Anatomy of an Epidemic (cont.)
In 1996 epidemiologist Don Burke’s research on emerging infectious diseases took him to Cameroon. When a vehicle he was in on that trip struck and killed a wild animal, Burke’s traveling companions threw the carcass in back so they could cook it up for dinner later.
When scientists identified a possible animal reservoir for the coronavirus behind SARS—a cat-sized creature called a civet—Burke searched for his old photos from Cameroon.
“The one and only road-kill meal of my career—and it was a civet,” he says. “It’s pretty good, actually—a little musky, but good.”
Burke’s civet dinner isn’t just an entertaining anecdote. The director of the Department of International Health’s Disease Prevention and Control Program uses it as a starting point in discussing the zoonotic diseases that move from animal reservoirs into human populations. SARS, of course, is just one example of the breed; others include AIDS, Ebola, mad cow disease, and numerous strains of influenza.
In some ways, SARS revealed the revolutionary progress of modern laboratory science. In a matter of a few weeks, researchers identified the mysterious new agent as a coronavirus, pinpointed its likely reservoir in the animal population, and decoded its genomic structure. Vaccine tests were under way in April—for an agent that no one knew existed in January.
And yet SARS simultaneously revealed gaping holes in our scientific knowledge. Virtually no one anticipated that a coronavirus, which previously had caused only minor human maladies, could wreak such havoc. One exception is Burke, who predicted such an outbreak in a 1997 lecture (see sidebar). Today, Burke is a strong advocate for expanding public health research on infectious diseases into animal populations. His own research focuses on the diseases of non-human primates in Africa.
“We know precious little about the reservoir of viruses that are in nature right now that could infect humans,” says Burke, MD. “We ought to do better at looking where the dangers could be. I want to go one step beyond surveillance. I think public health should be trying to understand the systems in which these things arise.”
Coronaviruses easily swap genes and mutate into new viruses. (Photo: Photo Researchers)
To many laypersons, the onset of a disease like SARS sounds like a simple matter—somebody caught a bug from an animal and passed it on. But in nature, such transmissions are anything but simple. After all, humans have been butchering and consuming civets for centuries, but no one contracted SARS before, at least as far as we know at the moment.
“This cross-species boundary has been there forever,” Burke says. “There’s nothing magic about this year.” One possible explanation, he explains, is that the virus arose because of a complex, one-of-a-kind chain of recombination or mutation events. “That’s the reason influenza epidemics emerge,” he says. “Flu goes hot when the virus reservoir in the animal population mixes with the viruses that are in humans. The new viruses that emerge from those combinations have mostly human virus and a little bit of animal virus.”
No one knows whether coronaviruses work the same way, but if they do, then SARS might be eradicable in the short term. Burke has been a leading voice in urging the international public health community to heighten its vigilance as SARS wanes, in an effort to catch and break the chain of transmission for every last case in the world.
If SARS, like most respiratory diseases, is a cold weather infection, then the warmer months offer a chance to beat it for good. Burke concedes that this may be a long-shot strategy, but the potential payoff is enormous. “If we can eradicate the agent that’s being transmitted now, that may be it,” Burke says. “If this was a chance recombination event, that means that just because there’s an animal reservoir doesn’t mean SARS is coming back any time soon.”