PLAGUES AND THE BUREAU OF ANIMAL INDUSTRY

I

n 1880 there was widespread criticism of the U.S. Veterinary Medical Asso-ciation from the pioneers in the field — from Law at Cornell, Huidekoper at Penn, and even from Liautard, director of the New York College of Veterinary Surgeons — that the organization was not effective in bringing about the federal regulations that were needed to control infectious diseases of livestock. At the annual meeting, state veterinarians from Nebraska, Minnesota, and the Dakotas complained. The territorial veterinarian of Wyoming was dismayed at the “apathy displayed by the association at the last annual meeting, as well as the lack of interest of veterinarians, in regard to . . . the necessity of whole-some sanitary laws and their enforcement.”³⁴

It had taken over a decade since agriculturalists in midwestern states proposed a federal agency to deal with the destructive plagues that were destroying the live-stock industry, but in 1881 the U.S. Congress created a new Cattle Commission, placing it in the Department of Treasury. Historically, Treasury’s Patent Office had evolved as the source of governmental information on agriculture; a report

by the commissioner in 1837 noted rapid improvements in agricultural imple-ments and suggested the Patent Office deal with livestock matters. When the Department of Interior was established ten years later, the Patent Office, includ-ing its agricultural work, was transferred there, and in 1861 the commissioner of patents had asked Congress to create a separate department to deal with agri-cultural matters.³⁵ After two years in the Patent Office, the Cattle Commission was moved as the Veterinary Division into to the new U.S. Department of Agri-culture — the USDA.

In early March of 1884 there was hysteria among ranchers in Coffey County, Kansas, when a report was publicized that a foot-and-mouth disease outbreak had occurred. Local cattle were developing ugly ulcerative lesions in the tongue and mouth and around the fetlock, pastern, and hoof areas of the lower leg.

It had been a cold, wet spring followed by a very hot early summer. The cattle had lost weight, had rough hair coats, and preferred to stand in water or in the shade when available on the Kansas plains. The hysteria might have been justified. Any diagnosis of foot-and-mouth disease would surely lead farm-ers to financial ruin with livestock deaths, quarantine of Kansas cattle, loss of export markets, and drop in market prices. Area stockmen and veterinarians from Leaven worth and Emporia traveled by train to Neosho Falls, convening to inspect the disease in Coffey and Woodson Counties. In their report the disease was pronounced to be the contagious foot and mouth disease.

The U.S. Department of Agriculture and the Army Veterinary Service were acti-vated. The USDA commissioner, George Loring, sent emissary M. R. Trumbower from Illinois to investigate but he failed to confirm the diagnosis. Loring then sent Daniel Salmon, who also wasn’t certain that this was foot-and-mouth disease. Salmon asked national leaders to convene in Kansas — state veter-inarians and professors of veterinary science (including Iowan Stalker, Paul Paquin from Missouri, George Faville from Colorado, and James Law all the way from Cornell). Of this large group, only two could rule out foot-and-mouth disease. Millikan Stalker and George Faville recognized the disease imme-diately; it was ergotism. There were no fevers or ulcers of the mouth. Cattle were being poisoned from a fungus growing on wheat and rye grass. Returning home, Salmon would take credit for the discovery, writing that “his team” had solved the problem, noting in the popular press — the Northwestern Live Stock Journal — that “Prof. Stalker of the Iowa University [sic], and Prof. Faville of the

Colorado Agricultural College have seen similar cases . . . and concurred in the opinion.” Trumbower’s official report never mentioned that it was Stalker and Faville who had made the diagnosis.³⁶

The foot-and-mouth disease scare seemed to have spurred politicians into action. Two months later, in a bill signed by President Chester Arthur on May 29, 1884, the Veterinary Division became the Bureau of Animal Industry. Daniel E. Salmon, the first head of the BAI, had been one of the first graduates of the DVM-granting department at Cornell University. Salmon’s assistant director was Theobald Smith, a PhB graduate of Cornell holding the MD degree from the Albany Medical College. Under their guidance, the BAI began dealing scientifically with the serious infectious diseases afflicting livestock. It was facing some serious plagues.

Texas cattle fever persisted as the major plague of cattlemen. BAI director Salmon mapped the flow of disease from south to north. In Nebraska, Frank Billings recorded the peculiar spread of Texas cattle fever in 1887 and published a report that ticks were responsible for perpetuating the disease, writing: “No ticks, no Texas fever.” English veterinarians noted Billings’s conclusions but Americans did not.³⁷ H. J. Detmers and Theobald Smith, following current dogma that arthropods did not cause disease, discredited the idea that ticks were involved in Texas cattle fever.

In 1889 the BAI assigned three scientists to investigate the disease: Theobald Smith; Cooper Curtice, a physician in charge of the BAI’s zoology department;

Veterinary Station, USDA, ca 1883: seven acres on Benning Road, a quarter mile from the northeast boundary of Washington, D.C. Main buildings at far right, background. At this site, director Fred Kilbourne planned the experiments that established ticks as the purveyor of Texas cattle fever. (U.S. Department of Agriculture drawing.)

and veterinarian Fred Kilbourne, head of its Experiment Station at Benning Road just outside the District of Columbia.

Working with blood from infected cattle, Theobald Smith soon discovered the protozoan parasite that destroyed red blood cells; he named it Pyrosoma bigeminum (now Babesia bigemina). It was a protozoan species that invaded, grew inside, and severely damaged the red blood cells which — misshapen and bearing “eat me” signals on their damaged surfaces — were removed by resident scavenger macrophages as they passed through the tortuous vascular passages through spleen and liver. Red blood cell destruction was so severe it led to lethal anemia. But how did this new protozoan parasite survive outside the cow host and how did it move from one cow to another?

Studying field cases, Fred Kilbourne was listening to western stockmen who were calling the disease tick fever, and it was his insistence that convinced Salmon and Smith that ticks were somehow associated with the disease.

Kilbourne planned and carried out the experiments that proved ticks were transmitting and perpetuating the disease in cattle. It was soon shown that a tick — it was named Boophilus annulatus — was the carrier. Kilbourne also discovered that newborn calves growing in an infected herd were resistant as adults because they developed immunity from their mother. The newborn calf would be infected but survive because of antibodies in its mother’s milk and would be solidly immune as an adult. Smith, senior to Kilbourne, took the lion’s share of the credit for the discovery of ticks in the disease.

Then the BAI research team discovered something entirely new — a tickwas not simply a mechanical bearer of the cause but was required as an intermedi-ate host for the perpetuation of the disease in cattle. Curtice worked out the life cycle of the tick and revealed that the protozoan parasite, after being sucked into the tick from an infected cow, not only replicated in the tick but passed its protozoan pathogen to its tick offspring. The next spring, when invading a new uninfected cow, the parasite caused the disease all over again. The study explained why Texas cattle fever occurred only in summer months and how it overwintered in the South.

This new discovery had a remarkable impact on medical science, opening the way for others to follow on insect-borne global diseases such as yellow fever, malaria, and typhus. Yellow fever, first documented in seventeenth-century Latin America, was a mosquito-borne disease of the Atlantic trade routes, caus-ing disastrous outbreaks in the U.S., Brazil, and Spain. In U.S. outbreaks it would kill thousands — in 1793, Philadelphia, still the U.S. capital, lost 10 percent of its

population. Other large metropolitan areas had similar outbreaks — Washington, Baltimore, Memphis, and New Orleans. The disease would travel northward with steamboats. Shreveport, Louisiana, lost a quarter of its population to yellow fever in 1873. After his discovery that female Aedes aegypti spread the virus as an intermediate host, the Army physician Walter Reed made it clear that his studies were predicated on the studies on Texas cattle fever.

“Our knowledge of yellow fever would in all likelihood have been delayed if the work of the Bureau of Animal Industry of the USDA on Texas fever had not been done,” so said Simon Flexner, MD, of the Rockefeller Institute of Medical Research in 1920.³⁸ The discovery of the role of the cattle tick as an intermediate host in the epidemics of Texas cattle fever was one of the most notable medi-cal achievements of the nineteenth century and made possible the methods of sanitary science that allowed the building of the Panama Canal.

Hog cholera research at the BAI was headed by Director Salmon;

investigations were run by Theobald Smith, head of the Pathological Div-ision, and Emil De Schweinitz, head of the Biochemic Division. From Wash-ington, D.C., in 1885, they announced the isolation of the hog cholera bacillus, which Smith named Salmonella cholera-suis in honor of his boss. When in-jected into pigs, the newly discovered bacillus produced hemorrhagic dis-ease and death.³⁹

At the time, two similar bacterial diseases of pigs were sweeping the coun-try: swine erysipelas and hemorrhagic septicemia, which both caused death with hemorrhages and other signs similar to those caused by the hog chol-era bacillus. And all three were confounding investigations into hog cholchol-era.

Adding to the confusion were the experiments on the hog cholera bacillus of Smith, which he published as a BAISpecial Report of the Cause and Prevention of Swine Plague — Smith was actually describing hemorrhagic septicemia.⁴⁰ Salmon finally recognized the dilemma and reported, not admitting any fail-ure, that there were actually two diseases that “are sometimes found to exist at the same time in the same herd.”

Detmers and Billings were at odds with Salmon over etiology; Detmers claimed that his Bacillus suis, reported years earlier, was the same bacterium reported by Salmon but could not prove the claim. From Nebraska, Billings claimed that Salmon had been wrong all along and that his own research had discovered the bacteria that caused swine plague. A native of Massachusetts,

Billings was an exceptional, energetic, and intelligent scientist with great powers of persuasive speech. He had enrolled at the Imperial Veterinary College of Berlin and, although unable to speak German well, graduated in 1878 with honors — the first American graduate of a German veterinary school. Returning to the U.S. to practice for a few years, he again went to Germany to visit Rudolf Virchow’s laboratory and tour German science faculties.

Billings was also an egocentric and snarky fellow, and he sent off a barrage of letters to the editor of the American Veterinary Review disparaging any scien-tist who disagreed with his findings. His prime targets were scienscien-tists of the BAI, especially Salmon, and a battle between the two of them would go on from 1886 to 1892.⁴¹ Perhaps Billings’s ferocity was stoked by Salmon’s rejection in 1886 of Billings’s application to work for the BAI. To defend his position on hog cholera, Billings produced a foolhardy four-hundred-page bulletin — an official publication of the University of Nebraska Experiment Station — de-nouncing the work of the BAI. Read worldwide, it produced contro versy that some approved, especially Detmers.

Billings went at Salmon with a vengeance. In the correspondence section of the American Veterinary Review for May 1887 Billings ridiculed Salmon’s report, and in the editorial section of the following January’s issue Salmon countered that Billings’s writings were the “product of a disordered brain” and that “he has proved nothing that was not previously reported from results of experiments in this Bureau.” Salmon complained to the commissioner of agri-culture, asking him to appoint a board of disinterested scientists to investigate the epidemic disease of swine. The board was appointed and visited Billings in Nebraska, Detmers in Ohio, and the BAI. An equivocal response was issued and the situation was unchanged.⁴²

Billings and Salmon continued the fight at meetings of the U.S. Veterinary Medical Association. Billings continued to be the big bad wolf of the era, and his eloquence seemed to frighten others from doing combat with him. But his reputation was badly mangled in 1887 by a letter to the editor that deni-grated the BAI and claimed that he had discovered a bacterium that caused Texas cattle fever. Salmon’s final retort was, “Unfortunately, the greater part of the bacteriological researches which are published . . . are absolutely value-less, and are a check to progress rather than an aid to it, because some one must disprove the conclusions which follow from them, and, even then, other workers must remain in doubt as to which observer is correct.”⁴³ But Billings’s

criticism had been valuable in wading through the complex of the diseases that were killing pigs.

In 1887 the U.S. Congress passed the Hatch Act, which gave $15,000 per year to each state land grant college to create agricultural experiment stations. Named for William Hatch, the chairman of the House Committee on Agriculture, it had been pushed strongly by Seaman Knapp, president of Iowa Agricultural College, who had written the first draft. One of the provisions of the Hatch Act of 1887 providing funds to establish agricultural experiment stations was that

“it shall be the object and duty of said Experiment Stations to conduct origi-nal researches or verify experiments on the physiology of plants and animals.”

Another provision was that annual reports be submitted to Congress.

As the century closed, eleven of the agricultural experiment stations had veterinarians attached to them. All reported work “in progress.” In those with official veterinary sections, few were involved in research. Most were overloaded with teaching or duties as state veterinarian. Half of the experiment station veterinarians were examining specimens for diagnostic purposes or answering letters of inquiry regarding treatment. Some were manufacturing vaccines for anthrax and blackleg, or producing tuberculin used in the diagnosis of tuber-culosis in cattle. The bulletins they produced only rarely contained “original researches.” Billings’s comment was that it was wasting money on petty sala-ries or equally petty experiments — “a sheer waste of money with no adequate results.”⁴⁴ That was not quite true: Hatch Act money did have an impact on state veterinarians and college diagnostic programs. Some of them were discov-ering new plagues.

In France, a venereal disease of horses named dourine, or maladie du coit, was being eliminated by a law that compelled veterinary officials to permanently brand affected horses with DN. Known as equine syphilis and covering sick-ness, the disease was passed during mating and began with chronic swelling of the genitals and progressed to silver-dollar-sized skin swellings and inflamma-tion of the nerves that led to hindquarter paralysis. There was no cure or vaccine, and condemned horses were to be destroyed. Dourine had not been reported in the United States, but in 1885 an imported Percheron stallion carrying the unmistakable condemnation brand DN had been found by Illinois assistant state veterinarian W. L. Williams to have spread dourine throughout DeWitt County. In 1888, Williams’s extensive report in the American Veterinary Review

led to the development of a test for antibodies in horse sera and a program to destroy affected horses with indemnity paid to owners.⁴⁵ The cause was identi-fied as a protozoan parasite, Trypanosoma equiperdum. It took a half-century, but dourine was eliminated from the U.S. in the 1940s.

Im Dokument AND THE GREAT PLAGUES (Seite 88-95)