Chapter 69

_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.

HORSESHOEING.

By JOHN W. ADAMS, A. B., V. M.,

_Professor of Surgery and Lecturer on Shoeing, Veterinary Department, University of Pennsylvania._

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.

GROSS ANATOMY OF THE FOOT.

(Pls. XXXII-XXXIV.)

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.