Cannibalism: A Perfectly Natural History(73)
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.
Meanwhile, Michael Alpers, who had been studying kuru since 1961 and who had taken time out from his own field work to collaborate with Gajdusek and Gibbs on the NIH primate study, waded through six years of Gajdusek’s epidemiological data on the Fore. After examining hundreds of Fore genealogies, he and Gibbs came up with a remarkable observation: Instances of kuru were beginning to decline in children, starting with the youngest age group. The question immediately became, “Why?” Shortly after conferring with Robert Glasse and his wife, Shirley Lindenbaum, Alpers came up with a hypothesis.
According to information gathered from interviews with the Fore, kuru victims were favored at mortuary feasts because the physical inactivity that characterized the latter stages of the disease left the stricken individuals with a tasty layer of subcutaneous fat. Starting in the 1950s, though, government authorities in New Guinea began cracking down on the practice of ritual cannibalism, and with mortuary feasts now forbidden by law, fewer people were eating infected tissue. As a result, incidents of the disease were decreasing. Additionally, since kuru had a shorter incubation period in children than it did in adults, the reduced occurrence of ritual cannibalism translated swiftly into a decreased incidence of kuru in the youngest sector of the population.
In a February 1966 article in Nature, Gajdusek, Gibbs, and Alpers described the experimental transmission of a “kuru-like syndrome” to their chimpanzees although the identity of the disease-causing agent was still unknown. Gajdusek, who still believed that they were dealing with a slow virus, was also reluctant to attribute the transmission of kuru to the consumption of infected flesh. Instead, he supported the view that during the process of handling and cutting up the dead, the kuru-causing agent was transmitted via cuts or across the thin mucous membranes that line the human mouth, eyes, and nose (a form of exposure known as inoculation).
By 1973, however, Gajdusek had come around to the idea that inoculation and consumption were both viable routes for kuru transmission.
The mechanism of spread of kuru is undoubtedly contamination of the population during their ritual cannibalistic consumption of their dead relatives as a rite of respect and mourning. They did the autopsies bare-handed and did not wash thereafter; they wiped their hands on their bodies and in their hair, picked sores, scratched insect bites, wiped their infants’ eyes, and cleaned their noses, and they ate with their hands.