Part 83

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.