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 (C3H4O(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.