TEXAS FEVER. Readers of the Veterinarian, an English journal, were informed in June 1868 that a "very subtle and terribly fatal disease" had broken out among cattle in Illinois. The disease killed quickly and was reported to be "fatal in every instance." The disease was very nearly as fatal as the Veterinarian claimed. Midwestern farmers soon realized that it was associated with longhorn cattle driven north by South Texas ranchers. The Texas cattle appeared healthy, but midwestern cattle, including Panhandle animals, allowed to mix with them or to use a pasture recently vacated by the longhorns, became ill and very often died. Farmers called the disease Texas fever or Texas cattle fever because of its connection with Texas cattle. Other names included Spanish fever and splenic or splenetic fever, from its characteristic lesions of the spleen. The disease is also known as hemoglobinuric fever and red-water fever, and formerly as dry murrain and bloody murrain. To protect their cattle, states along the cattle trails passed quarantine laws routing cattle away from settled areas or restricting the passage of herds to the winter months, when there was less danger from Texas fever. In 1885 Kansas entirely outlawed the driving of Texas cattle across its borders. Kansas, with its central location and rail links with other, more northern markets, was crucial to the Texas cattle-trailingqv business. The closing of Kansas, together with restrictive legislation passed by many other states, was an important factor in ending the Texas cattle-trailing industry that had flourished for twenty years. (see SHAWNEE TRAIL.)
Though Texas fever was clearly associated with Texas cattle, its cause remained for many years a mystery. Various theories were proposed to account for a fatal disease being transmitted by apparently healthy animals. One held that the longhorns ate poisonous plants that did not hurt them but that made their wastes so toxic that the smallest amount accidentally ingested by a nonimmune midwestern cow could cause illness and death. By the 1880s the work of pioneer bacteriologists Robert Koch of Germany and Louis Pasteur of France, among others, was widely known and accepted. These men had identified several specific disease-causing bacteria, and Pasteur had devised vaccinations to prevent chicken cholera and anthrax. Hoping for similar success, scientists studying Texas fever also were looking for a microorganism. In 1893 Theobald Smith and Fred Lucius Kilborne of the federal Bureau of Animal Industry in Washington, D.C., announced their isolation of the pathogen of Texas fever. They demonstrated that the disease is caused by a microscopic protozoan that inhabits and destroys red blood cells. Smith and Kilborne named the protozoan Pyrosoma bigeminum. It is now recognized that either of two species of the renamed genus Babesia, called Babesia bigemina and Babesia bovis, may be involved in Texas fever. From this is derived the modern name babesiosis, which is applied both to Texas fever and to infections caused throughout the world by these pathogens and other members of the same genus. Besides identifying the microorganism responsible for babesiosis, Smith and Kilborne discovered that the disease was spread by cattle ticks. After sucking blood from an infected animal, a tick would drop off into the grass and lay eggs from which would hatch young ticks already harboring the protozoan. Weeks after the original tick dropped from its longhorn host, its progeny were still capable of infecting other cattle. Several different species of tick are now known to spread babesiosis.
Identification of the pathogen and vector of babesiosis still did not explain the apparent good health of the Texas cattle that carried the disease. Modern research indicates that calves are born with a natural partial resistance to infection that lasts a month or two after birth and goes away gradually. In areas like nineteenth-century Texas (and other southern states), where the disease was widespread, the calf suffers a mild attack at an early age, then develops enough immunity to keep from being overwhelmed but not enough to rid itself of the pathogen. By the time the animal reaches adulthood, it has a shaky balance with its protozoan parasites that allows it to live in reasonably good health while remaining a carrier. Babesiosis is still a serious threat to livestock in many parts of the world. In the United States it has been eliminated by a vigorous program of cattle dipping, which eradicated the tick vector. King Ranch manager Robert J. Klebergqv is credited with building the first dipping vat in the state. Before the disease was eradicated in this country, nonimmune American cattle were protected from it by elaborate federal quarantine laws separating southern cattle from others in railway cars and stockyards. Northern cattle imported to the South for breeding purposes could be immunized by receiving injections of small amounts of blood from infected animals. Mark Francis of Texas A&M was a pioneer in the development of this method of immunization.
J. Evetts Haley, "Texas Fever and the Winchester Quarantine," Panhandle-Plains Historical Review 8 (1935). Miodrag Ristic and Julius P. Kreier, Babesiosis (New York: Academic, 1981). Jimmy M. Skaggs, The Cattle-Trailing Industry: Between Supply and Demand, 1866–1890 (Lawrence: University Press of Kansas, 1973).
The following, adapted from the Chicago Manual of Style, 15th edition, is the preferred citation for this article.Tamara Miner Haygood, "TEXAS FEVER," Handbook of Texas Online (http://www.tshaonline.org/handbook/online/articles/awt01), accessed May 24, 2013. Published by the Texas State Historical Association.