Chapter XXII: Part 22

Productive inflammations and tumors of the skin are common in domestic animals but as they are essentially surgical lesions, they will be better considered under that head. We may name papilloma, warts, fibroma, melanoma, epithelioma, sarcoma, adenoma, carcinoma, dermoid cysts. Parasitic and microbian diseases of the skin will be found under their respective headings.

ALOPECIA CONGENITA. CONGENITAL BALDNESS.

Cases of this kind have been met with in foals and calves, which were born entirely bald or with only a few thin delicate hairs scattered over the surface. In a calf observed by the author, and which lived for several months, the body was almost absolutely bald, and the mouth remained edentulous, a coincidence which has been observed in other cases. The teeth belong to the same class of embryonic tissues as the epidermis, and a failure in the development of the one is likely to entail a corresponding failure of the other. Schneidemühl observed that the few hairs present in such cases were especially delicate and brittle.

ALOPECIA. POST PARTEM. ALOPECIA AREATA.

Normal shedding. Shedding out of time; laminitis, dropsy, exudative
dermatitis, acariasis, ringworm, traumas, folliculitis. Debility,
excessive lactation, starvation, petechial fever, spoiled fodder.
Without apparent cause, alopecia areata, neurosis, micrococci, disease
of derma. Symptoms: general disorder has general shedding. Local
disorder extends from a centre. In horse with increased pigmentation.
Treatment: correct general causes, use hair stimulants, cantharides,
kerosene, tar, pilocarpin, mercuric chloride, cresol, iodine, balsam
of Peru, silver nitrate. Arsenic.

Acquired baldness is recorded in horse, cattle, sheep and dog.

_Causes._ The simple shedding of hair occurs physiologically in animals with the change of season, and if anything interferes with the growth of the new hair a transient baldness may ensue. If such shedding occurs from any cause at the wrong season, before the new hair has started, the baldness may be accentuated. Thus shedding may occur in some forms of indigestion, in laminitis, in dropsical swelling of the limbs or ventral aspect of the body, in dermatitis with an exudation which concretes around the hairs and raises them out of their follicles, in mange, in demodectic acariasis, in circinate ringworm, in traumas as on the elbows of dogs, etc., from lying on them, and in inflammation of the hair follicles from a variety of infections. It has been charged on general debility in excessive lactation, in gestation, and in starvation, on poisons in the blood as in petechial fever, and on musty or spoiled fodders in bad seasons, or from low damp lands.

When in the absence of such appreciable causes it commences at one or more points and gradually extends, and persists, it constitutes alopecia areata. This has been attributed to a disorder of the cutaneous nerves (tropho-neurosis), but the progressive advance of the disease, without limitation to areas representing the distribution of given cutaneous nerves, and the complete absence of other derangement of nerve function, throw doubt on this conclusion. Another doctrine attributes it to a microbe, but though micrococci and other organisms have been found, they have not been proved to be constant nor to be absolutely causative of the disease. Still another theory holds that it is a disease of the derma and not of the hair at all, the evulsion of the hair following the implication of the tissues around the follicles.

_Symptoms._ The baldness dependent on a general disorder occurs at once over an extended area. That of ringworm, acariasis, and of the specific alopecia areata, advances gradually and often slowly from a given point, until it may include a large area. Röll has seen it extend from a few points to nearly the whole body of the horse in a single year. In this, as in other cases in horse and dog, the baldness was followed by a considerable increase of the pigmentation of the skin.

_Treatment._ In cases that occur as the result of other diseases, the rational treatment is to deal with these diseases, and then to stimulate the growth of hair by some one or other of the known stimulants (dilute tincture of cantharides, kerosene, tar water, solution of pilocarpin hydrochlorate). In the more specific form, no treatment has been very successful, yet the best results on the whole appear to have come from local germicide applications. Mercuric chloride in alcohol and water (1 ∶ 500); cresol 1, alcohol 20; tincture of iodine reduced to half its strength by addition of alcohol; balsam of Peru 1, alcohol 5; nitrate of silver 1, alcohol 15, serve as examples.

As general treatment arsenic has been employed, but with no very encouraging results.

TRICHORRHEXIS NODOSA. NODULAR SWELLING AND SPLITTING OF HAIR.

Debility, ringworm, nodular hair. Hair bursts with brush like end.
Cases in horse like singed hair. Causes: infection probable, disturbed
innervation, dry air, impaired nutrition. Treatment: shave, oil,
vaseline, petroleum, cantharides, sulphur, tar, favor shedding coat.

In a variety of conditions the hairs split up and break, leading to bristling or baldness. In debilitated conditions, when the hair is badly nourished, in ringworm when it is invaded by a cryptogam, and in the various nodular or ringed conditions of the hair this brittleness and splitting appears. The term _Trichorrhexis_ (rexis a bursting forth) has been applied to one of these affections, in which the hair swells and bursts into a number of filaments giving it a broom-like termination. Trofimo describes this as affecting two-thirds of the horses of an artillery brigade, and showing upon the back, croup, mane and tail in isolated patches. Megnin, Trasbot and Roy have observed similar cases. The affected hair a short distance from the skin swells into a grayish white nodule and breaks across, leaving a tuft of fine filaments. The patches look to the naked eye as if singed, but when the hair is magnified the difference is easily made out, as there may be several nodular enlargements on the same hair, and the brushlike spread of filaments at the broken end is entirely unlike the solid node on the end of a singed hair.

The _causes_ of the affection have not been demonstrated, though indications point to an infection which gradually extends from the first point of attack. This extension is not limited to the area presided over by particular nerves, and there is no other indication of disordered innervation. Trasbot has seen the disease transmitted from horse to horse by the use in common of combs, brushes and rubbers, and in other cases experimentally by rubbing the scurf from a diseased animal on the skin of a healthy one. From observations on the human subject Montgomery looks on it as a result of extreme dryness and brittleness of the hair, and charges dry climates and seasons, and an abuse of soap in washing as conducive causes. Debility and impaired nutrition of the hair may operate in the same way. No specific microbe has been constantly found in these cases and until such factor can be proved, it may be held that among the etiological agents impaired nutrition and dry air are important.

In the way of _treatment_ shaving of the affected parts and oily or vaseline applications may be tried, together with such slight cutaneous stimulants as petroleum, weak tincture of cantharides, sulphur, tar ointment, etc. Roy noticed that cases that had lasted all winter recovered after shedding of the coat. It might be assumed that the evulsion of the infected hair, and the vascular stimulus necessary to the new growth contributed to the result.

CONSTITUTIONAL DISEASES.
RHEUMATISM.

Definition. Past views. Causes: heredity, age, cold, damp, cold
climates, seasons, exposure, buildings, cellars, night chills, weather
vicissitudes, valleys, wading, checked perspiration, lactic acid,
metabolic products, acid phosphate of soda, vegetable acids,
neuropathic causation, infection, microbes, injuries, overwork.
Lesions: in joints, synovia, serosa, articular cartilage,
fibro-cartilage, articular lamella, bone, eburnation, ligaments,
joints affected in horse and ox, blood changes, albumen, fibrine,
blood globules, pericardium, endocarditis, valvular disease,
myocarditis, embolisms in lungs, pleura, nervous lesions, digestive
system.

_Definition._ A constitutional, inflammatory affection, probably toxic, tending to localization in the joints, muscles, tendons, fascia, skin, heart and serous membranes and with a marked disposition to shift from place to place.

The word is derived from _rhein_ (γειν) to flow, and was originally employed to indicate that an acrid humor, generated in the brain or elsewhere escaped mainly by the nose and eyes as a catarrh. The idea naturally followed that the retention of this humor caused inflammation in the joints, muscles, heart or elsewhere. The connection of these various conditions with exposure to cold, led to the association of the name with the various internal inflammations in which chilling appeared to have been a factor, until it was difficult to limit it by any definite line. Finally infectious diseases implicating the joints or muscles (influenza, contagious pneumonia, omphalitis, gonorrhœal rheumatism), and diseases of metabolism (gout and possibly rheumatoid arthritis) have added to the general confusion.

GENERAL CAUSES. _Heredity._ This has been more definitely traced in man than in the lower animals, the line of family descent being more easily followed in man. Children of rheumatic parents are more obnoxious to the disease in the ratio of 5 to 1. In the absence of data for animals, we may say that it is probable that the influence of heredity will hold good for live stock in this matter. Whether the disease results from faulty metabolism or from microbian invasion or toxins, the hereditary defensive powers of the animal cell are likely to be an important factor.

_Age._ Genuine rheumatism is not common at a very early age, but in animals as in man, attacks especially those in the prime of life, accustomed to vigorous exercise, free perspiration and succeeding chills. There is as yet no direct evidence of an exhaustion of the susceptibility of early maturity and of any consequent immunity of the old.

_Cold and damp._ The association of rheumatism with cold and damp has always been so notorious that no argument is needed to enforce the truth. It is pre-eminently the disease of cold climates and cold situations exposed to the north and east in Europe, or to the north and west in North America on the Atlantic slope. It is very little prevalent in the tropics. Buildings and yards that lack sunshine and exposed storm-swept hillsides show cases most numerously. Dogs kept in cold, damp sunless cellars often suffer. Cold, damp or frosty nights start or aggravate cases in animals left out in the field, while warm sunshine usually brings immediate improvement. A sudden change of weather to cold and wet is the signal for aggravation of the existing disease, though this may have set in before the change of weather has been fully developed. Late autumn and early spring with their sudden changes, their sleet and rain are especially hurtful and particularly to chronic cases. The cold, raw ocean winds on the Pacific coast contrasting with the warm sunshine is a marked contributing cause. The currents of cold air that draw up through shaded valleys, gullies and ravines expose their denizens to attacks. Rheumatism is more rare among well housed and carefully treated family horses, and less so in draught, dray and other hard working horses that are made to cross streams and stand with feet and legs in cold water while the body is drenched with perspiration. Dogs suffer in the same way while hunting. Haycock attributes many attacks to washing the legs with ice cold water when the animal has just returned to the stable heated and perspiring. If then left undried and unbandaged in a cold draught these conditions are still farther aggravated. This was formerly attributed to the suppression of perspiration, but it occurs in an animal which has just perspired freely and is now in no special need of further elimination through the skin. It appears to be due rather to the action of the cold on the nerve endings, the susceptibility of which has been enhanced by the free secretion and general relaxation.

But potent as cold is in precipitating or aggravating an attack, it cannot be looked on as the sole or essential cause of rheumatism. The great majority exposed to the cold escape. The animal which has stood in the stall, or shed, is less likely to be attacked than the one at work in which the heat production has been more active. Indeed an immunity has been claimed for the Arctic regions, provided the subject is not exerted so as to cause perspiration. One might readily conclude that this apparent immunity, depended on the absence of an essential germ, as is also claimed for catarrhs, yet Nansen after his prolonged bath in the frigid waters seems to have had an attack of rheumatism. Cold appears to be one of the most potent accessory causes, but evidently not in itself the essential cause.

Cold undoubtedly affects profoundly the metabolism of the body and especially when the vital powers have been reduced by severe exertion, fatigue and perspiration. The same applies to many other affections especially such as are associated with an infecting element, which takes occasion of the debility caused by the cold to establish itself in the tissues.

_Lactic acid and other metabolic products._ Prout long ago claimed that rheumatism was caused by an excess of lactic acid in the system, and this was supported by the fact that an exclusive diet of buttermilk given in diabetes, is likely to produce acute articular rheumatism. Again the production of rachitis in the young can be traced in certain cases to excess of this acid. The strongly acid odor of the sweat in certain rheumatic attacks is thought to support this theory. The excess of lactic acid is variously explained by the overwork of the muscles of which it is the normal product, and by the imperfect oxidation of the muscular tissue and its product into lactic acid (C_{3}H_{4}O(OH)_{2}), instead of carbonic acid (CO(OH)_{2}). But in spite of the perfect theory, there is the fact that as a rule no special increase of lactic acid can be found in blood or urine in acute rheumatism and the improbability that an excess of this acid caused by sudden excessive muscular waste could be kept up during a long attack of acute much less of chronic rheumatism. Again the comparative immunity of sucklings in which there is the greatest opportunity for the production of lactic acid, would imply that that alone cannot be accepted, as the one essential cause of the affection. That its excess in the system will aggravate rheumatism, or even produce it under favorable circumstances must be freely acknowledged; also that acidity of the saliva is a marked feature of rheumatism.

The acid phosphate of soda may be assigned a somewhat similar rôle. In strongly predisposed subjects the ingestion of citric or other organic acid will sometimes precipitate rheumatic articular pains.

Still other products, the result of imperfect oxidation or metabolism must be allowed a place as probable factors in rheumatism. The occurrence of gout in connection with the excess of uric acid in the system is strongly suggestive of this, and the frequency of muscular rheumatism in pampered, overfed dogs with diseased livers and abnormal hepatic products, seems to give further support. Even in man, the subject of acute rheumatism, often leads a luxurious life and suffers from inactive or disordered liver, while in man and animals alike, a low grade of health and imperfect functional activity of important organs, are often precursors and accompaniments of acute rheumatism.

_Neuropathic theory._ The doctrine of a neurotic cause originated by Dr. Mitchell, of Philadelphia, has considerable basis in theory. The primary chill tends to nervous derangement, which may readily affect the overworked or already diseased and debilitated joints. Similar peripheric disturbance of nutrition occurs in locomotor ataxia in which the central nervous lesion is very evident. There is a strong disposition in rheumatism to show a bilateral symmetry, which points directly to a central nervous control. The frequent violence of the pain, disproportionate to the moderate structural changes, points in the same direction, and the free perspiration present in some severe attacks, points alike to its origin in cutaneous chill and to derangement of the centres presiding over perspiration. It may be added that the development of rheumatic symptoms in the advanced stages of infectious diseases, when the toxins are accumulating in the system, suggests that they are the direct result of a toxic action on the nerve centres. In man the influence of severe nervous shock in developing and maintaining rheumatism is recognized.

_Theory of infection._ This has been advocated by Cornil and Babes and Friedberger and Fröhner. The former quote the frequent presence of microörganisms and above all of micrococci in the liquids of the affected joints, serosæ and valvular exudates and ulcers, and even in the blood, and the occurrence of rheumatism in the course of various septic affections. The latter quote Auer and others as to the frequent supervention of articular rheumatism on the retention of the afterbirth in the cow. The weak point in these theories is the multiplicity and variety of the microbes found in the exudates. Either we must accept the rheumatic lesions as an occasional result of many microbes, which habitually act differently on the system, or we must look upon them as mere accessory causes or accidental complications. It might even be, that the invasion of these microbes are made possible by the inflammation and debility of the tissues, without being directly chargeable with the rheumatic process. Even then there remains the possibility that a specific microbe is present, which by reason of its infinitesimal size, or other physical property, has as yet escaped recognition. If such specific microbe is present, it manifestly requires a very special predisposition, since it is not seen to advance from one individual to another unless such favoring conditions are present. The symptoms and lesions of rheumatism are not incompatible with the idea of such an essential, specific germ, but as yet no such germ has been satisfactorily demonstrated as present in all cases.

_Local injuries._ Rheumatism seems to attack by preference parts that have already been debilitated by disease, a disposition which is also true of distinctly microbian infections. A pre-existing sprain, blow, bruise or an inflammation arising from any other cause seems to practically invite the localization of the morbid process at that point, and thus what was at first a purely traumatic lesion becomes the seat of active and perhaps permanent rheumatism. Unusual overwork and fatigue of given joints and muscles induce a similar predisposition, and habitual overexertion, sprain, injury or inflammation affecting repeatedly the rheumatic organ tends to fix the process in chronic form.

_Articular lesions._ These tend to concentrate as a form of inflammation in the synovial membranes, but usually implicate all the constituent structures of the joint, capsular and binding ligaments, cartilage and fibro-cartilage, articular lamella and osseous tissue. The synovial membrane may show only slight hyperæmia, or in severe cases it may be congested, red, thickened or even extensively infiltrated with a serogelatinoid liquid. These lesions are most marked around the line of attachment on the articular surface and in the synovial fringes. The synovia is usually in excess, distending the capsule and is whitish, opaque, flocculent or more or less deeply colored with red. It contains flakes of fibrine, leucocytes, albumen and it may be red blood globules. Pus cells are usually absent unless in distinctly infective cases. Coagula and false membranes floating from or adherent to the solid tissues, may be present in considerable amount and if these become organized they tend to lay the foundation for future stiffening and rigidity. In and beneath the serosa, cell proliferation may go on actively, especially in the synovial fringes. The synovia is usually neutral or slightly alkaline, though in rare instances it has proved to be acid.

The inflammation of the synovial membrane of the joint often extends to those of the adjacent tendons, implicating at the same time the tendons and their fibrous sheaths. Softening and rupture of the tendons have been noted by different observers (perforans, Oger; gastrocnemii, Trasbot; suspensory ligament, Olivier).

The articular cartilages and the fibro-cartilages may be the seat of congestion, with ramified or uniform redness, and areas of swelling, softening, absorption, erosion and ulceration, the ulcers varying in size from a millet seed upward. The nuclei increase in size and the cartilage cells multiply. In chronic forms calcification is not uncommon.

The articular lamella and subjacent bone may show inflammation with increased vascularity, softening and even ulceration. In the chronic forms on the parts denuded of cartilage, the surface of the bone may show the clear, polished condition known as eburnation.

The binding ligaments may show congestion, thickening, exudation, softening, with increased rigidity, or in some cases relaxation. Calcification is not uncommon in chronic cases. The soft parts around the joints are often extensively infiltrated and swollen.

In _horses_ these lesions are specially common in the fetlock, but occur also in the knee, elbow, shoulder, hips, stifle and hock. In _cattle_ they tend to attack the same parts with a preference perhaps for the hocks and fetlocks.

_Changes in the blood._ The blood becomes profoundly altered, the albumen reduced, the fibrinogenous elements increased (5 to 10 parts per 1000 instead of three), the red blood globules disappear (in man 2,850,000 per cubic millimeter instead of 4,500,000), the hæmoglobin and oxidizing power of the blood are reduced by about 50 per cent., the leucocytes are relatively increased, and coagulation takes place with unusual firmness, a cupped surface and an excess of buffy coat. No excess of urea, uric acid, nor lactic acid, has been found, nor has acidity been found save in very rare cases. In rare and severe cases petechiæ have appeared on the skin and mucosa.

_Lesions of the heart._ The implication of the fibrous structures of the pericardium and heart and especially of the valvular structures is a common lesion, and to be dreaded more than all others. In all animals this tendency to cardiac lesion is well marked, but especially in solipeds in which the great demands made on the heart during rapid paces, heavy draught, jumping, etc., severely strain the cardiac mechanism. In dogs there is not only the violent exertion and high blood pressure, but also the great irritability of the nervous mechanism presiding over the heart and the tendency to irregularity and intermissions in the rhythm and palpitations even when the organ is sound. There is every reason to conclude with Trasbot, Megnin, Heu and Laurent that in many cases the heart is primarily attacked, and that this heralds the articular rheumatism. In other cases undoubtedly the cardiac affection is secondary, following the articular attack.

Endocarditis is the most frequent, being found in a large proportion of fatal cases, and thickening of the valves, wart-like exudates and coagula are especially common. The clots may fill nearly the entire ventricular cavity, or at times the auricular, and show a preference for the left side, probably because of the more vigorous systole and the higher blood tension. The clots as a rule are firmly adherent to the diseased valve. Ulceration of the valve is rare in rheumatism. Other parts of the ventricular endocardium may be involved, becoming red, congested, rough or thickened, with adherent blood clots.

Pericarditis is less common though it may exist on either or both the cardiac and visceral folds. It is shown by vascularization, thickening, fibrinous exudate, and serous effusion. Haycock found in a horse a quart of reddish serous exudate with floating fibrous shreds and false membranes. Pus has been found in exceptional cases manifestly indicating a complex infection. Like endocarditis it may precede, follow, or coincide with an articular attack (Leblanc, Cadeac).

Myocarditis is usually seen as a complication and extension of rheumatic inflammation of the visceral pericardium, or of the ventricular endocardium. The muscular tissue may appear parboiled and friable, and shows granular or fatty degeneration.

_Pulmonic and pleuritic lesions._ Embolism of the lungs and pleura may occur from the transference of clots from the right heart, yet the sequence is much more commonly an articular rheumatism following infective disease of the lungs. Cadeac suggests that the impaired nutrition in pneumonic and pleuritic animals predisposes to the rheumatic arthritis, and again that the microbes of the infectious chest affection, colonizing the joints and other synovial sacs, determine the rheumatism. This last theory has the weakness of identifying influenza and contagious pneumonia with articular rheumatism, and is negatived by the experience that these two pulmonary affections never develop _de novo_ from simple rheumatism. The rheumatism which follows influenza and contagious pneumonia therefore must either be considered as a pseudo-rheumatism, or a rheumatism occurring only concurrently and accidently with the pulmonary affection. Apart from this, pleurisy or even pneumonia occurs as a simple extension from a rheumatic pericarditis.

The occurrence of the rheumatoid affection as a complication of influenza and contagious pneumonia in the horse, usually appears not earlier than 15 days after the outset of the pulmonary affection and may be delayed, according to Palat, for 102 days. Palat who had excellent opportunities for observation in army horses found that about one in ten was the ratio in which the rheumatic affection followed these pulmonary diseases.

The pulmonary lesions in these affections are essentially those of uncomplicated influenza, or contagious pneumonia.

_Cerebro-Spinal Lesions._ Nervous disorders are occasionally seen in rheumatism in man (dullness, prostration, delirium, coma, spasms) and traced in different cases to hyperthermia, congestion, exudation, embolism and toxins. In a few cases in the horse, cerebral complications have been observed. Olivier saw a horse with lachrymation, closed eyelids and hot, tender forehead, which showed at the necropsy articular inflammation, and sanguineous effusion in the cranium, encephalon, frontal and maxillary sinuses and ethmoid cells. Jacob records two cases (mare and horse) in which rheumatism was complicated by meningo-encephalic congestion but without necropsy as both recovered.

_Digestive system._ In man rheumatism has been exceptionally preceded by pharyngitis, dysphagia, and diarrhœa. In the horse Haycock has seen concurrent congestion of the pharyngeal mucosa, Olivier congestion of the stomach and intestine, and Jacob diarrhœa and abdominal pain, Leblanc and Palat record cases of peritonitis accompanying articular rheumatism in the horse.

SYMPTOMS OF ACUTE ARTICULAR RHEUMATISM IN THE HORSE.

Chill, hyperthermia, lameness in fetlock, hock, knee, shoulder,
stifle, hip, elbow, tendons, sheaths, bursæ, bilateral, shifting,
swelling, heat, tenderness, decubitus, joint semi-flexed, pain on
extension or flexion, signs of cardiac disease. Course: rapid to
recovery, improvements and relapses, metastasis, debility.

The attack is usually sudden and marked by a slight chill, shivering or staring coat with hyperthermia and lameness. The temperature may vary from normal to 107° or 108° F. in severe attacks. In many cases the fever and lameness appear simultaneously, the former being in ratio with the extent and severity of the latter, but not infrequently the elevation of temperature precedes the articular symptoms, and then it is to be considered as concurrent with the internal lesions—cardiac, pericardial or otherwise. In other cases the articular lesions and lameness precede by several days the appearance of the fever. So far as we know the fever never antedates the occurrence of some local lesion, external or internal.

The joints affected are very varied. The fetlock is the most frequently attacked, but some of the other larger joints, the hock, knee, shoulder, stifle, hip and elbow are often involved or exclusively affected. The adjacent tendons and their synovial sheaths are very often implicated; the attack is very prone to show a bilateral symmetry, the same joints (right and left) on the corresponding fore or hind limbs, suffering at once, or, as in the case of the fetlocks, all four are simultaneously attacked. A joint that is weak by reason of previous injury or disease is especially liable to suffer, and is then less likely than joints that had been previously healthy to undergo speedy improvement. When the symptoms wander from joint to joint or from joint to muscle, or fascia or tendon, the disease in its earlier seat seeming to undergo almost complete resolution, while it advances with great intensity in the newly affected joint or part, the occurrence is highly significant. These transitions often take place with great rapidity. Thus the centre of suffering may shift from one joint to another in an hour, (Megnin, Cadeac), or from a limb to the loins in a quarter of an hour (Lewis). The fact that the inflammation remains fixed in one or several joints, is not, however, proof of the absence of rheumatism. A joint with a primary weakness or injury may remain the seat of disease through even a chronic rheumatism.

The affected joint is usually swollen, hot and tender; the tenderness being as a rule greatest where the capsular ligament is pressed upon. These symptoms are very evident in joints that approach the surface, and obscure in such as are thickly covered by muscle (shoulder, hip). The swelling is soft, or tense and elastic (especially over the synovial membrane), or œdematous and pitting on pressure. On white skins sparsely covered by hair there is marked redness and congestion, the veins standing out prominently and the arteries above the joint pulsating strongly. When the tendinous sheaths are involved, they stand out as elastic lines following the course of the tendons, and with more or less pasty swelling adjacent.

In some cases, however, the swelling may be entirely absent, and the trouble is to be located only by the local tenderness and pain during motion.

Small, hard, pea like, subcutaneous nodosities were first noticed by Floriep, in 1843, in rheumatism in man, and have been met with in different cases in the horse. Rodet fils met with great numbers of these nodules crepitating under pressure, in a horse that had suffered for months from chronic rheumatism.

Acute pain on moving the affected joint or tendon is a most characteristic symptom. The horse goes dead lame, walks on three legs, or with great stiffness, and avoids as far as possible all flexion of the joint. If left alone the animal stands stock still, never moving from the place, or in the worst cases lies down and refuses to rise. If compelled to walk his suffering is shown by hastened breathing, dilated nostrils, anxious, pinched countenance and low plaintive neighing. The affected joint is held semi-flexed, to relieve the tension, the pastern is habitually more upright, and if the foot is lifted and the affected joint bent or extended, the animal winces, or resists, and tries to draw away the limb and groans. The movements of the affected joint in walking or under manipulation, are often attended by cracking which may be both felt and heard. It has been variously attributed to lack of synovial lubrication (Cadeac), and ulceration of the articular cartilage (Lafosse), yet it may occur from the constrained position assumed, as in the case of a man attempting to walk noiselessly on tip toe, and in other cases from the extension of false membranes, or of rigid or contracted binding ligaments.

Rheumatism of the fetlock and sesamoid pulley, as the most common form in solipeds, demands a special notice. The swelling of one fetlock, of the two fore, of the two hind or of all four at once, extends beyond the limits of both joint and sesamoid pulley and may form a general engorgement or _stocking_ which serves to hide the synovial distension. Pressure however shows that while all is tender, the extreme tenderness is referable to the joint, the synovial sheath of the flexors, to the flexors or suspensory ligaments. As the general swelling subsides the rounded or ovoid synovial distensions become more patent. The swelling and tenderness may extend to the knee in which case the synovial membrane of the carpal arch is especially distended and tender from the carpus down, or in the hind limb the synovial membrane of the tarsal arch is distended showing in this case on the inner and outer sides in front of the calcis, and not infrequently implicating the summit of that bone as a capped hock.

In rheumatism of the shoulder the coraco-radial tendon and pulley may be involved, causing a diffuse swelling on the point of the shoulder. If the hip is the seat of disease the median gluteal may suffer, causing an indefinite swelling over the joint. If the stifle is affected the patellar capsule suffers and not infrequently the tendon and pulley of the flexor metatarsi are involved.

The most important internal complications, pericarditis and endocarditis, are manifested by their usual symptoms, sharp, variable, irregular, unequal or intermittent pulse, blowing murmur usually with the first heart sound, oppressed breathing, and it may be muffled heart sounds, or dropsies.

_Course._ This is exceedingly uncertain. Some cases make a rapid progress to complete convalescence; others make partial improvements interrupted by relapses; others have the morbid process subside in great measure in one joint or organ only to reappear in full force in another; others leave complications on the part of the heart especially and are rendered permanently useless. Even should the heart escape, the health often suffers so much in connection with the destruction of the red globules, the malnutrition, and the local disease, swellings and distortions of the joints that a perfect recovery seems distant and problematical.

SYMPTOMS OF CHRONIC ARTICULAR RHEUMATISM IN THE HORSE.

Larger joints, muscles, heart, false membranes, indurations,
thickenings, calcifications, remittent, weather changes, cold, damp
beds, winds, open windows or doors, draughts, cold sponging, clipping.
Diagnosis: lameness variable, shifting, electric and meteoric storms.

Chronic rheumatism may be a sequel of the acute, or it may occur from the same causes acting with lessened force, or on a less susceptible animal. It tends to attack the larger joints especially, though it may implicate the muscles as well. Coincident affection of the heart is less common than in the acute, and when it does arise seems to advance slowly. It is liable to cause permanent distensions of the affected joint capsules, as well as false membranes, articular abrasions, degenerations and ulcerations and less frequently bony enlargements and calcifications, the latter implicating the soft tissues in the vicinity.

The attendant lameness is liable to be remittent or intermittent, subsiding in warm buildings and during genial, clear sunny weather, and relapsing in connection with cold, raw nights and mornings, exposure in the dew or rain, and before and during great changes of weather. Cold, damp beds, chilling draughts between open doors or windows, washing with iced water, sudden intense cooling of the body after perspiration, clipping during cold weather, any cause of sudden rigor, when followed by stiffness, lameness and articular swelling, serves to identify the latter as rheumatic. Even the warmth induced by judicious exercise, may cause improvement, so that a horse, starting out stiff or lame, may drive out of it after going a mile or two. The formation of subcutaneous nodules, though rare, appears to be more frequent than in acute rheumatism.

_Diagnosis_ is to be based largely on the variability of the lameness at different times, its propensity to shift from place to place, its manifest association with exposure to cold, and with the immanence of electric storms or change in the barometric pressure, and its improvement under genial weather, warmth and comfort.

SYMPTOMS OF MUSCULAR RHEUMATISM IN HORSES.

Under usual causes, muscles tender, stiffness, groaning, loins,
quarter, shoulder, neck, chest.

Developed under conditions similar to those causing rheumatism of the joints, rheumatism of the muscles tends to attack those of a particular region, and to continue in these throughout the attack rather than change to others. The affected muscles are very tender to the touch, but usually show no swelling nor heat. The muscles are relaxed and tend to atrophy, fever is little marked, there is comparatively little tendency to the implication of the heart, and the suffering and stiffness vary with the variation of the weather, or with electric or barometric changes. When generalized, however, fever may supervene, and the joints may be implicated (Thompson).

When the _loins_ are affected they become extremely tender to the touch, and the horse shows great stiffness, and groans when made to walk and above all when turned or backed. He does not, however, show the unsteadiness in gait and tendency to stagger that is shown in sprain of the loins, and there is no history of a slip, fall or injury, but an unmistakable connection with cold, exposure, change of weather, or overfeeding on grain.

When the _gluteal muscles_ are attacked there is intense lameness, and dragging of the hind limb, with an acute sensitiveness of the skin of the region, which characterizes neither disease of the hip nor of the trochanterean bursa.

When the _scapulo-humeral muscles_ are the seat of disease, there is a marked stiffness, shortness of step, drooping of the head, and great tenderness of the skin and muscles to manipulation or the use of the currycomb. Like the other cases named it occurs suddenly, without evidence of accident, but bearing a relation to cold or other change of the weather, and is better or worse as the weather is more or less genial.

When the _cervical muscles_ are affected (torticolis), the same features are noted, the absence of traumatic cause, the presence of a meteorological one, or at least of cold or wet, the responsiveness of the disease to the state of the weather, and to revulsive agents applied to the part. The neck may be held rigidly in one position, to one side or elevated so that there is great difficulty in getting the nose to the ground.

The _costal muscles_ are less frequently attacked (pleurodynia), but the same general principles guide in diagnosis.

Seidamgrotzky alleges the constant existence of acidity of the urine in muscular rheumatism. This may be attributed to the active trophic changes going on in the muscles.

SYMPTOMS OF ACUTE ARTICULAR RHEUMATISM IN CATTLE.

Sudden onset, hyperthermia, chill, fever, acid saliva, decubitus, does
not stretch on rising, lameness, joints involved, metastasis,
variability, morning and noon, suppuration, walking on toe, secondary
articular rheumatism. Course: muscular symptoms, cardiac, pleuritic,
digestive. Chronic. Muscular rheumatism: of back, loins, shoulder,
quarter, neck. Changes in blood and nutrition.

There is a sudden attack with constitutional disorder, chill, staring coat, cold horns and ears, dry muzzle, impaired appetite and rumination, acid saliva, constipation, thirst, hurried breathing, hard accelerated pulse and more or less hyperthermia. Then there may come reaction with surface heat and glow. The patient inclines to lie and when raised fails to stretch the back or the hind limbs, stands with arched back, and walks stiffly and with more or less lameness. The joints attacked may be determined by local strain, compression on concussion, hence the frequency of lesions of the knees and fetlocks. Yet any of the great joints of the limbs may suffer,—hip, stifle, hock, shoulder or elbow—or several may be affected at once. The disease may extend from one joint to another, may improve in one or more, only to suffer a relapse, and may oscillate better and worse according to the state of the weather or the exposure to cold or warmth. Often almost helpless in the early morning, the patient improves greatly in the heat of the sun.

The affected joint is swollen, distended with liquid, hot and tender with considerable infiltration of the surrounding tissues, including the tendons and their synovial sheaths. Suppuration is much more common than in the same affection of the horse appearing to be due to a complex infection with pus microbes. In walking in severe cases the foot of the affected limb is planted with great care and caution mainly on the toe and there appears to be exquisite suffering when weight is thrown on it, so that the fetlock and knee may knuckle over and the patient comes to the ground. Great infiltrations, fibroid, and other hyperplasias and even calcifications are not uncommon.

Cadeac describes as secondary articular rheumatism, those infective inflammations of the joints that follow on parturition, abortion, omphalitis, enteritis, etc., but it is manifest that these are special disorders due to the presence of the microbes of specific diseases or their toxins and should be described with these rather than with rheumatism.

The _course_ of acute rheumatism in the ox is very uncertain. Mild cases may recover in a few days. In others the lesions become extensive, great hyperplasia and induration occur around the joint and permanent stiffness and even anchylosis may supervene. The occurrence of temporary improvements and relapses is a common feature. The extension of the disease to other joints, tendinous sheaths, muscles and even internal organs is to be dreaded. Extreme tenderness of the back and loins when handled or pinched, with groaning is a marked feature especially in cold and damp times or in early morning. Cardiac complications show themselves by shortness of breath, palpitations, hard intermittent, irregular or unequal pulse, blowing murmur with the first heart sound, and other signs of circulatory trouble. Pleuritic, pulmonic and abdominal complications are also to be looked for. The costiveness by which acute rheumatism is ushered in, becomes complicated by congestion of stomach and intestine, and impaction of the first and third stomachs, great dullness, anorexia and even nervous disorder. Colic and even diarrhœa are occasional consequences.

Many cases subside into a _chronic form_ which shows a variable condition, better and worse, according to the condition of the weather, the exposure to cold and damp, and even the changes of diet. This may last throughout life.

SYMPTOMS OF MUSCULAR RHEUMATISM IN CATTLE.

This may set in with the same abruptness as articular rheumatism, the animal in the morning after a wet, dewy or frigid night showing general stiffness and lameness with extreme sensitiveness of the skin and muscles along the back and loins. The animal moves slowly and stiffly, grunting perhaps at each step and shows inappetence, fever, dry muzzle and costiveness. This is essentially _rachialgia_ or _lumbago._ Pandiculation on rising is entirely omitted.

Not infrequently the _muscles of the shoulder_ are mainly affected and become exceedingly tender to manipulation. The patient seeks to remain recumbent and when raised will get up on his hind parts and remain thus for some time resting on the knees before he can be made to get up in front.

When the _muscles of the croup_ are attacked the mode of getting up is reversed, the animal rising first on its fore feet and remaining for a time sitting on its haunches or resting on the hocks before it gets on the hind.

If the _muscles of the neck_ are involved there is the same stiffness, soreness, tenderness and twisting to one side or rigid elevation of the neck as seen in the horse in similar circumstances.

In any case there is a tendency to extension or shifting from one part to another, and notably to the implication of the tendons, synovial sheaths and joints. This is especially the case in the acute type, while chronic rheumatism may remain long confined to the groups of muscles which are first attacked. In the acute forms too there is the greatest liability to internal complications not only cardiac, but according to Cruzel abdominal and thoracic as well.

A fatal result is rare, but the impairment of appetite and digestion, the constant and often severe suffering, the destruction of the red globules, and the malnutrition, and increased and perverted metabolism as shown in the pallor of the visible mucous membranes, the steady loss of condition and advancing emaciation, the rigid, dry, scurfy, hidebound skin, tends to wear out the subject or render it unprofitable. In the chronic form it may last for months.

SYMPTOMS OF RHEUMATISM IN SHEEP.

Articular rheumatism seems to be very rare in mature sheep, while it has been recorded in lambs. Muscular rheumatism on the other hand has been seen in connection with untimely shearing, exposure to cold storms and cold, damp folds. The back and loins, are tender to the touch, or in other cases the neck or hind quarter, the limbs are carried straight and rigid, the animal moves slowly and stiffly, falls behind the flock, and is found alone, unthrifty and emaciated. It usually terminates in recovery though it may cause chronic disease and distortion of the affected joints or it may even prove fatal. The usual tendency of the morbid process to shift from joint to joint or to muscles, is here again characteristic.

SYMPTOMS OF ARTICULAR RHEUMATISM IN SWINE.

Climatic influences. Rheumatoid. Joints attacked. Muscles. Decubitus.
Stiff, rigid, steps on toes, grunts, swelling, heat, tenderness,
chaps, cracks, suppurations, inappetence, emaciation, metastasis,
cardiac disorder. Duration; course. Chronic form. Muscular form.
Diagnosis from trichinosis. Connection with arthritis. Metastasis.
Remissions.

The pig which shows an extreme sensitiveness to climatic vicissitudes and cold winds, fleeing instantly to his lair on their advent, is yet protected by his subcutaneous fat, so that he is not a frequent victim of simple rheumatism. Leblanc attributes it to unwholesome pens. Chaussade to too rapid fattening (overfeeding). Rheumatoid attacks are very common at the onset of hog cholera, swine plague and other infectious diseases, when they are probably but local manifestations of the general infection.

The lesions are mainly concentrated in the stifle, hock, knee and fetlock. In some cases the dorsal and lumbar muscles suffer and there is arching of the back with great tenderness on manipulation. In other cases the muscles of the quarter or shoulder are involved as shown by their stiffness and extreme sensibility to touch.

The pig is found down, indisposed to rise, and when up, stands drawn together with limbs rigid and feet resting on the toes. He will often point one toe to the ground repeatedly, before resting on the foot, or shift the weight uneasily from foot to foot. If moved he grunts plaintively and if handled squeals.

The affected joints may be surrounded by hot tender swellings or they may be nearly normal in outline, but they are always very sensitive to pressure and above all to flexion and extension, and the skin is usually hyperæmic and red. There may be engorgements of the lymphatics on the inner side of the limbs, and chaps and cracks in the flexures of the joints. Suppurations may follow (Graignard) suggesting a complex infection.

There is little appetite and though the disease becomes subacute or chronic there is a steady loss of condition or at least a failure to thrive.

Benion’s reference to a coincident or sequent inflammation of the respiratory or digestive organs and Spinola’s similar reference to pleurisy are strongly suggestive of swine plague and hog cholera. Any manifest disposition to shift from one part to another and any concurrent disorder of the heart, other than simple palpitation is strongly confirmatory of rheumatism.

The disease tends to recovery in from four to twenty days, or to pass into the _chronic form_. In this state the symptoms are materially mitigated. Fever is absent, but the appetite, digestion and assimilation are poor, the animal remains stunted, emaciated or unthrifty, there is a disposition to lie most of the time under the litter, and when up it moves stiffly with short steps, semi-flexed joints and upright digits. Sometimes the joints are permanently swollen and rigid by reason of thickening and shortening of the binding ligaments, by the organization of false membranes or by anchylosis.

=Muscular Rheumatism in Swine.= This appears to be rarely seen as an independent disease, but appears at times to coincide with the arthritic form. In such cases the back is arched and very sore to the touch or to pressure. It must be distinguished from the muscular soreness of trichinosis which occurs in infested localities, after trichinous food or water, is preceded by digestive disorder and diarrhœa, and by the passage of the nearly microscopic worms in the stools, and is independent of arthritis.

Muscular rheumatism leads to atrophy of the muscles, especially those of the quarters, and this may resemble, somewhat, partial paraplegia from disease of the spinal cord. Its connection with arthritis, its tendency to shift from place to place, to undergo ameliorations and relapses, and its exquisite tenderness, serve to distinguish it from paralysis.

SYMPTOMS OF ARTICULAR RHEUMATISM IN THE DOG.

Articular rheumatism rare. Femoro-tibial joints, bilateral,
remissions. Exudation, swelling of joint; muscular atrophy, weakness,
swaying, staggering, falling, paresis. Chronic, muscular rheumatism
common, back, loins, neck, general, stiff, painful movement,
decubitus, muscles tender, yelps, stiff neck, wry-neck. Masseteric.
Painful defecation and urination. Metastasis. Cardiac symptoms.
Pleurodynia. Digestive troubles. Emaciation, weakness, atony,
paraplegia. Diagnosis from strongylus, stephanurus, and cysticercus.

This affection seems to be rare in the dog. What is known as rheumatism in this animal, consists in an inflammation with hyperplasia around the articular ends of the long bones, the new material being partly fibrous and partly calcified. It shows a special predilection for the femoro-tibial and confines itself mainly to the inner side of the head of the tibia. Here the swelling may reach the size of a walnut, The whole head of the tibia and lower end of the femur are however often involved, entailing a general enlargement of the joint. It follows the general rule of rheumatism in usually attacking both stifle joints at once, and also in alternate ameliorations and relapses. Less frequently other joints are affected. In all such cases the joints become overdistended and swollen, partly by synovia, and partly by surrounding exudate, the muscles of the quarter and thigh become atonic, soft and flaccid, and are steadily atrophied. The dog shows a lack of strength in the hind parts, swaying, staggering or even falling, and advancing to a marked paresis. The malady follows a chronic course, lasting for months, a year, or more.

SYMPTOMS OF MUSCULAR RHEUMATISM IN THE DOG.

Muscular rheumatism is common in dogs. It is most common and most marked in the back and loins, though the neck may suffer, or the disease may be generalized. It is painful to move and the subject seeks to be as much as possible undisturbed. He walks stiffly and slowly, carrying the limbs with as little movement of the joints as possible, and in bad cases yelps occasionally from sudden pain. He can no longer be tempted to go up or down stairs or to make any special effort. When touched on the back or loins he will wince, cry out, or even snap at the offender. In some cases the pain is so acute that even a feint to touch the back will draw out a yelp. If the neck is affected it may be held so stiffly that the dog can barely reach the ground to find his food, or if unilateral the head is turned to one side. Even the muscles of the jaws may be affected, causing prehension and mastication to be difficult and imperfect. Defecation and urination are also interfered with and the straining may draw forth plaintive cries.

The rapid shifting of the morbid process from one group of muscles to another is often very striking, and if one pronounces on the exact seat of the disease, it is liable to be speedily rendered inexact by a sudden change of place. There is further a great disposition to the implication of the heart and especially the valves. This is shown by irregularity and inequality of the pulse by intermissions and palpitations, by a blowing murmur with the first heart sound and by oppressed breathing.

Short, shallow breathing is also caused when the intercostal muscles are attacked (pleurodynia). Various digestive troubles are also common, to which the difficult defecation and impacted rectum largely contribute.

Emaciation makes more or less progress, and the muscles of the hind parts especially become weak and atonic until marked paresis or actual paraplegia sets in, and the hind limbs are extended backward and dragged helplessly. In fat, sluggish, overfed and pampered animals the lack of control of the hind limbs may come on at an early stage. Stiffness due to strongylus gigas in the kidney or stephanurus or cysticercus cellulosa in the lumbar muscles must not be mistaken for rheumatism.

PREVENTION AND TREATMENT OF RHEUMATISM.

Prevention. Avoid known causes, untimely clipping, exposed buildings,
over-fatigue, chills, cold rains, dews and frosts, disorders of liver
and bowels, sweets, spiced food, overfeeding, constipation, torpid
liver, injuries to joints or tendons. Treatment: warm stall and
clothing, laxative food in moderation, purgatives, aloes, castor oil,
jalap, saline enemas, colchicum, alkalies, trimethylamine, acetate of
ammonia, salicylic acid, salicylates, salicine, oil of gaultheria,
salicine for debilitated. Large doses hourly or every two hours. Less
effective in chronic cases. Heart failure. Salol. Salophen. Phenocoll.
Antipyrin. Acetanilid. Pilocarpin. Tartar emetic. Dover’s powder.
Ammonium acetate. Chamomile. Boneset. Hot baths and packs, with cold
on head. Hand-rubbing. Hot drinks. Nauseants. Hot iron. Anodyne
liniments. Rubefacients. Blisters. Salicylate of methyl and other
salicylates. Quinine and potassium iodide. Tincture of muriate of
iron. In chronic cases, tonics, cod liver oil, arsenic, guaiacum,
potassium iodide. Essential oils. Electricity.

_Prevention._ This consists in the avoidance of all known causes of the disease and must vary to some extent for different genera of animals. The avoidance of cold and exposure, of clipping at unsuitable seasons, of exposed sites for buildings (north and northwest exposures, narrow valleys and ravines), of over-fatigue, of perspiration and subsequent chilling, of cold rains, dews and frosts, of inactivity, or habitual overloading of the liver and bowels, and of local injuries of joints or tendons. House dogs especially should be protected from sweets, spiced food, frequent feeding, constipation and torpid liver.

_Treatment._ One of the most important considerations is a warm stall or building, or warm clothing including loose woolen bandages on the legs, in the horse. Laxative food is called for.