Diseases of the Horse

Infectious Diseases

By Rush Shippen Huidekoper, M. D., Vet

[Revised by a. Eichhorn, D. V. S.]

General Discussion

An infectious disease may be defined as any malady caused by the introduction into the body of minute organisms of the vegetable or animal kingdom which have the power to multiply indefinitely and set free certain peculiar poisons which are chiefly responsible for morbid changes. Nearly all diseases of animals for which a definite cause may be attributed are caused by bacteria; such are tuberculosis, anthrax, blackleg, lockjaw, and others. There are some diseases, as, for instance, Texas fever and rabies, which are caused by a minute animal parasite known as protozoa, while others again, like lumpy jaw and aspergillosis, are caused by fungi. Besides there are infectious diseases in which the causative agents have never been successfully isolated, as they are so small that they can not be detected by the aid of the most powerful microscope, and accordingly they are termed as ultravisible viruses. Hog cholera, foot-and-mouth disease, smallpox, and others belong to this group.

Bacteria may be defined as very minute unicellular organisms of plantlike character. They multiply either by simple division or by spore formation, the latter usually taking place when the conditions pertaining to the growth of the bacteria become unfavorable. The spores are much more resistant to destruction than the bacteria which produce them.

Another group of parasites producing disease is known as protozoa. These are more complex than bacteria, and their artificial cultivation is also much more difficult than is the case with the bacterial parasites. Of the representatives of this group, causing disease in animals, are the trypanosomes, which are the causative factors of dourine and surra, and the piroplasma, which induce Texas fever in cattle and malaria or biliary fever of horses. There are also disease-producing fungi which are responsible for certain affections in horses; among these the most important are mycotic lymphangitis, or sporotrichosis, and streptotrichosis.

The introduction of the infection may take place in various ways. The most frequent method is by ingestion. Further, the entrance of the germs may occur by inhalation, skin abrasions, wounds of any kind, through the genital organs, and at times also through the milk ducts of the teats. As a general rule infectious diseases have a period of incubation which comprises the time elapsing between the exposure to the infection and the actual appearance of the disease. This period varies in the different diseases.

The treatment of infectious diseases is, as a rule, unsatisfactory. When the symptoms have once appeared a disease is liable to run its course in spite of treatment, and if it is one from which animals usually recover, all that can be done is to put them into the most favorable surroundings. Many infectious diseases lead sooner or later to death; treatment is useless so far as the sick animals are concerned, and it may be worse than useless for those not yet affected. All animals suffering with infectious diseases are more or less directly a menace to all others. They represent for the time being manufactories of disease germs, and they are giving them off more or less abundantly during the period of disease. They may infect others directly or they may scatter the virus about and the surroundings may become the future source of infection.

Therefore, in the control of infectious diseases prevention is the most important procedure. The isolation or segregation of healthy animals from infected ones should be primarily considered, and if at any time an animal manifests the symptoms of an infectious disease it is essential to protect the others from such a source of danger. In some of the infectious diseases it may become advisable to kill the infected animals in order to avoid the spread of the disease. This is especially important in diseases which are slow in their course, such as tuberculosis. At times when diseases appear in a country where they have not been prevalent it becomes advisable and necessary to protect the healthy herds by the slaughter of all the infected animals. Pursuance of this policy has resulted in control of the foot-and-mouth disease, and has proved to be a very satisfactory method of eradication.

Disinfection

Disinfection is a very important phase in the control of infectious disease. This consists in the use of certain substances which possess the power to destroy bacteria or their spores, or both. The cheapest and most available for animal diseases are ordinary freshly slaked lime, or unslaked lime in powder form, chlorid of lime, crude carbolic acid, corrosive sublimate, formalin, formaldehyde, gas, cresol, etc.

In the disinfection of stables and premises it is essential to execute the work in a most thorough manner. This may be satisfactorily accomplished by carrying out the following directions:

1. Sweep ceilings, side walls, stall partitions, floors, and other surfaces until free from cobwebs and dust.

2. Scrape away all accumulation of filth, and if woodwork has become decayed, porous, or absorbent, it should be removed, burned, and replaced with new material.

3. If floor is of earth, remove 4 inches from the surface, and in places stained with urine a sufficient depth should be replaced to expose fresh earth. All earth removed should be replaced with earth from an uncontaminated source; it would be better still to lay a new floor of concrete, which is very durable and easily cleaned.

4. All refuse and material from stable and barnyard should be removed to a place not accessible to cattle or hogs. The manure should be spread on fields and turned under, while the wood should be burned.

5. The entire interior of the stable, especially the feeding troughs and drains, should be saturated with a disinfectant, as liquor cresolis compositus (U. S. P.), or carbolic acid, 6 ounces to every gallon of water, to which 4 ounces of chlorid of lime should be added. The best method of applying the disinfectant and the lime wash is by means of a strong spray pump, such as those used by orchardists. This method is efficient in disinfection against most of the contagious and infectious diseases of animals, and should be applied immediately following any outbreak, and, as a matter of precaution, it may be used once or twice yearly.

6. It is important that arrangements be made to admit a plentiful supply of sunlight and fresh air by providing an ample number of windows, thereby eliminating dampness, bad odor, and other insanitary conditions. Good drainage is also very necessary.

If the use of liquor cresolis compositus, carbolic acid, or other coal-tar products is inadmissible because of the readiness with which their odor is imparted to milk and other dairy products, bichlorid of mercury may be used in proportion of 1 to 800, or 1 pound of bichlorid to 100 gallons of water. All portions of the stable soiled with manure, however, should first be thoroughly scraped and cleaned, as the albumin contained in manure would otherwise greatly diminish the disinfecting power of the bichlorid. Disinfection with this material should be supervised by a veterinarian or other person trained in the handling of poisonous drugs and chemicals, as the bichlorid is a powerful, corrosive poison. The mangers and the feed boxes, after drying, following spraying with this material, should be washed out with hot water, as cattle are especially susceptible to mercurial poisoning. The bichlorid solution should be applied by means of a spray pump, as recommended for the liquor cresolis compositus.

Vaccination

In recent years vaccination for the prevention of certain infectious diseases has been successfully developed, and without a doubt the future has a great deal in store for this phase of prevention. At the present time vaccination has been found effective against blackleg, hog cholera, anthrax, lockjaw, strangles, rabies, hemorrhagic septicemia, white scours, etc. It is always essential, of course, that the products used for the vaccination be pure and potent; also they should be employed only with the advice of competent authorities and with proper care. The biological products prepared for the cure and prevention of infections are prepared by manufacturers who, in order to conduct an interstate business, are required to obtain a license from the United States Department of Agriculture for the manufacture of such preparations.

Since July 1, 1913, the Department of Agriculture, by an act of Congress of March 4, 1913, has had control of the manufacture of biological products for the treatment of domestic animals. The numerous complaints which were received from time to time relative to the impotency of some of the preparations, and also the fact that in some instances the use of the products were directly responsible in causing outbreaks of disease, made the necessity for such control obvious. This supervision is no doubt of far-reaching importance, as it assures the users that the preparations are reliable.

Influenza

Synonyms.—Pinkeye, typhoid fever, epizooty, epihippic fever, hepatic fever, bilious fever, etc.; flèvre typhoide, grippe (French); Pferdestaupe (German); gastro-enteritis of Vatel and d’Arboval; febris erysipelatodes, Zundel; typhus of Delafond.

Definition.—The term influenza is applied to a febrile, contagious, infectious disease of horses, which is characterized by a blood infection, with inflammation of the mucous membranes, which frequently involves the lungs. Inflammatory complications also occur in the form of swellings of the subcutis, tendons, and tendinous sheaths and laminæ of the feet. The causative agent has not been satisfactorily established. One attack usually protects the animal from future ones of the same disease, but not always. An apparently complete recovery is sometimes followed by serious sequelæ of the nervous and blood-vessel systems. Under certain conditions of the atmosphere or from unknown causes, the disease is very liable to assume an epizootic form, with tendency to complications of especial organs, as, at one period, the lungs, at another the intestines, etc.

The first description of influenza is given by Laurentius Rusius in 1301, when it spread over a considerable portion of Italy, causing great loss among the war horses of Rome and the surrounding district. Later, in 1648, an epizootic of this disease visited Germany and spread to other parts of Europe. In 1711, under the name of “epidemica equorum,” it followed the tracks of the great armies all over Europe, causing immense losses among the horses, while rinderpest was scourging the cattle of the same regions. The two diseases were confounded with each other, and were, by the scientists of the day, supposed to be allied to the typhus, which was a plague to the human race at the same time. We find the first advent of this disease to the British Islands in an epizootic among the horses of London and the southern counties of England in 1732, which is described by Gibson. In 1758 Robert Whytt recounts the devastation of the horses of the north of Scotland from the same trouble. Throughout the eighteenth century a number of epizootics occurred in Hanover and other portions of Germany and in France, which were renewed early in the present century, with complications of the intestinal tract, which obtained for it its name of gastro-enteritis. In 1766 it first attacked the horses in North America, but is not described as again occurring in a severe form until 1870-1872, when it spread over the entire country, from Canada south to Ohio, and then eastward to the Atlantic and westward to California. It is now a permanent disease in our large cities, selecting for the continuance of its virulence young or especially susceptible horses which pass through the large and ill-ventilated and uncleaned stables of dealers, and assumes from time to time an enzootic form, when from some reason its virulence increases. It assumes this form also when, from reasons of rural economy and commerce, large numbers of young and more susceptible animals are exposed to its contagion.

Etiology.—The experiments of Dieckerhoff many years ago proved that the disease may be transmitted to healthy animals by intravenous injection of warm blood from affected horses.

Further investigations revealed the fact that blood from affected horses, even when passed through porcelain filters, may transmit the disease, thereby proving that the causative agent belongs to the so-called filterable viruses. This has been further substantiated by Gaffky, who showed in his recent experiments that the disease may be transmitted with defibrinated as well as with filtered blood, in which cases the typical form of influenza developed in inoculated animals in from five to six days. These findings were also substantiated by Basset. Further observations have also proved that apparently recovered animals may harbor the infection for a long time and still be capable of transmitting the disease. Such virus carriers are no doubt responsible for numerous outbreaks of this disease when, in a locality free from the disease, it certainly appears after the introduction of an apparently healthy animal.

As one attack is usually self-protective, numbers of old horses, having had an earlier attack, are not capable of contracting it again; but, aside from this, young horses, especially those about four or five years of age, are much more predisposed to be attacked, while the older ones, even if they have not had the disease, are less liable to it. Again, the former age is that in which the horse is brought from the farm, where it has been free from the risk of exposure, and is sold to pass through the stables of the country taverns, the dirty, infected railway cars, and the foul stockyards and damp stables of dealers in our large cities. Overfed, fat, young horses which have just come through the sales stables are much more susceptible to contagion than the same horses are after a few months of steady work.

Pilger, in 1805, was the first to recognize infection as the direct cause of the disease. Roll and others studied the contagiousness of influenza, and, finding it so much more virulent and permanent in old stables than elsewhere, classed it as a “stall miasm.” The contagion will remain in the straw bedding and droppings of the animal and in the feed in an infected stable for a considerable time and if these are removed to other localities it may be carried in them. It may be carried in the clothing of those who have been in attendance on horses suffering from the disease. The drinking water in troughs and even running water may hold the virus and be a means of its communication to other animals, even at a distance.

The studies of Dieckerhoff, in 1881, in regard to the contagion of influenza were especially interesting. He found that during a local enzootic, produced by the introduction of infected horses into an extensive stable otherwise perfectly healthy, the infection took place in what at first seemed to be a most irregular manner, but which was shown later to be dependent on the ventilation and currents of air through the various buildings. His experiments showed that the virus of influenza is excessively diffusible, and that it will spread rapidly to the roof of a building and pass by the apertures of ventilation to others in the neighborhood. The writer has seen cases that have appeared to spread through a brick wall and attack animals on the opposite side before others even in the same stable were affected. Brick walls, old woodwork, and the dirt which is too frequently left about the feed boxes of a horse stall will hold the contagion for several days, if not weeks, and communicate it to susceptible animals when placed in the same locality. On two successive mornings a 4-year-old colt belonging to the writer stood for about 10 minutes at the open door, fully 40 feet from the stalls, of a stable in which two cases of influenza had broken out the day before: in six days the colt developed the disease. On the morning when the trouble in the colt was recognized it stood in an infirmary with a dozen horses that were being treated for various diseases, but was immediately isolated; within one week two-thirds of the other horses had contracted the disease.

Symptoms.—After the exposure of a susceptible horse to infection a period of incubation of from four to seven days elapses, during which the animal seems in perfect health, before any symptom is visible. When the symptoms of influenza develop they may be intense, or so moderate as to occasion but little alarm, but the latter condition frequently exposes the animal to use and to the danger of the exciting causes of complications which would not have happened had it been left quietly in its stall in place of being worked or driven out to show to prospective purchasers. The disease may run a simple course as a specific fever, with alterations only of the blood, or at any period it may become complicated by local inflammatory troubles, the gravity of which is augmented by developing in an animal with an impoverished blood, an already irritated, rapid circulation, and defective nutritive and reparative functions.

The first symptoms are those of a rapidly developing fever, which becomes intense within a very short period. The animal becomes dejected and inattentive to surrounding objects; stands with its head down, and not back on the halter as in serious lung diseases. In the flanks, the muscles of the croup and of the shoulders, or of the entire body it has chills lasting from 15 to 30 minutes, and frequently a grinding of the teeth which warns one that a severe attack may be expected. The hairs become dry and rough and stand on end. The body temperature increases to 104°, 104.5°, and 105° F., or even in severe cases to 107° F., within the first twelve or eighteen hours. The horse becomes stupid, stands immobile with its head hanging, the ears listless, and it pays but little attention to the surrounding attendants or the crack of a whip. The stupor becomes rapidly more marked, the eyes become puffy and swollen with excessive lacrimation, so that the tears run from the internal canthus of the eye over the cheeks and may blister the skin in their course. The respiration becomes accelerated to 25 or 30 in a minute, and the pulse is quickened to 70, 80, or even 100, moderate in volume and in force. There is great depression of muscular force; the animal stands limp, as if excessively fatigued. There is diminution, or in some cases total loss, of sensibility of the skin, so that it may be pricked or handled without attracting the attention of the animal. On movement, the horse staggers and shows a want of coordination of all the muscles of its limbs. The senses of hearing, sight, and taste are diminished, if not entirely destroyed. The visible mucous membranes (as the conjunctiva), from which it received the name pinkeye, and the mouth, and the natural openings become of a deep saffron, ocher, or violet-red color. This latter is especially noticeable on the rim of the gums and is a condition not found in any other disease, so that it is an almost diagnostic symptom. In some outbreaks there is much more swelling of the lids and weeping from the eyes than in others. If the animal is bled at this period the blood is found more coagulable than normal, but at a later period it becomes of a dark color and less coagulable. There is great diminution or total loss of appetite, with an excessive thirst, but in many cases cold-blooded horses may retain a certain amount of appetite, eating slowly at hay, oats, or other feed. There is some irritation of the mucous membrane of the respiratory tract, as shown by discharge of mucus from the nose, and by cough. Pregnant mares are liable to abort.

We have, following the fever, a tumefaction, or edema, of the subcutaneous tissues at the fetlocks, of the under surface of the belly, and of the sheath of the penis, which may be excessive. The infiltration is noninflammatory in character and produces an insensibility of the skin like the excessive stocking which we see in debilitated animals after exposure to cold. In ordinary cases the temperature has reached its maximum of 105° or 106° F. in from 24 to 48 hours from the origin of the fever. It remains stationary for a period of from 3 to 4 days without so much variation between morning and evening temperature as we have in pneumonia or other serious diseases of the lungs. At the termination of the specific course of the disease, which is generally from 6 to 10 days, the fever abates, the swelling of the legs and under surface of belly diminishes, the appetite returns, the strength is rapidly regained, the mucous membranes lose their yellowish color, which they attain so rapidly at the commencement of the disease, and the animal convalesces promptly to its ordinary good condition and health, and rapidly regains the large amount of weight which it lost in the early part of the disease, a loss which frequently reaches 30, 50, or even 75 pounds each 24 hours. For the first three days of the high temperature there is a great tendency to constipation, which should be avoided if possible by the use of the means recommended below, for, if it has been marked, it may be followed by a troublesome diarrhea.

Terminations.—The terminations of simple influenza may be death by extreme fever, with failure of the heart’s action; from excessive coma, due generally to a rapid congestion of the brain; to the poisonous effects of the débris of the disintegrated blood corpuscles and the toxin of the disease; to an asphyxia, following congestion of the lungs; or the disease terminates by subsidence of the fever, return of the appetite and nutritive functions of the organs, and rapid convalescence; or, in an unfortunately large number of cases, the course of the disease is complicated by local inflammatory troubles, whose gravity is greater in influenza than it is when they occur as sporadic diseases.

Complications.—The complications are congestions, followed by inflammatory phenomena in the various organs of the body, but they are most commonly located in the intestines, lungs, brain, or vascular laminæ of the feet. Atmospheric influence or other surrounding influences of unknown quality seem to be an important factor in the determination of the local lesions. At certain seasons of the year, and in certain epizootics, we find 40 and 50 per cent or even a greater percentage of the cases rendered more serious by complication of the intestines; at other seasons of the year, or in other epizootics, we find the same percentage of cases complicated by inflammation of the lungs, while at the same time a small percentage of them are complicated by troubles of the other organs; inflammatory changes of the brain, of the laminæ, more rarely commence in epizootic form, but are to be found in a certain small percentage of cases in all epizootics.

Exciting causes are important factors in complicating individual cases of influenza, or in localizing special lesions, during either enzootics or epizootics. These exciting or determining causes act much as they would in sporadic inflammatory diseases, but in this case we find the animal much more susceptible and predisposed to be acted upon than ordinary healthy animals. With a temperature already elevated, with the heart’s action driving the blood in increased quantity into the distended blood vessels, which become dilated and lose their contractility, with a congestion of all the vascular organs already established, it takes but little additional irritation to carry the congestion one step further and produce inflammation.

Complication of the intestines.—When any cause acts as an irritant to the intestinal tract during the course of this specific fever it may produce inflammation of the organs belonging to it. This cause may be constipation, which can find relief only in a congestion which offers to increase the function of the glands and relieve the inertia caused by a temporary cessation of activity; or irritant medicines, especially any increased use of antimony, turpentine, or the more active remedies; the taking of indigestible feed, or of feed in too great quantities, or that has been altered in any way by fungus or other injurious alterations; the swallowing of too cold water; or any other irritant may cause congestion. This complication is ushered in by colics. The animal paws with the fore feet and evinces a great sensibility of the belly; it looks with the head from side to side, and may lie down and get up, not with violence, but with care for itself, perfectly protecting the surface of the belly from any violence. At first we find a decided constipation; the droppings if passed are small and hard, coated with a viscous varnish or even with false membranes. In from 36 to 40 hours the constipation is followed by diarrhea. The alimentary discharge becomes mixed with a sero-mucous exudation, which is followed by a certain amount of suppurative matter. The animal becomes rapidly exhausted and unstable, staggers on movement, losing the little appetite which may have remained, and has exacerbations of fever. The pulse becomes softer and weaker, the respiration becomes gradually more rapid, the temperature is about 1° to 1.5° F. higher. If a fatal result is not produced by the extensive diarrhea the discharge is arrested in from 5 to 10 days and a rapid recovery takes place.

Complication of the lungs.—If at any time during the course of the fever the animal is exposed to cold or drafts of air, or in any other way to the causes of repercussion, the lungs may become affected. In the majority of cases, however, after three, four, or five days of the fever, congestion of the lungs commences without any exposure or apparent exciting cause. Unless this congestion of the lungs is soon relieved it is followed by an inflammation constituting pneumonia. This pneumonia, while it is in its essence the same, differs from an ordinary pneumonia at the commencement by an insidious course. The animal commences to breathe heavily, which is distinctly visible in the heaving of the flanks, the dilatation of the nostrils, and frequently in the swaying movement of the unsteady body. The respirations increase in number, what little appetite remained is lost, the temperature increases from 1° to 2°, the pulse becomes more rapid, and at times, for a short period, more tense and full, but the previous poisoning of the specific disease has so weakened the tissues that it never becomes the characteristic full, tense pulse of a simple pneumonia.

On percussion of the chest dullness is found over the inflamed areas; on auscultation at the base of the neck over the trachea a tubular murmur is heard. The crepitant râles and tubular murmurs of pneumonia are heard on the sides of the chest if the pneumonia is peripheral, but in pneumonia complicating influenza the inflamed portions are frequently disseminated in islands of variable size and are sometimes deep-seated, in which case the characteristic auscultory symptoms are sometimes wanting. From this time on the symptoms of the animal are those of an ordinary grave pneumonia, rendered more severe by occurring in a debilitated animal. The cough is at first hacky and aborted; later, more full and moist. There is discharge from the nostrils, which may be mucopurulent, purulent, or hemorrhagic. As in simple pneumonia, in the outset this discharge may be “rusty,” owing to capillary hemorrhages. We find that the blood is thoroughly mixed with the matter, staining it evenly, instead of being mixed with it in the form of clots. At the commencement of the complication the animal may be subject to chills, which may again occur in the course of the disease, in which case, if severe, an unfavorable termination by gangrene may be looked for. If gangrene occurs it is shown by preliminary chills, a rapid elevation of temperature, a tumultuous heart, a flaky discharge from the nostrils, and a fetid breath; the symptoms are identical with those which occur in gangrene complicating other diseases.

Complication of the brain.—At any time during the course of the disease congestion of the brain may occur; at an early period if the fever has been intense from the outset, but in ordinary cases more frequently after three or four days. The animal, which has been stupid and immobile, becomes suddenly restless, walks forward in the stall until it fastens its head in the corner. If in a box stall and it becomes displaced from its position, it follows the wall with the nose and eyes, rubbing it along until it reaches the corner and again fastens itself. It may become more violent and rear and plunge. If disturbed by the entrance of the attendant or any loud noise or bright light, it will stamp with its fore feet and strike with its hind feet, but is not definite in fixing the object which it is resisting, which is a diagnostic point between meningitis and rabies and which renders the animal with the former disease less dangerous to handle. If fastened by a rope to a stake or post, the animal will wander in a circle at the end of the rope. It wanders almost invariably in one direction. The pupils may be dilated or contracted, or we may find one condition in one eye and the opposite in the other.

The period of excitement is followed by one of profound coma, in which the animal is immobile, the head hanging and placed against the corner of the stall, the body limp, and the motion, if demanded of the animal, unsteady. Little or no attention is paid to the surrounding noises, the crack of a whip, or even a blow on the surface of the body. The respiration becomes slower, the pulsations are diminished, the coma lasts for variable time, to be followed by excesses of violence, after which the two alternate, but if severe the period of coma becomes longer and longer until the animal dies of spasms of the lungs or of heart failure. It may die from injuries which occur in the ungovernable attacks of violence.

Complication of the feet.—The feet are the organs which are next in frequency predisposed to congestion. This congestion takes place in the laminæ (podophyllous structures) of the feet. The stupefied animal is roused from its condition by excessive pain in the feet and assumes the position of a foundered horse; that is, if the fore feet alone are affected, they are carried forward until they rest on the heels; and if the hind feet are affected, all the feet are carried forward, resting on their heels, the hind ones as near the center of gravity as possible. In some cases the stupor of the animal is so great that the pain is not felt, and little or no change of the position of the animal is noticeable. The foot is found hot to the touch, and after a given time the depressed convex sole of typical founder is recognized.

Pleurisy.—This is a rare complication, but when it does occur it is ushered in by the usual symptoms of depression, rapid pulse, small respiration, elevation of the temperature, subcutaneous edema of the legs and under surface of the belly, and we find a line of dullness on either side of the chest and an abscess of respiratory murmur at the lower part. If it is severe, there may be an effusion filling one-fourth to one-third of the thoracic cavity in from 36 to 48 hours.

Pericarditis is an occasional complication of influenza. It is ushered in by chills, elevation of the temperature; the pulse becomes rapid, thready, and imperceptible. The heart murmurs become indistinct or can not be heard. A venous pulse is seen on the line of the jugular veins along the neck. Respiration becomes more difficult and rapid. If the animal is moved the symptoms become more marked or it may drop suddenly dead from heart failure.

Peritonitis, or inflammation of the membranes lining the belly and covering the organs contained in it, sometimes takes place. The general symptoms are similar to those of a commencing pericarditis. The local symptoms are those of pain, especially to pressure on side of the flanks and belly, distention of the latter, and sometimes the formation of flatus, or gas, and constipation.

Other occasional complications are nephritis, hepatitis, inflammation of the flexor tendons and rupture of them, and abscesses.

Diagnosis.—The diagnosis of influenza is based upon continued fever, with great depression and symptoms of stupor and coma; the rapidly developing, dark-saffron, ocher, yellowish discoloration of the mucous membranes, swelling of the legs and soft tissues of the genitals. When these symptoms have become manifested the diagnosis of a local complication is based upon the same symptoms that are produced in the local diseases from other causes, but in influenza the local symptoms are frequently masked or even entirely hidden by the intense stupor of the animal, which renders it insensible to pain. The evidence of colic and congestion, which is followed by diarrhea, indicates enteritis. The rapid breathing or difficulty of respiration points to a complication of the lungs, but, as we have seen in the study of the symptoms, the local evidences of lung lesions are frequently hidden. Again, we have seen that inflammation of the feet, or founder, complicating influenza is frequently not shown on account of the insensibility to pain on the part of the animal, which indicates the importance of running the hand daily over the hoofs to detect any sudden elevation of temperature on their surface.

The diagnosis of brain trouble is based upon the excessive violence which occurs in the course of the disease, for during the intervening period or coma there is no means of determining that it is due to this complication. Severe cases of influenza may simulate anthrax in the horse. In both we have stupor, the intense coloration of the mucous membranes of the eyes, and a certain amount of swelling of the legs and under surface of the belly. The diagnosis here can be made only by microscopic examination of the blood. In strangles, equine variola, and scalma we have an intensely red, rosy coloration of the mucous membranes, full, tense pulse, and although in these diseases we may have depression, we do not have the stupor and coma except in severe cases which have lasted for several days. In influenza we have no evidence of the formation of pus on the mucous membranes as in the other diseases, except sometimes in the conjunctivæ.

In severe pneumonia (lung fever) we may find profound coma, dark-yellowish coloration of the mucous membranes, and swelling of the under surface of the belly and legs; but in pneumonia we have the history of the difficulty of breathing and an acute fever of a sthenic type from the outset, and the other symptoms do not occur for several days, while in influenza we have the history of characteristic symptoms for several days before the rapid breathing and difficulty of respiration indicate the appearance of the complication. Without the history it is frequently difficult to diagnose a case of influenza of several days’ standing, complicated by pneumonia, from a case of severe pneumonia of five or six days’ standing, but from a prognostic point of view it is immaterial, as the treatment of both are identical. The fact that other horses in the same stable or neighborhood have influenza may aid in the diagnosis.

Prognosis.—Influenza is a serious disease chiefly on account of its numerous complications. Uncomplicated influenza is a comparatively simple malady, and is fatal in but 1 to 5 per cent of all cases. In some outbreaks, however, complications of one kind or another preponderate; in such instances the rate of mortality is much increased.

Alterations.—The chief alteration of influenza occurs in the digestive tract, and consists in hyperemia, infiltration, and swelling of the mucous membrane, and especially of the Peyer’s patches near the ileocecal valve. The tissues throughout the body are found stained, and of a more or less yellowish hue. There is always found a congested condition of all the organs, muscles, and interstitial tissues of the body. The coverings of the brain and spinal cord partake in the congested and discolored condition of the rest of the tissues.

Other alterations are dependent entirely upon the complications. If the lungs have been affected, we find effusions identical in their intimate nature with those of simple pneumonia, but they differ somewhat in their general appearance in not being so circumscribed in their area of invasion. The alterations of meningitis and laminitis are identical with those of sporadic cases of founder and inflammation of the brain.

Treatment.—While the appetite remains the patient should have a moderate quantity of sound hay, good oats, and bran; or even a little fresh clover, if obtainable, can be given in small quantities. It is not so important that a special diet shall be observed as that the horse shall eat a moderate quantity of nourishing feed, and he may be tempted with any feed of good quality that he relishes. He should be placed in a well-ventilated box stall away from other horses. Grass, roots, apples, and milk may be offered and, if relished, allowed freely. To reduce the temperature the safest simple plan is to inject large quantities of cold water into the rectum. Antipyrene may be used with alcohol or strychnia. Derivatives in the form of essential oils and mustard poultices, baths of alcohol, turpentine, and hot water, after which the animal must be immediately dried and blanketed, serve to waken the animal from the stupor and relieve the congestion of the internal organs. This treatment is especially indicated when complication by congestion of the lungs, intestines, or of the brain is threatened. Quinin and salicylic acid in 1-dram doses will lower the temperature, but too continuous use of the former in some cases increases the depression. Iodid of potash reduces the excessive nutrition of the congested organs and thereby reduces the temperature; again, this drug in moderate quantities is a stimulant to the digestive tract and acts as a diuretic, causing the elimination of waste matter by the kidneys. Small doses of Glauber’s salt and bicarbonate of soda, used from the outset, stimulate the digestive tract and prevent constipation and its evil results.

In cases of severe depression and weakness of the heart digitalis can be used with advantage. At the end of the fever, and when convalescence is established, alcohol in one-half pint doses and good ale in 1-pint doses may be given as stimulants. To these may be added 1-dram doses of turpentine.

In complications of the intestines camphor and asafetida are most frequently used to relieve the pain causing the colics; diarrhea is also relieved by the use of bicarbonate of soda, nitrate of potash, and drinks made from boiled rice or starch, to which may be added small doses of laudanum.

In complication of the lungs iodid of potash and digitalis are most frequently indicated, in addition to the remedies used for the disease itself.

Founder occurring as a complication of influenza is difficult to treat. It is, unfortunately, frequently not recognized until inflammatory changes have gone on for several days. If recognized at once, local bleeding and the use of hot or cold water, as the condition of the animal may permit, are most useful, but in the majority of cases the stupefied animal is unable to be moved satisfactorily or to have one foot lifted for local treatment; the only treatment consists in local bleeding above the coronary bands and the application of poultices.

During convalescence small doses of alkalines may be kept up for a short time, but the greatest care must be used, while furnishing the animal with plenty of nutritious, easily digestible feed, not to over-load the intestinal tract, causing constipation and consequent diarrhea. Special care must be taken for several weeks not to expose the animal to cold.

Prevention.—In order to prevent the introduction of the disease it is advisable to isolate newly purchased animals for at least a week. Further, the stabling of healthy horses in sales and feed stables should also be guarded against. At the beginning of an outbreak the disease may be checked by immediate isolation of the affected horses, by taking the temperatures of the healthy animals, and by the segregation of those showing a marked elevation.

Bacterial vaccines are now being prepared for the prevention of this disease and also for its cure, but to date the results are not convincing as to the beneficial action of these products. Since the cause of the disease has not yet been satisfactorily determined it is difficult to conceive how immunity could be produced with the aid of the germs which enter into the preparation of these products. The reports would indicate, however, that vaccines exert a favorable influence upon the course of the disease, probably preventing severe complications which under ordinary conditions are the principal factors in determining the severity of the outbreak.

CONTAGIOUS PNEUMONIA.

Synonyms.—Edematous pneumonia; stable pneumonia; equine pleuropneumonia; influenza pectoralis equorum; pleuropneumonia; influenzal pneumonia; Brustseuche (German).

Contagious pleuropneumonia is an acute contagious disease of horses manifesting itself either as a croupous pneumonia or a pleuropneumonia with complications in the form of serous infiltrations of the subcutaneous tissues and tendons.

Etiology.—Investigators of this disease incriminated various kinds of microorganisms as the cause of this affection. Transmission experiments were usually negative with these organisms. This was also the case in attempts to transmit the disease by feeding with affected parts of the lungs, intestinal contents, and nasal discharge; likewise by intravenous or subcutaneous injections of blood and of emulsions made from nasal discharge, urine, the lung, and other organs.

The most recent experimental results of Gaffky and Lüber proved that at least at the beginning of the disease the bronchial secretion contains the infection. Upon killing horses affected with the typical forms of the disease on the third or fourth day of the affection the air passages are usually found to be filled with a yellowish, tenacious, germ-free secretion with which they succeeded in infecting healthy colts. The virus has not been isolated. The possibility of its being a protozoan is suggested by the above-named investigators through their observations of round or rod-shaped bodies in the round cells of the secretions.

Two organisms were formerly especially considered to play an important part in the cause of the disease, the Streptococcus pyogenes equi, which has been isolated from most cases of the disease, and the Bacillus equisepticus, which by some investigators was considered to be the cause of contagious pleuropneumonia. Although there is no doubt as to the presence of these microorganisms in most of the cases, their association with the cause of this disease, however, is now doubted, especially since attempts to transmit the disease with pure cultures of these germs failed to reproduce the typical form of the disease. They, however, are of great significance in connection with the pathological changes occurring in connection with the infection and probably are the determining factor in the course of the disease. They exert their action after the animal has already been attacked by the true virus, and then produce the inflammatory changes attributed to these secondary invaders.

This disease is the adynamic pneumonia of the older veterinarians, who did not recognize any essential difference in its nature from an ordinary inflammation of the lungs, except in the profound sedation of the force of the animal affected with it, which is a prominent symptom from the outset of the disease. Again, this same prostration of the vital force of the animal, combined with the staggering movement and want of coordination of the muscles, caused it for a long time to be confounded with influenza, with which at certain periods it certainly has a strong analogy of symptoms, but from which, as from sporadic pneumonia, it can be separated very readily if the case can be followed throughout its whole course.

Infectious pneumonia is a specific inflammation of the lungs, accompanied with interstitial edema and inflammation of the tissues of these organs and a constitutional disturbance and fever. It causes a profound sedation of the nervous system, which may be so great as to cause death. It is sometimes attended with pleurisy, inflammation of the heart or septic complications, which also prove fatal.

Old, cold, damp, foul, unclean, and badly drained and ventilated stables allow rapid dissemination of the disease to other horses in the same stable and act as rich reservoirs for preserving the contagion, which may be retained for over a year.

The virus is but moderately volatile, and in a stable seems rather to follow the lines of the walls and irregular courses than the direct currents of air and the tracts of ventilation. Prof. Dieckerhoff found that the contagion of influenza was readily diffusible throughout an entire stable and through any opening to other buildings, but he also found that the contagion of infectious pneumonia is not transmissible at any great distance, nor is it very diffusible in the atmosphere. A brick wall 8 feet in height served, in one instance, to prevent the infection of other animals placed on the opposite side from a horse ill with the disease, while others placed on the same side and separated from the focus of contagion only by open bars in the stall were infected and developed the disease in its typical form.

Symptoms.—The symptoms differ slightly from those of a frank, fibrinous pneumonia, but not so much by the introduction of new symptoms as by the want of or absence of the distinct evidences of local lesions which are found in the latter disease. All the pneumonias throughout the whole course of the trouble are less marked and less clearly defined.

The symptoms may develop slowly or rapidly. If slowly, there is fever and the animal gives a rare cough which resembles that of a heavy horse affected with a slight chronic bronchitis; it becomes somewhat dejected and dull, at times somnolent, and has a diminished appetite. This condition lasts for several days, or the disease may begin with high fever, and the symptoms described below are severe and develop in rapid sequence. The respiration increases to 24, 30, or 36 to the minute, and a small, running, soft pulse attains a rhythm of 50, 70, or even more beats in the sixty seconds. The heart, however, contrary to the debilitated condition of the pulse, is found beating violently and tumultuously, as it does in anthrax and septic intoxication. The mucous membranes of the eyes and mouth and of the genital organs are found somewhat edematous, and they rapidly assume a dirty, saffron color, at times approaching an ocher, but distinguishable from the similar coloration in influenza by the want of the luster belonging to the latter and by the muddy, dull tint, which is characteristic throughout the disease.

Suddenly, without the preliminary râles which precede grave lesions of the lungs in other diseases, the blowing murmur of pneumonia is heard over a variable area of the chest, usually, however, much more distinctly over the trachea at the base of the neck and directly behind the shoulder on each side of the chest. In some cases the evidence of lung lesion can be detected only over the trachea. The lesions of the lungs may be scattered throughout both lungs, involving numerous small areas, or they may be confined to and more or less fully occupy one or two lobes. Occasionally there is a general involvement of both lungs. The body temperature has now reached 104° or 105° F., or in extreme cases even a degree higher. The debility of the animal is great without the stupefaction or evidence of cerebral trouble, which is constant with such grave constitutional phenomena in influenza or severe pneumonia. The animal is subject to occasional chills, and staggers in its gait. The yellow coloration of the visible mucous membrane is rendered pale by infiltration of the liquid of the blood into the tissues; the pulse may become so soft as to be almost imperceptible, the heart movement and sounds being at the same time exaggerated. The animal loses flesh rapidly, and dropsies of the extremities, of the under surface of the belly, or of the internal organs may show themselves.

Terminations.—These symptoms may gradually subside after five to eight days, with an improved appetite the inanition may cease and the animal commence to nourish its impoverished blood and tissues; the pulse becomes stronger and the heart more regular and less tumultuous; the mucous membranes assume a brighter and more distinct color; the difficulty of respiration is removed, and the animal may make a recovery. When death occurs it is usually directly due to heart failure; in some cases it is caused by asphyxia, owing to the great amount of exudation into the lung tissue, rendering its further function impossible.

Complications.—The pulmonary complications of infectious pneumonia are secondary inflammatory or necrotic changes in the lungs themselves. Suppuration at times takes place in the bronchi and may extend to the lung tissue. In this case mucous râles develop which are most distinctly heard over the trachea and on the sides of the chest directly behind the shoulders. With the development of the mucous râles, to be heard on auscultation, we have a more purulent discharge from the nostrils, similar to that of a chronic or subacute bronchitis. If the inflammation has been of some standing, cavernous râles may be heard, indicating the destruction of a considerable portion of lung tissue and the formation of a cavity. The effects of this more acute inflammatory process are not appreciable in the general condition of the animal, except to weaken it still further and add to its debilitated and emaciated cachexia. Gangrene sometimes occurs. A sudden rise of the body temperature of 1° or 2°, with a more enfeebled pulse and a still more tumultous heart, develop simultaneously with the appearance of a discharge from the nostrils. This discharge is gray in color, serous or watery in consistency, mixed with the detritus of broken-down lung tissue, and sometimes contains clots of blood, or in more serious cases may be marked by a quantity of fluid blood from a hemorrhage, which proves fatal. The discharge is fetid to the smell. The animal emaciates rapidly. On examination of the lungs mucous râles are heard in the larger bronchi, cavities may be found at any part of these organs, and points of lobular pneumonia may be detected.

A very serious complication is an inflammation of the heart muscle. This is shown by a very weak and rapid pulse, great prostration, some filling of the lungs. This complication nearly always terminates in death. Other complications which may be mentioned are inflammation of the kidneys, blood poisoning, congestion of the brain, and inflammation of the tendinous sheaths and the tendons of the legs.

Diagnosis.—As fever is the first symptom of infectious pneumonia, it is useful during an outbreak of this disease to make daily temperature measurements of the exposed horses, so that the first indication of disease may be discovered and the horse removed from contact with those that are sound.

Prognosis.—The mortality in this disease may be as high as 25 per cent, but it is usually not more than 10 per cent. If there is a special tendency to complications of some sort, the mortality is increased.

Alterations.—At the time of death from infectious pneumonia we frequently find septic changes and the evidences of putrefaction. The solidification of the lung tissue is found irregular in shape and high around the root of the lungs and the large bronchi, and is generally covered by sound lung tissue. The anterior lobes of the lungs are usually entirely affected. The diseased portion appears of a gray-yellowish color, somewhat watery, and tears readily. Matter is found in the air tubes which form gutters through the jellylike mass of the diseased lung. Abscesses from the size of a nut to larger masses may be found throughout the lungs. The blood is dark in color, fluid, or only clotted into soft, jellylike masses. Masses of gangrenous or dead-black tissue may be present.

Treatment.—Bleeding is not to be used, because it would only still further weaken an already enfeebled animal; antimony or the alterants would increase the depression of a too-depraved constitution. There is in this disease no acute congestion of a particular organ to draw off by depletive measures, nor any violent blood current to be retarded, for fear of hypernutrition of any special part.

Revulsives do good, as they excite the nervous system and awaken the torpor of the weakened blood vessels, which aid in the reestablishment of the functions. As in other diseases, mustard poultices may be applied over the belly and sides of the chest, but caution must be used in the employment of blisters, as ugly ulcers may result from their action on a tissue of weakened vitality. Setons are dangerous from the great tendency in this disease to septic complications. Repeated friction of the legs by hand-rubbing and warmth by bandaging and by rubbing the surface of the body with turpentine and alcohol, which is immediately to be dried by rough towels, will excite the circulation and stimulate the emunctories of the skin.

Stimulants are given internally from the outset of the disease. Turpentine in 1-dram doses regulates the heart and excites the kidneys to carry off waste matter, but if repeated too frequently may disturb the already delicate digestive system. Alcohol rectifies the latter danger, and is a useful stimulant to the heart and digestive system, if given with care in small doses. It is an antiputrid, and is especially indicated when septic complications and gangrene are present. The aromatics and bitter tonics are useful; gentian and tea in warm decoction form a useful menstruum for other remedies. Digitalis is a useful remedy. Strychnin and quinin may be given throughout almost the whole course of the disease. The various preparations of iron are astringents and excitants to the digestive system. Carbolic acid is an antiputrid which is of marked benefit in edematous pneumonia; it should be given in small doses diluted in alcohol.

Salicylic acid may be given in 1 or 2 dram doses every few hours. It is much used for troubles of the serous membranes, lowers the temperature, and is of value in this disease in preventing the exudation into the tissue of the lungs. The alkalines, as the sulphate and bicarbonate of soda, the nitrate of potash, and very small doses of the iodid of potash, should be employed to regulate the digestive tract, the kidneys, and the other excreting glands, and to stimulate absorption of the waste matter.

The biological products enumerated under the treatment of the catarrhal form of influenza are also recommended for this disease. The bacterial vaccines in particular are being employed to a great extent, but the results are not uniformly satisfactory, especially with regard to prevention. They might, however, exert a beneficial influence against an attack of the secondary invaders and complications. A serum is also being prepared especially for the treatment of this disease, and since this is obtained from animals which have been highly immunized against the various organisms found in association with influenza it no doubt is beneficial, especially when the life of the animal is threatened. Such serum, however, should be used in sufficiently large doses, as repeated experience has proved that small doses have no beneficial action on the disease.

More recently salvarsan is being highly recommended for the treatment of the pneumonic form of influenza, and by many investigators it is considered as a specific for this affection. A single injection of this preparation is supposed to result in a rapid clearing of the lungs and the recovery of the animal is hastened. The cost of this product, however, at the present time, is exorbitant, and it should be considered only in the treatment of very valuable animals.

The same procedure as given for influenza should be carried out in the prevention of this affection.

The diet demands the strictest attention from the outset. In many of the fevers the feed has to be diminished in quantity and regulated in the quality of its heat-producing components during the acute part of the disease, so as to lessen the material for combustion in the inflamed organs. In edematous pneumonia, on the contrary, all the feed that can possibly be digested and assimilated must be given. Choice must be made of the richest material which can be handled by the weakened stomach and intestines without fatiguing them. Good, sound hay should be chopped short and dampened or partly boiled; in the latter case the hay tea can be reserved to use as a drink. Oats may be preferred dry or in other cases are taken better scalded; in most cases, however, it is better to give slops of oatmeal, to which may be added a little bran, barley flour, or boiled milk and wheat flour. Pure cow’s milk, not too rich in fatty matter, may be given alone or with beaten eggs; frequently the horse has to be coaxed with the milk diluted with several parts of water at first, but will soon learn to drink the pure milk. Apples and carrots cut up raw or boiled are useful, and fresh clover in small quantities will frequently stimulate the appetite. In other words, various feeds and combinations should be given to the horse. Throughout the course of the disease and during convalescence the greatest attention must be taken to cleaning the coat thoroughly so as to keep the glands of the skin in working order, and light, warm covering must be used to protect the animal from cold or drafts of air.

Strangles

Synonyms.—Distemper; colt-ill; catarrhal fever; one form of shipping fever; febris pyogenica.

Definition.—Strangles is an infectious disease of the horse, mule, and ass, seen most frequently in young animals, and usually leaving them immune from future trouble of the same kind.

It appears as a fever lasting for a few days, and is usually associated with an abscess formation of lymph glands, especially those under the jaw, which have a tendency to break on the outside. It usually leaves the animal after convalescence perfectly healthy and as good as it was before, but sometimes leaves it a roarer or is followed by the development of deep-seated abscesses which may prove fatal.

Causes.—The cause of strangles is infection by direct contact with an animal suffering from the disease, or indirectly through contact with the discharges from an infected animal, or by means of the atmosphere in which an infected animal has been. There are many predisposing causes which render some animals much more subject to contract the disease than others. Early age, which has given it the popular name of colt-ill, offers many more subjects than the later periods of life do, for the animal can contract the disease but once, and the large majority of adult and old animals have derived an immunity from previous attacks. At 3, 4, or 5 years of age the colt, which has been at home, safe on a meadow or in a cozy barnyard, far from all intercourse with other animals or sources of contagion, is first put to work and driven to the market town or county fairs to be exposed to an atmosphere or to stables contaminated by other horses suffering from disease and serving as infecting agents. If it fails to contract it there, it is sold and shipped in foul, undisinfected railway cars to dealers’ stables, equally unclean, where it meets many opportunities of infection. If it escapes so far, it reaches the time for heavier work and daily contact on the streets of towns or large cities, with numerous other horses and mules, some of which are sure to be the bearers of the germs of this or some other infectious disease, and at last it succumbs.

The period of the eruption of the last permanent teeth, or the end of the period of development from the colt to an adult horse, at which time the animals usually have a tendency to fatten and be excessively full-blooded, also seems to be a predisposing period for the contraction of this as well as of the other infectious diseases. Thoroughbred colts are very susceptible, and frequently contract strangles at a somewhat earlier age than those of more humble origin. Mules and asses are much less susceptible and are but rarely affected. Other animals are not subject to this disease, but there is a certain analogy between it and distemper in dogs. After exposure to infection there is a period of incubation of the disease, lasting from two to four days, during which the animal enjoys its ordinary health.

Symptoms.—The horse at first is a little sluggish if used, or when placed in its stable is somewhat dejected, paying but moderate attention to the various disturbing surroundings. Its appetite is somewhat diminished in many cases, while in some cases the animal eats well throughout. Thirst is increased, but not a great deal of water is taken at one time. If a bucket of water is placed in the manger the patient will dip its nose into it and swallow a few mouthfuls, allowing some of it to drip back and then stop, to return to it in a short time. The coat becomes dry and the hairs stand on end. At times the horse will have chills of one or the other leg, the fore quarters, or hind quarters, or in severe cases of the whole body, with trembling of the muscles and dryness of the skin.

If the eyes and mouth are examined the membranes are found reddened to a bright rosy color. The pulse is quickened and the breathing may be slightly accelerated. At the end of two days a cough is heard and a discharge begins to come from the nostrils. This discharge is at first watery; it then becomes thicker, somewhat bluish in color, and sticky, and finally it assumes the yellowish color of matter and increases greatly in quantity.

At the outset the colt may sneeze occasionally and a cough is heard. The cough is at first repeated and harsh, but soon becomes softer and moist as the discharge increases. Again, the cough varies according to the source of the discharge, for in light cases this may be only a catarrh of the nasal canals, or it may be from the throat, the windpipe, or the air tubes of the lungs, or even from the lungs themselves. According to the organ affected the symptoms and character of cough are similar to those of a laryngitis, bronchitis, or lung fever caused by ordinary cold.

Shortly after the discharge is seen a swelling takes place under the jaw, or in the intermaxillary space. This is at first puffy, somewhat hot and tender, and finally becomes distinctly so, and an abscess is felt, or having broken itself the discharge is seen dripping from a small opening. When the discharge from the nostrils has fully developed the fever usually disappears and the animal regains its appetite, unless the swelling is sufficient to interfere with the function of the throat, causing pain on any attempt to swallow. At the end of four or six days the discharge lessens, the soreness around the throat diminishes, the horse regains its appetite, and in two weeks has regained its usual condition. Old and strong horses may have the disease in so light a form that the fever is not noticeable; they may continue to eat and perform their ordinary work as usual and no symptom may be seen beyond a slight discharge from the nose and a rare cough, which is not sufficient to worry any but the most particular owner. But, on the other hand, the disease may assume a malignant form or become complicated so as to become a most serious disease, and even prove fatal in many cases. Inflammation of the larynx and bronchi, if excessive, produce violent, harsh coughing, which may almost asphyxiate the animal. The large amount of discharge may be mixed with air by the difficult breathing, and the nostrils, the front of the animal, manger, and surrounding objects become covered with a white foam. The inflammation may be in the lung itself (lobular pneumonia) and cause the animal to breathe heavily, heave at the flanks, and show great distress. In this condition marked symptoms of fever are seen, the appetite is lost, the coat is dry, the horse stands back in its stall at the end of the halter strap with its neck extended and its legs propped apart to favor breathing. This condition may end by resolution, leaving the horse for some time with a severe cough, or the animal may die from choking up of the lungs (asphyxia).

The swelling under the jaw may be excessive, and if the abscess is not opened it burrows toward the throat or to the side and causes inflammation of the parotid glands and breaks in annoying fistulas at the sides of the throat and even up as high as the ears. Roaring may occur either during a moderately severe attack from inflammation of the throat (larynx), or at a later period as the result of continued lung trouble. Abscesses may develop in other parts of the body, in the poll, in the withers, or in the spaces of loose tissue under the arms, in the fold of the thigh, and, in entire horses, in the testicles.

During the course of the disease, or later, when the animal seems to be on the road to perfect recovery, abscesses may form in the internal organs and produce symptoms characteristic of disease of those parts.

Roaring, plunging, wandering in a circle, or standing with the head wedged in a corner of the stall indicate the collection of matter in the brain. Sudden and severe lung symptoms, without previous discharge, point to an abscess between the lungs, in the mediastinum; colic, which is often continuous for days, is the result of the formation of an abscess in some part of the abdominal cavity, usually in the mesentery.

Pathology.—The lesions of strangles are found on the surface of the mucous membranes, essentially of the respiratory system, and in the loose connective tissue fibers of the internal organs and glands, and consist of acute inflammatory changes, tending to the formation of matter. The blood is unaltered, though it is rich in fibrin, and if the animal has died of asphyxia it is found dark colored and uncoagulated when the body is first opened. If the animal has died while suffering from high fever the ordinary alterations throughout the body, which are produced by any fever not attended by alteration of blood, are found.

Prevention.—Healthy horses should be separated from the infected animals, and the stables in which the disease has occurred should be thoroughly disinfected. Since the disease frequently occurs annually on infected premises, systematic disinfection should be practiced after an outbreak. The stables, as well as all utensils which might have come in contact with the infection, should be thoroughly disinfected. By such practices recurrences of the disease may be prevented.

Treatment.—Ordinary light cases require but little treatment beyond diet, warm washes, moistened hay, warm coverings, and protection from exposure to cold. The latter is urgently called for, as lung complications, severe bronchitis, and laryngitis are often the results of neglect of this precaution. If the fever is excessive, the horse may receive small quantities of Glauber’s salt (handful three times a day) as a laxative, bicarbonate of soda or niter in one-dram doses every few hours, and small doses of antimony, iodid of potash, aconite, or quinin. Steaming the head with the vapor of warm water poured over a bucket of bran and hay, in which belladonna leaves or tar have been placed, will allay the inflammation of the mucous membranes and greatly ease the cough.

The swelling of the glands should be promptly treated by flaxseed poultices and bathing with warm water, and as soon as there is any evidence of the formation of matter it should be opened. Prompt action in this will often save serious complications. Blisters and irritating liniments should not be applied to the throat. When lung complications show themselves the horse should have mustard applied to the belly and to the sides of the chest. When convalescence begins great care must be taken not to expose the animal to cold, which may bring on relapses, and while exercise is of great advantage it must not be turned into work until the animal has entirely regained its strength.

Bacterial vaccines are now being extensively used for the prevention and treatment of this disease. They are prepared from the specific germ of the disease and frequently exert a very beneficial influence. A serum is also being prepared from horses, which is injected with gradually increasing doses of this germ. This serum possesses considerable curative value and may prove especially valuable in cases in which the animals have failed to respond to other forms of treatment, or when valuable animals are affected with the disease.

Purpura Hemorrhagica

Synonyms.—Anasarca; petechial fever; morbus maculosus.

Definition.—This disease is a septic bacterial intoxication, acute and infectious in character, and is manifested by edematous swellings of the subcutaneous connective tissue, and hemorrhages on the mucous membrane and in the internal organs.

A previous attack of influenza is a common predisposing cause of this disease, which appears most frequently a few weeks after convalescence is established. It occurs more frequently in those animals which have made a rapid convalescence and are apparently perfectly well than it does in those which have made a slower recovery.

Anasarca commences by symptoms which are excessively variable. The local lesions may be confined to a small portion of the animal’s body and the constitutional phenomena be nil. The appearance and gravity of the local lesions may be so unlike, from difference of location, that they seem to belong to a separate disease, and complications may completely mask the original trouble.

In the simplest form the first symptom noticed is a swelling, or several swellings, occurring on the surface of the body—on the forearm, the leg, the under surface of the belly, or the side of the head. The tumefaction is at first the size of a hen’s egg; not hot, little sensitive, and distinctly circumscribed by a marked line from the surrounding healthy tissue. These tumors gradually extend until they coalesce, and in a few hours we have swelling of the legs, legs and belly, or the head, to an enormous size; they have always the characteristic constricted border, which looks as if it had been tied with a cord. In the nostrils are found small reddish spots, or petechiæ, which gradually assume a brownish and frequently a black color. Examination of the mouth will frequently reveal similar lesions on the surface of the tongue, along the lingual gutter, and on the frænum. If the external swelling has been on the head, the petechiæ of the mucous membranes are liable to be more numerous and to coalesce into patches of larger size than when the dropsy is confined to the legs. The animal may be rendered stiff by the swelling of the legs, or be annoyed by an awkward swollen head, which at times may be so enormous as to resemble that of a hippopotamus rather than that of a horse. During this period the temperature remains normal; the pulse, if altered at all, is only a little weaker; the respiration is only hurried if the swelling of the head infringes on the caliber of the nostrils. The appetite remains normal. The animal is attentive to all that is going on, and, except for the swelling, apparently in perfect health.

In from two to four days, in severe cases, the tissues can no longer resist the pressure of the exuded fluid. Over the surface of the skin which covers the dropsy we find a slight serous sweating, which loosens the epidermis and dries so as to simulate the eruption of some cutaneous disease. If this is excessive we may see irritated spots which are suppurating. In the nasal fossæ the hemorrhagic spots have acted as irritants, and, inviting an increased amount of blood to the Schneiderian membrane, produce a coryza or even a catarrh. We may now find some enlargement and peripheral edema of the lymphatic glands, which are fed from the affected part. The thermometer indicates a slight rise in the body temperature, while the pulse and respiration are somewhat accelerated. The appetite usually remains good. In the course of a few days the temperature may have reached 102°, 103°, or 104° F.

Fever is established, not an essential or specific fever in any way, but a simple secondary fever produced by the dead material from the surface or superficial suppuration, and by the oxidization and absorption of the colloid mass contained in the tissues. The skin may suppurate or slough more or less over the areas of greatest tension or where it is irritated by blows or pressure. The great swelling about the head may by closure of the nostrils interfere seriously with breathing. Internal edema may occur in the throat, lungs, or intestines. Septicemia, or blood poisoning, may result from anasarca.

Terminations.—The simple form of the disease most frequently terminates favorably on the eighth or tenth day by resolution or absorption of the effusion, with usually a profuse diuresis, and with or without diarrhea. The appetite remains good or is at times capricious.

Death may occur from mechanical asphyxia, produced by closure of the nostrils or closure of the glottis. Metastasis to the lungs is almost invariably fatal, causing death by asphyxia, Metastasis to the intestines may cause death from pain, enteritis, or hemorrhage.

Excessive suppuration, lymphangitis, and gangrene are causes of a fatal termination by exhaustion. Mortal exhaustion is again produced by inability to swallow in cases of excessive swelling of the head.

Peritonitis may arise secondary to the enteric edema, or by perforation of the stomach or intestines by a gangrenous spot. Septicemia terminates fatally with its usual train of symptoms.

Alterations.—The essential alterations of anasarca are exceedingly simple; the capillaries are dilated, the lymphatic spaces between the fibers of the connective tissue are filled with serum, and the coagulable portion of the blood presents a yellowish or citrine mass, jellylike in consistency, which has stretched out the tissue like the meshes of a sponge. Where the effusion has occurred between the muscles, as in the head, these are found dissected and separated from each other like those of a hog’s head by the masses of fat. The surface of the skin is desquamated and frequently denuded of the hair. Frequently there are traces of suppuration and of ulceration. The mucous membrane of the nose is found studded with small, hemorrhagic spots, sometimes red, more frequently brown or black, often coalesced with each other in irregular-sized patches and surrounded by a reddish zone, the product of irritation. If edema of the intestines has occurred, the membrane is found four or five times its normal thickness, reddish in color, with hemorrhages on the free surface. Edema of the lungs leaves these organs distended. The secondary alterations vary according to the complications. There are frequently the lesions of asphyxia; externally we find ulcers, abscesses, and gangrenous spots and the deep ulcers resulting from the latter. The lymphatic cords and glands are found with all the lesions of lymphangitis. Again are found the traces of excessive emaciation, or the lesions of septicemia. Except from the complications the blood is not altered in anasarca.

Diagnosis.—The diagnosis of anasarca must principally be made from farcy or glanders. In anasarca the swelling is nonsensitive, while sensitive in the acute swelling of farcy. The nodes of farcy are distinct and hard and never circumscribed, as in the other disease. The eruption of glanders on the mucous membranes is nodular, hard, and pelletlike. The redness disappears on pressure. In case of excessive swelling of the head in anasarca, there may occur an extensive sero-fibrinous exudation from the mucous membranes of the nose, poured out as a semifluid mass or as a cast of the nasal fossæ, never having the appearance or typical oily character which it has in glanders. The inflammation of the lymphatic cords and glands in anasarca does not produce the indurated character which is found in farcy.

Prognosis.—While anasarca is not an excessively fatal disease, the prognosis must always be guarded. The majority of cases run a simple course and terminate favorably at the end of 8 or 10 days, or possibly, after one to two relapses, requiring several weeks for complete recovery. Effusion into the head renders the prognosis much more grave from the possible danger of mechanical asphyxia. Threatened mechanical asphyxia is especially dangerous on account of the risk of blood poisoning after an operation of tracheotomy. Edema of the viscera is a most serious complication. The prognosis is based on the complications, their extent, and their individual gravity, existing, as they do here, in an already debilitated subject.

Treatment.—The treatment of anasarca may be as variable as are the lesions. The indications are at once shown by the alterations and mechanism of the disease, which we have just studied.

Hygiene comes into play as the most important factor. Oats, oat-and-hay tea, milk, eggs—anything which the stomach or rectum can be coaxed to take care of—must be employed to give the nutriment, which is the only thing that will permanently strengthen the tissues; they must be strengthened in order to keep the capillaries at their proper caliber.

Laxatives, diaphoretics, and diuretics must be used to stimulate the emunctories so that they may carry off the large amount of the products of decomposition which result from the stagnated effusions of anasarca. Of these the sulphate of soda in small, repeated doses, the nitrate of potash and bicarbonate of soda in small quantity, or the chlorate of potash in single large doses will be found useful. Williams cites the chlorate of potash as an antiputrid. Stimulants and astringents are directly indicated. Spirits of turpentine serves the double purpose of a cardiac stimulant and a powerful, warm diuretic, for the kidneys in this disease will stand a wonderful amount of work. Camphor can be used with advantage. Coffee and tea are two of the diffusible stimulants which are too much neglected in veterinary medicine; both are valuable adjuncts in treatment of anasarca, as they are during convalescence at the end of any grave disease which has tended to render the patient anemic. Dilute sulphuric and hydrochloric acids are, perhaps, the best examples of a combination of stimulant, astringent, and tonic which can be employed. The simple astringents of mineral origin, sulphates of iron, copper, etc., are useful as digestive tonics; I doubt whether they have any constitutional effect. The vegetable astringents, tannic acid, etc., have not proved efficacious in my hands. Iodid of potash in small doses serves the triple purpose of digestive tonic, denutritive for inflammation, and diuretic. Among the newer forms of treatment are diluted Lugol’s solution injected into the trachea, anti-streptococcus serum and colloidal silver solution injected into the circulation. No one but a qualified veterinarian would be competent to apply these remedies.

Externally.—Sponging the swollen parts, especially the head, when the swelling occurs there, is most useful. The bath should be at an extreme of temperature—either ice cold to constrict the tissues or hot water to act as an emollient and to favor circulation. Vinegar may be added as an astringent. When we have excessively denuded surfaces, suppuration, or open wounds, disinfectants should be added to the wash.

In cases of excessive swelling, especially of the head, mechanical relief may be required. Even in country practice, punctures of the part should be made with the hot iron, as no other disease so predisposes to septic contamination. When mechanical asphyxia is threatened tracheotomy may be demanded. With the first evidence of dyspnea, not due to closing of the nostrils or glottis, or with the first pawing which gives rise to a suspicion of colic, a mustard plaster should be applied over the whole belly and chest. The sinapism will draw the current of the circulation to the exterior, the metastasis to the lungs or intestines is prevented, and the enfeebled nervous system is stimulated to renewed vigor by the peripheral irritation. The organs are encouraged by it to renewed functional activity; the local inflammation produced by it favors absorption of the exudation. The objection to the use of blisters is their more severe action and the danger of mortification. Septicemia, when occurring as a complication, requires the ordinary treatment for the putrid diseases, with little hope of a good result.

After recovery the animal regains its ordinary health, and there is no predisposition to a return of the disease.

Horsepox, or Equine Variola

Synonyms.—Variola equina; pustular grease; phlyctenold herpes.

Definition.—Horsepox is a specific, infectious fever of the horse, attended by an eruption of pustules, or pocks, over any part of the skin or on the mucous membranes lining the various cavities in the body, but chiefly, and often exclusively, upon the pasterns and fetlocks. The eruption may commence upon the lips, or about the nostrils or eyes.

This disease was described by the early Roman agricultural writers and by the veterinarians of the eighteenth century. It received its first important notice from the great Jenner, who confounded it with grease in horses, since animals with this disease are very liable to have the eruption of variola appear on the fetlocks. He saw these cases transmit the disease to cattle in the byres and to the stablemen and milkmaids who attended them, and furnish the latter with immunity from smallpox, which led to the discovery of vaccination. Horsepox is also frequently mistaken for the exanthemata attending some forms of venereal disease in horses.

Variola in the horse, while it is identical in principle, general course, complications, and lesions with variola in other animals, is a disease of the horse itself, and is not transmissible in the form of variola to any other animal; nor is the variola of any other animal transmissible to the horse. Cattle and men, if inoculated from a case of horsepox, develop vaccinia, but vaccinia from the latter animals is not so readily reinoculated into the horse with success. If it does develop, it produces the original disease.

Causes.—The direct cause of horsepox is infection. A large number of predisposing causes favor the development of the disease, as in the case of strangles, and this trouble, like almost all contagious diseases, renders the animal which has had one attack immune. The chief predisposing cause is youthfulness. Old horses which have not been affected are less liable to become infected when exposed than younger ones. The exposure incident to shipment, through public stables, cars, etc., acts as a predisposing cause, as in the other infectious diseases. The period of final dentition is a time which renders it peculiarly susceptible.

Dupaul states that the infection is transmissible through the atmosphere for several hundred yards. The more common means of contagion is by direct contact or by means of fomites. Feed boxes and bridles previously used by horses affected with variola are probably the most frequent carriers of the virus, and we find the lesions in the majority of cases developed in the neighborhood of the lips and nostrils. Coition is a frequent cause. A stallion suffering from this disease may be the cause of a considerable epizootic, as he transmits it to a number of brood mares and they in turn return to the farms where they are surrounded by young animals to which they convey the contagion. The saddle and croup straps are frequent agents of infection. The presence of a wound greatly favors the inoculation of the disease, which is also sometimes carried by surgical instruments or sponges. Trasbot recites a case in which a set of hobbles, which had been used on an animal suffering from variola, were used on a horse for a quittor operation and transmitted the disease, which developed on the edges of the wound.

Symptoms.—There is a period of incubation, after an animal has been exposed, of from five to eight days, during which there is no appreciable alteration in the health. This period is shorter in summer than in winter. At the end of this time small nodes develop at the point of inoculation and the animal becomes feverish. The horse is dull and dejected, loses its appetite, and has a rough, dry coat with the hairs on end. There is moderate thirst. The respirations are somewhat quickened and the pulse becomes rapid and full. The body temperature is elevated, frequently reaching 104° or 105° F. within 36 or 48 hours from the appearance of the first symptoms.

The visible mucous membranes, especially the conjunctivæ, are of a bright rosy red. In the lymphatic, cold-blooded, and more common horses these symptoms of fever are less marked; even with a comparatively high temperature the animal may retain its appetite and work comparatively well, but these cases, if worked and overheated, are liable to develop serious complications.

At the end of from three and a half to four days the eruption breaks out, the fever abates, and the general symptoms improve. The eruption in severe cases may be generalized; it may be confined to the softer skin of the nose and lips, the genital organs, and the inside of the thighs, or it may be localized in the neighborhood of a wound or in the irritated skin of a pair of greasy heels. It consists of a varying number of little nodes which, on a mucous membrane, as in the nostrils or vagina, or on soft, unpigmented skin, appear red and feel at first like shot under the epidermis. These nodes soften and show a yellowish spot in the center when they become pustules. The epidermis is dissolved and the matter escapes as a viscid fluid at first citrine and later cloudy and purulent, which dries rapidly, forming scabs; if these fall off or are removed they leave a little shallow, concave ulcer which heals in the course of five or six days. In the softer skin if pigmented the cicatrices are white and frequently remain so for about a year, when the pigment returns. The lips or genital organs of a colored horse, if covered with a number of small white spots about the size of a pea, will usually indicate that the animal has been affected with the horsepox.

At times the pustules may become confluent and produce large, superficial, serpentine ulcers on the membrane of the nostrils, around the lips or eyelids, or on the borders of wounds and in greasy heels; in this case the part becomes swollen, hot, painful, and is covered with a profuse discharge of matter. In this form there is frequently a secondary fever lasting for a day or two.

In severe cases there may be a suppurative adenitis, or inflammation of the lymphatic glands which are fed from the affected part. If the eruption is around the nostrils and lips, the glands between the jaws (submaxillary) form abscesses as in a case of strangles; if the eruption is in a pair of greasy heels abscesses may form in the fold of the groin (inguinal). There may be so much tumefaction of the nostrils as to produce difficulty in breathing.

Complications.—A case of horsepox may be attended with various complications of varying degrees of importance. Adenitis, or suppuration of the glands, has just been mentioned. Confluent eruptions irritate the part and induce the animal to rub the inflamed part against the manger or scratch it in other ways and thus produce troublesome ulcers, which may leave ugly scars. Irritation of the mucous membrane of the nose causes severe coryza with purulent discharge.

The eruption may occur in the throat or in the air tubes to the lungs, developing an acute laryngitis or bronchitis. If the animal is exposed to cold, or worked so as to engorge the lungs with blood at the termination of the specific fever, just when the eruption is about to localize, it may be determined to the lungs. In this case we have a short, dry cough, labored breathing, the development of a secondary fever of some gravity, and all the external symptoms of a pneumonia. This pneumonia differs, however, from an ordinary pneumonia in the symptoms furnished by the examination of the lungs themselves. In place of a large mass of the lung tissue being affected the inflammation is disseminated in smaller spots over the entire lung.

Diagnosis.—The diagnosis of horsepox is to be based on the presence of a continuous fever, with rosy mucous membranes, for several days and the appearance of the characteristic eruption. If the eruption is in the nasal cavities, marked by a considerable discharge and attended with submaxillary abscesses, it may be confounded with strangles. If the throat is affected, it may be confounded with an angina (laryngitis or pharyngitis), but in the latter the local trouble precedes or is concomitant with the fever, while in the former the fever precedes the local trouble by several days. Variola may be confounded with bronchitis or pneumonia if complicated with these troubles and the eruption is absent from the exterior, but it is of little moment, as the treatment for both is much the same. When the eruption is in the neighborhood of the genital organs the disease has been mistaken for dourine. In variola the eruption is a temporary one; the nodes and pustules are followed by shallow ulcers and rapid cicatrization unless continued in the vagina or on the penis by the rubbing of the walls and filth which accumulates; there are apt to be pustules at other parts of the body. In the venereal disease the local trouble commences as a papule and breaks into an ulcer without having formed a pustule. The ulcer has not the convex rosy appearance of that of the less serious discharge; the symptoms last for a longer period, by which time others aid in differentiating the two. In glanders the tubercle is hard and, after breaking into an ulcer, the indurated bottom remains, grayish or dirty white in color, ragged, and exuding a viscous, oily discharge. There is no disposition to suppuration of the neighboring glands. In variola the rosy shallow ulcer and healthy pus, with the acutely tumefied glands, should not be mistaken, at least after a day. I have seen in mules acute glanders which required a day’s delay to differentiate from strangles; at that time the farcy buds appeared.

Prognosis.—The average case of horsepox runs a course of dejection, loss of appetite, and more or less fever for about four days, followed by a rapid convalescence, and leaves the animal as well and as sound as before. If the eruption has been excessive or confluent, the ulcerations may act as irritants and render the animal unfit for use for several weeks. Laryngitis, pharyngitis, bronchitis, and pneumonia in this disease are not of greater gravity than they are when occurring from other causes. The spots denuded of pigment left by the pustules on the lips and genitals may temporarily depreciate the value of the animal to a slight degree.

Treatment.—As this is a disease unattended by alterations of the blood itself, although a specific fever, and is of a sthenic type, active remedies are admissible and indicated. The horse should be placed on a low diet (little or no oats)—bran mashes, a moderate quantity of good, sound hay, a few carrots or apples, which will act as laxatives; also slop feed. Barley flour is more cooling for mashes than bran or oatmeal. Water may be given as the animal desires it, but it should not be cold; if a half bucketful of water is kept in the manger, the horse will take but a few swallows at a time. One-dram doses of nitrate of potash or 1-ounce doses of sweet spirits of niter are useful in the drinking water. If the fever is high, the antipyretics are indicated: Sulphate of quinin in 1-dram doses; iodid of potash in 1-dram doses; infusion of pine tops, of juniper leaves, of the aromatic herbs, or of English breakfast tea are useful in the later stages. If complications of the air passages or lungs are threatened, a large mustard poultice should be applied to the belly and sides of the chest. Oxid of zinc ointment should be used on confluent eruptions, and if the ulceration is excessive it may have to be touched with caustic.

Great care must be taken to keep the animal protected from cold drafts of air or other exposure. Blankets or sheets should be used on the body and bandages on the legs. After convalescence is established, nutritious feed of easy digestion and walking exercise are all that is needed, except perhaps a little Glauber’s salt to prevent constipation.

Prophylactic treatment.—When horsepox breaks out among a large number of horses, especially on a farm where there are a number of colts, it may be assumed that the greater majority will contract the disease, and it is more economical that they should have it and be through with it at once. If the weather is moderate, all the animals which have not been affected can be inoculated, which will produce the disease in a mild form, with the eruption at a point of election, and render the danger of complication a minimum one. For inoculation the discharge from the pustules of a mild case should be selected and inoculated by scarification on the belly or the under surface of the neck.

ANTHRAX.

Synonyms: Carbuncle, splenic fever, splenic apoplexy, etc.; charbon, sang de rate (French); Miltzbrand (German).

Definition.—Anthrax is a severe and usually fatal contagious disease, characterized by chills, great depression and stupor of the animal, and a profound alteration of the blood. It is caused by the entrance into the animal’s body of a bacterium, known as the Bacillus anthracis, or its spores.

Practically all animals are susceptible to anthrax. The herbivora are especially susceptible, in the following order: The sheep, the ox, and the horse. The guinea pig, the hog, the rabbit, mice, and other animals die quickly from its effects. Man, the dog, and other omnivora and carnivora may be attacked by it in a constitutional form as fatal as in the herbivora, but fortunately in many cases develop from it only local trouble, followed by recovery.

Anthrax has been a scourge of the animals of the civilized world since the first written history we have of any of their diseases. In 1709-1712 extensive outbreaks of anthrax occurred in Germany, Hungary, and Poland. In the first half of the nineteenth century it had become an extensively spread disease in Russia, Holland, and England, and for the last century has been gradually spreading in the Americas, more so in South America than here. In 1864, in the five governments of Petersburg, Novgorod, Olonetz, Twer, and Jaroslaw, in Russia, more than 10,000 horses and nearly 1,000 persons perished from the disease.

Causes.—The causes of anthrax were for a long time attributed entirely to climatic influence, soil, and atmospheric temperature, and they are still recognized as predisposing factors in the development of the disease, for it is usually found, especially when outbreaks in a great number of animals occur, in low, damp, marshy countries during the warm seasons. It is more frequent in districts where marshy lands dry out during the heat of summer and are then covered with light rains. Decaying vegetable matter seems most favorable for nourishing and preserving the virus.

The direct cause of anthrax is always infection of a previously sound animal, either directly from a diseased animal or through various media which contain excretions or the débris from the body of one previously infected.

The specific virus of anthrax was first discovered by Davaine in 1851. He recognized microscopic bodies in the form of little rods in the blood of animals suffering from anthrax. It was not, however, till a quarter of a century later that Pasteur defined the exact nature of the bacillus, the mode of its propagation, and its exact relationship to anthrax as the sole cause of the disease. In the animal body the bacilli have a tendency to accumulate in the spleen, liver, and elsewhere, so that these organs are much more virulent than the muscles or less vascular tissues. When eliminated from the animal in the excretions, or when exposed to outside influences by the death of the animal and the disintegration of the tissues, the body of the rod is destroyed and the spores only remain. These spores, which may be called the seeds of the bacilli, retain their vitality for a long period; they resist ordinary putrefaction; they are unchanged by moisture; and they are not affected by moderate heat. If scattered with the débris of a dead animal on the surface of the ground, they may remain around the roots of the grass in a pasture or may be washed to the nearest low-lying ground or marsh. If buried in the body of an animal dead from anthrax, they may be washed deep into the ground, and in later years (in one proved case 17 years) be brought to the surface and infect other animals. They are frequently brought to the surface of the earth, having been swallowed by earthworms, in the bodies of which they have been found.

This accounts for the outbreaks at the time of the first rains after a dry season. During the latter the earthworm goes deep in the ground in search of moisture; it finds the spore which has been washed there in past years, swallows it, and afterwards brings it to the surface. The virus is carried with the wool from infected sheep and remains in it through the process of manufacture into cloth. The spores remain in the hides of animals which have died of anthrax and retain their vitality throughout months of soaking in the tanners’ pits, the working of the harness maker or the cobbler, and after the oiling of the completed leather. The dried spores in the dust from any of these products may be carried by the atmosphere.

Infection of an animal takes place through inoculation or contact of the bacillus or its spores with an abraded surface or mucous membrane, on a sound animal. In an infected district horses may eat with impunity the rich pasturage of spring and early summer, but when grass gets low they crop it close to the ground, pull up the roots around which the virus may be lodged, and under these conditions the animals are more apt to have abrasions of the lips or tongue by contact with dried stubble and the dirt on the roots; this favors the introduction of the germs into the system. The virus may be introduced with feed and enter the blood-vessel system from the stomach and intestines. If in the dust, dried hay, or on the parched pasture of late summer, the virus may be inhaled and be absorbed from the lining of the lungs. If in harness leather, it needs but an abrasion of the skin, as the harness rubs it, to transfer the spore from the leather to the circulation of the animal.

The writer saw a case of anthrax occur in a groom from the use of a new horse brush. The strap which passes over the back of the hand inoculated an abrasion on the knuckle of the first finger, and in 12 hours a “pustule” had formed and the arm had become infected.

Symptoms.—The symptoms of anthrax usually develop with extreme rapidity. The horse is dejected and falls into a state of profound stupor, attended with great muscular weakness. The feeble, indolent animal, if forced to move, drags its legs. There are severe chills, agitation of the muscles, symptoms of vertigo, and at times colicky pains. The mucous membranes turn a deep ocher or bluish-red color. The body temperature is rapidly elevated to 104° or 105° F. The breathing is increased to 30 or 40 respirations in the minute and the pulse is greatly accelerated, but while the arteries are soft and almost imperceptible, the heart beats can be felt and heard, violent and tumultuous. In some cases, when inoculation is through the skin, large subcutaneous swellings appear; these may involve a leg, a shoulder, one side of the body, or the neck or head. The swelling is at first hot and painful, but afterwards it becomes necrotic and sensation is lost. The symptoms last but two, three, or four days at most, when the case usually terminates fatally. An examination of the blood shows a dark fluid which will not clot, and which remains black after exposure to the air. After death the bodies putrefy rapidly and bloat up; the tissues are filled with gases, and a bloody foam exudes from the mouth, nostrils, and anus, and frequently the mucous membranes of the rectum protrude from the latter. The hairs detach from the skin. Congestion of all the organs and tissues is found, with interstitial hemorrhages. The muscles are friable and are covered with ecchymotic spots. This is especially marked in the heart.

The black, uncoagulated, and incoagulable blood shows an iridescent scum on its surface, which is due to the fat of the animal dissolved by the ammonia produced by the decomposed tissues. The serum oozes out of every tissue and contains broken-down blood, which, when examined microscopically, is found to have the red globules crenated and the leucocytes granular. A high power of the microscope also reveals the bacteria in the shape of little rodlike bodies of homogeneous texture with their brilliant spores.

The lymphatic ganglia are increased four, five, six, or ten times their natural size, enlarged by the engorgement of blood. The spleen shows nodulated black spots containing a muddy blood, which is found teeming with the virus. This organ is much enlarged and is quite friable. The mucous membranes of the intestines are congested and reddish brown; the surface of the intestines is in many places denuded of its lining membrane, showing fissures and hemorrhagic spots. The liver has a cooked appearance; the kidneys are congested and friable; the urine is red; the pleura, lungs, and the meninges are congested, and the bronchi of the lungs contain a bloody foam.

Treatment.—Treatment of anthrax in animals by medicinal means has not proved satisfactory. In cases of local anthrax an incision of the swelling followed by the application of disinfectants sometimes causes good results. In such cases, however, the danger of disseminating the infection from the wounds tends to make this procedure inadvisable unless great care is taken.

Good results are obtained from the use of serum in the treatment of the disease. For this purpose 30 to 100 cubic centimeters should be administered subcutaneously or intravenously. If no improvement is noticed within 24 hours the injection should be repeated. In a number of instances afforded to test the curative value of the serum in cases of anthrax in man and animals splendid results were obtained.

The prophylactic treatment formerly consisted in the avoidance of certain fields and marshes which were recognized as contaminated during the months of August and September and had been occupied the years in which the outbreaks usually occurred. It underwent, however, a revolution after the discovery by Pasteur of the possibility of a prophylactic inoculation or vaccination which granted immunity from future attacks of the disease similar to that granted by the recovery of an animal from an ordinary attack of the disease.

This treatment consists in the use of a vaccine which is made by the artificial cultivation of the virus of anthrax in broth and in the treatment of it by means of continued exposure to a high temperature for a certain time, which weakens the virus to such extent that it is capable of producing only a very mild and not dangerous attack of anthrax in the animal in which it is inoculated, and thus protects it from inoculation of a stronger virus. The production of this virus, which is carried on in some countries at the expense of the governments and is furnished at a small cost to the farmers in regions where the disease prevails, in this country is made in private laboratories only.

At the present time very good results are being obtained with vaccination consisting of an injection of highly potent anthrax serum on one side of the animal and a vaccine on the other side. This method of treatment requires only a single handling of the animals and further possesses advantages over the Pasteur treatment in that it immediately makes animals immune. In the numerous applications of this form of treatment very good results have been obtained and the immunity produced thereby visually lasts at least one year. The vaccinated animals should be kept for a period of ten days to two weeks from exposure, since during that period they are at times even more susceptible to the disease, and therefore care should be taken not to reduce their vitality.

Prevention.—In attempts to control the disease it is essential, aside from protective vaccination, to prevent the reinfection of localities. For this purpose it is essential, if possible, to drain thoroughly and keep under cultivation the infected areas before animals are permitted to pasture on them. The complete destruction of all anthrax carcasses is also very important. This is best accomplished by burning, but as this method of disposal is impracticable in many localities, deep burial may be found to be better. Covering the carcasses within their graves with quicklime adds another valuable precaution against further dissemination of the infection. No animal dying from anthrax should ever be skinned or cut open, as the blood from these sources is one of the most dangerous means of spreading the infection, being charged, while in the animal, with great numbers of bacilli, which quickly turn into spores as soon as spread about upon the face of the ground. All discharges from the body openings should also be burned or buried deeply, as they are frequently of a virulent character.

Glanders and Farcy

(Pls. Xl-Xlii.)

Definition.—Let it be understood at the outset that glanders and farcy are one and the same disease, differing only in that the first term is applied to the disease when the local lesions predominate in the internal organs, especially in the nostrils, lungs, and air tubes, and that the second term is applied to it when the principal manifestation is an outbreak of the lesions on the exterior or skin of the animal. The term glanders applies to the disease in both forms, while the term farcy is limited to the visible appearance of external trouble only; but in the latter case internal lesions always exist, although they may not be evident.

Glanders is a contagious constitutional disease of the genus Equus (the horse, ass, and mule), readily communicable to man, the dog, the cat, the rabbit, and the guinea pig. It is transmitted with difficulty to sheep and goats, and cattle seem to be entirely immune. It runs a variable course and usually produces the death of the animal affected with it. It is characterized by the formation of neoplasms, or nodules, of connective tissue, which degenerate into ulcers, from which exude a peculiar discharge. It is accompanied with a variable degree of fever, according to the rapidity of its course. It is subject to various complications of the lymphatic glands, of the lungs, of the testicles, of the internal organs, and of the subcutaneous connective tissue.

History.—Glanders is one of the oldest diseases of which we have definite knowledge in the history of medicine. Absyrtus, the Greek veterinarian in the army of Constantine the Great, described it with considerable accuracy and recognized the contagiousness of its character. Another Greek veterinarian, Vegetius Renatus, who lived in the time of Theodosius (381 A. D.), described, under the name of “malleus humidus,” a disease of the horse characterized by a nasal discharge and accompanied by superficial ulcers. He recognized the contagious properties of the discharge of the external ulcers, and recommended that all animals sick with the disease be separated at once with the greatest care from the others and should be pastured in separate fields, for fear the other animals should become affected.

In 1682 Sollysel, the stable master of Louis XIV, published an account of glanders and farcy, which he considered closely related to each other, although he did not recognize them as identical. He admitted the existence of a virus which communicated the disease from an infected animal to a sound one. He called special attention to the feed troughs and water buckets as being the media of contagion. He divided glanders into two forms—one malignant and contagious and the other benign—and he stated that there was always danger of infection.

Garsault in 1746 said that “as this disease is communicated very easily and can infect in a very short time a prodigious number of horses by means of the discharges which may be licked up, animals infected with glanders should be destroyed.”

Bourgelat, the founder of veterinary schools, in his “Elements of Hippiatry,” published in 1755, establishes glanders as a virulent disease.

Extensive outbreaks of glanders are described as prevailing in the great armies of continental Europe and England from time to time during the periods of all the wars of the last few centuries.

Glanders was imported into America at the close of the eighteenth century, and before the end of the first half of the last century had spread to a considerable degree among the horses of the Middle and immediately adjoining Southern States. This disease was unknown in Mexico until carried there during the Mexican War by the badly diseased horses of the United States Army. During the first half of the last century a large body of veterinarians and medical men protested against the contagious character of the disease, and by their opinion prevailed to such an extent against the common opinion that several of the Governments of Europe undertook a series of experiments to determine the right between the contesting parties.

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 râles. 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°, 104°, or 105° 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 râles 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 pharmacopœia 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° 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° 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 coït, 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 Rivière, 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 rôle 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° 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. Petechiæ, 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 petechiæ, 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 petechiæ, with a serous exudate present in the thoracic cavity. In addition to the petechiæ 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 petechiæ. 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 µ long by 1 to 2 µ 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° to 104° 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 petechiæ 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 petechiæ 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° or 105.8° 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 petechiæ 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. Pétrone 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 vertebræ 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.

The animal becomes poor in flesh, the coat is rough and lusterless, and the skin tight and harsh, producing a condition termed “hidebound,” with considerable “tucking up” of the abdomen. The horse shows a short, stilted, choppy gait, which later becomes stiffer and more restricted, while on standing a position simulating that in founder is assumed, with a noticeable drop to the croup. The animal at this stage usually lies down and remains recumbent for several days at a time. Bed sores frequently arise and fractures are not uncommon in consequence of attempts to arise, which complications, in addition to emaciation, result in death.

The disease may exist in this manner for variable periods extending from two or three months to two years. The termination of the disease is uncertain at best, but is likely to be favorable if treatment and a change of feed, water, and location is adopted in the early stages of the malady.

Lesions.—As has been stated, the bones are the principal tissues involved. The nutrition of the bone is disturbed, as is indicated by the diminished density or rarefaction of the bony substances, the increase in the size or widening of the Haversian canal and the medullary cavity, and the enlargement of the network of spaces in the spongy tissue, the absorptive changes following the course of the Haversian system. In this process of absorption there are formed within the substance of the bone areas of erosion, indentations, or hollow spaces of irregular shape. These spaces increase in size and become confluent, causing an appearance resembling some varieties of coral. The affected bone may be readily incised with a knife, the cut surface appearing finely porous. This porous area is soft, pliable, and yields easily to the pressure of the finger. It has been shown by chemical analysis that the bone of an osteoporotic horse, when compared with that of a normal horse, shows a reduction in the amount of fat, phosphoric acid, lime, and soda, but a slight increase in organic matter and silicic acid. The bones lose their yellowish-white appearance, becoming gray and brittle. The affected bones may be those of any region or portion of the body. Besides the change already noted in the bones of the face, the ends of the long bones, such as the ribs, are involved, and may be sectioned, though not so readily as the facial bones. The bones of the vertebræ are also frequently involved, necessitating great care in casting a horse, as the writer has seen several cases of broken backs in casting such animals for other operations. The marrow and cancellated tissue of the long bones may contain hemorrhages and soft gelatinous material or coagulated fibrin. The internal organs are usually normal, but a catarrhal condition of the gastrointestinal tract may be noted as the result of the improper mastication, resulting from the enlargement of the jaws and soreness of the teeth.

Treatment.—The affected animal should be immediately placed under new conditions, both as to feed and surroundings. If the horse has been stable fed, it is advisable to turn it out on grass for two or three months, preferably in a higher altitude. If the disease has been contracted while running on pasture, place the animal in the stable or corral. In the early stages of the disease beneficial results have followed the supplemental use of lime given in the drinking water. One peck of lime slaked in a cask of water and additional water added from time to time is satisfactory and can be provided at slight expense. This treatment may be supplemented by giving a tablespoonful of powdered bone meal in each feed, with free access to a large piece of rock salt, or the bone meal may be given with four tablespoonfuls of molasses mixed with the feed. Feeds containing mineral salts, such as beans, cowpeas, oats, and cottonseed meal, may prove beneficial in replenishing the bony substance that is being absorbed. Cottonseed meal is one of the best feeds for this purpose, but it should be fed carefully. The animal should not be allowed to work at all during the active stage of the disease, nor should it be used for breeding purposes.

Footnotes

7 This summary of symptoms is based upon work by Lingard.