkins Hospital Reports, Bulletin 100.

2. Varying Malignancy of the Tubercle Bacillus in Man. Nothing is more familiar to physicians than the slow progress of tuberculosis of the lymph-glands and bones, on the one hand, and its frequent rapid progress in pulmonary, abdominal, or encephalic organs on the other. It has on this account been rather difficult to persuade many of the etiological identity of scrofula and consumption. In experimental tuberculosis the same truth constantly crops up. Arloing and his followers found that the tubercle bacillus from the lymph-glands of man proved less virulent and deadly than that from the human lungs (Lecons sur la Tuberculose). As early as 1880, Creighton drew attention to this in his work on Bovine Tuberculosis in Man.

But the bacillus from the lungs is subject to variations of this kind. Among seven specimens of human sputum, cultivated by Theobald Smith, six had a fair average vitality, while the seventh failed to perpetuate itself on dog serum.[4]

Footnote 4:

Journal of Experimental Medicine, 1898, No. 111.

It should be strongly emphasized in this connection that the failure of extension and generalization of the sputum germ when transferred to cattle does not distinguish it from the tubercle bacillus as conveyed from ox to ox. Everyone at all experienced with the tuberculin test well knows that in most herds the majority of the tuberculous animals show no generalization, but only a localized tuberculosis. There is reason to believe that even recoveries take place after slight infection, and it is certain that many tuberculous cattle continue for years in what appears to be good general health. Unless in particularly susceptible subjects or under specially poor hygienic conditions, or unless in case of reinfection, the average bacillus of bovine origin habitually fails to produce in other cattle a rapid extension and generalization.

3. Interchangeability of Bacillus of Man and Bird. Of all known forms of tubercle bacillus that of birds is the most distant from that of man or ox, and yet the beautiful experiments of Nocard[5] serve to establish their essential identity. Taking the bacillus of human sputum, which would not infect the fowl, he enclosed it in collodion capsules, which confined the bacilli while allowing transudation of the animal fluids, and left these in the abdomen of the chicken for not less than four months. He repeated this three times in succession with the product of the original sputum germ, and obtained a bacillus which was actively pathogenic for the chicken, though it had been harmless after the sojourn of four and eight months respectively.

Footnote 5:

Annales de l’Institut Pasteur, September, 1898.

This may explain the reported cases in which a flock of poultry have developed tuberculosis a few months after they were placed in the hands of a consumptive caretaker. That such transmission does not always occur is not surprising, considering that transmission between man and man is infrequent in comparison with the number of exposures. So in cattle the majority of exposed animals usually escape, although in such a case there can be no plausible explanation on the ground of a difference of germ. We have in every case to consider the necessity for receptivity as well as infectivity, and the lack of either is a bar to infection. When, however, we assume that the most diverse tubercle bacilli are descendent’s of one original stock, that a large herd must furnish some animals of more than usual susceptibility, and that such animals are subjected to continuous accessions of both bacilli and toxins, we can easily understand how some of the more adaptable germs will in time accommodate themselves to the new medium. A Pettinkoffer, with an immune constitution or a specially vigorous gastric digestion, may with impunity drink a culture of cholera spirillum, but the same is not true of the drunkard fresh from a spree and with seriously impaired digestion.

Bacillus Tuberculosis in Man and Ox. Points of Similarity. The bacillus tuberculosis of cattle is in general shorter and thicker than those of man, but many in both subjects are morphologically indistinguishable. Such differences are often far exceeded by different specimens of one stock of germ seeded on different media. There is no great difference in the thermal death point, and the viability in light, dryness, cold and putrefaction. The tendency is in all cases to colonize the lymph plexus or glands and to develop the specific lesions, with slight variation in detail. The slow development of the lesions from both forms of bacilli and their histological similarity is another argument for their essential identity. The slow growth of both on artificial media, the demand of each for a medium having the same approximate composition, and the similar pathogenic and diagnostic characters of the toxic matters elaborated by both germs bespeak a primary identity. The very remarkable staining qualities of tubercle bacillus, from whatever source it may be drawn, are no less remarkable.

Tuberculosis of Man and Ox Coextensive. The prevalence of tuberculosis in man and ox in the same country and district is so frequent that it may be safely set down as the rule. Among ichthyophagists and great fishing communities, like the people of the Hebrides, Iceland, Newfoundland, Greenland, and the coasts of Hudson Bay, tuberculosis is rare. In these countries cattle are few or absent, or, like the hardy highland kyloes of the Hebrides, they are kept in the open air. The immunity of the people is not due to insusceptibility, since they fall ready victims to tuberculosis when removed to infected countries and cities.

In Northern Sweden, Norway, Lapland and Finland, where cattle are scarce and reindeer plentiful, tuberculosis is said to be rare, though the inhabitants live in the closest of dwellings through the long winter. In most of the Pacific islands there are no cattle, and the natives are comparatively free from consumption. In Hawaii, since the introduction of cattle, consumption has increased. Australia and Tasmania, which forty years ago were the great resorts for English consumptives, have become increasingly the homes of infection since the development of the cattle industry and the influx of phthisical subjects. Minnesota and Dakota, in the early days, were held to be incompatible with tuberculosis, but since the advent of the white man and his stabled herds they have largely lost their sanitary reputation. The highest known mortality from tuberculosis to-day is that of the reservation Indians of these States, who feed on raw, diseased beef. In the Kighiz steppes the Tartars subsist on the flesh and milk of their solipeds, and largely escape consumption. In Japan, Dr. Ashmead tells us that the common people escape tuberculosis, while the aristocracy suffer severely. He attributes this mainly to the debauchery of the ruling class; but it must not be overlooked that they eat freely of beef and dairy products, which the rice-eating poorer population do not. The same remarks apply in measure to the mandarin and plebian classes in China. Holden tells us that tuberculosis is rare in Columbia, Ecuador and on the eastern slopes of the Andes, where little or no milk or butter is used. It must be further borne in mind that in these countries all herds live in the open air, and practically escape infection.

These examples must be contrasted with the consumers of beef and milk in civilized temperate countries, where the stock are largely kept indoors. A general average mortality of 7 or 8 per cent. from tuberculosis, and the post mortem evidence in European and American hospitals of 33 to 50 per cent. which show tubercular lesions, recent or remote, cannot be lightly passed over. The contrast with our reservation Indians is still more striking. Holden and Treon testify that the meat furnished to the Indians is always poor and often diseased, and that when the stock arrives our hungry wards devour the internal organs raw, or, later, the flesh as pounded preserved meat, and still uncooked. The deaths of these Indians from tuberculosis is 50 per cent. of the total mortality.[6] Dr. Washington Matthews, who spent twenty-one years among the Indians, gives their food as the main cause of the disease, and states that when the supply of fresh meat is liberal the death rate from tuberculosis is highest (Census of 1880).

Footnote 6:

Medical Record, August 13, 1883.

If we now contrast this fearful mortality with the immunity of the Indians of Hudson Bay, Great Slave Lake, Alaska, and the North generally, we have a most suggestive picture. It may be conceded that the extreme Northern Indians, being beyond the cereal region, have a slight measure of protection in their meat diet; but the recent spread of tuberculosis, like a plague, among the inhabitants of Barrow Straits, when introduced by the frozen-in whalers and the relief party, is sufficient disproof of any claim of special insusceptibility. There can be no doubt that in this, as in other virulent diseases, the rule holds that the long absence of the infection secures the preservation of the susceptible lines of blood, so that when the contagion does come it finds a more inviting field than in countries in which the more susceptible strains have been killed off and the comparatively immune have survived. Toward the Arctic circle the Indian must crowd into closer quarters in winter than his brother further south; but, in spite of all, the beef-eating Indian is being rapidly exterminated by tuberculosis, to which his brother of the north is a comparative stranger.

Exceptions: Their Explanation. This statement would be incomplete without a notice of exceptions to the rule. The Cape Town branch of the British Medical Association reports “that tuberculosis is rapidly increasing there in the human population, while tubercle in cattle is almost nonexistent.” This finds an abundant explanation in the different conditions of life. The men live indoors and concentrate the infection, whereas the cattle enjoy an outdoor life and escape. In a latitude of 30° south, where frost is rare, and with a dry climate (12 to 30 inches of rain per annum), the colonists find no occasion for housing their cattle, so that the conditions for the prevention of tuberculosis are ideal. It may be added that cattle are far less numerous in Cape Colony than they formerly were. The destruction first by lung plague and later by rinderpest has made the cattle industry extremely hazardous, and even before the advent of the rinderpest many had abandoned cattle and taken to sheep.

Parallel cases can be found in other countries. In Egypt, the great resort of consumptives, cattle are almost immune, the abattoirs furnishing about one tuberculous ox in ten thousand killed.[7] From Tunis (Alix), Algiers (Sarciron, Plaise), and Senegambia (Lenoir) a similar testimony comes. Cattle imported from Europe may die of tuberculosis, which is liable to assume a rapidly fatal type; but the native cattle, kept in the open air, are practically exempt.

Footnote 7:

Danzon. Études Expérimentale et Cliniques sur la Tuberculose, vol. i. p. 350.

Jersey cattle in their native island, staked out at pasture all the year round, show little or no tuberculosis, whereas the housed Jerseys of England and America suffer severely. The cattle of our Gulf Coast States, kept on ranches in the open air, are largely immune, and the cattle of Columbia, Ecuador, Peru, and the Argentine Republic largely escape; but the housed dairy cows of our Southern cities show a very high ratio of consumptives. Consumption becomes more and more deadly in the Southern negro even in the country localities, while the outdoor cattle of the same districts escape.

The absence of tuberculosis from the sanitarium herd at Saranac requires to be explained on a different basis. This herd is housed in winter, and infection, once introduced, would have opportunity to spread. The absence of tuberculosis is highly complimentary to the management of the establishment. But a similar immunity is the rule for all well-managed sanitariums, and not as regards cattle only, but man as well. At Argeles no case of tuberculosis contagion to attendants occurred in ten years (Ferrand). At Soden baths, in a village of 1500, there were in thirty-four years 65 deaths, 15 from consumption (Hopt). At Falkenstein, in fifteen years, one attendant became tuberculous (Jousset). At Görbersdorf the cases of consumption in the village and environs decreased (Knopf). At Brompton, London, in thirty-six years, among 150 attendants, but one became consumptive, though they individually served for from fifteen to twenty-four years, and nearly 40,000 patients had been received.[8] A well-conducted sanitarium is and should be a safer place than the average community, in which 15 per cent. and upward are tuberculous. The educational influence of such an institution should decrease tuberculosis in the surrounding districts.

Footnote 8:

Études Expérimentale et Cliniques sur la Tuberculose, vol. iii. p. 408.

Cases of Direct Infection from Man to Ox. Chauveau induced tuberculosis in cattle by feeding the tubercle from the lungs of man.[9]

Footnote 9:

Arloing. Tuberculosis Congress of 1891.

Nocard relates that a Beauce farmer, with a finely appointed stable and healthy herd, in 1883 employed a dairyman who had cough, profuse expectoration, and occasional hæmoptysis, and who had been several times in the hospital in consequence. He slept in the cow stable directly over the cows. In 1886 two cows, stalled immediately beneath him, showed ill health and were put up to fatten, but did badly and showed extensive tuberculosis when butchered. The dairyman stayed until 1891, having to go to the hospital several times in the interval. In 1892 the tuberculin test was applied and seven more cows were found to be tuberculous.

Huon tells of a cow bought to furnish milk for calves used to raise vaccine. She stood the tuberculin test, and was carefully secluded from all other cattle, but soon began to fall off, and in six months was very much emaciated, responded to the tuberculin test, and when killed showed extensive tuberculosis. Her caretaker at the vaccine establishment had what was believed to be chronic bronchitis, but when he died, soon after, this was found to be extensive pulmonary tuberculosis.

Bollinger inoculated a three-months’ calf with liquid from human tubercle and killed it seven months later. Fibroid pedunculated tumors, from a pea to a walnut in size, hung from the mesentery and spleen, and the mesenteric and retroperitoneal glands were tubercular.[10]

Footnote 10:

Münchener medicinische Wochenschrift, 1894.

Sidney Martin furnishes the following: Four calves were fed 70 c.c. of sputum containing a large number of bacilli. Three were killed after four, eight, and twelve months respectively, and had severally 53, 63 and 13 nodules on the small intestine, mostly on Peyers’ patches. Two calves received at one dose 440 c.c. of tuberculous sputum, and were severally killed after eight and nineteen weeks. The first had tubercular nodules in the intestine and mesenteric glands.[11]

Footnote 11:

Report of Royal Commission of 1895.

Frothingham injected into the peritoneum of two calves, three and thirteen weeks old, a culture of tubercle bacilli isolated one year before from the liver of a child. Slight local nodules were produced, some like spontaneous tubercle, others granulation tissue.

Theobald Smith inoculated sputum into the chest and abdomen of the following:

1. A yearling heifer, which was killed two months later and showed on the pleura near the seat of infection a mass of tubercles, one by one and a half inch in diameter, with partly caseated centres; also a nodule one-eighth of an inch on the right lung, and small tubercles attached to the diaphragm and omentum.

2. A yearling injected in the same way showed in two months on the diaphragm a mass of tubercles two inches in diameter, and a second mass one inch in diameter on the ribs near the seat of infection. Microscopical examination failed to detect bacilli, but there is no evidence that they were sought by culture or inoculation.

3. A cow injected in the chest and killed after two months showed tubercles of the lungs, pleura, and mediastinal glands, partly caseated and containing bacilli. Vascular fringes hung from the pleura.

4. A cow receiving a chest injection of sputum culture and killed in two months showed fringes and pendulous masses on the pleura, with small tubercles containing cheesy matter and a few bacilli.[12]

Footnote 12:

Journal of Experimental Medicine, 1898, vol. iii. p. 482.

Crookshank injected tubercular sputum into the peritoneum of a calf, which died of streptococcus infection on the forty-second day. It showed extensive tubercular deposits in the seat of injection and an abscess the size of a walnut. Nodular fleshy neoplasms in hundreds studded the mesentery, omentum, liver, spleen, and diaphragm, and small tubercles disseminated through the lungs and liver contained tubercle bacilli. Three abscesses contained streptococci.[13]

Footnote 13:

Transactions of the Pathological Society of London, 1891, p. 332.

The experimental inoculations of cattle with sputum by T. Smith, Kruse, and Adami showed a decided lack of potency in the bovine system, but (1) they do not show that the germ at once perishes in the system of cattle; (2) they do not prove that this germ, if returned from the ox to man, would prove less pathogenic than if carried from man to man without the intervention of the ox. (3) The observations of Bollinger, Baumgarten, and Crookshank show that under certain conditions the sputum bacillus can and does produce generalized tuberculosis in cattle. (4) Diminished pathogenesis of the germ when passed from man to cattle is no guarantee that this germ, or the slightly modified germ of casual bovine tuberculosis will prove equally mild if transferred from the bovine to the human patient.

Cases of Infection of Man from Ox. Tscherning, of Copenhagen, attended a young veterinarian who had cut his finger in dissecting a tuberculous cow. The skin wound healed in three weeks, but a subcutaneous swelling persisted, an ulcer formed, and a tuberculous mass containing bacilli was removed. No secondary tubercles formed.[14] A parallel case occurred to a prominent American veterinarian. The diseased tissue was excised and the bacilli identified by the bacteriologist of the university with which the patient was connected, and a permanent recovery ensued.

Footnote 14:

Nocard. Dictionnaire de Med. Veterinaire. Article, Tuberculosis.

Pfeiffer, of Weimar, attended a veterinarian who had been similarly inoculated from a tuberculous cow. The patient, aged thirty-four years, had a good constitution and no tuberculous taint. The cutaneous lesion healed, but six months later there was tuberculosis in the cicatrix; pulmonary tuberculosis followed, and the patient died of this two years later. At the necropsy were found tubercular arthritis of the wounded thumb and many vomicæ in the lungs.[15]

Footnote 15:

Zeitschrift für Hygiene, Band iii.

The post-mortem wart (tuberculosis verrucosa cutis) is familiar to surgeons as occurring in butchers and tanners, and there is every presumption that in many cases this is of bovine origin (Martin du Magny, Hanot, Senn, Riehl, Paltauf, Osier). Gerber testifies that in exceptional cases this extends to the lymph-glands and becomes generalized.

Dr. Stang, of Amorbach, had a five-year-old, finely developed boy patient, of healthy parents, destitute of hereditary taint. He died after a few weeks’ illness with miliary tuberculosis of the lungs and enormously enlarged tubercular mesenteric glands. The cow which supplied his milk had been killed a short time before with pulmonary tuberculosis.[16]

Footnote 16:

Lydtin. Veterinary Congress, Brussels, 1883.

Dr. Demme, of the Children’s Hospital, Berne, had four infants, the offspring of sound parents, with no hereditary taint of tubercle, die of intestinal and mesenteric tuberculosis, having been fed on the milk of tuberculous cows. Among 2,000 tuberculous infants treated in twenty years these were the only ones in which he could exclude the probability of hereditary and other causes.[17]

Footnote 17:

Nocard. Dictionnaire de Med. Veterinaire. Article, Tuberculosis.

Mr. Howe, of North Hadley, Mass., lost a son, aged twenty months, from abdominal tuberculosis, three months after he had paid a week’s visit to his uncle and had been fed the milk of the uncle’s tuberculous cow. The cow showed at death generalized tuberculosis. The child had been strong and well, as were his parents.

The four-year-old son of Colonel Beecher, of Yonkers, died March, 1894, of tubercular meningitis, and the two Alderney cows which had supplied him with milk were then proved consumptive by the tuberculin test and post-mortem examination.[18]

Footnote 18:

New York Sun, March 29, 1894.

The child of Dr. Brown, U. S. A., and now of Cornell University Medical School, was similarly cut off by tuberculosis, having been fed on the milk of a tuberculous cow.

Dr. C. H. Peabody had a child patient die of tubercular meningitis three months after the family cow had been killed for generalized tuberculosis. There had been previously no tuberculosis in the family (Ernst, Infectiousness of Milk).

A. H. Rose, of Littleton, Mass., gives the case of a child which was fed for three years on the milk of a tuberculous cow and died with abdominal tuberculosis (Ernst).

Gordon, of Quincy, Mass., records the case of a ten months old child of healthy parents and ancestry which had been fed on the milk of a cow with advanced tuberculosis, and which died after a few weeks with acute tuberculosis (Ernst).

Gage, of Lowell, Mass., had an infant patient of healthy parents and surroundings, but which subsisted exclusively on a cow’s milk that contained bacilli and infected Guinea pigs. The child died of tubercular meningitis. A second child fed the same milk suffered in a similar way (Ernst).

Andersen, of Seeland, reports the death from tuberculosis of a six months old child which had fed on the milk of a cow having tuberculosis of the udder. The mother developed symptoms of tuberculosis after the death of the child.[19]

Footnote 19:

Hatch Experiment Station, Massachusetts Agricultural College, Bulletin No. 3.

Dr. Gosse, of Geneva, Switzerland, spent his Sundays with his family on an estate in the hills, and his daughter, aged seventeen years, took great pleasure in drinking milk warm from the cows. Early in 1893 she sickened with an obscure illness, and after ten months died, revealing at the necropsy intestinal and mesenteric tuberculosis. The five cows on the estate were tested with tuberculin; four reacted and were killed; two showed tuberculous udders (Nocard).

Dr. H. M. Pond reports four cases of tuberculosis in one family, three of them fatal. The cows supplying the family with milk were tuberculous.[20]

Footnote 20:

Pacific Medical and Surgical Journal, 1888.

Dr. Faust, veterinarian, of Poughkeepsie, records the case of a family on Long Island that lost from tuberculosis 139 cows. A three-year-old child and two grown sons died of tuberculosis. Tuberculosis was unknown in the parents’ families.[21]

Footnote 21:

Report to the Board of Health.

Dr. Kelly, veterinarian, Albany, gives the following: In a family of five a son, aged nineteen years, was very fond of milk and drank it fresh from the cow, and contracted tuberculosis. Some months later the farm herd of seventeen registered Jerseys were tested with tuberculin, and thirteen reacted and showed extensive tuberculosis when killed.

Dr. Cooper, veterinarian, Paterson, N. J., furnishes this: A child, fed on the milk of a cow, contracted tabes mesenterica. Examination revealed the presence of tubercle bacilli in the milk. The milk was then fed to ten kittens, all of which became ill and emaciated, and when killed showed tuberculosis.

Such cases, in connection with the experimental inoculations, furnish more than mere circumstantial evidence. They are corroborated and strengthened by the very uniform diffusion of tuberculosis in man and stalled cattle in practically all civilized countries. Of the closer connection in individual cases one or two instances may here be added as drawn from personal observation:

1. In one case a family cow and the owner’s wife had both advanced tuberculosis. The lady consumed a good deal of the cow’s milk, but when she gave up its use she felt decidedly better.

2. The owner of a thoroughbred herd of sixty head had suffered for years from consumption, and attributed the poor condition of the animals to lack of care since he had been laid aside. Without the tuberculin test, I diagnosed tuberculosis in fifty-nine of the animals.

3. In a second thoroughbred herd there never lacked one or two cases of advanced tuberculosis, two of the family suffered, and the eldest son, who was fond of milk and vegetable food, died of pulmonary tuberculosis.

4. A dairy of common cows had seventeen out of twenty-six destroyed for tuberculosis, and the farmer’s wife, father-in-law, and two brothers-in-law had shortly before died of consumption. The wife felt ill in the close house air, and with her father occupied herself much about the cattle.

5. A veterinary professor, who was meat inspector of the city abattoir, died a few years ago of tuberculosis, which he handled so constantly in his daily duties.

Stalker and Niles report that 5 persons, 20 to 30 years of age, of healthy ancestry, died of tuberculosis within two years, on a farm where 17 tuberculous cattle were found, and others had died in previous years, (Bull. Ia. Agr. Exp. Stat., 29).

Leonhardt reports the death from tuberculosis, abdominal and meningeal, of two children, fed on the milk of a tuberculous cow, (Rep. N. H. Bd. of Health, 1892).

Sontag reports the death by tuberculosis of a six months old child of healthy parents, that had been fed the milk of a tuberculous cow, (Rep. N. H. Board of Health, 1892).

Dr. E. Pearson quotes the following:

“A well known veterinarian wounded in the hand in opening a tuberculous cow, had a tumid, intractable sore, the tissues of which when excised showed tubercle bacilli.

A veterinarian, of Chester Co., Pa., in opening a tuberculous cow, cut his knuckle, which healed tardily, remained swollen and when excised, showed typical tubercular lesions including giant cells.”

He quotes from Hartzell the cases of two men wounded in cleaning cattle cars, both of whom had resulting tubercle, arrested in one case by excision, but in the other advanced to generalized tuberculosis and death.

Bang gives the following Danish cases:

A merchant having two chlorotic daughters secured a fine cow to feed them fresh milk. The cow was killed tuberculous and was replaced by another which also showed tuberculosis, this time affecting the udder. The girls died of tuberculosis at 16 and 18 years. Two younger children fed on the milk of sound cows grew up healthy.

A healthy cow became tubercular, after having been placed in the same stall in which another had died of tuberculosis. A child fed almost exclusively on the milk of these two cows died of tuberculosis.

A peasant at Silkeborg drank freely of milk freshly drawn. He died of tuberculosis, as did also a cow, and later in the same stable, a pig.

A peasant had an 11 year old cow with generalized tuberculosis, implicating the udder. The wife of the peasant, formerly healthy, became tuberculous shortly after the udder became affected and died at 45. A daughter who, like her mother, used the milk of this cow, died consumptive in the same year. The husband who drank beer, and not milk, remained well.

A physician fed his two children on the milk of his tubercular cow, and lost both from tuberculosis. Neither parents nor grand-parents were tuberculous. (L. Pearson in Bull. 75, Tuberculosis of Cattle).

Thorne had reports from twenty-two Ohio physicians to the effect that they had traced tuberculosis in their patients to the use of the milk of tuberculous cows, and thirty-three who believed they had reason to suspect the meat and milk supply as the source of cases of consumption. (Ohio Exp. Stat. Bull. 108).

To these may be added the cutaneous forms of tuberculosis (tuberculosis verrucosa cutis), which occur on the hands of persons (butchers, tanners, coachmen, cooks, etc.), who handle infected products of animals. These have been described by Riehl and Paltauf, Senn, and a number of surgeons and dermatologists and the relation of the occupation to the seat of the disease is conclusive as to the source of the infection. It is the exact counterpart of the verrucosa necrogenica of the hands of persons working in the dissecting rooms of medical schools, and the source of infection is equally well established in both cases.

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