Spillover - By David Quammen Page 0,158

of its 2002–2003 emergence in Guangdong and Hong Kong. SARS-CoV has it, no matter where or why SARS-CoV may be hiding since then. Hendra virus does not have it. Hendra achieves fluent transmission among horses but not among humans. Of course, a pathogen may also acquire that capacity by mutation and adaptation within human hosts. Have you noticed the persistent, low-level buzz about avian influenza, the strain known as H5N1, among disease experts over the past fifteen years? That’s because avian flu worries them deeply, though it hasn’t caused many human fatalities. Swine flu comes and goes periodically in the human population (as it came and went during 2009), sometimes causing a bad pandemic and sometimes (as in 2009) not so bad as expected; but avian flu resides in a different category of menacing possibility. It worries the flu scientists because they know that H5N1 influenza is (1) extremely virulent in people, with a high lethality though a relatively low number of cases, and yet (2) poorly transmissible, so far, from human to human. It’ll kill you if you catch it, very likely, but you’re unlikely to catch it except by butchering an infected chicken. Most of us don’t butcher our own chickens, and health officials all over the world have been working hard to assure that the chickens we handle—dead, disarticulated, wrapped in plastic or otherwise—have not been infected. But if H5N1 mutates or reassembles itself in just the right way, if it adapts for human-to-human transmission, then H5N1 could become the biggest and fastest killer disease since 1918.

How does a pathogen acquire such an adaptation? The process of genetic variation (by mutation or other means) is random. A game of craps. But an abundance of opportunity helps to increase a virus’s likelihood of rolling its point—that is, chancing into a highly adaptive change. The more rolls before sevening out, the more opportunities to win. And there’s Jon Epstein’s word again: opportunity.

Back in Dhaka after my nights of bat catching with Epstein, I returned to the ICDDR,B for some further conversations, because I wanted to learn more about the capacity for human-to-human transmission in Nipah. I spoke with a handful of people from Steve Luby’s program on infectious diseases. One was an American epidemiologist named Emily Gurley, who had spent several years of her youth as a diplomat’s kid in Bangladesh and then returned as an adult to work in public health. Gurley is in her middle thirties, with curly brown hair, pale freckles, and blue eyes that widen when she discusses important details of disease sleuthing. She had helped investigate the outbreak in Faridpur District in 2004, the one with thirty-six identified case patients, of whom twenty-seven died. The most notable aspect of the Faridpur episode was that many of those people had evidently been infected by contact with a single person, a superspreader, who sat like a spider at the center of a web of transmissions.

This man was a religious leader, the venerated head of an unorthodox Islamic sect, an informal group that seems to have been nameless, with a small number of fervent followers in a village called Guholaxmipur and roundabouts. Unlike orthodox Muslims, the sect members declined to pray five times a day or to fast during Ramadan, and they sometimes sat up all night, men and women together, praying, smoking cigarettes (or stronger weed), and singing. Their ecstatic practices offended the conventionally pious believers around them, and so when the leader died of a brief, mysterious illness, and then his family and followers started dying too, neighbors attributed the deaths to asmani bala: a curse from above.

Okay, that was one possible explanation. Epidemiology would offer another.

The religious leader had already died and been buried, his grave made a shrine, the outbreak underway, by the time Gurley’s group arrived. She and some colleagues drove out from Dhaka, in early April, in response to an urgent if belated call from the Faridpur civil surgeon, who alerted them that people were dying and the cause seemed to be Nipah. (The surgeon would have been at least roughly aware of what Nipah looked like from the outbreak in that neighboring district, Rajbari, just four months earlier.) As their car reached Guholaxmipur, Gurley told me, “it was very dramatic. We were met by a funeral procession coming out of the village, body wrapped in a white shroud. Which didn’t bode well.” People began carrying comatose relatives out of their homes, imploring the visitors for help. “There were a lot

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