Chapter C: F. Dawson, in investigating a wasting disease of well fed Brahma (7)

_Symptoms in Rabbits._ Rouget found in inoculated rabbits, extensive gangrene of the skin, involving even the cranial bones, ulcerative keratitis, hypopion, panophthalmia, following on the earlier genital troubles of vaginitis, swelling and discharge.

_Treatment._ Some cases recover spontaneously a few may be aborted in the earliest stage of the disease, but cases that have advanced to any extent and assumed a grave character are practically hopeless.

An important element in treatment is to do away as far as possible with the cause of generative excitement since the disease is aggravated and more rapidly advanced by frequent copulation. Rodloff from a very wide experience speaks highly of castration of the stallion. Castration of the mare has not been specially advocated and the absence of marked lesions in the ovaries, may deter the veterinarian, yet whatever promises to lessen in any degree the genesic excitement is not to be despised, and the measure has besides a sanitary value for other animals.

Early local treatment is the most promising, and especially if it can be applied to exposed animals during apparent incubation. Injection of the urethra, sheath, vulva, vagina and uterus with antiseptic lotions, and apply them to the external sores. Mercuric chloride 1:2000, carbolic acid 2:100, silver nitrate 1:250, calcium chloride 1:100, or chlorine water may be taken as examples. When local swellings have supervened it would be entirely appropriate to incise them freely or even to excise them and cauterize thoroughly with stronger agents.

Internal treatment by mercuric chloride 1½ to 3 grains, potassium iodide 2 to 5 drs., arsenic 7 to 14 grains, has been widely used but to little purpose. The same may be said of Rodloff’s treatment by tonics and carminatives (sal ammoniac, camphor, iron, angelica, gentian, ginger and valerian.)

_Prevention._ The one thing to be secured is the prevention of copulation with any animal that has been affected, or exposed to this disease in the past three years.

1st. Any stallion or mare once affected must be excluded from breeding for at least three years after apparent recovery.

2d. Every such animal that has been exposed by copulation with a suspected animal must be excluded from breeding for the same period even if no active symptoms have been shown.

3d. Every affected or exposed animal, should be quarantined in the hands of his or her owner and placed on an official register and the sale, gift or loan of such an animal, or its movement to a new place where it might propagate the disease should be made a misdemeanor.

4th. In any county or district in which the disease exists all stallions and mares should be registered and none should be allowed to be used for breeding purposes without an official certificate showing that each of the animals mated is free from all suspicion of having been exposed to this infection.

5th. If any stallion or mare is imported from a country in which dourine exists it should be accompanied by an official certificate showing that it has not in the past three years been exposed to the possibility of infection with dourine.

6th. In the absence of such certificate the imported animal (capable of breeding) should be kept in strict quarantine for the period of three years.

7th. A much more radical measure, which may be made to supersede all of the above, would be to castrate every soliped (stallion or mare) which has suffered from the disease in the past three years, and every such animal that has by coition been exposed during that length of time to even a remote opportunity for contagion. This would embrace all apparently sound mares that had been served by a stallion which had shown slight symptoms of the disease, or by a stallion which had not himself shown such symptoms, but which had served a mare that had shown such symptoms; or one that had served a mare that had not shown such symptoms, but that had been previously served by a stallion which had shown such symptoms, or that previously covered a mare that had shown such symptoms. In such cases the State might well afford to indemnify the owner for any reduction in value of the castrated stallion from that borne by the animal as a prospective breeder, the breeding for which indemnity is sought being understood to count only from a date of three years after the sanitary castration. A mare once attacked should be remorselessly castrated or killed. A perfect recovery in a horse can be better attested; that of a mare is always uncertain, and most secondary outbreaks after the apparent extinction of the poison have come from breeding mares that have apparently recovered, or that after exposure have shown no appreciable symptoms.

When a State is so lost to all sanitary considerations as to abandon an affection of this kind to take its course, the owners of stallions and mares cannot be too careful to avoid the exposure of their valuable breeders to the risk of infection. Each mare brought for service should be admitted only when accompanied by a certificate showing all previous services in the last three years, with the identification of the stallion, and this irrespective of whether the service has been fruitful or not. In such certificate the owner of the mare should bind himself to make good all damage or loss that may accrue from his failure to set forth in the certificate every such service and every symptom of illness affecting the generative organs from which the mare has suffered in the three years antecedent.

The owner of the stallion should give a similar guarantee that the horse has in the past three years served no mare that was in any way open to suspicion, and that the animal has not suffered from any affection of the generative organs which had any of the characteristics of dourine.

No mare should be served which shows swelling, nodules, distortion, or gaping vulva, a muco-purulent discharge, or too frequent or too prolonged _heats_.

No stallion in such locality should be allowed to serve which shows pasty swelling of the sheath, swelling, shrinking or distortion of the penis, red, angry, tender meatus urinarius, or a muco-purulent discharge.

Unless in case of Arabian horses the appearance of white spots on the dark ground of the sheath, penis, vulva, or perineum, should be ground for debarring from service until an absolutely stainless record covering a number of years has been shown.

MAL DE CADERAS.

This is a disease caused by _Trypanosoma Equinum_ described by Voges who studied the affection in the Argentine Republic as it exists in a region extending from Santa Fe, and Corrientes on the south to Bolivia on the north. It resembles surra in prevailing in tropical heat, during wet weather, in its intermittent character, in the presence of the mature trypanosomata in the blood at the beginning of a paroxysm and their disappearance toward the end of it, in the supervention of rapid and extreme emaciation, debility and anæmia, in the destruction of red blood globules and the passage of the coloring matter by the kidneys, in the presence of paresis and œdemas, in its expending its energy mainly on the soliped and in the constancy of the mortality. Death occurs in two to five months in horses, and six to twelve months in asses and mules. Swine and water hogs contract the disease casually and it is inoculable on white and gray rats, mice, rabbits, dogs, goats, sheep, chickens, turkeys, ducks and monkeys, (Nyctipithecus felinus), and exceptionally on Guinea pigs. The same measures of prevention would be indicated as in cases of surra and dourine.

INFECTIOUS PARAPLEGIA OF SOLIPEDS IN MARAJA.

Synonym. Definition: Infectious, anæmic, dropsical paraplegia. Origin:
Decomposition of myriads of horse carcasses in torrid heat; rodents;
swine; horses. Causes: Microbe uncertain; infection in corral and
vicinity; manure; rubbish; flies; hot dry weather. Symptoms:
Decreasing severity; preliminary weakness, dulness, emaciation,
dyspnœa. Paresis: Fifty per cent. paraplegic; marasmus; difficult
defecation or urination; paretic penis; anorexia; ardent thirst with
diuresis; rumbling of bowels. Œdema, epigastrium, abdomen, sheath,
mammæ, head. Cutaneous sloughing, stupor, asthenia, rapid emaciation,
hemiplegia, impaired peristalsis. Blood dark, viscid. Lesions:
Intestinal congestion; petechiæ of serosæ; icterus; enlarged, soft,
congested liver; spleen engorged, softened; kidneys swollen,
congested; petechiæ on bladder; congested lungs, thoracic serosæ,
cerebral meninges. Relation to surra. Mortality excessive or constant.
Treatment hopeless. Prevention: Keep sound from sick and from infected
places and things; kill and bury sick; disinfect harness, trappings,
wagons, utensils, buildings, manure and rubbish heaps; destroy flies
and mosquitoes, vermin (rodents), etc.

_Synonym._ Quebra Bunda: Broken Buttock.

_Definition._ An acute infectious disease of horses characterized by a condition of fever, with rapid loss of condition, resulting in rapid and extreme emaciation, local dropsies, cutaneous eruptions and ulcers, a rapidly advancing anæmia and debility, with lessening control of the hind quarters and death in almost all instances.

_History of the Disease._ Luis Calendrini da Silva Pacheco says the malady was unknown on the island until 1830, when, on account of the great excess of wild horses and their devouring the pastures needed for the more valuable cattle, great numbers were killed and their hides marketed. This continued for over a year without any attempt to dispose of the carcasses. These accordingly lay in heaps in a damp climate, under the equatorial sun, in a condition of putrefaction, exhaling the most offensive odors. Stimulated by frequent complaints, the government ordered that the carcasses should be burned to ashes, but no success was accomplished, in one case 800 bodies having been merely roasted a little on the surface. The district around Chaves contained the greatest number of horses, there the greatest number were killed, and there the disease broke out. A number, variously estimated at from 25,000 to 60,000 were driven into the little bay of Juncal and killed by burning the grass, which, however, did not at all consume the bodies. The disease attacked first the capivaras (rodents) in the district of Chaves, killing off the whole race; then the wild and domestic swine suffered, and finally it ravaged the equine race, and though confined to Chaves for two years it was extended through sales of horses and raged with such fury that in five years not a horse was left alive in the island, except a small remnant of a few hundreds in Chaves, where the infection started.

_Causes._ The microbian cause of the disease has not been definitely ascertained, so it is idle to speculate whether we have to deal with a saprophyte which has taken on deadly pathogenic properties, or whether the infection was carried to the island by winged insects or birds attracted by the decaying carcasses.

Certain conditions may be named as accessory or favoring causes. The wild horse often escapes so long as he is on the pasture, but when lassoed, taken to the corral and broken, he will die in four to six days. This suggests that the infection is laid up and preserved in the corrals or stables, the mangers or racks, or possibly in the water supplies. The contact with even the reins (harness) of other horses is alleged to be a prominent cause of infection. Another significant point is that around every hacienda, within a radius of a mile, there are numbers of carcasses, so that there is every opportunity for the infection of the wild and susceptible horses caught and brought in. Near the buildings, too, are accumulations of horse and cattle manure and rubbish heaps of all kinds, the breeding places of the flies, which are probably important factors in conveying the infection. Again, the attacks are more numerous and severe and death earlier in the hot, dry summer weather, while there is a pause and a lesser intensity in the cool or rainy season. All domestic animals, save when kept up for breaking or work, live in the open field day and night and subsist on the green food (capine, gramineæ), and are thereby exposed to all climatic changes.

_Symptoms._ At the first appearance of the disease (1830) it proved fatal in a few hours, but after a year’s prevalence, when the more susceptible animals had been killed off, the progress of the malady became slower, death being deferred to the 8th or 15th day, so that the symptoms could be more definitely followed. From 7 to 14 days before the more obvious symptoms, there were lifelessness, tardy movement, hurried breathing, debility, weakness and emaciation without work or other obvious cause. Exercise caused difficult breathing, dilated nostrils and great agitation of the flanks.

One of the most constant symptoms was the loss of power of the hind limbs which would sway and stagger, the femurs turning inward, as if dislocated, and on uneven ground the animal could not walk without falling. When down, he could not rise without assistance. In the earlier experience of the malady (1835) only 8 to 16 per cent. failed to show these paraplegic symptoms, whereas in recent years 50 per cent. or more escape them. In these cases the emaciation goes on alone, gradually encreasing until the patient appears like a living skeleton. Some retain an appearance of liveliness, yet all stand on three limbs, and change from one hind limb to the other every six or eight seconds.

The retraction of the abdomen is a marked feature, yet expulsive contraction is defective, the patient fails to put himself in the position for urination or defecation, and there is more or less detention of urine or fæces, the latter being dry, moulded, covered with mucus and of a reddish yellow color. After a time the urine escapes in fine jets, so small that in the absence of stretching to urinate, or raising of the tail, they are easily overlooked. The urine may be normally clear, or dark colored. The penis hangs out of the sheath several inches farther than in health.

Appetite is sometimes impaired, or completely lost, but usually the patient eats and drinks to the last, but without proper digestion or assimilation. It does not check the advance of marasmus. Thirst often becomes excessive and in such cases, there is diuresis together with frequent and excessive rumbling of the bowels. The loins are very sensitive to pinching.

About sixty to seventy per cent. in different outbreaks show œdema, in the epigastric region it may be six inches in diameter, or it may extend from the sternum back so as to include the abdomen, sheath, or mammæ, and perineum, and even the hind limbs. Considerable serous oozing takes place from this for four or five days after which it dries up.

In about seven to fourteen per cent. the head became œdematous and swollen, with an abundant fœtid purulent discharge from the nose and eyes, and extensive ulceration of the pituita and conjunctiva. Such cases became completely blind prior to death. In other cases extensive ulceration of the skin set in with the formation of most repulsive sores.

The nervous symptoms assumed various forms; in some there was stupor with head resting on the ground; in others extreme debility and paraplegia with phenomenally rapid emaciation; in a few hemiplegia, or even delirium was shown; in all there was a marked paresis of the digestive organs and especially impairment of peristalsis. The blood assumed a dark gluey aspect.

The most constant symptoms appear to be dyspnœa under exercise, paresis of the hind limbs and intestines, genital atony, a wonderfully rapid and extreme emaciation, œdema, and a tendency to impaired nutrition or ulcerous degenerations of the pituita, conjunctiva or skin.

_Lesions._ Congestion or inflammation of the intestines was usually noted, with petechiæ on the peritoneum, especially the omentum, and on other serosæ. The serosæ, mucosæ and other normally white tissues were of a yellowish color, more or less deep. The liver was enlarged, much softened, gorged with black blood, and sometimes of a greenish color. The spleen was more or less black, and friable sometimes coming to pieces in handling. The kidneys were always enlarged and gorged with black blood. The bladder was usually distended and showed petechiæ on its mucosa. The lungs and bronchia bore evidences of congestion, and the pericardium had become dull, rough and lusterless. The horses that had rested their heads on the ground showed meningeal congestion.

Sr. Calendrini claims to have had recoveries in some cases, followed by relapses, and states that a second relapse is usually fatal. Many features of the disease reminds one of surra—for example its relation to hot weather, its relation to buildings and enclosures with their accumulations of decomposing organic matter and swarms of flies, the decomposition of the blood, anæmia, icterus of the white tissues, petechiæ, extreme weakness, muscular atrophy, and marasmus. Calendrini’s cures followed by relapses suggest the further coincidence of intermissions. If now the trypanosoma were discovered in the blood it might be recognized as at least a near ally of surra.

_Mortality._ _Prognosis._ The disease is nearly always fatal. At the time of its first appearance (1830) Calendrini had 5,000 horses, and in 1835 he mounted his last horse a half-tamed animal lassoed on the Campo. One Haziendiero invested $25,000 in horses and in 30 days he had lost $18,000 worth. Others with 35,000 head lost the whole.

_Treatment_ proved one continuous failure. Bleeding, purgatives, coloquintidas, saltpeter, cream of tartar, lemon, vinegar, nicotine, buchu, by mouth and rectum, strychnia, camphor, caustics, prolonged baths in the river, and a great variety of other measures, only seemed to hasten a fatal result.

_Prevention._ Calendrini finally struck the true note of rational prophylaxis, in the immediate killing and burial of all affected animals, and the strict separation of all sound horses from the places where they had been, together with the thorough disinfection of all harness, utensils, wagons, etc. For a number of years his district (Soure) had by this means been kept free from the plague.

This might be profitably extended so as to include the thorough disinfection of any buildings and yards where the sick had been, the removal of manure heaps and disinfection of their sites, also of all rubbish heaps as breeding places of flies, the use of petroleum on all stagnant water devoid of fishes and frogs as being the sources of mosquitoes, and the application of suppressive measures which would include the rodents (capivaras), and swine which have been shown to propagate the infection.

INFECTIOUS PARAPLEGIA IN SOLIPEDS IN EUROPE.

Definition: Infectious, non-febrile affection of solipeds with lesions
of the genito-urinary mucosa and nerve centres, paresis and paralysis.
History. Causes: Microbes varying; bacteria of colon group; infected
urine, genital mucus, brushes, combs, rubbers, mares especially
exposed; infection local or general. Lesions: Congestion, exudation,
swelling, discharge from vulva, vagina, bladder, ureter, kidneys;
lumbar spinal cord, brain. Symptoms: Mare, swollen open vulva,
congestion and petechiæ, bloody mucus; horse, swollen sheath, pendant
penis, congested papilla, discharge; paresis of hind limbs, falls,
inability to get up, incontinence of urine; paresis of fore limbs, of
thoracic muscles, asphyxia, fever in late stages. Recovery. Diagnosis:
From hæmoglobinuria by absence of dietetic cause, the infectious
progress and genital lesions. Prognosis: One-fourth to one-third die
or fail to recover. Treatment: Antiseptic washes and irrigations of
vagina, urethra, bladder, skin; internally oil of turpentine; slings.
Prevention: Isolation, disinfection, separate attendants, litter,
sponges, etc., fly nets, screens, insect powder, removal and
disinfection of manure and garbage.

_Definition._ A contagious, non-febrile affection of solipeds, characterised by congestive and hæmorrhagic lesions of the genito-urinary mucosa, the spinal cord and its meninges, and by paraplegia or paresis of the hind limbs.

_History._ This was described in 1888 by Comeny, as occurring in a regiment of French cavalry. Other outbreaks have been observed in 1892 (Rancoule); in 1896 (Blin and Lambert). Earlier outbreaks have doubtless been confounded with cerebro-spinal meningitis, hæmoglobinuria or simple paraplegia, the genito-urinary symptoms having been overlooked or viewed as secondary.

_Causes._ The disease, as hitherto observed, has been invariably associated with microbian infection of the genito-urinary mucosa, but no one microörganism has been found to be constantly present. In the 1888 cases, Nocard isolated from the kidneys and lumbar cord a small, motile bacillus which was not stained by Gram’s method and the inoculation of which proved fruitless. Zschokke, in 1889, found in the kidneys, lungs, liver and spleen of both horses and cattle, the victims of a progressive infectious paralysis, a bacterium coli commune 1.5μ long by 0.7μ broad, which stained in methylin blue and grew in agar and gelatine, and when inoculated under the skin of a goat provoked paralysis. It had no effect on a pig. In keeping with this, Thomassen, in 1893, alleged that the bacillus coli communis in certain conditions, when colonized in the solid organs, produced a toxin which caused paresis and paraplegia. Blin and Lambert, in 1896, found in the urine, in pure cultures, a short ovoid microbe, motile, non-liquefying and bleached by Gram’s solution. It grew on gelose and peptonized gelatine as a creamy surface layer which did not extend into the medium, and assumed a brownish color as it became older. On potato it formed a superficial bright yellow film. In bouillon the surface film which formed gradually precipitated to the bottom of the vessel.

This microörganism was not found in the blood, liver, muscles nor spinal cord.

Inoculation into the pleural cavity of the horse induced pleuro-pneumonia.

The contagion appears to be transmitted through the urine and morbid discharges of the urino-genital canal, falling on the litter and floor and thus contaminating the tail, and indirectly the generative organs. The brushes, combs and rubbers used on one horse after another are similarly incriminated. The mares, having a wider exposure to infection, appear to suffer most. Comeny saw eighty sick mares to twenty-eight horses, and the mortality was thirty-four mares to three horses. The smallness and length of the male urethra and its frequent flushing throughout its whole length with urine seems to give a greater measure of immunity to the horse.

In the Blin and Lambert cases the indications pointed to a local infection and to the presence in the spinal cord of the toxins alone. It may be assumed that in such cases there was a purely local infection. In the Zschokke cases on the other hand, with microbian infection of internal parenchymatous organs the presumption is that the paralysis was due to a totally different infection, as appears to be further indicated by the morphology of the microbe. They may have been, however, but the advanced and generalized stages of a primary local infection.

_Lesions._ These appear to vary with the progressive advance of the malady. In an ass which was killed as soon as paraplegia appeared and the necropsy made at once, the lesions were confined to the vulva, vagina and bladder. In advanced cases the ureters and kidneys are visibly involved together with the spinal cord, especially in the lumbar region, and in certain instances the brain.

The vulva is swollen, held habitually open so as to expose the erect clitoris; the mucosa is irregularly swollen and petechiated, and there is a glairy or bloody discharge. The swelling usually extends to the inner side of the thighs, the mammary glands and the adjacent wall of the abdomen. The vaginal mucosa is congested, swollen so as to bulge irregularly at intervals and covered with a glairy muco-purulent matter often mingled with clots of blood. The urethra and bladder are red and congested, with marked thickening and ecchymosis of the mucosa and an abundant serous exudate which extends into the muscular and peritoneal coats as well. Minute extravasations are found in the two outer coats and petechiæ of the serosa is the rule. In fatal cases the ureters and kidneys are involved, the renal parenchyma is greatly congested and softened, the cortical part especially being of a dark red, and the glomeruli distinctly enlarged. An oily sanguineous liquid can be squeezed from the cut surface. The lumbar portion of the spinal cord together with its meninges, is congested and arborescent, and in bad cases this may extend upward to the head and involve the brain and its coverings.

There is general congestion of the venous system with black blood, especially noticeable in the arborescent lines on the inner surface of the skin and in the serosæ, and the liver and spleen are gorged with black blood, which, however, reddens on exposure to the air. Muscles and parenchymatous organs may show a parboiled appearance. In the male the swelling appears about the sheath and penis, the papilla, the urethral mucosa and that of the bladder are deeply congested and petechiated, and the kidneys and medulla may be implicated as in the mare.

_Symptoms._ In the _mare_ the early symptoms are the swelling and gaping of the vulva, with the muco-purulent or sanguineous discharge and the presence of redness, congestion and petechiæ of the mucous membrane.

In the _horse_ there is swelling of the sheath and a pendant condition of the penis, which in its turn may be irregularly reddened and swollen, and the papilla and orifice of the urethra are deep red and angry.

Most commonly these early local symptoms are overlooked until attention is drawn by some lack of control of the hind quarters. When moved the animal sways or staggers behind, knuckles forward at the fetlocks and drags the toe along the ground. This weakness encreases, and although for a time the animal can stand steadily, he is liable to fall when we make him take a step, and when down he will require help to get up. In advanced stages the animal remains recumbent and cannot be made to stand even with help, the fore limbs have become implicated in the paralysis, and in the end the respiratory muscles are involved and the patient dies asphyxiated. This marks the occurrence of severe lesions in the medulla oblongata. Incontinence of urine is a frequent symptom. Fever usually sets in, in advanced cases. Recoveries may take place from the first and second stages, the control of the muscular system improves, the animal lies down and rises with greater ease, the drooping penis is retracted within the sheath, incontinence of urine ceases, micturition becoming less frequent and more abundant at a time, and finally muscular control becomes once more perfect. Convalescence may be complete in eight days if it begins early, while it may require two or three months when the disease has been more advanced.

Some subjects survive without overcoming the paralysis, so that they simply _eat their heads off_ if preserved.

_Diagnosis._ From hæmoglobinuria this disease is to be distinguished by the history which fails to show its supervention on a period of hard work and high feeding, followed by one or more days of rest and then sudden exercise; by the swelling ecchymosis and discharge from the vulva or sheath, and by the occurrence of several cases in animals that have had an opportunity for a common infection. In case of death the condition of the kidney, bladder and urethra, and the marked congestion of the lumbar portion of the cord is significant, the congestion, petechiæ and extravasations are deeper and the glairy discharge is present.

_Prognosis._ From one-fourth to a third of the animals attacked either die or are rendered permanently useless.

_Treatment._ Antiseptic washes and irrigations of the genito-urinary passages, and the adjacent parts, if employed early enough, would tend to abort the disease. Even if resorted to later, they would be of some value in limiting the multiplication of the microbe and the absorption of its toxins. For this purpose boric or salicylic acid, salicylate of soda, permanganate of potash, or silver nitrate may be taken as examples. They should be as thoroughly applied as possible, the bladder being thoroughly evacuated and injected several times a day. As internal medication, oil of turpentine and other stimulant antiseptics that are eliminated by the kidneys might be tried in small doses frequently repeated. Keep in slings. The patient that cannot stand up is lost.

_Prevention._ This consists in isolation of the healthy, thorough disinfection of the stalls, gutters, combs, brushes, rubbers, blankets, and the hands of attendants. Litter used for the sick should be burned and manure piles secluded and disinfected. Even flies are to be dreaded, so that darkness in the stable, fly nets, fly screens, and insect powder and other means of insect destruction will be in order. Sponges and other means of dressing should not be used indiscriminately on different animals.

PROTOZOAN CATTLE FEVER. TEXAS FEVER. PALUDISM OF CATTLE.

Symptoms. Definition: protozoan, tick-borne, febrile, affection, of
wild damp lands, and warm seasons, with enlarged spleen and liver and
hæmolysis. Historic Notes; Old World; Australia; tropical and
subtropical America. Causes: contact of cattle from salubrious
districts with the insalubrious or with cattle from such; Piroplasma
bigeminum; a bovine parasite, reducing red globules by ¾ths.;
successive forms of piroplasma; the cattle tick, boöphilus bovis,
bearer of piroplasma; demonstration of the tick agency; toxic saliva
of tick; toxic property in blood; question of identity of
infection-bearing ticks. Lesions: putrefaction rapid, icterus, ticks,
blood oozing in skin, hydræmia, hæmoglobinæmia, few red globules,
small petechiæ, slight serous exudates and effusions: congestion,
petechiation, sloughing, perforation of gastric mucosa, congestion of
intestinal mucosa, in rectum like port wine; liver enlarged,
congested, biliary radicles in acini gorged with bile; spleen
enlarged, engorged; kidneys œdematous, blood-stained; bladder
petechiated; urine opaque or red, in convalescence watery; womb;
fœtus. Incubation three to ten days; delays due to hatching of ticks.
Symptoms: Acute case: anamnesis; hot season; hyperthermia 104° to 109°
F.; hurried breathing and pulse; anorexia; dulness; costiveness;
icterus; prostration; weakness; delirium; urine turbid, red; blood
hydræmic; diarrhœa; emaciation. Duration one to seven days. Fatal
(90%) to exotic cattle; mild in indigenous, or cool season. Mild case;
temperature 103°, anorexia, dulness, costiveness, enuresis,
albuminuria, pallid mucosæ, emaciation, round protozoön in globules,
ticks, oligocythemia. Differential diagnosis, from anthrax. Treatment:
laxative; antiseptic; mucilaginous food; picking off ticks;
anti-ixodic lotion; tick-free pasture or place. Prevention:
destruction of ticks; picking; dipping or smearing with tick killing
preparation, paraffin or extradynamo oil and sulphur, danger with
shipping; dressing of all cattle at intervals during warm season;
cultivation of tick-infected land; exclusion of cattle for one summer
and two winters; soil cattle for three weeks in each of two tick free
pens, to let ticks drop; danger of nonimmunized cattle in infested
area; suggestions for extinction by States. Immunization: Infection of
sucking calf; infecting by a few ticks: by graduated injections of
piroplasma blood; technique; injection of blood from body of tick.
Limited value of artificial tolerance. Marketing of the beef. Federal
restrictions.

_Synonyms._ Splenic fever; Spanish fever; Mexican fever; Southern cattle fever; Australian tick fever; Tristeza; Red water; Black water; Bovine periodic fever; Bovine yellow fever; Maladie du bois; Holzkrankheit; Moor evil; Wood-ill; Ixodic Anæmia; Roumanian hæmoglobinuria.

_Definition._ A specific fever of cattle, enzoötic during the warm seasons in the low, malarious grounds and wooded or uncultivated districts of different countries, caused by a protozoön in the blood and red globules, which is conveyed from animal to animal by ticks, and leading to engorgement of the spleen and liver, destruction of the red globules, hæmoglobinuria, and oligocythemia.

_Historic Notes._ This malady has doubtless existed from time immemorial in different malarial districts of the Old World, where the wood and moor ill is now coming to be recognized as a protozoan tick-borne disease. The malady exists in Roumania (Starcovici, Babes, Gavrilescu), Turkey (Nicolle, Adil-Bey), Sardinia (San Felici, Loi), Southern France (Lignieres), Italy (Celli, Santori), Algiers, Tunis (Lignieres), Finland (Krogins, Von Hollens), West Indies, Mexico, Nicaragua, United States of Columbia, South America as far south as the Argentine Republic, German East Africa (Koch), Transvaal (Theiler), S. Australia (Pound). In Australia imported European cattle found the infection waiting for them in the uncultivated bottoms. In America it doubtless prevailed on the seaboard and islands of the Gulf of Mexico from the time of the importation of Spanish cattle, but for the first definite account of it we are indebted to Dr. James Pease, who records the widespread destruction of the native herds in Lancaster, Co., Penn., in connection with the introduction of cattle from the south. None of the southern cattle died, but wherever they traveled, the native stock perished all but universally. Other droves from South Carolina were equally destructive to all cattle along their track. The recorded symptoms of anorexia, great weakness, often inability to stand, trembling, groaning, bloody urine, bleeding from the nose, costiveness, congested kidneys, and decomposed, incoagulable blood serve to identify the disease.

Later, whenever southern cattle were moved north, the disease followed their trail. Florida cattle left infection along their route until they reached the border of Virginia, where it usually ceased. When taken from the Georgia mountains to the lowlands, they died without infecting the native stock, and, when such native stock of the lowlands were moved to the hills or the north, they conveyed the fever to the stock among which they came, though themselves well and improving all the time (Wilkinson). Similar experiences were had in all the middle states up to the war of 1861, but, in too many cases, the real source of infection was overlooked. It was observed that the disease was confined to the vicinity of the main highways and drove roads running north, and spared the lands lying somewhat back of these routes. Attention was drawn to the Texas cattle in 1853 when a herd of 450 which had wintered in Jasper Co., Mo. moved north passing through Vernon Co. in June, and causing losses of 50 to 90 per cent. of the native cattle along their course, and only along that line. Such invasions occurred yearly, and in 1858 $200,000 worth of native cattle perished from this cause in Vernon Co. alone (A. Badger). During the war (1861–64) the cattle, in Texas especially, encreased without meeting with an adequate market, and, on the opening of the trade once more, they were sent north in large numbers carrying infection with them. When Forts Smith and Gibson had been occupied by the Union soldiers, the southern cattle poured in along the military road and the Kansas farmers along this route suffered severe losses, as well as those to whom the southern cattle were finally distributed (Bray).

_Causes._ Up to 1889 the true cause of Texas fever was unknown. It was well established that cattle brought from the lowlands of the southern states, during the warm season, though themselves in apparently the best of health, proved deadly to northern cattle with which they came in contact, to those that followed them in the same pasture during the same warm season, and even in many cases to the mountain cattle of the south. In the same way northern cattle, removed to the infected regions in the south, contracted the fever and almost all perished. This was equally true of cattle taken from the northern states to Jamaica or other islands in the Gulf. In the winter season, after the first severe frosts of autumn and before the last keen frosts of spring, the southern cattle could be safely introduced into the northern states and on this a modus vivendi, for a trade in southern cattle in the winter only, was based.

_Microbiology._ _Piroplasma bigeminum_: _Apiosoma bigeminum_. (Apios pear, geminus twin). In 1888 Starcovici discovered pyriform organisms (_Babesia bigeminum_) in the red blood globules of Roumanian cattle suffering from hæmoglobinuria, and Babes, after a study of the organisms, named them _Hœmatococcus_. The following year Theobald Smith found them in the Texas fever blood, and recognized them as protozoa (_Pirosoma bigeminum_). Wadoleck proposed _Apiosoma_, Bonome _Amœbosporidia_, and Patton, _Piroplasma_. The latter pointed out that _Pirosoma_ was already in use for another organism. Th. Smith’s discovery identified Texas fever with the Roumanian hæmoglobinuria, and stimulated the Bureau of Animal Industry to an extended research which, in the main, elucidated the true nature of the disease. In a long series of experiments the observers produced the disease in healthy susceptible cattle, by injecting them, in the warm season with the blood of sick animals, and as constantly failed in the experimental inoculation of similar blood on non-bovine animals such as sheep, rabbits, Guinea pigs and pigeons. In Australia, Pound had violent fever in two injected sheep but no pyroplasma, and their blood injected on the ox, had no effect. In none of these latter were the blood globules invaded by the parasite, nor were the corpuscles lessened in number. In the affected cattle, the red cells were reduced from the normal 7,000,000 per cubic mm. to 1,800,000 and even lower in some cases.

The _Piroplasma Bigeminum_ passes through a series of forms in the blood. Theobald Smith found in the red globule and attached to its margin a _pale round body_ 0.5μ in diameter, and staining freely in _alkaline methylene blue_ and other basic anilin dyes and in _hæmatoxylin_, but not in acid coloring fluids. These he found in the red globules in acute cases, often in company with the pear-shaped bodies, and usually in the absence of the piriform bodies in chronic cases, in non-fatal relapses, in cases occurring in cooler weather, (late autumn or early winter) and in immune southern cattle. The red cells containing these rounded organisms were not crenated nor distorted, though 50 per cent. of them might contain the parasite. He looked on these as the earlier stage of the organism which later developed into the _piriform body_, by segmentation of its substance. The _piriform_ or _spindle-shaped bodies_ were usually found in pairs connected at their pointed ends by a filament and extending across nearly the whole breadth of the red globule. _Free microörganisms_, pear-shaped or round, he failed to find in the blood of the large vessels, but saw them only in the cardiac capillaries and especially in the kidneys. In some cases the dim remnant of the disintegrated blood globule could still be detected around the parasite.

Laveran and Nicolle, examining the blood of Italian cases by fixing and staining, found the two forms, round or oval, and piriform, and claimed that the first passed into the second by segmentation.

Lignieres working in Buenos Ayres with the most ample opportunity as regards fresh material and authority to use it, watched the successive changes in the living organisms, and reached further conclusions. He diluted the blood with a 7 per cent. salt solution, or with ox serum or both, until the globules stood apart in the field. The blood can be kept under observation for days under a cover glass luted with sterile paraffin, and the changes clearly traced. Securing the blood from a subject having a great abundance of infected globules (usually at the height of the hæmoglobinuria) he found mainly the _piriform parasite_ intraglobular and free, and in the latter an active whirling motion was kept up by means of the flagellum at its pointed end. As usually arranged in pairs (gemina), whether inside or outside the globule, they are connected by the flagellum attached to their pointed ends. Careful observation enables one to detect in the pyriform mass a small brightly refrangent point like a nucleus. In this form the piroplasma is 3 to 4μ in length.

After 4 or 5 hours, and on toward the 8th, the piroplasma has assumed the _round_ or _oval form_ with a small linear prolongation (flagellum) and shrunken to 1 to 1½μ in diameter. All the piriform bodies pass into the rounded so that this last is the second stage of their development and not the first as was formerly supposed. The round forms are always present in great numbers in the cortex of the kidney in the second stage of the disease (toward the subsidence of the hæmoglobinuria). The refrangent nucleus is no longer to be seen.

After, one, two or more days there appears in the round parasite a _chromatine mass_, which breaks up into 2, 3, 4 or 5 smaller _chromatic bodies_, which Lignieres considers as germs. He has seen no division of the protoplasm, but on the contrary the germs escape, yet remain for a time attached to the outer surface of the parent organism. They show rapid jerking movements.

Lignieres claims to have followed all these changes in the blood kept in a sterilized glass cup at room temperature or in the thermostat, and in the stomach of the tick, as well as on the warm stage of the microscope.

He claims to have made a further success in cultivating the parasite in ox-blood serum highly charged with hæmoglobin. It was only occasionally, and by the use of blood extraordinarily rich in the parasites, that success was obtained. In one such case he produced five successive cultures, the product being the rounded forms only and within these the germs. There were no piriform bodies. These are not formed outside of the red globules. The third successive culture in this medium grew with great readiness, producing larger parasites with less disposition to contract, but the fourth and fifth cultures were encreasingly poor. Inoculation with these cultures failed to produce the disease. To explain this the doctrine of passive germs, strong for survival, but weak pathogenically, is hazarded.

To summarize, the successive stages of the piroplasma are: 1st. The intraglobular _pear-shaped bodies_, with flagellum often connecting two bodies. 2nd. The _rounded bodies with refrangent nucleus_—intraglobular or extraglobular. 3d. The _free round bodies_ with the nucleus divided into 2 to 5 _chromatin masses_. 4th. The _free chromatin masses_, large, _active_, _infecting germs_, and small, _passive_, _noninfecting germs_. The insuccess of inoculations of cattle with the last-named bodies throws an air of doubt upon them as links in the pathogenic chain. Definite information on the antecedents, environment, food, etc., of the cattle unsuccessfully inoculated, including the season, shelter and meteorological conditions might have brought us a step nearer to the full life history of the piroplasma.

_The Cattle Tick_: _Boöphilus Bovis_: _Ixodes Bovis_: _I. Dugesii_: _The Invertebrate Host of the Texas Fever Organism_. As early as 1868 shrewd observers had noticed that in all outbreaks of Texas fever the affected animals were covered with ticks, and drew the natural inference that the disease was due to the bites of these insects. But the prevalence of ticks in localities where the disease was unknown served to draw attention away from the important fact that was suggestive of the true explanation of the disease. The truth, however, constantly obtruded itself that casual cases were never found in the absence of the tick. Finally, in 1889, Kilborne conceived the idea of putting the matter to the test, and with the approval of the Chief of the Bureau of Animal Industry, set aside special paddocks for this purpose. Five native cattle were placed, at midsummer, with three South Carolina cattle, from which all ticks had been carefully picked, and they completely escaped infection.

After seventy-one days, on September 6th, when the hottest weather had passed, two were turned into a lot with four South Carolina cattle of the original herd which had stocked the pasture with ticks. Of the two one died of Texas fever, September 20th, and the other sickened in the last week of September, and had a relapse in October, but finally recovered. Of eleven other native cattle placed in this tick-infested field up to September 30th, ten sickened and one escaped. One animal placed in the field October 19th escaped.

Again three North Carolina cattle and three natives were placed in a field September 14th and 15th. The new generation of ticks was retarded by the cool season, so that few larvæ appeared on the native stock yet one of the three sickened.

These results were confirmed by a series of other similar experiments.

In a further experiment, September 13th, thousands of ticks, mostly mature, from North Carolina, were scattered over a second lot and four native cattle turned into it next day. Three sickened and one, to outward appearance, escaped.

These results were corroborated by experiments made in succeeding years. In addition the disease was produced regularly in native stock by placing on their skin the six-legged larvæ of boöphilus bovis, which had been hatched in glass vessels in the laboratory. It was also shown that the Washington winter destroyed the ticks in infected pastures so that native cattle could be safely turned on them the following spring or summer.

To summarize:—

1. The blood of southern cattle containing the piroplasma produced the disease when injected into a healthy susceptible animal.

2. The animal with piroplasma in its blood, did not convey the disease, in the absence of ticks, to a susceptible animal kept with it.

3. The animal with piroplasma in its blood and covered with ticks conveyed the disease to a susceptible animal kept with it.

4. The ticks hatched and raised in glass vessels in the laboratory, when put on susceptible animals, infected them.

5. Ticks taken from cattle harboring the piroplasma, and put on the skin of susceptible animals, or on their pastures in the warm season, infected the exposed stock.

6. The six-legged larvæ developed in the laboratory from the eggs of mature ticks, taken from cattle having the piroplasma, conveyed the disease.

7. On bare pastures as far south as Washington the winter frosts destroyed the ticks so as to render the pastures safe on the following season.

8. Ticks artificially raised in a warm laboratory, produced the disease when placed on susceptible cattle in a warmed stable (65° to 80° F.) in winter.

9. In the Gulf states, in stables which the cattle occupy constantly or enter twice daily for milking or feeding, the ticks may live through the entire winter. The same has occurred in the warm swill stables in the north.

10. When taken into a new locality, it is rarely the mature ovigerous ticks that bite and infect the native cattle of the place, but the next generation of larvæ, so that time must be allowed for the laying and hatching of ova.

11. Ovipositing usually occupies about a week, while hatching varies with the temperature from two to six weeks.

12. Cases can be adduced in which native cattle followed, on the same pasture, the tick-bearing infecting cattle, and remained for a week or more, and yet escaped, the larvæ being as yet unhatched from the ova. Other native cattle, following these two or three weeks later, perished almost without exception.

13. This delay in the hatching may be indefinitely prolonged, and thus in the southern states, the winter may be tided over, without the loss of vitality in the ova, especially if it is covered by leaves, moss, wood, or decaying vegetable matter.

14. When dealing with lung plague in Chicago in 1888, I noted the facts that every cow that entered a city stable through the stock yards during the dry, hot, midsummer weather died of Texas fever within a month, while those that passed through the same yards during a particular rainy week, all escaped. Berkau has shown that, in the absence of the coating of the glutinous saliva, the eggs do not hatch, and here we may assume that this covering was washed off by the rains and the eggs perished.

15. It has long been noticed that the ticks are scarcely at all dangerous to young calves living on milk. This applies not only to calves born of cows native to infected localities, and therefore possibly having a congenital immunity, but also to the calves of northern and susceptible cows, and which were exposed simultaneously with their dams. It suggests a special defensive power in even the bovine system when sustained on animal food. In the Bureau of Animal Industry experiments, calves of four months, already using vegetable food freely, sickened but still, as a rule, recovered.

16. The Bureau fed three cattle with adult live ticks (2000 to one animal) but no infection resulted.

17. Four cattle were injected intravenously with the liquid charged by crushing ticks in a mortar with distilled water. In some cases the liquid was put through a Pasteur filter, in others only through two thicknesses of filter paper. No infection ensued.

18. Lignieres injected, subcutem, in different animals the pulp of the ticks at all stages of life, ground in a mortar with distilled water, but found in no case tristeza as the result nor any destruction of red globules.

The apparent paradox involved in the last three items probably finds its explanation in the statement of Nicolle and Adil-Bey that, in biting, the tick instils into the wound a venomous saliva which causes local congestion and infiltration and presumably operates on the blood globules as well. Curtice describes the two racemose glands situated under the head shield, the secretions of which are pressed out by the movements of the mouth ring and appendages. How much of this irritant and toxic action is inherent in the saliva, and how much due to the protozoan contained in it, has not been shown. Nicolle, Adil-Bey and, later, Lignieres showed a similar toxic property in the blood. Three to five cc. of blood taken from an acute case at the crisis and injected into the marginal vein of the ear in a rabbit, killed the subject in a few seconds. A similar amount thrown into the peritoneum of a Guinea pig destroyed life in a few minutes. It is probable that the dilution of the venom in the mass of tick pulp and distilled water reduced its toxic quality to such a low ebb that the red globules were comparatively unaffected by it and successfully resisted the attacks of the microbe.

The name _Boöphilus bovis_ was given to the bearer of the Piroplasma by Cooper Curtice who made a special study of the tick, and its development. For the description see _Parasites, Ixodes_. Among the most marked and distinctive features of the female are the extreme shortness and relative breadth of the rostrum, the slender palpi, the eight rows of spines on the lower surface of the labium, the smooth mandibles with terminal hooks, the limbs long, slender, in seven segments, and each furnished with a terminal pad (pulvillus) and one hook (fore limbs) or two hooks (hind). Curtice has identified the ticks of hæmoglobinuria in various other countries with the boöphilus. The _Garrapata_ of Mexico and the West Indies, the Hæmaphysalis rosea of Cuba (Koch), the Ixodes Annulata of Florida (Say), the Ixodes Dugesii of Italy (Nequin), the Ixodes Algeriensis and the Ixodes Egypti he found to be identical. There may be some doubt as to the Rhipicephalus Annulatus Microplus of Buenos Ayres, but as it agrees with the boöphilus in size, in the thickness of its rostrum, in the eight rows of hooks on the lower surface of the labium, in its host and habits, in the fact that it transfers the piroplasma to cattle, and that it prevails on the same continent in what were formerly colonies of Spain it is in all probability the same tick. Curtice holds that it was originally a North African tick, which was carried by the Spaniards to their American colonies. The Rhipicephalus Annulatus of Roumania is probably the same, together with the ticks that convey the Piroplasma in the other countries of Europe. There remain the Hæmaphysalis of South Africa and the “Scrub-tick” of Australia to be identified with, or differentiated from the Boöphilus. The life history of the Queensland “scrub” tick coincides with that of the boöphilus of America (Pound). As Australia derived her cattle from Britain it is improbable that the tick was imported from Europe.

_Lesions._ If the course of the disease has been short, followed by an early death, the carcass may be full and rounded, but if the animal has been sick for five or six days there is marked loss of condition and weight—emaciation. As after any other affection occurring during very hot weather, decomposition sets in early, though not quite so speedily as in anthrax, in which the subject dies full of rich blood. Something, too, depends on the condition at death, putrefaction being manifestly slower in protracted and debilitated cases. The color of the skin, the mucosæ and normally white tissues varies in the same way. As it has been largely seen in our northern States (and Australia) in fat cattle, which contracted the disease in railway cars, cattle markets, or dealers’ or butchers’ parks, etc., the deep orange hue of the white tissues is one of the most marked features, and even the muscles have a deep mahogany yellow hue. In poor milch cows and stock cattle in the South, on the other hand, the icteric hue is often conspicuous by its absence. Cattle killed early for experimental purposes may also show less icterus. The color appears to be influenced largely by the abundance of red globules in the blood when the animal was attacked, by the rapid destruction of these globules, and the saturation of the blood and tissues with hæmoglobin in solution. The presence of ticks on the skin, especially along the ventral aspect, inside of the thighs, on the scrotum, udder or perineum, sufficiently explains the number of minute infiltrations into the derma, the oozing of blood or serum, and the matting of the hairs into little tufts.