Wilesmith and his team learned from herdsmen that several recent changes had been made to livestock diets. The first was a significant increase (from 1 percent to 12 percent) in the amount of meat and bone meal added to dairy cow feed. Calves were also receiving the protein supplement at an earlier age. As in other spongiform encephalopathies, there appeared to be a direct correlation between the amount of contaminated material ingested and the likelihood of contracting BSE. Similarly, the incubation period for BSE was apparently shorter in younger animals. In theory, then, before industry-wide changes in diet were implemented, calves received less of the contaminated supplement and did not start ingesting it until later in their lives. As a consequence, infected animals would have been slaughtered before they had a chance to get sick.
The results of Wilesmith’s epidemiological study were presented to ministry officials in May 1988. He told them that the BSE problem could be traced to the popular nutritional supplement that had been contaminated with sheep scrapie. This material had subsequently been fed to cows, sickening them. In retrospect, Wilesmith’s detective work was remarkably efficient, but ultimately his belief that BSE and scrapie were one in the same disease would place British consumers in peril for over a decade.
Back from New Guinea in 1963, Carleton Gajdusek realized that his fellow researchers had been correct about the striking similarities between kuru-infected brains, brains from victims of Creutzfeldt-Jakob disease, and those from sheep with scrapie. The puzzle was just beginning to come together when yet another piece was discovered—but this one was several decades old.
In 1947, an outbreak of what would become known as transmissible mink encephalopathy (TME) in farm-raised mink led investigators to search for links between the ranches where infected animals had been identified. They discovered that it was a common practice for adjacently located ranches to share animal feed. In these instances, when mink from one ranch came down with TME, invariably so did animals from the adjacent ranch. The feed itself was a vile mess composed of cereal, fish, meatpacking plant by-products like sheep entrails and other internal organs, and flesh from downer cattle. By the time another outbreak of TME occurred in 1963, veterinary researchers suspected that something very strange had happened—the disease had been transmitted across species, in this case from sheep to mink.
By September 1963, similarities in kuru-, scrapie-, and TME-infected brain tissue, coupled with the discovery that TME and scrapie could be transmitted within and between species, led Gajdusek and NIH researcher Joe Gibbs to an important experiment. At the Patuxtent, Maryland, lab they inoculated a trio of chimpanzees with liquefied brain tissue from kuru victims. If the chimps came down with the disease, it would prove once and for all that kuru was not a genetic abnormality or a stress-related psychosis, but an infectious or transmissible agent. As the antsy Gajdusek left the U.S. for another field season in New Guinea, he worried about the long, symptom-free incubation period for scrapie, which sometimes extended up to five years post-exposure. What if his experimental animals didn’t get sick for five years or more?
Gajdusek need not have worried. Less than two years after being inoculated, two of the chimps, Georgette and Daisy, began showing the telltale signs of kuru—at first a drooping lower lip in Georgette, and then changes in behavior as both primates became more lethargic. Eventually the apes began to show even more clear symptoms of the disease: occasional unsteadiness and trembling followed by a gradual loss of balance.
When informed of these developments, Gajdusek was excited but cautious, worrying that the chimps might have been accidentally contaminated with scrapie. His coworkers assured him that there had been no contamination. As the researcher alternated between elation and skepticism, back in Maryland the physical deterioration of the chimps continued at a frightening pace. Only four months after the first symptoms appeared, Georgette and Daisy were almost completely paralyzed. With Gajdusek carrying out field work in one of the most isolated regions in the world, his coworkers called in a neuropathologist from London to assist with the post-mortem analysis.
On October 28, 1965, Georgette was anesthetized and sacrificed by the heartbroken researchers. Her entire body was deconstructed, fixed, and preserved, and her brain was sectioned for microscopic analysis. The results were 100 percent conclusive. Slides of Georgette’s cerebellum were indistinguishable from those of human kuru victims.
Carleton Gajdusek and his colleagues had discovered a brand new disease.