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 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 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.
[7] This summary of symptoms is based upon work by Lingard.
Bad and indifferent shoeing so frequently leads to diseases of the feet and in irregularities of gait, which may render a horse unserviceable, that it has been thought appropriate to conclude this book with a brief chapter on the principles involved in shoeing healthy hoofs.
In unfolding this subject in the limited space at my disposal, I can only hope to give the intelligent horse owner a sufficient number of facts, based on experience and upon the anatomy and physiology of the foot and leg, to enable him to avoid the more serious consequences of improper shoeing.
Let us first examine this vital mechanism, the foot, and learn something of its structure and of the natural movements of its component parts, that we may be prepared to recognize deviations from the normal and to apply the proper corrective.
The bones of the foot are four in number, three of which—the long pastern, short pastern, and coffin bone, placed end to end—form a continuous straight column passing downward and forward from the fetlock joint to the ground. A small accessory bone, the navicular, or "shuttle," bone, lies crosswise in the foot between the wings of the coffin bone and forms a part of the joint surface of the latter. The short pastern projects about 1-/2 inches above the hoof and extends about an equal distance to it. (See also page 395.)
The pastern and the coffin bone are held together by strong fibrous cords passing between each two bones and placed at the sides so as not to interfere with the forward and backward movement of the bones. The joints are therefore hinge joints, though imperfect, because, while the chief movements are those of extension and flexion in a single plane, some slight rotation and lateral movements are possible.
The bones are still further bound together and supported by three long fibrous cords, or tendons. One, the extensor tendon of the toe, passes down the front of the pasterns and attaches to the coffin bone just below the edge of the hair; when pulled upon by its muscle this tendon draws the toe forward and enables the horse to place the hoof flat upon the ground. The other two tendons are placed behind the pasterns and are called flexors, because they flex, or bend, the pasterns and coffin bone backward. One of the tendons is attached to the upper end of the short pastern, while the other passes down between the heels, glides over the under surface of the navicular bone, and attaches itself to the under surface of the coffin bone. These two tendons not only flex, or fold up, the foot as the latter leaves the ground during motion, but at rest assist the suspensory ligament in supporting the fetlock joint.
The foot-axis is an imaginary line passing from the fetlock joint through the long axes of the two pasterns and coffin bone. This imaginary line, which shows the direction of the pasterns and coffin bone, should always be straight—that is, never broken, either forward or backward when viewed from the side, or inward or outward when observed from in front. Viewed from one side, the long axis of the long pastern, when prolonged to the ground, should be parallel to the line of the toe. Viewed from in front, the long axis of the long pastern, when prolonged to the ground, should cut the hoof exactly at the middle of the toe.
Raising the heel or shortening the toe not only tilts the coffin bone forward and makes the hoof stand steeper at the toe, but slackens the tendon that attaches to the under surface of the coffin bone (perforans tendon), and therefore allows the fetlock joint to sink downward and backward and the long pastern to assume a more nearly horizontal position. The foot-axis, viewed from one side, is now broken forward; that is, the long pastern is less steep than the toe, and the heels are either too long or the toe is too short. On the other hand, raising the toe or lowering the heels of a foot with a straight foot-axis not only tilts the coffin bone backward and renders the toe more nearly horizontal, but tenses the perforans tendon, which then forces the fetlock joint forward, causing the long pastern to stand steeper. The foot-axis, seen from one side, is now broken backward—an indication that the toe is relatively too long or that the heels are relatively too low.
The elastic tissues of the foot are preeminently the lateral cartilages and the plantar cushion. The lateral cartilages are two irregularly four-sided plates of gristle, one on either side of the foot, extending from the wings of the coffin bone backward to the heels and upward to a distance of an inch or more above the edge of the hair, where they may be felt by the fingers. When sound, these plates are elastic and yield readily to moderate finger pressure, but from various causes may undergo ossification, in which condition they are hard and unyielding. The plantar cushion is a wedge-shaped mass of tough, elastic, fibro-fatty tissue filling all the space between the lateral cartilages, forming the fleshy heels and the fleshy frog, and serving as a buffer to disperse shock when the foot is set to the ground. It extends forward underneath the navicular bone and perforans tendon, and protects these structures from injurious pressure from below. Instantaneous photographs show that at speed the horse sets the heels to the ground before other parts of the foot—conclusive proof that the function of this tough, elastic structure is to dissipate and render harmless violent impact of the foot with the ground.
The horn-producing membrane, or "quick," as it is commonly termed, is merely a downward prolongation of the "derm," or true skin, and may be conveniently called the pododerm (foot skin). The pododerm closely invests the coffin bone, lateral cartilages, and plantar cushion, much as a sock covers the human foot, and is itself covered by the horny capsule, or hoof. It differs from the external skin, or hair skin, in having no sweat or oil glands, but, like it, is richly supplied with blood vessels and sensitive nerves. And, just as the derm of the hair skin produces upon its outer surface layer upon layer of horny cells (epiderm), which protect the sensitive and vascular derm, so, likewise, in the foot the pododerm produces over its entire surface soft cells, which, pushed away by more recent cells forming beneath, lose moisture by evaporation and are rapidly transformed into the corneous material which we call the hoof. It is proper to regard the hoof as a greatly thickened epiderm having many of the qualities possessed by such epidermal structures as hair, feathers, nails, claws, etc.
The functions of the pododerm are to produce the hoof and to unite it firmly to the foot.
There are five parts of the pododerm, easily distinguishable when the hoof has been removed, namely: (1) The perioplic band, a narrow ridge from one-sixteenth to one-eighth of an inch wide, running along the edge of the hair from one heel around the toe to the other. This band produces the perioplic horn, the thin varnishlike layer of glistening horn, which forms the surface of the wall or "crust," and whose purpose seems to be to retard evaporation of moisture from the wall. (2) The coronary band, a prominent fleshy cornice encircling the foot just below and parallel to the perioplic band. At the heels it is reflected forward along the sides of the fleshy frog, to become lost near the apex of this latter structure. The coronet produces the middle layer of the wall, and the reflexed portions produce the "bars," which are, therefore, to be regarded merely as a turning forward of the wall. (3) The fleshy leaves, 500 to 600 in number, parallel to one another, running downward and forward from the lower edge of the coronary band to the margin of the fleshy sole. They produce the soft, light-colored horny leaves which form the deepest layer of the wall, and serve as a strong bond of union between the middle layer of the wall and the fleshy leaves with which they dovetail. (4) The fleshy sole, which covers the entire under surface of the foot, excepting the fleshy frog and bars. The horny sole is produced by the fleshy sole. (5) The fleshy frog, which covers the under surface of the plantar cushion and produces the horny frog.
The horny box or hoof consists of wall and bars, sole and frog. The wall is all that part of the hoof which is visible when the foot is on the ground (see fig. 8). As already stated, it consists of three layers—the periople, the middle layer, and the leafy layer.
The bars (see fig. 1c) are forward prolongations of the wall, and are gradually lost near the point of the frog. The angle between the wall and a bar is called the "buttress." Each bar lies against the horny frog on one side and incloses a wing of the sole on the other, so that the least expansion or contraction of the horny frog separates or approximates the bars, and through them the lateral cartilages and the walls of the quarters. The lower border of the wall is called the "bearing edge," and is the surface against which the shoe bears. By dividing the entire lower circumference of the wall into five equal parts, a toe, two side walls, and two quarters will be exhibited. The "heels," strictly speaking, are the two rounded soft prominences of the plantar cushion, lying one above each quarter. The outer wall is usually more slanting than the inner, and the more slanting half of a hoof is always the thicker. In front hoofs the wall is thickest at the toe and gradually thins out toward the quarters, where in some horses it may not exceed one-fourth of an inch. In hind hoofs there is much less difference in thickness between the toe, side walls, and quarters. The horny sole, from which the flakes of old horn have been removed, is concave and about as thick as the wall at the toe. It is rough, uneven and often covered by flakes of dead horn in process of being loosened and cast off. Behind the sole presents an opening into which are received the bars and horny frog. This opening divides the sole into a body and two wings.
The periphery of the sole unites with the lower border of the wall and bars through the medium of the white line, which is the cross section of the leafy horn layer of the wall and of short plugs of horn which grow down from the lower ends of the fleshy leaves. This white line is of much importance to the shoer, since its distance from the outer border of the hoof is the thickness of the wall, and in the white line all nails should be driven.
The frog, secreted by the pododerm covering the plantar cushion or fatty frog, and presenting almost the same form as the latter, lies as a soft and very elastic wedge between the bars and between the edges of the sole just in front of the bars. A broad and shallow depression in its center divides it into two branches, which diverge as they pass backward into the horny bulbs of the heel. In front of the middle cleft the two branches unite to form the body of the frog, which ends in the point of the frog. The bar of a bar shoe should rest on the branches of the frog. In unshod hoofs the bearing edge of the wall, the sole, frog, and bars are all on a level; that is, the under surface of the hoof is perfectly flat, and each of these structures assists in bearing the body weight.
With respect to solidity, the different parts of the hoof vary widely. The middle layer of the wall is harder and more tenacious than the sole, for the latter crumbles away or passes off in larger or smaller flakes on its under surface, while no such spontaneous shortening of the wall occurs. The white line and the frog are soft-horn structures, and differ from hard horn in that their horn cells do not under natural conditions become hard and hornlike. They are very elastic, absorb moisture rapidly, and as readily dry out and become hard, brittle, and easily fissured. Horn of good quality is fine grained and tough, while bad horn is coarse grained and either mellow and friable or hard and brittle. All horn is a poor conductor of heat, and the harder (drier) the horn the more slowly does it transmit extremes of temperature.
A hoof while supporting the body weight has a different form, and the structures inclosed within the hoof have a different position than when not bearing weight. Since the amount of weight borne by a foot is continually changing, and the relations of internal pressure are continuously varying, a foot is, from a physiological viewpoint, never at rest. The most marked changes of form of the hoof occur when the foot bears the greatest weight, namely, at the time of the greatest descent of the fetlock. Briefly, these changes of form are: (1) An expansion or widening of the whole back half of the foot from the coronet to the lower edge of the quarters. This expansion varies between one-fiftieth and one-twelfth of an inch. (2) A narrowing of the front half of the foot, measured at the coronet. (3) A sinking of the heels and a flattening of the wings of the sole. These changes are more marked in the half of the foot that bears the greater weight.
The changes of form occur in the following order. When the foot is set to the ground the body weight is transmitted through the bones and sensitive and horny leaves to the wall. The coffin bone and navicular bone sink a little and rotate backward. At the same time the short pastern sinks backward and downward between the lateral cartilages and presses the perforans tendon upon the plantar cushion. This cushion being compressed from above and being unable to expand downward by reason of the resistance of the ground acting against the horny frog, acts like any other elastic mass and expands toward the sides, pushing before it the yielding lateral cartilages and the wall of the quarters. This expansion of the heels is assisted and increased by the simultaneous flattening and lateral expansion of the resilient horny frog, which crowds the bars apart. Of course, when the lateral cartilages are ossified, not only is no expansion of the quarters possible, but frog pressure often leads to painful compression of the plantar cushion and to increase of lameness. Frog pressure is therefore contraindicated in lameness due to sidebones (ossified cartilages). Under the descent of the coffin bone the horny sole sinks a little; that is, the arch of the sole around the point of the frog and the wings of the sole become somewhat flattened. All these changes of form are most marked in sound unshod hoofs, because in them ground pressure on the frog and sole is pronounced; they are more marked in fore hoofs than in hind hoofs.
The movement of the different structures within the foot and the changes of form that occur at every step are indispensable to the health of the hoof, so that these elastic tissues must be kept active by regular exercise, with protection against drying out of the hoof. Long-continued rest in the stable, drying out of the hoof, and shoeing decrease or alter the physiological movements of the hoof and sometimes lead to foot diseases. Since these movements are complete and spontaneous only in unshod feet, shoeing must be regarded as an evil, albeit a necessary one, and indispensable if we wish to keep horses continuously serviceable on hard, artificial roads. However, if in shoeing we bear in mind the structure and functions of the hoof and apply a shoe whose branches have a wide and level bearing surface, so as to interfere as little as may be with the expansion and contraction of the quarters, in so far as this is not hindered by the nails, we need not be apprehensive of trouble, provided the horse has reasonable work and his hoofs proper care.
All parts of the hoof grow downward and forward with equal rapidity, the rate of growth being largely dependent upon the amount of blood supplied to the pododerm, or "quick." Abundant and regular exercise, good grooming, moistness and suppleness of the hoof, going barefoot, plenty of good feed, and at proper intervals removing the overgrowth of hoof and regulating the bearing surface, by increasing the volume and improving the quality of the blood flowing into the pododerm, favor the rapid growth of horn of good quality; while lack of exercise, dryness of the horn, and excessive length of the hoof hinder growth.
The average rate of growth is about one-third of an inch a month. Hind hoofs grow faster than fore hoofs and unshod ones faster than shod ones. The time required for the horn to grow from the coronet to the ground, though influenced to a slight degree by the precited conditions, varies in proportion to the distance of the coronet from the ground. At the toe, depending on its height, the horn grows down in 11 to 13 months, at the side wall in 6 to 8 months, and at the heels in 3 to 5 months. We can thus estimate with tolerable accuracy the time required for the disappearance of such defects in the hoof as cracks, clefts, etc.
Irregular growth is not infrequent. The almost invariable cause of this is an improper distribution of the body weight over the hoof—that is, an unbalanced foot. Colts running in soft pasture or confined for long periods in the stable are frequently allowed to grow hoofs of excessive length. The long toe becomes "dished"—that is, concave from the coronet to the ground—the long quarters curl forward and inward and often completely cover the frog and lead to contraction of the heels, or the whole hoof bends outward or inward, and a crooked foot, or, even worse, a crooked leg, is the result if the long hoof be allowed to exert its powerful and abnormally directed leverage for but a few months upon young plastic bones and tender and lax articular ligaments. All colts are not foaled with straight legs, but failure to regulate the length and bearing of the hoof may make a straight leg crooked and a crooked leg worse, just as intelligent care during the growing period can greatly improve a congenitally crooked limb. If breeders were more generally cognizant of the power of overgrown and unbalanced hoofs to divert the lower bones of young legs from their proper direction, and, therefore, to cause them to be moved improperly, with loss of speed and often with injury to the limbs, we might hope to see fewer knock-kneed, bow-legged, "splay-footed," "pigeon-toed," cow-hocked, interfering, and paddling horses.
If in shortening the hoof one side wall is, from ignorance, left too long or cut down too low with relation to the other, the foot will be unbalanced, and in traveling the long section will touch the ground first and will continue to do so till it has been reduced to its proper level (length) by the increased wear which will take place at this point. While this occurs rapidly in unshod hoofs, the shoe prevents wear of the hoof, though it is itself more rapidly worn away beneath the high (long) side than elsewhere, so that by the time the shoe is worn out the tread of the shoe may be flat. If this mistake be repeated from month to month, the part of the wall left too high will grow more rapidly than the low side whose pododerm is relatively anemic as a result of the greater weight falling into this half of the hoof, and the ultimate result will be a "wry," or crooked foot.
The colt should have abundant exercise on dry ground. The hoofs will then wear gradually, and it will only be necessary from time to time to regulate any uneven wear with the rasp and to round off the sharp edge about the toe in order to prevent breaking away of the wall.
Colts in the stable can not wear down their hoofs, so that every four to six weeks they should be rasped down and the lower edge of the wall well rounded to prevent chipping. The soles and clefts of the frog should be picked out every few days and the entire hoof washed clean. Plenty of clean straw litter should be provided. Hoofs that are becoming "awry" should have the wall shortened in such a manner as to straighten the foot-axis. This will ultimately produce a good hoof and will improve the position of the limb.