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.