At the veterinary school at Alfort and at the farm of Lamirault in France several hundred horses which had passed examination as sound had placed among them glandered horses under various conditions. The results of these experiments proved conclusively the contagious character of the disease.

In 1881 Bouchard, of the faculty of medicine in Paris, assisted by Capitan and Charrin, undertook a series of experiments with matter taken from the farcy ulcer of a human being. They afterwards continued their experiments with matter taken from horses, and in 1883 succeeded in showing that glanders is caused by a bacterium which is capable of propagation and reproduction of others of its own kind if placed in the proper media. In 1882 the specific germ of glanders was first discovered and described by Loeffler and Schuetz in Germany.

When we come to study the etiology of glanders, the difference of susceptibility on the part of different species of animals, or even on the part of individuals of the same species, and when we come to find proof of the slow incubation and latent character of the disease as it exists in certain individuals, we understand how in a section of country containing a number of glandered animals others can seem to contract and develop the disease without having apparently been exposed to contagion.

Causes.—The contagious nature of glanders, in no matter what form it appears, being to-day definitely demonstrated, we can recognize but one cause for all cases, and that is contagion by means of the specific virus of the disease. The causative organism is known as the Bacillus mallei.

In studying the writings of the older authors on glanders, and the works of those authors who contested the contagious nature of the disease, we find a large number of predisposing causes assigned as factors in the development of the malady.

While a virus from a case of glanders if inoculated into an animal of the genus Equus will inevitably produce the disease, we find a vast difference in the contagious activity of different cases of glanders. We find a great variation in the manner and rapidity of the development of the disease in different individuals and that the contagion is much more liable to be carried to sound animals under certain circumstances than it is under others. Only certain species of animals are susceptible of contracting the disease, and while some of these contract it as a general constitutional malady, in others it develops as only a local sore.

In acute glanders the contagion is found in its most virulent form, as is shown by the inevitable infection of susceptible animals inoculated with the disease, while the discharge from chronic semilatent glanders and farcy may at times be inoculated with a negative result; again, in acute glanders, as we have a free discharge, a much greater quantity of virus-containing matter is scattered in the neighborhood of an infected horse to serve as a contagion to others than is found in the small amount of discharge of the chronic cases.

The chances of contagion are much greater when sound horses, asses, or mules are placed in the immediate neighborhood of glandered horses, drink from the same bucket, stand in the next stall, or work in the same wagon, or are fed from feed boxes or mangers which have been impregnated by the saliva and soiled by the discharge of sick animals. Transmission occurs by direct contact of the discharges of a glandered animal with the tissues of a sound one, either on the exterior, when swallowed mixed with feed into the digestive tract, or when dried and inhaled as dust.

The stable attendants serve as one of the most common carriers of the virus. Dried or fresh discharges are collected from the infected animals in cleaning, harnessing, feeding, and by means of the hands, clothing, the teeth of the currycomb, the sponge, the bridle, and the halter, and are thus carried to other animals.

An animal affected with chronic glanders in a latent form is moved from one part of the stable to another, or works hitched with one horse and then with another, and may be an active agent in the spreading of the disease without the cause being recognized.

Glanders is found frequently in the most insidious forms, and we recognize that it can exist without being apparent; that is, it may affect a horse for a long period without showing any symptoms that will allow even the most experienced veterinarian to make a diagnosis. An old gray mare belonging to a tavern keeper was reserved for family use with good care and light work for a period of eight years, during which time other horses in the tavern stable were from time to time affected with glanders without an apparent cause. The mare, whose only trouble was an apparent attack of heaves, was sold to a huckster who placed her at hard work. Want of feed and overwork and exposure rapidly developed a case of acute glanders, from which the animal died, and at the autopsy were found the lesions of an acute pneumonia of glanders grafted on chronic lesions, consisting of old nodules which had undoubtedly existed for years.

In a case that once came under the care of the writer, a coach horse was examined for soundness and passed as sound by a prominent veterinarian, who a few months afterwards treated the horse for a skin eruption from which it recovered. Twelve months afterwards it came into the hands of the writer, hidebound, with a slight cough and a slight eruption of the skin, which was attributed to clipping and the rubbing of the harness, but which had nothing suspicious in its character. The horse was placed on tonics and put to regular light driving. In six weeks it developed a bronchitis without having been specially exposed, and in two days this trouble was followed by a lobular pneumonia and the breaking of an abscess in the right lung. Farcy buds developed on the surface of the body and the animal died. The autopsy showed the existence of a number of old glanderous nodules in the lungs which must have existed previous to purchase, more than a year before.

Public watering troughs and the feed boxes of boarding stables and the tavern stables of market towns are among the most common recipients for the virus of glanders, which is most dangerous in its fresh state, but cases have been known to be caused by feeding animals in the box or stall in which glandered animals had stood several months before. While the discharge from a case of chronic glanders is much less liable to contain many active bacilli than that from a case of acute glanders, the former, if it infects an animal, will produce the same disease as the latter. It may assume from the outset an acute or chronic form, according to the susceptibility of the animal infected, and this does not depend upon the character of the disease from which the virus was derived.

The animals of the genus Equus—the horse, the ass, and the mule—are those which are the most susceptible to contract glanders, but in these we find a much greater receptivity in the ass and mule than we do in the horse. In the ass and mule in almost all cases the period of incubation is short and the disease develops in an acute form. We find that the kind of horse infected has an influence on the character of the disease; in full-blooded, fat horses of a sanguinary temperament, the disease usually develops in an acute form, while in the lymphatic, cold-blooded, more common race of horses the disease usually assumes a chronic form. If the disease develops first in the chronic form in a horse in fair condition, starvation and overwork are liable to bring on an acute attack, but when the disease is inoculated into a debilitated and impoverished animal it is apt to start in the latent form. Inoculation on the lips or the exterior of the animal is frequently followed by an acute attack, while infection by ingestion of the virus and inoculation by means of the digestive tract is often followed by the trouble in the chronic latent form.

In the dog the inoculation of glanders may develop a constitutional disease with all the symptoms which are found in the horse, but more frequently the virus pullulates only at the point of inoculation, remaining for some time as a local sore, which may then heal, leaving a perfectly sound animal; but while the local sore is continuing to ulcerate, and specific virus exists in it, it may be the carrier of contagion to other animals. In man we find a greater receptivity to glanders than in the dog, and in many unfortunate cases the virus spreads from the point of inoculation to the entire system and destroys the wretched mortal by extensive ulcers of the face and hemorrhage or by destruction of the lung tissue; in other cases, however, glanders may develop, as in the dog, in local form only, not infecting the constitution and terminating in recovery, while the specific ulcer by proper treatment is turned into a simple one. In the feline species glanders is more destructive than in the dog. The point of inoculation ulcerates rapidly and the entire system becomes infected.

While a student the writer saw a lion in the service of Prof. Trasbot, at Alfort, which had contracted the disease by eating glandered meat and died with the lung riddled with nodules. A litter of kittens lapped the blood from the lungs of a glandered horse on which an autopsy was being made, and in four days almost their entire faces, including the nasal bones, were eaten away by rapid ulceration. Nodules were found in the lungs. A pack of wolves in the Philadelphia Zoological Garden died in 10 days after being fed with the meat of a glandered horse. The rabbit, guinea pig, and mice are especially susceptible to the inoculation of glanders, and these animals are convenient witnesses and proofs of the existence of suspected cases of the glanders in other animals by the results of successful inoculations.

The primary lesion in any form is a local point in which occurs a rapid proliferation of the cell elements which make up the animal tissue with formation of new connective tissue, with a crowding together of the elements until their own pressure on one another cuts off the circulation and nutrition, and death takes place in them in the form of ulceration or gangrene. Following this primary lesion we have an extension of infection by means of the spread of the bacilli into those tissues immediately surrounding the first infected spot, which are most suitable for the development of simple inflammatory phenomena or the specific virus. The primary symptoms are the result of specific reaction at the point of inoculation, but at a later time the virus is carried by means of the blood vessels and lymphatic vessels to other parts of the body and becomes lodged at different places and develops in them; again, when the disease has existed in the latent form in the lungs of the animal and the virus is wakened into action from any cause, we have it carried to various parts of the body and developing in the most susceptible regions or organs. The points of development are most frequently determined by the activity of the circulation and the effects of exterior irritants. For example, if a horse which has been so slightly affected with the virus of glanders that no symptoms are visible is exposed to cold, rain, or sleet, or by the rubbing of the harness on the body and the irritation of mud on the legs, the disease is liable to develop on the exterior in the form of farcy, while a full-blooded horse which is employed at speed and has its lungs and respiratory tract gorged with blood from the extreme use of these organs will develop glanders as the local manifestation of the disease in the respiratory tract.

The previous reference to the existence of glanders under the two forms more commonly differentiated as glanders and as farcy, and our reference to the various conditions in which it may exist as acute, chronic, and latent, show that the disease may assume several different phases. Without for a moment losing sight of the fact that all these varied conditions are identical in their origin and in their essence, for convenience of study we may divide glanders into three classes—chronic farcy, chronic glanders, and acute glanders with or without farcy.

CHRONIC FARCY.

Symptoms.—In farcy the symptoms commence by formation of little nodes on the under surface of the skin, which rapidly infringe on the tissues of the skin itself. These nodes, which are known as farcy "buds" and farcy "buttons," are from the size of a bullet to the size of a walnut. They are hot, sensitive to the touch, at first elastic and afterwards become soft; the tissue is destroyed, and infringing on the substance of the skin the disease produces an ulcer, which is known as a chancre. This ulcer is irregular in shape, with ragged edges which overhang the sore; it has a gray, dirty bottom and the discharge is sometimes thin and sometimes purulent; in either case it is mixed with a viscous, sticky, yellowish material like the white of an egg in consistency and like olive oil in appearance. The discharge is almost diagnostic; it resembles somewhat the discharge which we have in greasy heels and in certain attacks of lymphangitis, but to the expert the specific discharge is characteristic. The discharge accumulates on the hair surrounding the ulcer and over its surface and dries, forming scabs which become thicker by successive deposits on the under surface until they fall off, to be replaced by others of the same kind; and the excess of discharge may drop on the hairs below and form similar brownish yellow crusts. The farcy ulcers may retain their specific form for a considerable time—days or even weeks—but eventually the discharge becomes purulent in character and assumes the appearance of healthy matter. The surface of the gangrenous bottom of the ulcer is replaced by rosy granulations, the ragged edges are beveled off, and the chancre is turned into a simple ulcer which rapidly heals.

The farcy buttons occur most frequently on the sides of the lips, the sides of the neck, the lower part of the shoulders, the inside of the thighs, or the outside of the legs, but may occur on any part of the body.

We have next an irritation of the lymphatic vessels in the neighborhood of the chancres. Those become swollen and then indurated and appear like great ridges underneath the skin; they are hot to the touch and sensitive. The cords may remain for a considerable time and then gradually disappear, or they may ulcerate like a farcy bud itself, forming elongated, irregular, serpentine ulcers with a characteristic, dirty, gray bottom and ragged edges, and pour out a viscous, oily discharge like the chancres themselves.

The essential symptoms of farcy are, as above described, the button, the chancre, the cord, and the discharge. We have in addition to these symptoms a certain number of accessory symptoms, which, while not diagnostic in themselves, are of great service in aiding the diagnosis in cases where the eruption takes place in small quantities, and when the ulcers are not characteristic.

Epistaxis, or bleeding from the nose without previous work or other apparent cause, is one of the frequent concomitant symptoms in glanders, and such hemorrhage from the nostrils should always be regarded with suspicion. The animal with farcy frequently develops a cough, resembling much that which we find in heaves—a short, dry, aborted, hacking cough, with little or no discharge from the nostrils. With this we find an irregular movement of the flanks, and on auscultation of the lungs we find sibilant or at times a few mucous rales. Another common symptom is a sudden swelling of one of the hind legs; it is found suddenly swollen in the region of the cannon, the enlargement extending below to the pastern and above as high as the stifle. This swelling is hot and painful to the touch, and renders the animal stiff and lame. On pressure with the finger the swelling can be indented, but the pits so formed soon fill again on removal of the pressure. In severe cases we may have ulceration of the skin, and serum pours out from the surface, resembling the oozing which we have after a blister or in a case of grease. This swelling is not to be confounded with the stocking in lymphatic horses or the edema which we have in chronic heart or in kidney trouble, as in the last the swelling is cool, not painful, and the pitting on pressure remains for some time after the latter is withdrawn. It is not to be confounded with greasy heels. In these the disease commences in the neighborhood of the pastern and gradually extends up the leg, rarely passing beyond the neighborhood of the hock. The swollen leg in glanders almost invariably swells for the entire length in a single night or within a very short period. When greasy heels are complicated by lymphangitis we have a condition very much resembling that of farcy. The swelled leg in farcy is frequently followed by an outbreak of farcy buttons and ulcers over its surface. In the entire horse the testicles are frequently swollen and hot and sensitive to the touch, but they have no tendency to suppuration. The acute inflammation is rapidly followed by the specific induration, which corresponds to the local lesions in other parts of the body.

Chronic farcy in the ass and mule is an excessively rare condition, but sometimes occurs.

CHRONIC GLANDERS.

Symptoms.—In chronic glanders we find the same train of inflammatory phenomena, varying in appearance from those of chronic farcy only by the difference of the tissues in which they are situated. In chronic glanders there is first the nodule, from the size of a shot to that of a small pea, which forms in the mucous membranes of the respiratory tract. This may be just inside the wings of the nostrils or on the septum which divides the one nasal cavity from the other, and may be easily detected, or it may be higher in the nasal cavities on the turbinated bones, or it may form in the larnyx itself or on the surface of the trachea or deep in the lungs.

The nodules, which are first red and hard and consist of new connective tissue, soon soften and become yellow; the yellow spots break and we have a small ulcer the size of the preceding nodule, which has a gray, dirty bottom and ragged edges and is known as a chancre. This ulcer pours from its surface a viscous, oily discharge similar to that which we have seen in the farcy ulcer. The irritation of the discharge may ulcerate the lining mucous membrane of the nose, causing serpentine gutters with bottoms resembling those of the chancres themselves. If the nodules have formed in large numbers, we may have them causing an acute inflammation of the Schneiderian membrane, with a catarrhal discharge which may mark the specific discharge, or that which comes from the ulcers and resembles the discharge of strangles or simple inflammatory diseases.

The eruption of the ulcers and discharge soon cause an irritation of the neighboring lymphatics; and in the intermaxillary space, deep inside of the jaws, we find an enlargement of the glands, which for the first few days may seem soft and edematous, but which rapidly becomes confined to the glands, these being from the size of an almond to that of a small bunch of berries, exceedingly hard and nodulated. This enlargement of the glands is found high on the inside of the jaws, firmly adherent to the base of the tongue. It is not to be confounded with the puffy, edematous swelling, which is not separated from the skin and subcutaneous connective tissues found in strangles, in laryngitis, and in other simple inflammatory troubles.

These glands bear a great resemblance to the indurated glands which we find in connection with the collection of pus in the sinuses; but in the latter disease the glands have not the extreme nodulated feel which they have in glanders. With the glands we find indurated cords, feeling like balls of tangled wire or twine, fastening the glands together.

The essential symptoms of glanders are the nodule, the chancre, the glands, and the discharge. With the development of the nodules in the respiratory tract, according to their number and the amount of eruption which they cause, we may find a cough which resembles that of a coryza, a laryngitis, a bronchitis, or a broncho-pneumonia, according to the location of the lesions. In chronic glanders we find the same accessory symptoms that occur in chronic farcy, the hemorrhage of the nose, the swelling of the legs, the chronic cough, and, in the entire horse, the swelling of the testicles.

On healing, the chancres on the mucous membranes leave small, whitish, star-shaped scars, hard and indurated to the touch, and which remain for almost an indefinite time. The chancres heal and the other local symptoms disappear, with the exception of the enlargement of the glands, and we find these so diminished in size that they are scarcely perceptible on examination. During the subacute attacks, with a minimum quantity of local troubles, in chronic glanders and in chronic farcy the animal rarely shows any degree of fever, but does have a generally depraved appearance; it loses flesh and becomes hidebound; the skin becomes dry and the hairs stand on end. There is a cachexia, however, which resembles greatly that of any chronic, organic trouble, but is not diagnostic, although it has in it certain appearances and conditions which often render the animal suspicious to the eye of the expert veterinarian, while, without the presence of local lesions he would be unable to state on what he has based his opinion.

ACUTE GLANDERS.

Symptoms.—In the acute form of glanders we find the symptoms which we have just studied in chronic farcy and in chronic glanders in a more acute and aggravated form. There is a rapid outbreak of nodules in the respiratory tract which rapidly degenerate into chancres and pour out a considerable discharge from the nostrils. There is a cough of more or less severity according to the amount and site of the local eruption. Over the surface of the body swellings occur which are rapidly followed by farcy buttons, which break into ulcers; we find the indurated cords and enlargement of the lymphatics.

Bleeding from the nose, sudden swelling of one of the hind legs, and the swelling of the testicles are liable to precede an acute eruption of glanders. As the symptoms become more marked the animal has difficulty of respiration, the flanks heave, the respiration becomes rapid, the pulse becomes quickened, and the temperature becomes elevated to 103 deg., 104 deg., or 105 deg. F.

With the other symptoms of an acute fever the general appearance and station of the animal is that of one suffering from an acute pneumonia, but upon examination, while we may find sibilant and mucous rales over the side of the chest, and may possibly hear tubular murmurs at the base of the neck over the trachea, we fail to find the tubular murmur or the large area of dullness on percussion over the sides of the chest which belongs to simple pneumonia.

Diagnosis.—When there is doubt as to the diagnosis, the mallein test, the inoculation test, or the complement-fixation test may be employed. The mallein test is made by injecting mallein (a sterilized extract from a culture of glanders bacilli) beneath the skin. If the horse has glanders there results a febrile reaction and a swelling at the point of injection. If the horse does not have glanders the mallein has no effect or, at most, it produces a slight swelling only at the point of injection. The inoculation test consists in the inoculation of a susceptible animal (usually a guinea pig) with some of the suspected discharge from the nose or a farcy ulcer. If the material is properly used, and if it contains bacilli of glanders, the experimental animal will develop the disease.

The eye test is now universally accepted as a very satisfactory means of diagnosing glanders. This consists in dropping into an eye of a suspected animal a specially prepared solution of mallein, as a result of which in an infected animal the inflammation develops in the eye, resulting in a discharge which varies in intensity from a mucopurulent character to a thick, sticky pus. The eyelids may also swell and many times become glued together. The reaction usually appears in from 8 to 20 hours after the introduction of the mallein.

Neither of these tests should be put into use except by a competent veterinarian. The complement-fixation test is a highly specialized laboratory test and can be carried out only by one versed in laboratory technique. (See Bureau of Animal Industry Bulletin 136.)

The post-mortem examination of the lungs shows that the pneumonia of glanders is a lobular, V-shaped pneumonia scattered throughout the lungs and caused by the specific inflammatory process taking place at the divergence of the smaller air tubes of the lungs. In some cases of acute glanders the formation of nodules may so irritate the mucous membrane of the respiratory tract and cause such a profuse discharge of mucopurulent or purulent matter that the specific character of the original discharge is entirely masked. In this case, too, for a few days the submaxillary space may so swell as to resemble the edematous, inflamed glands of strangles, equine variola, or laryngitis. This condition is especially liable to be marked in an acute outbreak of glanders in a drove of mules.

Cases of chronic farcy and glanders, if not destroyed, may live in a depraved condition until the animal dies from general emaciation and anemia, but in the majority of cases, from some sudden exposure to cold, it develops an acute pneumonia or other simple inflammatory trouble which starts the latent disease and the animal has acute glanders.

In the ass, mule, and plethoric horses acute glanders usually terminates by lobular pneumonia. In other cases the general symptoms may subside. The symptoms of pneumonia gradually disappear, the temperature lowers, the pulse becomes slower, the ulcers heal, leaving small, indurated cicatrices, and the animal may return to apparent health, or may at least be able to do a small amount of work with but a few symptoms of the disease remaining in a chronic form. During the attack of acute glanders the inflammation of the nasal cavities frequently spreads into the sinuses or air cells, which are found in the forehead and in front of the eyes on either side of the face, and causes abscesses of these cavities, which may remain as the only visible symptom of the disease. An animal which has recovered from a case of acute glanders, like the animals which are affected by chronic glanders and chronic farcy, is liable to be affected with emphysema of the lungs (heaves), and to have a chronic cough. In this condition it may continue for a long period, serving as a dangerous source of contagion, the more so because the slight quantity of discharge does not serve as a warning to the owner or driver as profuse discharge does in the more acute cases.

At the post-mortem examination of an animal which has been destroyed or has died of glanders we find evidences of the various lesions which we have studied in the symptoms. In addition to this, we find nodules similar to those which we have seen on the exterior throughout the various organs of the body. Nodules may be found in the liver, in the spleen, and in the kidneys. We may find inflammation of the periosteum of the bones, and we have excessive alterations in the marrow in the interior of the bones themselves. Both these conditions during the life of the animal may have been the cause of the lamenesses which were difficult to diagnose.

In one case which came under the observation of the writer, a lame horse was destroyed and found to have a large abscess of the bone of the arm, with old nodules of the lungs. When an animal has died immediately after an attack of a primary, acute case of glanders, we find small V-shaped spots of acute pneumonia in the lungs. If the animal has made an apparent recovery from acute glanders, and in cases of chronic farcy and chronic glanders, no matter how few the external and visible symptoms may have been, there is a deposit of nodules—small, hard, indurated nodes—of new connective tissue to be found in the lungs. When these have existed for some time we may find a deposit of lime salts in them. These indurated nodules retain the virus and their power to give out contagion for almost an indefinite time, and predispose to the causes which we have studied as the common factors in developing a chronic case into an acute case; that is, an inflammatory process wakens their vitality and produces a reinfection of the entire animal. The blood of an animal suffering from chronic glanders and farcy is not virulent and is unaltered, but during the attack of acute glanders, while the animal has fever, the blood becomes virulent and remains so for a few days.

Treatment.—Almost the entire list of drugs in the pharmacopoeia has been tested in the treatment of glanders. Good hygienic surroundings, good feed, with alteratives and tonics, frequently ameliorate the symptoms, and often do so to such an extent that the animal would pass the examination of any expert as a perfectly sound animal. While in this case the number of nodules of the lungs, which are invariably there, may be so few as not to cause sufficient disturbance in the respiration as to attract the attention of the examiner, yet they exist, and will remain there almost indefinitely, with the constant possibility of a return of acute symptoms.

It is probable that some horses may recover from glanders if the infection is slight, but it will not do to depend upon this except under the most stringent veterinary supervision. With good care, good feed, good surroundings and little work, an animal affected with glanders may live for months or even years in a state of apparently perfect health, but with the first deprivation of feed, with a few days of severe hard work, with exposure to cold or with the attack of a simple fever or inflammatory trouble from other causes, the latent seeds of the disease break out and develop the trouble again in an acute form.

In several celebrated cases horses which have been affected with glanders have been known to work for years and die from other causes without ever having had the return of symptoms; but allowing that these cases may occur, they are so few and far between, and the danger of infection of glanders to other horses and to the stable attendants is so great, that no animal which has once been affected with the disease should be allowed to live unless repeated mallein tests have shown him to have become free from taint of glanders.

In all civilized countries, with the exception of some of the States in the United States, the laws are most stringent regarding the prompt declaration on the part of the owner and attending veterinarian at the first suspicion of a case of glanders, and they allow indemnity for the animal. When this is done, in all cases the animal is destroyed and the articles with which it has been in contact are thoroughly disinfected. When the attendants have attempted to hide the presence of the disease in a community, punishment is meted out to the owner, attending veterinarian, or other responsible parties. Several States have passed excellent laws in regard to glanders, but these laws are not always carried out with the rigidity with which they should be.

SPOROTRICHOSIS (MYCOTIC LYMPHANGITIS).

By JOHN R. MOHLER, V. M. D., Assistant Chief, Bureau of Animal Industry.

This disease has previously been known in this country as epizootic lymphangitis, or pseudo-farcy. It is a chronic, contagious disease, particularly of equines, caused by a specific organism, the Sporotrichum schenckii, and characterized by a suppurative inflammation of the subcutaneous lymph vessels and the neighboring lymph glands. Owing to the fact that this affection does not spread as an epizootic and that its causal factor is a fungus, the name sporotrichosis has been suggested.

The disease in man was first described by Schenck and by Beurmann and Gougerot. Carougeau observed its occurrence among horses and mules in Madagascar, while in the United States it was first observed by Pearson in Pennsylvania in 1907, although it is probable that it had existed for many years in various parts of this country. Page and Frothingham were first to recognize its mycotic nature in the United States. More recently Meyer has also made valuable contributions with regard to the existence of this affection. Its presence has been definitely established in Ohio, Iowa, California, and North Dakota, and there is a probability of its existence in Indiana and several Western States.

Bacteriology.—The sporotrichum is 2 microns thick, cylindrical and segmented, having more or less branching threads, which bear spores at the end. In the pus they occur as slightly ovoid bodies 3 to 5 microns long, which are somewhat pointed toward the poles, have a sharp double contour, and only on artificial cultivation at a temperature of over 18 deg. do they develop into the characteristic spore-carrying threads.

The period of incubation varies greatly, extending from three days to four months, or even longer. In artificial inoculations with pus through wounds in the skin, inflammation and swelling of the lymph vessels may be noticed in ten to sixty days; these vessels show in their course a development of hard nodules, from which abscesses form.

The natural infection without doubt is caused through superficial wounds, such as galls, barbed-wire cuts, or through various stable utensils, harness, bandages, insects, etc. Solipeds are mostly susceptible, but cattle may also be infected.

Symptoms.—The inflammation of the lymph vessels is usually first observed on the extremities, especially on one or both hind legs; it may also appear on the forelegs, shoulder, or neck, and more rarely on the rump, udder, and scrotum. The lesions, as a rule, develop in the tissue adjacent to the place of inoculation. In the early stages of the disease the lymph vessels appear very hard and thickened, and along their course hard nodules develop, ranging in size from a pea to a hen's egg. Later these nodules soften, burst spontaneously, and discharge a thick, yellowish pus. The surface of the resulting ulcers or abscess cavities soon fills up with exuberant granulations which protrude beyond the surface of the skin, giving it a fungoid appearance. The affected extremities are considerably enlarged, similar to cases of simple lymphangitis. In rare cases the mucous membrane of the nostrils may also become affected, showing yellowish flat elevations and ulcerations, and these may extend by metastasis to internal organs. In cases in which the mucous membrane is affected, the submaxillary lymph gland may also become enlarged and suppurate.

The constitutional symptoms accompanying this disease are not very marked and may be altogether absent. There is usually only a very slight fever, which seldom runs over 102 deg. F. The appetite is not impaired except in the advanced cases.

Lesions.—The anatomical changes are most marked in the skin and the subcutaneous tissues. They may become 2 to 3 inches thick and indurated as the result of fibrous-tissue formation, owing to the inflammation present. On the baconlike cut surface suppurative areas and granulating sores may be noticed of various sizes, also enlarged lymph vessels filled with clotted lymph mixed with pus. The neighboring lymph glands are usually enlarged and frequently contain suppurating foci. Rarely the internal organs may show metastatic abscesses.

Diagnosis.—The diagnosis is based on the characteristic appearance of the ulcerations, which show exuberant granulation of a bright red color, inverted edges, and a thick, creamy, glutinous discharge. These manifestations differentiate the disease from glanders, in which the ulcers are craterlike, do contain exuberant granulations, and the discharge is of a viscous, oily character. The submaxillary and other nodes as well as the corded lymphatics in glanders are more firmly attached to the adjacent tissues, and are therefore less movable. In some chronic cases of sporotrichosis, however, the lesions may closely resemble those of farcy, and in these cases the microscopical examination of the pus will disclose the nature of the affection. In the pus the causative organism can be easily seen in the unstained specimen, and is recognized by its size, shape, and highly refractory double outline. Furthermore, the injection of mallein in cases of sporotrichosis will be attended with negative results.

Treatment.—At the onset of the disease treatment consists in entire extirpation of the nodules, in case the lesions are localized. In cases in which the nodules have formed abscesses, their opening is recommended, followed by the application of the actual cautery or a 1 to 250 solution of bichlorid of mercury. It must be borne in mind that the organism is quite resistant to antiseptics, and the best results will be obtained from the application of a solution of a strong antiseptic following the opening of the lesions. Internally, potassium iodid is recommended in 2-dram doses, dissolved in drinking water, twice a day.

In the most favorable cases recovery results in from five to seven weeks; as a rule, however, it requires several months.

In order to prevent the spreading of the disease the affected animals should be isolated, the products of the disease should be destroyed, and the stable should be disinfected with very strong liquid disinfectants in consideration of the resistance of the causative organism.

RABIES, HYDROPHOBIA, OR MADNESS.

Rabies is a contagious disease, which is usually transmitted by a bite and by the introduction of a virus contained in the saliva of an affected animal. It may, however, be transmitted in other ways. It is characterized by symptoms of aberration of the nervous system and invariably terminates fatally. It is accompanied with lesions, inflammation, and degeneration in the central nervous system. It is a disease that is most common in the dog, but is transmitted to the horse, either from dogs or from any other animal affected with it. (See also remarks on page 244.) As a disease of the horse it is invariably the result of the bite of a rabid animal, usually a dog.

Perhaps no disease in medicine has been the object of more controversy than rabies. Certain medical men of prominence have even doubted its existence, and many others have claimed for it a spontaneous origin. The experience of ages, however, has shown that contagion can be proved in the great majority of cases, and, by analogy with other contagious diseases, we may only believe that the development of one case requires the preexistence of a case from which the virus has been transmitted. Pasteur has further added to our knowledge of the disease by showing that a virus capable of cultivation exists in the nervous system, especially in the lower part of the brain (medulla oblongata) and in the anterior part of the spinal column. He has further shown that that portion of the nervous system which contains the virus, the exact nature of which has not yet been demonstrated, will retain it for a very long time if kept at a very low temperature or if left surrounded by carbolic acid; but if the nerve matter, which is virulent at first, is exposed to the air and is kept from putrefaction by substances which will absorb the surrounding moisture, it will gradually lose its virulence and become inoffensive in about fifteen days. He has also further shown that the action of a weak virus on an animal will prevent the development of a stronger virus, and from this he has formulated his method of prophylactic treatment. This treatment consists in the successive inoculation of portions of the nerve matter containing the virus from a rabid animal which has been exposed to the atmosphere for thirteen days, ten days, seven days, and four days, until the virulent matter which will produce rabies in any unprotected animal can be inoculated with impunity. A curious result of the experiments of Pasteur is that an animal which has first been inoculated with a virus of full strength can be protected by subsequent inoculations of attenuated virus repeated in doses of increasing strength.

Innumerable attempts have been made to discover the causative agent, and investigators have announced the finding of many of the lower forms of animal and vegetable life as the pathogenic factor. Among the recently described causes, certain protozoanlike bodies found in the ganglionic cells in 1903 by Negri, and termed Negri bodies, are of a very suggestive nature. Negri claims that these bodies are not only specific for rabies, but that they are protozoa and the cause of the disease. His work has been corroborated by investigators in all parts of the scientific world. An examination of the vitality of these bodies will show a striking resemblance to the vitality of an emulsion of the virulent tissue. Thus, they have been found to be quite resistant to external agencies, such as putrefaction, drying, etc., and are about the last portion of the nerve cell to survive the advance of decomposition. They are also found in more than 96 per cent of the cases of rabies examined, but have not been proved to exist in other diseases.

Valenti states, as his strongest evidence of the protozoan nature of the bodies, that the virus of rabies is neutralized in test tubes by quinin, while no other alkaloid has this property. As a result of the work performed in the New York City Board of Health laboratory, Park claims that Negri bodies are found in animals before the beginning of visible symptoms, and evidence is given that they may be found early enough to account for the infectiousness of the central nervous system. These bodies are now almost universally considered as diagnostic of rabies, and in the pathological laboratory of the Bureau of Animal Industry their detection in the nerve cells of the brain suffices for a diagnosis of rabies without animal inoculations. In case these granular bodies are not found in a suspected animal, the plexiform ganglion is next examined, and should negative results still be obtained, the inoculation of rabbits is then made as a last resort. It is indeed rare that positive results are obtained from the latter method after the first two methods have been negative, but it has occurred occasionally in cases in which the animal had been killed in the early stages of the disease.

Symptoms.—From the moment of inoculation by the bite of a rabid dog or other rabid animal or by other means, a variable time elapses before the development of any symptoms. This time may be eight days or it may be several months; it is usually about four weeks. The first symptom is an irritation of the original wound. This wound, which may have healed completely, commences to itch until the horse rubs or bites it into a new sore. The horse then becomes irritable and vicious, and it is especially susceptible to moving objects, excessive light, noises, the entrance of an attendant, or any other disturbance will cause the patient to be on the defensive. It apparently sees imaginary objects; the slightest noise is exaggerated into threatening violence; the approach of an attendant or another animal, especially a dog, is interpreted as an assault and the horse will strike and bite. The violence on the part of the rabid horse is not for a moment to be confounded with the fury of the same animal suffering from meningitis or any other trouble of the brain. But in rabies there is a volition, a premeditated method, in the attacks which the animal will make, which is not found in the other diseases. Between the attacks of fury the animal may become calm for a variable period. The writer attended a case in which, after a violent attack of an hour, the horse was sufficiently calm to be walked 10 miles and only developed violence again an hour after being placed in the new stable. In the period of fury the horse will bite at the reopened original wound; it will rear and attempt to break its halter and fastenings; it will bite at the woodwork and surrounding objects in the stable. If the animal lives long enough it shows paralytic symptoms and falls to the ground, unable to use two or more of its extremities, but in the majority of cases in its excesses of violence it does physical injury to itself. It breaks its jaws in biting at the manger or fractures other bones in throwing itself on the ground and dies of hemorrhage or internal injuries. At times throughout the course of the disease there is an excessive sensibility of the skin which, if irritated by the touch, will bring on attacks of violence. Throughout the course of the disease the animal may have appetite and desire water, but on attempting to swallow has a spasm of the throat which renders the act impossible. This latter condition, which is common in all rabid animals, has given the disease the name of hydrophobia (fear of water).

In a case under the care of the writer a horse, four weeks after being bitten on the forearm by a rabid dog, developed local irritation in the healed wound and tore it with its teeth into a large ulcer. This was healed by local treatment in 10 days, and the horse was kept under surveillance for more than a month. On the advice of another practitioner the horse was taken home and put to work; within 3 days it developed violent symptoms and had to be destroyed.

Diagnosis.—The diagnosis of rabies in the horse is to be made from the various brain troubles to which the animal is subject; first by the history of a previous bite of a rabid animal or inoculation by other means; second, by the evident volition and consciousness on the part of the animal in its attacks, offensive and defensive, on persons, animals, or other disturbing surroundings. The irritation and reopening of the original wound or point of inoculation is a valuable factor in diagnosis. Diagnosis after death may be made by microscopic examination for Negri bodies or by the inoculation of rabbits, as already mentioned.

Recovery from rabies may be considered as a question of the correctness of the original diagnosis. Rabies is always fatal.

Treatment.—No remedial treatment has ever been successful. All the anodynes and anesthetics, opium, belladonna, bromid of potash, ether, chloroform, etc., have been used without avail. The prophylactic treatment of successive inoculations is being used on human beings, and has experimentally proved efficacious in dogs, but would be impracticable in the horse unless the conditions were quite exceptional.

DOURINE.

By JOHN R. MOHLER, V. M. D., Assistant Chief, Bureau of Animal Industry.

Dourine (also known as maladie du coit, equine syphilis, covering disease, breeding paralysis) is a specific infectious disease affecting under normal conditions only the horse and ass, transmitted from animal to animal by the act of copulation, and due to an animal parasite, the Trypanosoma equiperdum.

History.—It is described as having existed as early as 1796 in the Eastern Hemisphere, and was more or less prevalent in several of the European countries, including France, Germany, Austria, and Switzerland, during the first half of the nineteenth century. Its presence was recognized for the first time in the United States in 1886, when an outbreak occurred in Illinois. Since then the existence of the disease has been observed at irregular intervals in numerous other States, including Nebraska, Iowa, Montana, Wyoming, New Mexico, North Dakota, and South Dakota.

Symptoms.—There are many variations in the symptoms of dourine, and this is particularly true of the disease as it occurs in this country. Two distinct stages may be noted which vary somewhat from those described in textbooks, but probably no more than could be expected when differences of climatic conditions and methods of handling are taken into consideration.

The first stage chiefly concerns the sexual organs and therefore differs somewhat in the male and female. In the second stage the symptoms indicating an affection of the nervous system are more prominent and are not dependent upon the sex of the animal.

Following a variable period of incubation of from 8 days to 2 months, there is seen in the stallion an irritation and swelling about the penis and sheath. In a few days small vesicles or blisters may appear on the penis, which later break, discharging a yellowish, serous fluid and having irregular, raw ulcers. The ulcers show a tendency to heal rapidly, leaving scars which are permanent. There may be more or less continuous dripping from the urethra of a yellowish, serouslike fluid. Stallions may show great excitement when brought in the vicinity of mares, but service is often impossible because of the fact that a complete erection of the penis does not occur.

In the mare the first symptoms may be so slight as to be overlooked. The disease, being the result of copulation, usually begins with inflammation of the vulva and vagina. There may be a mucopurulent discharge, which may be slight or profuse in quantity, agglutinating the hairs of the tail. The mare may appear uneasy and urinate frequently. Vesicles may appear on the external vulva and mucous membrane of the vulva and vagina which later rupture and form ulcers. On the dark skin of the external vulva the scars resulting from healing of the ulcers are white, more or less circular in outline, from one-eighth to half an inch in diameter, and pitlike. This depigmentation of the skin about the external genitals is permanent.

Urticarial eruptions or plaques which break out over various parts of the body are a frequent symptom seen in animals of either sex. These are sharply defined and edematous swellings of the skin about the size of a half dollar or may be even larger. The usual locations of these plaques are the croup, belly, and neck.

The intensity of the symptoms mentioned which are significant of the early stage of the disease may vary to a wide extent and in many instances be so mild as to escape the attention of any but the most careful observer. They commonly disappear after a brief period. The apparent recovery, however, is not permanent, for such animals after a period of variable length manifest constitutional or nervous symptoms. These may not appear for several months or even years. They consist of a general nervous disorder with staggering, swaying gait, especially in the hind limbs. The animal generally becomes emaciated, the abdomen assuming a tucked-up appearance. The first indication of paralysis will be noted in traveling, when the animal fails to pick up one of the hind feet as freely as the other, or both may become affected at the same time, at which time knuckling is a common symptom. Labored breathing is occasionally noted. When the paralysis of the hind limbs starts to appear the disease usually progresses rapidly. The horse goes down, is unable to rise, and dies in a short time from nervous exhaustion. The appetite usually remains good up to the last.

Although a case of dourine may now and then recover, as a rule the disease is present in the latent stage. Bad weather, exposure, insufficient feed, and complicating diseases like influenza, distemper, or in fact any condition which tends to lower the vitality of the animal, may hasten the termination of the disease.

Diagnosis.—The complement-fixation test furnishes by far the most reliable means of diagnosis and is especially valuable in a chronic affection of this character, when the symptoms manifested are variable and frequently so obscure as to escape observation. This is a laboratory test requiring special facilities and the services of a trained bacteriologist.

Treatment.—Little benefit can be obtained from medicinal treatment, nor is such treatment desirable in this country, where the disease has existed only in restricted areas, and where sanitary considerations demand its prompt eradication.

INFECTIOUS ABORTION IN MARES.

Infectious abortion (also known as contagious abortion, epizootic abortion, enzootic abortion, slinking of colts) is a disease of mares which from a specific cause results in the premature expulsion of the fetus and its membranes from the uterus. It is characterized by an inflammatory condition of the female reproductive organs.

The contagious nature of the disease had not been recognized until recently, the disease being principally attributed to various conditions, such as traumatic influences, various infectious diseases, spoiled feed, drugs, and other factors. Ostertag was the first to study premature births in mares, attributing as the cause of the same a streptococcus, which he was supposed to have been able to use successfully in artificially producing abortion, either by inoculations or feeding. His findings could not be substantiated by other investigators.

The earliest appearance of the disease in this country was in 1886, at which time it caused considerable damage to the horse-breeding industry in the Mississippi Valley. Smith and Kilbourne investigated an outbreak in Pennsylvania in 1893, at which time they incriminated another germ belonging to the paratyphus B group as the causative factor of the disease. These findings have been subsequently substantiated by many investigators abroad, as well as in this country, notably so by De Jong, Dassonville, and Riviere, and by Good and Meyer. More recently very valuable information was contributed to our knowledge on this disease by Schofield, of Canada, especially with regard to the biological tests for diagnosis. Good suggested "Bacillus abortivus equinus" as the name for the specific organism.

The causative agent of this disease is not identical with the germ causing abortion in cattle. It exerts its action, however, in a similar manner, and appears to have, under certain conditions, a predilection for the genital organs of the mare, where it induces certain morbid changes whereby a premature expulsion of the fetus is the result. The germ is usually present in the fetal membranes and also in the aborted fetus. Mares may harbor the infection without disclosing any apparent ill effects. It appears to exert its influence mainly upon the female genital organs, where it may induce an inflammatory condition of the uterus.

The infected animals may carry the fetus through the normal period of pregnancy, giving birth to either a normal or a weak colt, or again abortion may take place at any time during pregnancy, mostly, however, from the sixth to the ninth month.

Symptoms.—The symptoms suggestive of abortion are frequently entirely absent. At times the abortion may be ushered in by symptoms of colicky pains, restlessness, and periodical straining; these, however, are by no means constant, especially if the abortion takes place in the early months of pregnancy. The genital organs are usually swollen, showing a mucous discharge. Immediately before abortion the symptoms are more aggravated. Following abortion the discharge is more characteristic, being of a dark-brown color, sometimes even bloody, and contains streaky or flaky pus. The fetal membranes in all cases are not expelled with the aborted fetus, but there is a tendency toward retention of these membranes, which frequently has serious consequences upon the health of the animal. At times it becomes necessary to resort to manual removal of the afterbirth, and the inflammation of the uterus and a chronic discharge usually follow such conditions. The expelled fetuses, as a rule, die soon after the abortion, and if the expulsion has taken place at a time close to its full term the fetuses are usually poorly developed and subject to various kinds of digestive and septic disorders. The fetuses do not disclose any particular abnormal appearance on external examination; in many cases, however, the post-mortem examination reveals inflammatory changes of various organs.

The method of infection has not yet been satisfactorily established; nevertheless it is essential that we consider as the principal mode of infection the ways which have been proved for the contagious abortion in cattle. These are especially by ingestion; that is, by taking up the germs with the feed, water, or other means, which have become contaminated with the germs. The infection through the genital organs is probably not so frequent, but in this regard the stallion no doubt plays an important role in the spreading of the disease. Schofield considers this method of infection as the principal source of spreading the disease.

It must be considered that in infected stables the germs may be present throughout the premises, and by keeping animals which have aborted in such stables a contamination of feed and utensils may continually take place, since the aborted mares usually discharge a considerable quantity of material which is often heavily charged with the germs. The germ is taken up by the body with the feed or water, passing from the intestines into the blood, and from there is carried to the genital organs, where it finds suitable conditions for its development. Milk from an infected mare may also contain the germ, and colts may become infected by sucking the milk of infected mothers. In such instances the infection may remain dormant until the colt develops and becomes pregnant, when the organism, finding a condition suitable for its development, produces the disease.

On the other hand, stallions used in covering infected mares may be carriers of the germs, and when used for the breeding of healthy animals may in this manner readily transmit the disease to them.

Diagnosis.—Contagious abortion may be diagnosed by the changes which occur in the fetal membranes, and also in the expelled feces. In order, however, to substantiate a diagnosis with certainty, demonstration of the germ by microscopical examination is necessary. The occurrence of frequent abortions among the mares in a stable is also an additional evidence of the contagious character of the malady. It must be considered that at times infected mares may carry the fetus to full maturity, in which case the diagnosis is possible only by blood examinations in a laboratory.

Infected animals usually abort only once; however, in a certain proportion of cases they may abort even two, three, or four times in succession.

Animals which establish a tolerance for the infection, and carry the fetus to full maturity, may nevertheless remain a source of danger for spreading the disease.

The tests used in laboratories for the diagnosis are the agglutination and complement-fixation tests, by which the disease may be diagnosed from a sample of blood from a suspected animal. Such tests, however, have to be confined to the laboratories, which are equipped for such work.

Treatment and prevention.—Medicinal treatment is usually of no avail, and all efforts should be directed toward the prevention of the disease. Various medicinal agents have been recommended and are being exploited for the treatment, but to the present time no satisfactory evidence has been established as to their merits. Bacterial vaccines prepared from the specific organism have been given limited trials, but to date they can not be considered as entirely satisfactory, since it will require considerable experience with them before their usefulness can be definitely established.

The prevention should consist largely in sanitary measures directed toward the disinfection of premises and animals. (For a method for disinfection of premises see article under that heading.)

The following procedure is advised for the disinfection of animals: To prevent a stallion from carrying the infection from a diseased mare to a healthy one the sheath and the penis should be disinfected with a solution of 1/2 per cent of compound cresol solution, lysol, or trikresol, or a 1 per cent carbolic acid or 1 to 1,000 potassium permanganate solution in warm water. For this purpose it is advisable to use a soft-rubber tube with a large funnel attached to one end, or an ordinary syringe and tube would serve the purpose. The tube should be inserted into the sheath, and the foreskin held with the hand to prevent the immediate escape of the fluid. In addition to this the hair of the belly and inner side of the thighs should be sponged with an antiseptic. This disinfection should invariably precede and follow every service.

With regard to the mares, a period of three months should elapse between abortion and a subsequent breeding, and especially if there is any evidence of a discharge the breeding of the animal should not be undertaken. The mare showing signs of abortion should be immediately isolated and the fetus and membranes should be burned. The fetus should never be dragged across a barnyard or stable, but should be removed by other means by which the contamination of the premises may be prevented. The stall in which the animal aborted should be thoroughly disinfected and the genital organs of the mare washed daily with a disinfectant. The antiseptic washing recommended for the treatment of the stallions prior to and after breeding should be also used for the irrigation of the uterus of mares which have aborted. This treatment should be continued daily until all evidence of discharge has ceased. The isolation of the animal should be carried out for at least one month after the evidence of a discharge has ceased.

By carefully and persistently carrying out the sanitary measures it may be possible to control and finally eradicate the disease.

NAVEL ILL OF COLTS.

Navel ill of colts is also known as joint ill, omphalophlebitis, septic arthritis of sucklings, and pyosepticemia of the newly born. The unfavorable outlook after the appearance of the disease, together with the fact that the disease when present requires the attention of a veterinarian, demands that the breeder concern himself with its prevention.

The disease is caused by a microorganism and several bacteria have been suspected of being responsible. Every one of the suspected organisms is found abundantly in manure and objects contaminated with manure. The infective material gains entrance into the colt through the open umbilical cord as a result of its coming into contact with litter, floors, or discharges from its dam contaminated by one of the organisms which cause the trouble. There are cases on record in which the infection has taken place before birth, and while some investigators assert that this method is the principal mode of infection still, in a large number of cases, the prophylactic measures adopted to guard against the infection through the navel cord have given good results. Since infection before birth can not be controlled satisfactorily, we are justified, for all practical purposes, in preventing navel ill by guarding against the infection through the cord at birth or soon afterwards.

Cleanliness of stables where pregnant mares are kept must be insisted upon. This is especially necessary where outbreaks of navel ill have been known to exist. Mares in the last stages of gestation should be placed in a box stall which has previously been cleaned and disinfected. The bedding should be frequently renewed and the external genitals and neighboring tissues should be kept clean and disinfected with a 2 per cent solution of carbolic acid or 1 per cent liquor cresolis compositus, or any other reliable disinfecting agent. Operations for opening abscesses and removal of afterbirths from cows should not be executed in the immediate vicinity of mares in an advanced stage of pregnancy.

The foal when dropped should be placed on clean bedding. In any event the cord of the foal should be washed in a disinfectant solution and tied at about 1-1/2 inches from the navel with a band or string which has previously been soaked in a disinfectant solution. With a sharp pair of scissors the navel cord is then severed about one-half inch below the band and again disinfected. The ligature should not be tightened, however, until pulsation of the vessels in the cord has ceased. The stump of the cord is then painted with strong carbolic-acid solution, tincture of iodin, or a mixture of equal parts of tincture of iodin and glycerin. The stump should be washed daily with a disinfectant and either painted with iodin mixture or carbolic acid or dusted with some reliable antiseptic healing powder. After five days the parchmentlike dried stump may be cut off and the navel wound washed with a disinfectant solution and dusted with powder until healed.

The cases of navel ill resulting from infection before birth can not well be guarded against. By keeping mares, advanced in pregnancy, in good physical condition, the fetus will be expelled immediately upon the opening of the uterine cavity.

Once the infection of the navel cord has set in, the cord should not be ligated but should be washed in a disinfectant solution and a veterinarian called for the subsequent treatment.

INFECTIOUS ANEMIA OR SWAMP FEVER.

By JOHN R. MOHLER, V. M. D., Assistant Chief, Bureau of Animal Industry.

Infectious anemia of horses, known also by a number of other names, as swamp fever, American surra, malarial fever, typhoid fever of horses, the unknown disease, no-name disease, plains paralysis, and pernicious anemia, has recently been the subject of much investigation. The cause of the disease has now been definitely determined as an invisible virus, which is capable of passing through the pores of the finest porcelain filters, like the infection of foot-and-mouth disease, rinderpest, hog cholera, and similar diseases. The disease is most prevalent in low-lying and badly drained sections of the country, although it has been found on marshy pastures during wet seasons in altitudes as high as 7,500 feet. Therefore proper drainage of infected pastures is indicated as a preventive. It is also more prevalent during wet years than in dry seasons. It usually makes its appearance in June and increases in frequency until October, although the chronic cases may be seen in the winter, having been contracted during the warm season.

Cause.—It has been conclusively proved that infectious anemia is produced by an invisible filterable organism which is transmissible to horses, mules, and asses by subcutaneous inoculation of blood serum. The virus which is present in the blood may be transmitted to a number of equines in a series of inoculations by injecting either the whole blood, the defibrinated blood, or the blood serum which has been passed through a fine Pasteur filter, thus eliminating all the visible forms of organismal life, including bacteria, trypanosoma, piroplasma, etc. This virus has also been found to be active in the carcass of an affected animal 24 hours after death.

Following the injection of the infectious principle there is a period of incubation which may extend from ten days to one and one-half months, at the end of which time the onset of the disease is manifested by a rise of temperature. If uncomplicated, the infection runs a chronic course, terminating in death in from two months to one and one-half years, or even longer. The probability of the virus being spread by an intermediate host, such as flies, mosquitoes, internal parasites, etc., is now receiving careful investigation.

From experiments already conducted it appears that this disease, formerly supposed to be confined to Manitoba and Minnesota, is more or less prevalent in Kansas, Nebraska, Colorado, Wyoming, Montana, North Dakota, Virginia, Texas, and New York. It also occurs in Europe, having been reported in Germany under the name of infectious anemia and in France as infectious typho-anemia.

Symptoms.—The disease is characterized by a progressive pernicious anemia, remittent fever, polyuria, and gradual emaciation in spite of a voracious appetite. It begins to manifest itself by a dull, listless appearance and by general weakness, the animal tiring very easily. This stage is followed closely by a staggering, swaying, uncertain gait, the hind legs being mostly affected. There is also noted a weakness and tenderness in the region of the loins, and at the same time the pulse, though weak, stringy, and intermittent, increases in rapidity and may run as high as 70. The temperature may rise to 103 deg. F. or higher, remaining high for several days, and then dropping to rise again irregularly. Toward the end of the disease the temperature occasionally remains persistently high. The horse may improve for a time, but usually this improvement is followed by a more severe attack than the first. Venous regurgitation is sometimes noticed in the jugular before death. The quantity of urine passed is enormous in some cases. Death finally occurs from exhaustion or syncope.

The blood shows a slight decrease in the number of white blood cells, while there is a gradual but marked diminution of red corpuscles, the count running as low as 2,000,000 per cubic millimeter, the normal count being 7,000,000. If the blood is drawn from such an animal, the resulting red clot will be about one-fifth of the amount drawn. Occasionally a slow dripping of blood-tinged serum from the nostrils is observed as a result of this very thin blood oozing from the mucous membranes. Petechiae, or small hemorrhagic points, are sometimes noticed on the nictitating membrane and conjunctiva, while paleness of the visible mucous membranes of the nose and mouth is usually in evidence, although they may have a yellow or mahogany tinge. Often a fluctuating, pendulous swelling may appear on the lower lip, point of elbow, sheath, legs, under the belly, or on some other pendent portion, especially late in the disease, which is indicative of poor circulation, thinning of the blood, and consequent loss of capillary action.

Lesions.—After death the carcass is found to be very much emaciated and anemic, the visible mucosa being very pale. This marked absence of adipose tissue makes the skinning of the animal a difficult task. Subcutaneous and intermuscular edema and hemorrhages are frequently observed, although in many cases it is remarkable to see how few macroscopic lesions may be present. The predominating and most constant lesion is probably the petechiae, so often observed in the muscle or on the serous membranes of the heart. The heart is generally enlarged and may be the only organ to show evidence of disease. In other cases the lungs may be studded with petechiae, with a serous exudate present in the thoracic cavity. In addition to the petechiae already noted, the pericardial sac generally contains an increased quantity of fluid. The abdominal cavity may show peritonitis and a hemorrhagic condition of the intestines, which probably result from overfeeding in consequence of the ravenous appetite. The liver, although usually normal, sometimes presents a few areas of degeneration. The spleen is at times found to be enlarged and covered with petechiae. The kidneys may appear normal or anemic and flaccid, but microscopically they usually show a chronic parenchymatous degeneration. The lymph glands may be enlarged and hemorrhagic.

Diagnosis.—The diagnosis of the disease is not difficult, especially in advanced stages. The insidious onset, remittent fever, progressive emaciation and anemia, unimpaired or ravenous appetite, staggering gait and polyuria are a train of symptoms which make the disease sufficiently characteristic to differentiate it from other diseases affecting horses in this country. The peculiar relapsing type of fever, the great reduction in the number of red blood cells, and the absence of eosinophila are sufficient to differentiate it from the anemias produced by internal parasites, while it may be readily distinguished from surra by the nonsusceptibility of cattle and by the great ease with which the trypanosoma may be found in the latter affection.

Prognosis.—The prognosis of the disease is very unfavorable. Veterinarians in different sections of the country where it is prevalent report a mortality of 75 per cent or even higher. Recovery takes place only when treatment is begun early or when the animal has a long convalescent period.

Treatment.—The treatment of the disease has so far been far from satisfactory. The iodid, permanganate, and carbonate of potash have been used. Arsenic, axytol, quinin, and silver preparations have been suggested, but all have been uniformly without success. Intestinal antiseptics have been resorted to, and the results are encouraging but not altogether satisfactory. Symptomatic treatment seems to be the most dependable. For instance, Davison, of this bureau, was able to reduce greatly the mortality from this affection by giving an antipyretic of 40 grains of quinin, 2 drams of acetanilid, and 30 grains of powdered nux vomica four times daily. In the late stages, with weak heart action, alcohol should be substituted for acetanilid. Cold-water sponge baths may be given, and in addition frequent copious injections of cold water per rectum, which has a beneficial effect in reducing the temperature and in stimulating peristalsis of the bowels, which, as a result of the disease, show a tendency to become torpid during the fever. Purgatives, on account of their debilitating effect, should not be given unless absolutely necessary, but laxatives and easily digested feeds should be given instead. Not infrequently a dirty yellowish tinge of the visible mucous membranes has been observed, in which cases 20 grains of calomel in from 2 to 4 drams of aloes in a ball, or 2-dram doses of fluid extract of podophyllin, may be given. Following the subsidence of the fever, a tonic should be administered, composed of the following drugs in combination:

Arsenious acid grams 2 Powdered nux vomica do 28 Powdered cinchona bark do 85 Powdered gentian root do 110

These should be well mixed and one-half teaspoonful given to the affected animal at each feed.

As in the case of all other infectious diseases, the healthy should be separated from the sick horses and thorough disinfection of the infected stables, stalls, litter, and stable utensils should be carried out in order to prevent the recurrence of the disease. As a disinfectant the compound solution of cresol, carbolic acid, or chlorid of lime may be used, by mixing 6 ounces of any one of these chemicals with 1 gallon of water. One of the approved coal-tar sheep dips may also be used to advantage in a 5 per cent solution (6 ounces of dip to 1 gallon of water). The disinfectant solution should be applied liberally to all parts of the stable, and sufficient lime may be added to the solution to make the disinfected area conspicious.

Investigations are now in progress with a view of producing a vaccine or serum that will protect horses that have been exposed to the disease.

SURRA.

By CH. WARDELL STILES, PH. D.

Professor of Zoology, United States Public Health Service.

Surra is not known to occur in the United States, but it is more or less common in the Philippine Islands and India. It is caused by a microscopic, flagellate animal parasite, known as Trypanosoma evansi, 20 to 34 mu long by 1 to 2 mu broad, which lives in the blood and destroys the red blood corpuscles. In general the disease is very similar to and belongs in the same general class with tsetse-fly disease, or nagana, of Africa and mal de caderas, of South America.

Surra is a wet-weather disease, occurring chiefly during or immediately after heavy rainfalls, floods, or inundations.

Surra attacks especially horses, asses, and mules, but it may occur in carabao, camels, elephants, cats, and dogs, and has been transmitted to cattle, buffaloes, sheep, goats, rabbits, guinea pigs, rats, and monkeys. No birds, reptiles, amphibia (frogs, etc.), or fish are known to suffer from it. It attacks both male and female animals, young and old. Australian breeds of horses and white and gray mules are said to be more susceptible than animals of other breeds and color.

Surra in equines and camels is said to be an invariably fatal disease, but cattle occasionally recover from it. There is no history of a definite onset of the disease, and the condition is progressive, usually with a number of relapses. The period of incubation may vary somewhat; in experimental cases it is from 2 to 75 (usually 6 to 8) days, according to conditions. The duration varies with the species of animal attacked, their age, and general condition. The average duration in the horse is reported at less than two months, though some cases may terminate fatally in less than one to two weeks.

Method of infection.—All evidence now available seems to indicate that surra is strictly a wound disease, namely, that the parasite may enter the body only through a wound of some kind. Apparently by far the most common method is through wounds produced by biting flies whose mouth parts are moist with the infected blood of some animal bitten by the same flies immediately before biting the healthy animal. Crows may also transmit the infection by pecking at sores on a diseased animal, soiling their beaks with blood, and transferring this infected blood to a healthy animal. Likewise, if a scratch is made on a horse and then infected blood is rubbed on the scratch, the horse will become diseased. If, in experiment, infected blood is fed to a healthy animal, the latter may contract surra in case it has an abraded or wounded spot in the mouth; but if no part of the lining of the alimentary canal is wounded, infection does not take place. Thus dogs and cats may contract the disease by wounding the lining of the mouth (as with splinters of bone) while feeding on the carcasses of surra subjects. All available evidence indicates that under normal conditions of pregnancy the disease is not transmitted from mother to fetus.

There is a popular view that surra may be contracted by drinking stagnant water and by eating grass and other vegetation grown upon land subject to inundation, but there is no good experimental evidence to support this view: Probably the correct interpretation of the facts cited in support of this theory is that biting flies are numerous around stagnant water and in inundated pastures; hence, that a great number of possible transmitters of the disease are present in these places.

Symptoms.[7]—The invasion of this disease when contracted naturally is usually marked by symptoms of a trivial character; the skin feels hot, and there may be more or less fever; there is also slight loss of appetite, and the animal appears dull and stumbles during action; early a symptom sometimes appears which may be the first intimation of the animal's indisposition, and which, as a guide to diagnosis, is of great importance; it is the presence of a general or localized urticarial eruption. If the blood is examined microscopically, it may be found to present a normal appearance; but in the majority of cases a few small, rapidly moving organisms will be observed, giving to the blood, as it passes among the corpuscles, a peculiar, vibrating movement, which if once observed will not easily be forgotten. If the parasite has not been discovered in the blood for several days, the symptoms mentioned above may be the only ones noticed, and, as a rule, when treated with febrifuges, the horse quickly improves in health and the appetite returns. This condition does not last for more than a few days, when the animal is again observed to present a dull and dejected appearance, and on examination well-marked symptoms are found; the skin is hot, the temperature more or less elevated—101.7 deg. to 104 deg. F.; the pulse full and frequent—56 to 64 beats a minute; the visible mucous membranes may appear clean, but the conjunctival membranes, especially those covering the membrana nictitans, are usually the seat of dark-red patches of ecchymosis, varying in size in different animals. There is more or less thirst and slight loss of appetite; the animal eats its grain and green grass, but leaves all or a portion of the hay with which it has been supplied. At the same time there are slight catarrhal symptoms present, including lacrimation and a little mucous discharge from the nostrils. Occasionally at this period of the disease the submaxillary glands may be found enlarged and perhaps somewhat tender on manipulation. One symptom is markedly absent, namely, the presence of rigors or the objective sign of chilliness. In addition, it will be noted that there is some swelling and edema of the legs, generally between the fetlock and the hock, which pits but is not painful on pressure, and in case of horses there may be also some swelling of the sheath at this stage of the disease. When the fever and concomitant symptoms have declared themselves for a short period, one thing becomes especially noticeable in every animal attacked, namely, the rapidity with which it loses flesh. If the blood has been examined microscopically during the second period of fever, at first a few parasites will have been observed in it, which day by day increase in number and reach a maximum, where they remain for a varying period, or at once suddenly or gradually disappear during the period of apyrexia. After the fever and the accompanying symptoms have for the second time been present for a few days—the period varying from one to six—the animal is found to have lost the dull, dejected appearance and to look bright. The temperature has fallen and, in some cases, has attained normal or even subnormal limits. The visible mucous membranes are clean, and the conjunctival petechiae begin to fade; the pulse, however, will be found to be weak and thready in character, but the appetite excellent, and, in fact, if it were not for the loss of flesh and slight edema of the legs, there would be little to show that the animal was sick. Unfortunately, however, this condition does not continue for any great length of time, for again the temperature is elevated; in the course of a few hours the thermometer registers a still higher degree, the animal is dull and dejected, and by the following day the visible mucous membranes present a yellow tinge; large ecchymoses, dark in color, appear on the conjunctival membranes, the action of the heart is irritable, the pulse full and quick, or at times intermittent, and regurgitation may be observed in the jugulars, the breathing is quickened, and the individual respirations are shallow. On watching an animal in this condition it may be noticed that it takes seven or eight very short inspirations, followed by a much more prolonged and sonorous one; at the same time the breathing is more abdominal than thoracic in character. On examination of the legs it will be found that the swelling and edema have increased considerably, and that on the under surface of the abdomen, where previously it was confined to the sheath, it has now commenced to spread forward along the subcutaneous tissue between the skin and the muscles. During the whole of this time the appetite will have varied little, and the evacuations will be only slightly, if at all, altered in character. In the blood a repetition of the previous events takes place, the parasites make their appearance and increase to a maximum and again suddenly or gradually disappear, according to the length of the fever period. These periods, alternating with and without fever, may go on for a considerable time. The progress of the disease is variable and greatly depends upon the condition of the animal attacked, the weak one succumbing very rapidly, but each return of the fever brings with it, as a rule, an increase in the severity of the symptoms. There is increased yellowness of the membranes, fresh crops of petechiae on the conjunctiva, a collection of gelatinous material at the inner angle, which at times becomes red in color from an admixture of blood, and which on microscopic examination is found to contain a varying number of the surra parasites; increased swelling and edema of the extremities and abdomen, which now extends between the fore limbs and up the chest. During this time the wasting has been steadily progressive, especially of the muscles of the back and those surrounding the hip joint and the glutei.

Toward the termination of the disease it will be noticed that an animal is disinclined to move, and when made to do so there is manifest loss of power over the hind quarters, somewhat simulating a slight partial paralysis, and the hind quarters of the animal reel from side to side. In connection with this it may be noted that frequently there is paralysis of the sphincter ani and a dilated condition of the anus. These symptoms taken together point to some interference with the normal functions of the spinal cord in the lower dorsal and lumbar regions, and are probably owing to pressure caused by an exudation within the spinal membranes. In many cases shortly before death the heart's action becomes exceedingly violent, shaking the whole frame at each beat, so that the sound can be heard at some distance from the animal. In some of these cases the animal may suddenly drop dead; in others the emaciation and weakness become so pronounced that it falls to the ground, and, after a short struggle, succumbs to the disease. In other cases, again, the animal falls to the ground and appears to be suffering from acute pain, struggles violently, sweat covers the body, and respiration is very hurried. The struggles soon exhaust the patient's strength, and for a time it lies quiet; soon, however, the struggles commence again, continuing until death occurs. In some cases the appetite is voracious.

The symptoms of the disease as observed in experimentally inoculated animals are as follows: Twenty-four hours after the subcutaneous injection of a small quantity of surra blood, in the great majority of cases, a small circumscribed and somewhat raised swelling is noticed at the seat of the inoculation. After forty-eight hours the tumor has increased in size and is accompanied with some edema; it presents a certain amount of tension of the parts involved, and is generally tender on manipulation. These conditions continue to increase, until by the fourth day the tumor may measure 3 or 4 inches in; one direction by 2 or 3 in the other, and raised to the extent of an inch or an inch and a half above the surrounding tissues, or in some cases the tumor presents an almost circular form throughout. It will be also found that, if the tumor is firmly grasped, it is not fixed, but can be lifted up from the subcutaneous tissue. According to the nature and quantity of the inoculated blood, these symptoms rapidly present themselves, and either attain a maximum or are retarded until, varying from the fourth to the thirteenth day, the tumor at the seat of inoculation will be found to have lost a certain amount of its tension and tenderness. From this date the swelling and edema gradually begin to grow less, until finally, after a period of 10 to 14 days, the only sign left of the former swelling is a slight thickening of the skin over the point of the injection; but at the moment when the tension and tenderness of the parts at the seat of inoculation become suddenly decreased a symptom of the utmost clinical importance takes place, namely, at that moment the parasite of surra enters the blood of the general circulation.

The temperature on the day of inoculation, and, in fact, for several days afterwards, may remain normal in character, there being only a few degrees difference between the morning and evening observations. In other cases there may be a slight rise from the first evening, and a gradual progressive rise until the swelling at the seat of inoculation shows signs of reduction in size, when the temperature generally takes a decided rise again, and may attain 104 deg. or 105.8 deg. F. This elevation will last a varying period of from two to six days, and on the day following its onset the ordinary symptoms of fever will be noticed, and in addition there will be petechiae on the conjunctival membranes, lacrimation, a slight mucous discharge from the nose, and in severe cases some edema of the lower portion of the legs, and perhaps of the sheath in horses. At the termination of the period of fever the temperature will be found to have fallen to normal or nearly so; the animal will present a brighter aspect, and there is every appearance of its return to health; in a few days, however, the animal again appears dull and half asleep; the temperature is elevated, a relapse takes place, and a repetition of all the symptoms in the primary paroxysm, including the reappearance of the parasite, is observed.

Diagnosis.—A diagnosis may also be established by the complement-fixation or agglutination tests with the sera from suspected animals. This, however, can be carried out only in laboratories and requires special facilities for its execution.

Treatment.—No satisfactory treatment is known. Intravenous injections of Fowler's solution of arsenic give temporary relief, but relapses occur. In view of the great economic importance of this disease, it would not be advisable to attempt to treat any sporadic cases should they occur in this country. On the contrary, the animals should be slaughtered immediately and their carcasses promptly burned.

OSTEOPOROSIS OR BIGHEAD.

By JOHN R. MOHLER, V. M. D., Assistant Chief, Bureau of Animal Industry.

Osteoporosis is a general disease of the bones which develops slowly and progressively and is characterized by the absorption of the calcareous or compact bony substance and the formation of enlarged, softened, and porous bone. It is particularly manifest in the bones of the head, causing enlargement and bulging of the face and jaws, thereby giving rise to the terms "bighead" and "swelled head," which are applied to it. The disease affects horses, mules, and asses of all ages, classes, and breeds, and of both sexes, and is found under all soil, dietetic, and climatic conditions. It may occur in sporadic form, but in certain regions, such as South Africa, Australia, Madagascar, India, Hawaii, and in this country it seems to be enzootic, several cases usually appearing in the same stable or on the same farm, and numerous animals being affected in the same district. In the United States the disease has been found in all the States bordering the Delaware River and Chesapeake Bay, in some of the New England States, and in many of the Southern States, especially in low regions along the coast. In Europe the disease appears to be quite rare, and is usually described as a form of osteomalacia, a disease which is not uncommon among cattle of that continent. The opinion that bighead is only a form of osteomalacia, however, can not be accepted, nor can the infrequency of the former among European horses and the frequency of the latter among other live stock be conceded on the argument which has been presented, namely, that the better care which horses receive prevents them from becoming affected. In the Southwest, where osteomalacia, or creeps, has not infrequently been observed among range cattle by the writer, no case of osteoporosis of the horses using the same range has been noted, although the latter animals are given no more attention than the cattle.

The appropriate treatment of osteomalacia in cattle is so effective that if osteoporosis were a similar manifestation of disease a similar line of treatment should prove equally efficacious. However, this is not the fact. On the other hand, the occurrence of osteomalacia on old, worn-out soil, or on land deficient in lime salts, or from eating feed lacking in these bone-forming substances, or drinking water with a lime deficiency, is in perfect accord with our knowledge of the disease. But osteoporosis may occur on rich, fertile soil, in the most hygienic stables, and in animals receiving the best of care and of bone-forming feeds with a proper amount of mineral salts in the drinking water.

Cause.—The cause of this disease still remains obscure, although various theories have been advanced, some entirely erroneous, others more or less plausible; but none of them has been established. Thus the idea that feeding fodder and cereals poor in mineral salts and grazing in pastures where the soil is poor in lime and phosphates will cause the disease has been entirely disproved in many instances. Others have considered that the disease starts as a muscular rheumatism which is followed by an inflammatory condition of the bones, terminating in osteoporosis. The idea that the disease is contagious has been advanced by many writers, although no causative agent has been isolated. Numerous experiments have been made by inoculating the blood of an affected horse into normal horses without results. A piece of bone taken by Pearson from the diseased lower jaw of a colt was transplanted into a cavity made for it in the jaw of a normal horse, but without reproducing the disease. Petrone believes that the Micrococcus nitrificans causes osteomalacia in man as a result of its producing nitrous acid, which dissolves the calcareous tissues, and when injected into dogs in pure culture a similar disease is produced. It is probable that if this work is confirmed a somewhat similar causative factor will be discovered for osteoporosis.

Elliott considers the latter disease to be of microbic origin, the result of climatic conditions, and divides the island of Hawaii into two districts, in one of which the rainfall is 150 inches annually, where bighead is very prevalent, and the second of which is dry and rarely visited by rain, where the disease is unknown. Removal of animals from the wet to the dry district is followed by immediate improvement and frequently by recovery. In the wet district horses in both good and bad stables take the disease, but in the dry districts no unfavorable or unhygienic surroundings produce the affection. As both native and imported horses are equally susceptible, there is no indication of an acquired immunity to be observed.

Theiler has recently stated that his experiments in transfusing blood from diseased to normal horses were negative, and has suggested that the causative agent may be transmitted by an intermediate host only, as in the case of Texas fever. He draws attention to this method of spreading East African coast fever, although blood inoculations, as in osteoporosis, are always without result. We know that coast fever is infectious, and that it can not be transmitted by blood inoculations, but is conveyed with remarkable ease by ticks from diseased cattle. That the cause has not been observed may be accounted for by its being invisible even to the high magnification of the microscope.

On some farms and in some stables bighead is quite prevalent, a number of cases following one after another. On one farm of Thoroughbreds in Pennsylvania all the yearling colts and some of the aged horses were affected during one year, and on a similar farm in Virginia a large proportion of the horses for several years were diseased, although the cows and sheep of this farm remained unaffected.

Symptoms.—The commencement of the disease is usually unobserved by the owner, and these symptoms which do develop are generally not well marked or are misleading unless other cases have been noted in the vicinity. Until the bones become enlarged the symptoms remain so vague as not to be diagnosed readily. The disease may be present itself under a variety of symptoms. If the bones of the hock become affected, the animal will first show a hock lameness. If the long bones are involved, symptoms of rheumatism will be the first observed, while if the dorsal or lumbar vertebrae are affected indications of a strain of the lumbar region are in evidence. Probably the first symptom to be noticed is a loss of vitality combined with an irregular appetite or other digestive disturbance and with a tendency to stumble while in action. These earlier symptoms, however, may pass unobserved, and the appearance of an intermittent or migratory lameness without any visible cause may be the first sign to attract attention. This shifting and indefinite lameness, involving first one leg and then the other, is very suggestive, and is even more important when it is associated with a tendency to lie down frequently in the stall and the absence of a desire to get up, or the presence of evident pain and difficulty in arising.

About this time, or probably before, swelling of the bones of the face and jaw, which is almost constantly present in this disease, will be observed. The bones of the lower jaw are the most frequently involved, and this condition is readily detected with the fingers by the bulging ridge of the bone outside and along the lower edge of the molar teeth. A thickening of the lower jawbone may likewise be identified by feeling on both sides of each branch at the same time and comparing it with the thinness of this bone in a normal horse. As a result mastication becomes difficult or impossible and the teeth become loose and painful. The imperfect chewing which follows causes balls of feed to form which drop out of the mouth into the manger. Similar enlargements of the bones of the upper jaw may be seen, causing a widening of the face and a bulging of the bones about midway between the eyes and the nostrils. In some cases the nasal bones also become swollen and deformed, which, together with the bulging of the bones under the eyes, gives a good illustration of the reason for the application of the term bighead.

Other bones of the body will undergo similar changes, but these alterations are not so readily noted except by the symptoms they occasion. The alterations of the bones of the spinal column and the limbs, while difficult of observation, are nevertheless indicated by the reluctance of the animal to get up and the desire to remain lying for long periods of time. The animal easily tires, moves less rapidly, and if urged to go faster may sustain a fracture or have a ligament torn from its bony attachments, especially in the lower bones of the leg. An affected horse weighing 1,000 pounds was seen by the writer to fracture the large pastern bone from rearing during halter exercise.