Chapter C: F. Dawson, in investigating a wasting disease of well fed Brahma (6)

_Prevention._ As the ticks are the chief media of infection, the disease may be eradicated by their destruction. The burning of all withered grass and brush during the winter months will do much in this direction. Their destruction is rendered even more complete by ploughing and putting the land under a series of cultivated crops. By this means not only is the winter shelter of the tick removed, but the animal host which it requires for its complete development is denied it, and it must perish before the land is again seeded to grass. When the land is unsuited to cultivation, the same end may be in some measure secured by fencing off half the pasture, and leaving it unpastured for a season, meanwhile burning the dry grass or temporarily suppressing it by a liberal application of salt. The following year the pasture so treated may be restored to pasturage, and the other half subjected to the same course of treatment. In the absence of such thorough treatment, a liberal application of lime to a virgin soil will often bring a growth so fresh and appetizing that the stock keeps it closely cropped and thus removes the shelter for the offensive ticks. Finally, the ticks may be prevented from attacking the animals, by repeated use during April, May and June of a dip in which tar oil, cade oil, heavy petroleum or other odorous insecticide forms a component part (see the dip of Meek and Greig-Smith).

A very obvious precaution is to avoid the movement of sheep during April, May and June, from tick-infested pastures to others which furnish rank grass, brush or other suitable shelter for the preservation of the parasite.

It has been noticed that sheep indigenous to the tick-infested and louping-ill pastures are less susceptible than those that have been introduced from outside, but, as yet, no attempt appears to have been made to secure immunity by the use of sterilized products of the microbe, nor therapy by the resort to antitoxin. A liberal and tonic diet is an important element in prevention. Grain and hay should therefore be allowed whenever necessary to bring the sheep to early summer in good condition.

_Treatment_ can hardly be said to have been attempted, though mild cases are allowed by the shepherds to recover. According to Meek, the deaths often average 10 to 20 per cent. of the flock.

BRAXY, BRADSOT, GASTRO-MYCOSIS OVIS.

Definition: Acute, infectious, bacteridian disease of sheep, with
colic, enteritis, emphysematous swellings, dark, diffluent blood, and
after death rapid putrefaction. Geographical distribution: Iceland,
Norway, Faroe Islands, Scotland. Causes: inclement weather, exposed
localities, low condition, winter food, chill, frosted grass.
Bacteriology: Bacillus gastromycosis ovis: 2 to 6 μ by 1 μ, in pairs
or filaments, sporogenous, polar staining, anærobic liquefying,
gasogenic, found in the gastro-intestinal congested mucosa, serosa,
liver, kidneys, blood. Pure cultures by boiling five minutes.
Pathogenic to sheep, Guinea pig, mice, pigeons, hens and less
certainly rabbits. Symptoms: resemble blackquarter, sudden, rapid,
fatal, back arched, stiff hind parts, crepitating swellings on hind
parts or elsewhere, colics, tympany, anorexia, pulse and breathing
hurried, separation from flock, lying, drooping head, ears and eyelid.
Usually found dead in morning when apparently well previous night.
Lesions: early putrefaction, slight, transient rigor mortis, tympany,
fœtor, sero-sanguineous exudates under skin, on fourth stomach and
bowels, and elsewhere. Contents of large intestine dry, hard.
Effusions in serosa. Spleen enlarged or not. Liver and kidneys
congested, softened, small, pale necrotic areas containing bacillus.
Prevention: drainage and cultivation, winter feeding, abandon infected
pastures in late fall and winter as pasture for young, avoid
overstocking, burn old fibrous heather. Immunization by sterilized
kidney extract. Treatment.

_Definition._ An acute infectious disease of sheep, manifested by sudden attack, colicy pains, inflammatory and sero-hæmorrhagic lesions of the bowels, and sanguino-emphysematous swellings occurring subcutaneously and especially in the hind quarters. The blood is dark, tarry and comparatively incoagulable and after death putrefaction advances with extraordinary rapidity.

_Geographical Distribution._ Braxy is generally prevalent in Iceland where it was described over a century ago (1778) by Ketilson as “vinstrarfár” or “vinstrarplága” (“Omasum disease”). In Norway it prevails on the whole Atlantic border to as far north apparently as the sheep industry extends (Stavanger to Tromso Amt). The Faroe Islands are said to be affected throughout. In Scotland it prevails like louping-ill along the west coast especially, and embraces Caithness, Ross, Cromarty, Banff, Inverness, Aberdeen, Argyle, Bute, Ayrshire, Lanark, Galloway, Dumfries, Peebles, Selkirk and Roxburgh.

_Causes._ Like louping-ill this affection is associated with inclement seasons, exposed localities, and insufficient or indigestible food, but it differs in being an affection of autumn and winter rather than spring. It is rarely seen in summer. At a time when it was looked upon as an acute indigestion, its coincidence with hard frost or deep snow, was explained on the basis that the victim had been driven to eat dry, fibrous, indigestible grasses, brakens and heather. W. Williams who formerly identified the disease with anthrax, seemed to go back to this theory of indigestion. Though that is no longer tenable, yet it would be wrong to ignore the effect of inclement weather and unwholesome food in predisposing the animal system, and robbing it of the healthy tone which would otherwise have successfully resisted the infection in many cases. The occurrence of deaths after frosty mornings more than during mild weather, suggests at once the chill effected in the animal, the chilling of the paunch by the frosted grass eaten producing a subsequent congestive reaction, and the known facility with which frozen vegetables undergo rapid fermentation.

Cowan and Borthwick, (Transactions of Highland Society 1863) agree that the disease is especially prevalent when the land has been overstocked in summer, or when there has been a drought which withered up the pastures, and later a free growth of green herbage from the autumn rains. This they attribute to the “foul and unwholesome” character of the autumn growth, but it suggests no less the low condition of the sheep on the overstocked lands and the soft, aqueous character of the herbage grown rapidly in a comparatively cold season. Cowan quotes cases in which the lambs, weaned early and put in a separate pasture (hogg hirsel), suffered a mortality of 50 per cent., while in later years when allowed to remain with the ewes until winter, the deaths were reduced to 10 or 15 per cent. Here the more rugged health and vigor were manifestly strong prophylactic factors.

Both Cowan and Borthwick incriminate the withered heather and the dry, fibrous (“tathy”) and innutritious tufts of grass which make up a large proportion of many hill pastures in autumn and winter.

Cowan strongly condemns heavy smearing with tar, which he believes to encrease the mortality, by lowering the general tone of the system: “Hoggs are very dull and listless for some time after being smeared with tar, more especially if heavily smeared; ... when the skin is taken off, every shed or opening in the wool where the tar has been laid on, is as distinctly visible upon the flesh as the stripes upon a piece of printed calico.”

It has been further alleged that the deaths are especially common during the full of the moon, the usual explanation being that the sheep are tempted to feed in the night and overload the stomach. It may be added that at such times the grass is taken in a cold—(often frosted) condition so as to chill the stomach and cause a congestive reaction, and that short of this, under the night dews the microbian ferments are moist and ready to start into full activity, while the herbage if it has been partly frosted is particularly susceptible to bacteridian attack.

_Bacteriology of Braxy._ The essential cause of braxy was revealed by Ivar Nielson in 1888, who demonstrated on the local lesions of the alimentary canal and the capillaries of various internal organs a bacillus which he named _bacillus gastromycosis ovis_. This is 2 to 6μ long by 1μ broad, occurring in pairs or filaments. The organism has an elliptical form and stains deeply at the extremities, while the central, bulging portion fails to take the color, is highly refrangent, and represents the spore. The non-spore-bearing bacilli are long, uniform rods with rounded ends. The germ is anærobic, grows readily in serum glycerine agar, and is gas producing and foul smelling. Liquefies gelatine. It is found abundantly in the congested parts of the abomasum and to a less extent in the bowels, in the mucosa, and in the submucous and subserous tissues. It was also found in the blood and in the small areas of degeneration in the liver and kidneys. Jensen obtained pure cultures through the survival of the spores when impure cultures were boiled for a few minutes.

_Animals Susceptible._ Inoculation of the cultures subcutem produces an affection resembling malignant œdema, or braxy, in sheep, Guinea pigs, mice, pigeons and hens, and less certainly in rabbits. Inoculation of a calf had no deleterious effect, while a second succumbed in forty-eight hours. In its pathogenesis this microbe appears to be more closely allied to that of malignant œdema than that of black quarter, as the latter attacks cattle very readily and has little effect on rabbits, pigeons and chickens.

_Symptoms._ The more obvious manifestations of braxy bear a resemblance to those of black quarter, so that the two affections have been often confounded. In both the attack is sudden, the course rapid and fatal, the back arched, the step short, especially with the hind limbs, and there are swellings which crepitate on pressure on the hind quarters or some other part of the body. Symptoms of colic soon appear, the sheep lying down and rising frequently and moving the hind limbs uneasily, and the abdomen becomes distended, tympanitic and tender. Rumination and feeding are promptly suspended, and as a rule defecation as well. Urine may be passed frequently in small amounts and of a high color. The pulse is rapid and often irregular and the breathing hurried and labored. In some cases the abdominal pain is less acute, the animal standing apart with drooping head, ears and eyelids and frothy lips, or lying by itself at a distance from the flock. Sooner or later emphysematous swellings appear on some part of the body, but most commonly on the hind quarter, which have a soft, doughy feeling and crackle or gurgle on pressure. In the great majority of cases, however, the disease runs a rapid course and ends in death in a few hours, and as the attacks are mostly in the cold of the night, the victim, which appeared well at night, is found dead in the morning. Cowan has often noticed that those that stepped short at night were dead next morning. In certain cases the sheep stood obstinately to the end and fell dead as if shot. When death was deferred for several days a common result was shedding of the wool.

_Pathological Anatomy._ A marked feature of braxy is the early putrefaction of the carcass. The rigor mortis quickly passes and the carcass bloats up and exhales a putrid odor. On removing the skin one sees extensive sero-sanguineous exudations, mixed with bubbles of gas of an offensive odor. The abdomen is tense and tympanitic and the anus protrudes. Visceral lesions are especially marked in the fourth stomach, the walls of which are thickened in patches or throughout by a hæmorrhagic or sero-hæmorrhagic exudation of a dark purplish color. If killed in the early stages this may be very restricted in area, but becomes general in animals that have died of the disease. Similar exudations are found on the walls of the first three stomachs, or on the small or large intestines. The fourth stomach and duodenum are, as a rule, empty of food, though containing a sanguineous liquid. The contents of the large intestines are usually dry and hard. Some serous exudate is usually present in the peritoneum, pleura and pericardium. The spleen may be normal or slightly enlarged. The liver is pale, soft and friable. The kidneys may be congested and swollen and usually show brownish areas of necrosis in which the bacillus is readily found. The blood is dark, and though it may be coagulated, the clot is usually soft and diffluent.

_Prevention._ Much may be done in the way of drainage and above all cultivation and liming of the braxy pastures, and again laying them down in grass. Cowan found that braxy diminished largely in ratio with the improvement and cultivation of the soil. A rotation of crops and the free æration of the soil tends to destroy an anærobic microbe or to render it non-virulent. Winter feeding is another well attested source of protection. Hay with turnips, oats, linseed cake or oil cake seems to encrease the tone and vigor, and to counteract the fermentations in the digestive organs which lay the system open to attack. Wholesome and nutritious food then must be a main stay whenever the health threatens to be undermined by insufficient or unwholesome pasture, by dried or withered grass, ferns or heather, by the watery grass of recent and rapid growth, by frosted and partially decayed herbage, or by pasture exhausted by overstocking or drought.

Fields and hills known to be infecting must be abandoned especially in late fall and winter and in the case of the younger and more susceptible sheep. Understocking is always better than overstocking as the flock is kept better nourished, stronger and with a greater measure of tolerance and resistance. Upon land covered with old, fibrous, astringent heather, burning is often of great value. The new growth of young heather is much more digestible and nutritious, and destitute of injurious astringency, and maintains a stronger and healthier flock.

Finally the question of _immunization_ arises. Nielsen attempted this by drying and heating to sterilization the diseased kidney and injected small quantities of this suspended in water. Sheep treated in this way in Norway and Iceland have had a circumscribed inflammatory swelling and afterward appeared to resist casual infection when placed on the braxy fields. Jensen carried the experiment a step farther and inoculated his artificially immunized sheep with 2½ cc. of a virulent serum-gelatine-agar culture. It was rather unwell for half a day and walked lame but soon recovered. A dose of ¹⁄₃₀ cc. of the same culture killed in fifteen hours a larger sheep that had not been artificially immunized.

_Treatment._ Though some cases of braxy recover yet the treatment of the disease can hardly be seriously considered as yet. A disorder which is so rapid in its progress, so early associated with such great and rapidly extending lesions of the most vital organs, and which proves fatal so early and almost invariably, leaves little room for a successful treatment. In the milder cases, likely to recover of their own accord, this may be hastened by the internal use of antiseptics and purgatives, and perhaps even by antitoxic serum from the blood of an immunized animal.

SOUTH AFRICAN HORSE SICKNESS. ŒDEMA MYCOSIS. DUNPAARDZIEKTE.
DIKKOPZIEKTE.

Definition: Geographical distribution: S. Africa; enzoötic or
epizoötic on damp soils; damp, humid atmosphere. Pathogenesis: horses,
and more mildly mules and asses, quagga; (cattle and goats?). Causes:
green forage, from rich, damp lands, eaten dewy; cut and fed with dew
on; dried in sun safe; so of horses stabled or corralled; in hot
summer only; inoculable; penicillium; cultures cause the disease;
debility. Forms: lung sickness—head sickness—blue tongue. Symptoms:
incubation 8 days. Fulminant form asphyxiates in an hour. Acute lung
form has rigor; remittent hyperthermia; prostration; dyspnœa;
cyanosis; serous nasal discharge; frothing; gurgling breathing; cough;
death in 3 or 4 days. Head œdema; general swelling and oozing of
serum. Blue tongue: great lingual swelling; cyanosis; coldness;
projection from mouth; salivation; stertor; asphyxia. Three forms
combined. Mortality. Lesions: serous exudate coagulates with heat or
blood; intermuscular exudates; whole head densely infiltrated;
excessive bloody pleural effusion; punctiform petechiæ; lungs pale,
yellow, great interlobular infiltration; or, if worked, hepatization;
dark, congested mucosæ; blood diffluent; heart pale; spleen enlarged,
blood-gorged; kidneys infiltrated; gastro-intestinal congestions;
cerebro-spinal effusion. Prevention: keep indoors during summer and
autumn; allow no fresh damp forage; or cut only after dew is off;
check rein or muzzle; pastured horses must be stabled at night or in
damp weather. Immunization: by protective inoculations; recovered
horse is re-inoculated until a high grade of resistance is secured and
his blood used to immunize.

_Definition._ An ectogenous, infective disease of solipeds in South Africa, characterized by intense vascular congestions, destructive changes in the blood and the profuse exudation of liquor sanguinis into the tissues of the affected parts.

_Geographical Distribution._ The affection is not known out of South Africa, where it has been observed since 1780. It appears yearly in certain areas in the Transvaal, Orange River Colony, Natal, and adjacent States, but only in certain years in Cape Colony and especially in its southern portion. In certain years it makes wide extensions so that it has appeared to become epizoötic instead of enzoötic. The habitual enzoötic prevalence is in the areas that are relatively lower, damper and richer than the surrounding country, where the vegetation is luxuriant and the surface of the ground moist. Thus it is a disease of low meadows, basins, river bottoms, drying marshes or ponds, and the Boers have been in the habit of protecting their horses by sending them to high, dry tablelands, from the first appearance of the disease until the first frost. Yet elevation in itself is no protection, thus Johannisburg, 6000 feet above the sea, is habitually ravaged and Rhodesia loses 90 per cent. annually. A humid atmosphere, mist, or rain with a high temperature are directly connected with the outbreaks.

_Animals susceptible._ Horses take the disease in its most fatal form. Mules suffer like horses, while in asses the disease is relatively somewhat more benign, and the virus after having passed through the ass, has lost part of its potency. A disease of a similar nature is seen in cattle and goats. The quagga is also alleged to suffer (Edington).

_Causes._ The disease has been traced to the green forage, grown in damp, hot seasons on the rich moist bottom lands, in basins, gullies, etc., and which has been consumed while damp with night dews or fog. Few suffer that are only turned out to pasture after the sun has dried up the dew, and that are shut in the stable or kraal before sunset. Coley who witnessed a loss of 60 per cent. of the stabled horses at Eshowe, Zululand, found that the deaths were among horses that had been allowed to eat their fodder wet. The Guinea or Ubaaba grass and Indian corn were cut at night and fed to the horses next day. The horses that ate this wet from the bundles were attacked, while those that had it only after it had been opened and dried in the sun escaped. Race horses that receive no green fodder very rarely suffer. Horses that are corralled (in kraal) at night escape.

The hot season is the season of greatest prevalence, the disease beginning in November and proving especially fatal from the end of December to the first of March. It appears in a modified form until May when the first frosts appear.

Though the disease can be fatally inoculated by transferring the blood from one horse to another, it is the rarest possible occurrence to have it propagated in this way. It can be absolutely prevented therefore by attention to the diet.

The real cause of _horse sickness_ is a mold having the general characters of a penicillium, and which enters the system with the moist, dewy food. Edington, who discovered this cryptogam, has found it in the blood in all his necropsies of horses dying of horse sickness. Why this should be no longer infecting when dried does not clearly appear. It has been alleged that the disease has gradually extended to the higher grounds which were formerly free from it, and the introduction of diseased or infected horses has been advanced as the cause, but in the unfenced state of the veldt and the former abundance of wild animals this should have ensured such extension long ago, if it is really a permanent one. The deadly prevalence of the malady in particular areas in given years, and its entire absence from such localities in others may explain the instances of apparent extension. The dryness and cold of winter is the factor which usually extinguishes the poison in a given district. We have as yet no absolute proof of a progressive acclimatisation of the germ in a colder and drier region. Wittshire observes that it will prevail on one side of a narrow river, while the other at an equal elevation is practically free from it. There is no mention of shade which might have explained such a difference in the growth of cryptogams on the right and left banks.

Such limitations, together with the activity of the infection in damp seasons, and during damp hours of the day, and its inactivity in dry air and vegetation, would strongly suggest a microbe which is conveyed in the body of some invertebrate, but this appears to be nonessential because Edington has cultivated his mold in vitro and inoculated its products on horses so as to secure immunity.

Debility doubtless renders an animal more susceptible, yet the disease usually kills nearly all horses attacked, excepting such as have been immunized. This is the same for casual and inoculated cases. When, however, the virulence has been lessened by culture or by passing through the body of an unsuitable animal the results are very uncertain; some horses it will kill, while in others it produces a slight and harmless fever.

_Forms._ Two leading forms of the disease are known: 1st, the _lung sickness_ (_Dunpaardziekte_), and 2nd, the _head sickness_ (_Dikkopziekte_). A variety of this last is _blue tongue_ (Blautong), which has been confounded with gloss-anthrax.

_Symptoms._ The _lung sickness_ may appear as a fulminant affection following on the usual _incubation_ of about eight days. Suddenly, in the midst of apparently full health and vigor, the breathing becomes accelerated and dyspnœic; this encreases for about an hour, then the patient staggers, falls, ejects a mass of white froth from mouth and nostrils and dies. When death is more delayed, there may be noted a rigor, and in the evening a rise of temperature to 103° F., lowering a little next morning and rising again toward night, yet making an encrease day by day until near the end, when it becomes subnormal. Death in such cases occurs on the third or fourth day, preceded by great prostration, hurried, labored breathing, dark red or cyanosed mucosæ, loud rattling over the large bronchia or lower end of the trachea, coughing and dropping of a serous fluid from the nose, or accumulation of white froth around nostrils and mouth. The froth soon condenses in part into a straw-colored liquid, which collects in considerable quantity. The abundance of froth blocking the air passages produces death by suffocation.

In the _head œdema_, the muzzle, lips, head and neck become the seat of excessive exudation, the swelling of the face drawing back the lips so as to expose the teeth of the lower jaw. The skin is rendered tense and exudes the straw-colored serum, as do also the buccal and pituitary mucosæ.

In _blue tongue_ the exudate is concentrated in the lingual organ, which swells to an enormous size, forcing the jaws and lips apart, and hanging out as a dark blue, cold mass. A foul, liquid mixture of saliva and exudate drivels from the mouth. The pressure on the larynx may cause marked stertor, advancing to asphyxia.

While these three types may seem to be distinct and uncomplicated in some cases, more commonly the exudation appears to a slight extent in all three situations, and it is only the predominance of the symptoms in one particular part that assigns the attack to one type rather than another. All are very fatal, but the lung sickness is preëminently so, very few such surviving.

_Lesions._ There is usually a mass of white froth around the mouth and nostrils. The serous exudate coagulates readily in the presence of minute traces of blood, and forms a solid mass of clot when heated. A yellow gelatinoid exudate is found in streaks or patches, subcutaneously and between the muscles, but especially along the jugular furrow. In the _head sickness_ the whole subcutaneous and intermuscular tissue in the head and neck are infiltrated, and the straw-colored liquid escapes abundantly when the part is scarified. The same is true of the tongue, which is stained throughout with blood that has gravitated into it.

The pleuræ contain an abundant exudate more or less deeply stained with blood. The same is true of the pericardium. In the latter Edington has found 140 fluid ounces. On the surface of the lungs and pericardium are extensive yellowish exudates. They are covered with petechiæ mostly small or punctiform. If the horse has stood at rest throughout the illness the lungs seem pale, yellowish, yet swollen and indisposed to collapse. The interlobular tissue especially is infiltrated with serum so that toward the free margin the lobules may be separated by intervals of half an inch in breadth as in lung plague of cattle. In horses that have been worked during the illness the whole organ is congested and firm, resembling the condition of croupous pneumonia. The trachea and bronchia show dark congestion of the mucosæ and a mixture of froth and serous exudate. The large blood vessels contain diffluent blood clots of an intensely dark color. In the vascular furrows of the heart and along the large vessels are yellow exudates or blood extravasations. The muscular tissue of the heart appears normal or rather pale, and under the microscope the striæ are found to be obscured by cloudy swelling, and minute blood extravasations and hæmatin are met with. The endocardium is cloudy, with blood extravasations, and exceptionally ante-mortem clots are found. The spleen is usually swollen, very dark, blood gorged and covered with petechiæ. On section there are found extensive extravasations, with masses of blood pigment and crystals. The kidneys are enlarged, the capsule easily detached, the epithelium of the glomeruli and convoluted tubes swollen and their nuclei multiplied. A gelatinoid exudate is usually present in the renal pelvis. Congestions have been found in the right gastric _cul-de-sac_ and less frequently in the intestines. Exudations have also been found in the cerebro-spinal nervous system, the laryngeal mucosa and the conjunctiva. The latter is usually cyanosed.

_Prevention._ The first consideration is to keep work horses indoors or in a kraal during the summer or sickly season. Here they must be fed on dry hay and grain only, grass being strictly withheld. If it becomes absolutely necessary to feed green fodder of any kind it should not be cut until all dew or rain has completely dried off in the heat of the sun, and if kept over night should be kept under cover and again dried before feeding. When taken out to work the animal should wear a check rein or muzzle so that he cannot by any chance reach the green vegetation. This rule must be most strictly adhered to at night or during damp weather.

For horses turned to pasture a fair amount of protection may be secured by shutting them in a stable or kraal before sundown, and until the vegetation has been thoroughly dried by the sun the next morning.

_Immunization._ A horse that has recovered from the _sickness_ has been long held to be immune and will bring from six to ten times its former price. As any disease is liable to be called the sickness this enhanced value is too often insubstantial. Wiltshire even says that all “salted” horses eventually die of _horse sickness_ if allowed to live long enough. Be this as it may Edington appears to have established a reasonable measure of immunity by his protective inoculations. He takes a recovered (‘salted’) animal and reinoculates it at intervals with encreased doses of virulent blood. After the last of these inoculations the subject is allowed to rest for a long period of time, and is then re-inoculated with a small dose of virulent blood. A definite amount of this horse’s virulent blood is mixed with 50cc. of serum and injected subcutaneously; some days later 30cc. of the same serum with the same dose of blood is injected; at a later date the procedure is repeated, with a reduced dose of serum, and fourteen days later pure virulent blood is injected.” The result has been perfectly satisfactory.

DOURINE.

Synonyms. Definition: Contagious disease of breeding solipeds, with
special lesions in generative and nervous system, and skin, and caused
by a trypanosoma. Susceptible animals: horse, dog, rabbit, rat, mouse,
ass. History: in Europe and America. Causes: contagion; coition;
microbiology; trypanosoma equiperdum; its successive stages: 1.
granules and refrangent spherules; 2; chromatin bodies with two
prolongations; 3. fusiform body with nucleus and nucleolus and two
flagella; 4. pyriform bodies with flagella; 5. fusiform body with
nucleus, nucleolus and undulating membrane: in blood, sperm, milk,
vaginal mucus, sores; disappears from blood in intermissions and
rapidly after death. Lesions: phlegmons of generative organs, papules,
vesicles, mottling, swollen inguinal glands, penis, testicles,
caseation or atrophy, thickened lymphatics, nervous lesions, friable
bones, arthritis, liver, spleen, kidneys, lungs, lack of red globules,
anæmia, muscular atrophy; in mare, in dog. Symptoms: _Horse_:
incubation 11 days, variable; preputial, scrotal, sub-abdominal
swelling, catarrh of genital mucosa, vesicles, sores, swollen penis,
semierections; paraphymosis, slight fever, tender loins, frequent
micturition, paresis, swollen joints, tendons, emaciation marked
anæmia, apathy, dementia, nasal ulcers, submaxillary swellings.
_Mare_: vulvar swelling, distortion, leucorrhœa, eruption, spots of
depigmentation, erection of clitoris, urine in driblets often,
inguinal swellings, sterility or abortion, lameness, trembling, great
anæmia and emaciation. Diagnosis: from urticaria: from glanders,
generative lesions, no response to mallein, paresis: from chronic
paraplegia, by its coition cause, and in horses only; from vesicular
exanthema by gravity and nervous phenomena. Prognosis: Mortality 70
per cent. and upwards. Symptoms in ass slight: in dog severe and
fatal; in rabbits severe. Treatment: prevent copulation, castration,
local antiseptics early. Prevention: prevent copulation of infected
and suspected animals, castrate, import only on certificate and on
long quarantine.

_Synonyms._ _Venereal Disease of Solipeds_; _Equine Syphilis_; _Maladie du Coit_; _Chancrous Epizoötic_; _Breeding Paralysis_; _Epizoötic Paraplegia_.

_Definition._ A contagious affection of solipeds, transmitted by copulation, and attended by specific lesions in the generative organs and nervous system, such as local venereal swellings, chancrous ulcers and cicatrices, dementia and paralysis.

_Susceptibility._ As occurring casually the disease is essentially an equine one, yet the following species are susceptible to experimental inoculation in the order named: dogs, rabbits, rats, mice, asses. While the horse shows the greatest susceptibility, the ass is comparatively very resistant to the poison.

_History._ The malady has probably long prevailed in the east, yet it was first clearly distinguished in 1796 when described by Ammon as prevailing in the royal stud at Trakehnen in Northern Prussia. We have later descriptions of the disease in the same locality in 1801 (Hertwig), and 1807 (Ammon). It was found in Bromberg in 1817 to 1820 (Waltersdorf), also in Hanover (Haveman), in Austria and Bohemia in 1821–8 (Fischer), in Styria in 1821, in Switzerland in 1830, in France in 1830–2 (Lautour), in Silesia and Pomerania in 1833–40 (Fischer), in Italy in 1836, in Russia in 1843, (Fischer), in Silesia and Poland in 1830–40 (Freidberger and Fröhner), in Algiers in 1847–55, and in Syria and Asia generally and perennially (Daumas and Signol).

It appeared at Bloomington, Ill., in 1882, the first affected animal being a brown stallion that had been imported from France and which bore on his neck a brand like the letter D. In this locality it extended to a considerable number of breeding mares and stallions, and having been recognized by Dr. W. L. Williams, was largely stamped out by a rigid quarantine of diseased and exposed animals. Some exposed animals had, however, left the district, and isolated centres of infection have been since found in Nebraska and elsewhere in the United States.

It is not known to have invaded Belgium, Scandinavia, England, South America nor Australasia.

All indications point to Asia or North Africa as the primal home of the disease, as they still prove its perennial one.

_Causes._ The disease is transmitted by contagion and almost exclusively in the act of coition. Hayne has seen the affection in geldings, and Haxthausen in mares that had never been served. Schneider, Buffard, Nocard, Blaise and others have transmitted it freely by inoculation of blood and nervous matter, so that the possibility of infection through other channels than the generative organs must be admitted. But such irregular means of casual infection are so rare, and the probability of transmission of the virus from a non-breeding animal is so remote that in the practical measures of sanitary police, the breeding horses alone need be taken into account.

The extra vascularity of the male and female generative organs at the period of coition undoubtedly favors infection, as a latent or apparently recovered case will relapse under its frequent repetition. The abrasion of the epithelial surface also forms infection atria and favors new multiple points of infection.

The disease has occurred congenitally (Rodolff, Jessen). It has been claimed that the higher bred horses with lighter frames are the more susceptible (Fischer), but this is probably a delusion, the disease having been often introduced by the Barb and Arabian and propagated among their grade descendants. The heavy Percheron shows a very ready susceptibility and a virulent and fatal form of the affection.

_Microbiology._ That the affection was due to a microbe was clearly shown by its absence from every part of the world into which infected horses had not been brought. The secluded countries, Belgium, England, Scandinavia, that breed their own horses, the distant Australia, New Zealand and South America remained free in face of the constant presence of the infection in different parts of Central and Southern Europe, in Africa and Asia. The horses of America and South Africa showed a ready susceptibility to the virus brought by infected horses, and rigorous sanitary police control speedily cleared a district of the trouble.

Thanhoffer found in the blood, vaginal mucous, testicle, semen, spinal fluid, myelon, and roots of the dorsal and lumbar nerves cocci, especially streptococci and less constantly bacilli, to which he attributed the malady. More recently Schneider and Buffard have apparently demonstrated that an infusorian, the _trypanosoma of dourine_, is the essential pathogenic agent.

The _Trypanosoma Equiperdum_ varies greatly in form at different stages of its growth or in different media. In the exudate of the slight early tumefaction, without as yet other symptoms, it is found as minute granules in groups, as larger spherical very refrangent bodies like very large cocci, each having a strongly staining nucleus, and as larger bodies in which a delicate membranous covering encloses one, two or three masses of chromatin and extends to form one or more points (club-shaped or fusiform). Each chromatin mass has a nucleolus on its outer surface or slightly apart from it. Twenty-four hours later there may be added: First, short, thick chromatin bodies, with two slightly undulating, pointed, membranous prolongations. Second, more delicate, fusiform bodies, each with one chromatin nucleus, a detached nucleolus, and the membrane prolonged into two actively moving flagella. Third, larger pyriform bodies with chromatin nuclei and nucleoli and the membrane prolonged into one or several flagella. Fourth, fusiform bodies, thick or delicate, each having a chromatin nucleus and nucleolus, and arranged singly or in groups of two, four, six or more, united together at one end and diverging at the other to form a stellate mass. These last, 20 to 30μ long by 1.5 to 2μ broad, may perhaps be the adult form of the parasite from which the small granular or spore forms found in the most recent lesions are derived. The fusiform outline, the deep staining central mass, with its adjacent nucleolus, and the pointed or flagellate membranous prolongations, more or less motile or undulating, are characteristic features.

In its morphology and evolutionary forms the trypanosoma of dourine has not been shown to differ from that of surra, nor the nagana or Tsétsé disease, the granule form, the spherical, the club-shaped or pyriform, the fusiform with more or less stellate grouping, are characteristic of all (Lydia Rabinowitsch, Kemper, Schneider, Buffard). The distinction is found in the pathogenesis of the two diseases.

With active cutaneous or mucous lesions, the parasite is usually found abundantly in the blood, sperm, milk, vaginal secretions, and the erosions of the vaginal mucosa or penis. During intermissions, however, and in the absence of local lesions, examination of the blood may fail to detect it, yet its inoculation on a dog will usually produce the affection. It disappears from the blood and tissues with great rapidity after death, so that, to prove successful, inoculations should be made before death or immediately after. They are ineffective after 48 hours.

Schneider and Buffard, Nocard and others found the trypanosoma in the blood and exudates of horses, asses and dogs, suffering from dourine, and failed to find it, in the same localities, in animals of the same species which were free from dourine. The infected blood, preserved for 24 hours in sealed glass tubes, and then inoculated on two dogs produced characteristic dourine, with the extensive production of trypanosoma in the blood, the destruction of blood globules, and the pathognomonic local lesions. Inoculation of two other dogs, with the same material, at the end of 48 hours produced a slight transient hyperthermia only, without local lesions or propagation of the parasite in the blood. The same blood inoculated after 15 days produced neither local lesion nor fever.

_Lesions._ _Horse._ In the early stages are found a phlegmonous or œdematous swelling of the _sheath_, _scrotum_, _penis_ and _inguinal glands_ and a yellowish liquid effusion into the scrotal cavity. The skin covering these parts may show a papular or vesicular eruption or if this has passed, a mottling with white spots shows where the lesions have been. Later still the _inguinal glands_ are shrunken and have undergone fibroid degeneration and induration and the testicles, swollen or shrunken, contain centres of caseation. The connective tissue of the epididymus and cord is the seat of a gelatinoid exudation. The _walls of the scrotum_ may be greatly thickened and the seat of abscess or of caseous degenerated hyperplasia. In advanced cases the _testicles_ are usually abnormally small even if the scrotal mass is enormously distended. The _sheath_ and _penis_ may be the seat of more or less numerous ulcers, and swellings, contractions and distortions of the latter organ are not uncommon. The penis may, however, retain its normal dimensions. The walls of the _lymphatics_ in the inguinal region may be the seat of hyperplasia, the thickening causing them to stand out like cords as in glanders. In the advanced stages the _muscles_, especially those of the hind limbs, become pale and atrophied.

The _nerve centres_ undergo profound changes which have been studied by Thanhoffer. The _pia mater_ in the affected parts of the spinal cord is the seat of active congestion and thickening. The central canal of the cord is dilated (syringomyelia) more at one point than another, contains more than the normal amount of liquid, and the neuroglia around it is thickened and fibrous (sclerosed). The _substance of the cord_, both white and gray, shows congestion, blood staining, at points foci of softening, and at others induration (hyperplasia of the neuroglia). The _nerve cells_ are modified in various ways, some being granular, some discolored by fine granular pigment, some having enlarged and multiplied nuclei, and some show vacuoles. The _nerve filaments_ often show a granular degeneration extending from the nerve cell into the axis cylinder, and the latter is liable to be varicose or uneven in size. In the affected portion of the cord leucocytes are numerous and hyperplasia is often present. The neuroglia especially tends to encrease, and apart from the foci of softening tends to give a special firmness to the substance. At intervals, in the perivascular spaces, may often be found minute (microscopic or macroscopic) blood clots. The subarachnoid and subdural fluid is encreased and may be pinkish. At the roots of spinal nerves, especially in the dorsal and lumbar regions, a gelatinoid exudate may invest the nerve, distending the connective tissue beneath the neurilemma and even occupying the interval between the nerve filaments. Sometimes large corpuscular bodies are found between the nerve fibres.

The _cerebral meninges_, especially the _pia mater_, are congested and opaque. Foci of softening are by no means uncommon and the cerebral ventricles contain an abnormal quantity of fluid.

The _bony tissue_ generally has lost its consistency and the medullary matter may be unduly reddened. The large joints contain an excess of synovia somewhat pinkish in color, and the ligaments of the hip joints are often congested, thickened and softened. The articular cartilage may even show patches of blood staining.

The _intestines_ are usually nearly empty, soft, pale and flaccid, and Ruthe has in one case observed rounded ulcers on the mucosa. Fibroid thickening on the peritoneal surface may indicate a previous exudate.

The _mesentery_ is thickened, with infiltration and has a yellowish discoloration and the _mesenteric glands_ are usually enlarged, softened and friable, though sometimes firm and contracted. The _lymph glands_ adjoining the generative organs are often swollen, pigmented and studded with foci of caseation, varying in size from a pea upward.

The _liver_ is softened and congested or fatty. The _spleen_ is small.

The _kidneys_ are usually large, but flaccid, pale and bleached.

The _thoracic organs_ may show little change, though hypostatic inflammation and foci of caseation or suppuration may be present.

The _blood_ is pale and watery and forms a loose, pale, diffluent clot, while there is an extraordinary diminution of red globules and a relatively great encrease of leucocytes.

In advanced stages the _muscles_ are pale, anæmic and shrunken especially those of the hind limbs.

_Mare._ In the mare in addition to the lesions of the internal organs and blood, the following may be noted in connection with the generative system. Phlegmonous or œdematous swellings, sores or ulcers on the lips of the vulva, and on the vulvar and vaginal mucosæ. The parts become variously distorted, and the vulva, habitually open may expose the swollen and ulcerated clitoris. A crop of papules or vesicles, running into sores or ulcers may appear on the urethral orifice, the vulva and adjacent skin, and even though overlooked, their seats are marked later by loss of cutaneous pigment and the formation of small white spots. The mammæ are sometimes inflamed, œdematous and tender, with suppurative or necrotic foci and the adjacent lymph glands are enlarged by infiltration or contracted by sclerosis.

_Dog._ These resemble those in horses. In the bitch genito-urinary congestion, inflammation and catarrh, subcutaneous infiltration under the belly and inside the thighs, swelling of the inguinal lymph glands, emaciation, and pallor and atrophy of the voluntary muscles are marked features.

_Symptoms._ _Horse._ Incubation may last from one to eight weeks (Maresch), but is usually 11 days from the infecting service. It may be abridged by a special susceptibility, and by repeated infections and hence the more acute cases are especially seen in the male in daily service. In some such subjects local genital infiltrations are speedily followed by paralysis or vertigo which cuts off the patient in a few days.

More commonly the malady is _chronic_ though varying in different countries, epizoötics or even in particular cases.

The first _symptom_ is slight swelling of the anterior border and raphe of the sheath, which gradually extends backward to the scrotum and inguinal region and forward on the abdomen it may be as far as the brisket. This may be hot and painful, but is usually œdematous, cool and painless. The infiltration affects the end of the penis, the meatus may be red and angry with a slight muco-purulent discharge, and red spots vesicles and ulcers may stand out clearly on the pigmented surface. Williams never saw such eruptions in the American cases and doubts their existence except as the result of injuries. There are frequent semierections and service is still possible. Later the engorgement extends to the specially pendent testicles, inguinal glands and others adjacent. Paraphymosis is occasionally seen or, more commonly, the penis hangs out of the sheath soft and flaccid and erection seems impossible. The local swelling may become excessive, pressing the testicles up against the inguinal ring, or suppuration and extensive abscess may follow. Appetite is retained and the temperature remains moderate (100° to 102° F.).

The local swellings may almost completely subside, except a slight tumefaction of the end of the penis, hence some (Fischer) have held that the cutaneous lesions are the primary ones, yet the start of infection at the generative organs and the fact that a stallion often infects a number of mares before there is any suspicion of his own infirmity is evidence enough of the genital seat of the earliest lesions.

The cutaneous lesions, which are essentially secondary, but highly characteristic, appear from forty to sixty days after the infection (Schneider and Buffard). They are from a quarter of a dollar and upward in size (in some old horses much smaller), and rise abruptly from the healthy skin, becoming the more marked that the hairs upon them stand erect. These may arise suddenly and subside again in one day, or give out a serous exudate which mats the hairs into a tuft. They may, however, last four or five days. These are more patent after a full drink of water, or after sprinkling or sponging with water. Even when they have been overlooked these results may often be seen later on colored skins, in the presence of many circular white spots entirely devoid of pigment. The most common seat of these cutaneous lesions is the hind parts (anus, tail, croup, quarters), but they may appear on the sides, neck, shoulder or thighs.

Tenderness of the loins may now be shown, with frequent, painful micturition, but the penis becomes more and more paretic, so that coition becomes encreasingly difficult or impossible. Paresis also shows in the hind limbs, the animal remains recumbent a great part of the time, rises with difficulty, starts suddenly forward at the fetlock, and drags the toe on the ground in walking. Swelling of the joints and tendinous sheaths, with attendant lameness, is not uncommon. The appetite remains good, yet emaciation and weakness make marked progress.

The advanced stages are characterised by marked anæmia, paraplegia and dementia. The visible mucosæ are pale, emaciation advanced, the patient stubs his toes and sways in walking, and finally drops unable to rise; or he stands with hind legs straddled and semi-bent, and largely oblivious of all around him. He may be too stupid to eat unless the food is placed in his mouth, and yet the neigh of another horse or a mare may draw forth a feeble retort, as if the deranged generic instincts remained. Swelling, or even abscess of the lymph glands, axillary, submaxillary or inguinal, is usually present, and muco-purulent discharge with ulceration of the nose or eyes is not uncommon. The joints crack when moved and fractures are common.

The duration of the disease is two or three months, the progress being more rapid in winter.

_Mare._ Vulvar swelling eight or nine days after service, with ejection of urine in jets, contraction of the vulva, redness, swelling and erection of the clitoris, and a muco-purulent discharge are marked symptoms. European observers note nodules, vesicles and ulcers on the mucosa and adjacent skin, but these were not observed in the American cases (Williams). Yet later they showed the characteristic white spots. Switching of the tail, stamping of the hind feet and painful straining to urinate are followed in certain cases by ejection of the urine forcibly in jets or in small dribblets. The catarrhal discharge is at first watery, but later becomes viscid, sticky and white, yellow or grayish, or even red. It mats together the hair of the tail and thighs, and putrefies, exhaling a repulsive odor. The swelling involves the space between the thighs and often implicates the mammary glands and even the floor of the abdomen. The inguinal glands are often involved, and hyperplasias with degenerations and even abscesses may appear in this region. As in the stallions the local lesions may have periods of advance and subsidence, and in favorable cases, that are not again served, there may seem to be a temporary recovery. The mare, however, remains infecting, and if served the local disease is at once roused into activity. The button-like skin eruptions appears on the quarter as already noticed of the horse and in grave cases may caseate or suppurate and burst, forming an indolent and intractable sore. The dark skin of the vulva and perineum becomes marked by white spots or by irregular patches caused by the confluence of several such spots, which for ordinary breeds of horses are highly characteristic of this disease. Many Arabian horses naturally acquire such white spots on the dark skin, and in pure Arabs and grades this appearance need not be held as evidence of dourine.

Infected mares rarely conceive, and any that do so are likely to abort before the sixth month.

The systemic symptoms, nervous, paralytic, tremulous, dyspeptic, atrophic, cerebral and cachectic follow a similar course as in the stallion.

In grave and progressive cases the lesions of the generative organs become very marked. The lips of the vulva become rigid and distorted so that it remains constantly open and the erect clitoris continually exposed. The skin of the vulva is tense, dry and shining. Lameness is shown in one or both hind limbs, knuckling over at the fetlock, shortening of the step, planting the toe first and the heel later with a jerk, lack of balance, paresis and even inability to rise.

A disposition to trembling is common to both sexes, as is also an intolerable itching of the skin which may make the animals tear the lower parts of the limbs with the teeth. In either there may be a local paralysis of a lip, an ear, an eyelid, or some other part of the body. In both sexes the disease tends to extreme anæmia, debility and emaciation, and to infective internal inflammations (lungs, bronchia) or septic or purulent infections.

_Diagnosis._ From _urticaria_ this disease is to be distinguished by the absence of lesions of the generative organs in the former, by its association with change of food and digestive disorder and by the absence of all evidence of contagion.

From _glanders_ it is to be distinguished in the same way by its casual transmission by sexual connection only, by its restriction to breeding animals, and by the irresponsiveness of the victim to the mallein test. The progressive paresis and hebetude are valuable diagnostic phenomena.

From _chronic paraplegia_ it is distinguished by the same prevalence in breeding solipeds only, and by its mode of transmission.

The greatest difficulty is experienced with the slight and comparatively occult cases, and in some of these the history of the infection of a number of breeding animals, which have been served by the same horse may be the one guiding point for a number of the cases. For sanitary purposes it is well to treat as suspicious animals all mares that have been served by a stallion which is in the line of infection. This suspicion would attach also to any stallion that had served a mare which had been to a diseased or suspected stallion, and to all mares that have been served by the suspected stallion after he had been to the suspected mare.

From _simple vesicular exanthema_ dourine is to be distinguished by its comparatively slow progress, and by the uniformity of the lesions of the generative organs and nervous system, which are lacking in the vesicular affection.

_Prognosis._ A certain number of animals recover from the milder attacks which have not become complicated by the grave trophic and nervous lesions, but as in glanders, recovery from severe attacks and in the advanced stages is practically unknown. The mortality is set at 70 per cent. and upward.

_Symptoms in the Ass and Mule._ The disease usually remains discrete, the lesions in the generative organs or other seat of infection being the marked symptoms, and recovery the rule. Œdema of the end of the penis, obliteration of the folds around the orifice of the urethra and eversion of the urethral mucosa are the most constant features, distinct even in semi-erection. Œdema of the sheath and skin eruption may follow. Exceptionally a mule proves as susceptible as the horse, and shows the disease with the same fatal severity.

_Symptoms in Dog._ A bitch, 15 days after vaginal injection of the infected equine blood, showed severe vaginitis and hyperthermia (100°). On the 23d day she aborted, followed by muco-purulent discharge, vulvar œdema, pallor of the mucosæ, anæmia, rapid emaciation, paresis and occasional convulsions. Blood drawn from the vulva contained the trypanosoma. She died on the 66th day. The temperature rose to 103°.

Two male dogs that lined the above infected bitch showed after 12 days, engorgement of the sheath and scrotum, muco-purulent discharge, and abundance of the trypanosoma in the blood of the affected parts. Cutaneous lesions on the loins, thighs, sides or forehead, showed erection of the hair, with infiltration, or shrivelling and bloodlessness.

Other dogs showed arthritis, corneal opacities and ulcers, hypopion, cataract, nasal discharges, facial periostitis, dyspnœa and syncope.