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.

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