Spillover: Animal Infections and the Next Human Pandemic

by David Quammen

Bangladesh is at special risk from infectious disease outbreaks for several reasons, most obvious of which is the density of its population.

two risk factors worth mentioning. Some of the victims had lived with or cared for other victims, suggesting the possibility of person-to-person transmission, which was new. And more than a few of them had had contact with a sick cow.

trees? That was puzzling. Although the Montgomery group documented a strong correlation, their results didn’t explain why tree climbing might expose young Bangladeshis to Nipah infection. They could only make a calculated guess: It put the boys closer to bats.

none of those questions—not even the one about tree climbing, this time—yielded any statistically significant distinction between those who had gotten sick and those who hadn’t. Only one question asked by the Luby team did: Have you drunk any raw date-palm sap recently?

Nipah is important because of what might happen and because we understand little about how it might happen.

He gets God’s grace and the customer gets Nipah.

How have changes to Bangladesh’s landscape, and the density of people upon it, affected the fruit bats, the virus they carry, and the likelihood of spillover?

two distinct but interconnected dimensions of zoonotic transfer: ecology and evolution.

Habitat disturbance, bushmeat hunting, the exposure of humans to unfamiliar viruses that lurk in animal hosts—that’s ecology.

Rates of replication and mutation of an RNA virus, differential success for different strains of the virus, adaptation of the virus to a new host—that’s evolution.

“Tony, what do you know about bats?” Schountz thought Charlie meant Louisville Sluggers. “They’re made of ash.” “Hello, Tony? I’m talkin’ about bats.” Wing-flapping gesture. As distinct from: DiMaggio gesture. “Oh. Uh, nothing.”

“Tony said, ‘Are you crazy? We don’t know anything!’ ” “Well, she doesn’t know anything, you don’t know anything, and I don’t know anything. This is great. We don’t have any biases.” “Biases?” said Schountz. “We don’t have any information!” “I said, ‘Tony, that shouldn’t hold us back.’ ” Thus the workings of science.

The paper made a handful of salient points, the first of which put the rest in perspective: Bats come in many, many forms.

One in every four species of mammal is a bat.

their viral burden is proportional to their share of all mammal diversity, and thus just seems surprisingly large.

bats are very abundant and very social.

R0 increases with the lifespan of a persistently infected bat. And a bigger R0, as you know, is always good for the pathogen.

What it means is: Hello, people? We’ve gotta grow these bugs the old-fashioned way, we’ve gotta look at them in the flesh, if we’re gonna understand how they operate. And if we don’t, the paper added, “we are simply waiting for the next disastrous zoonotic virus outbreak to occur.”

Later, because of the cut, Amman would get a postexposure shot against rabies, though Marburg was a more immediate concern. “Yeah,” he thought, “this could be a really good place for transmission.”

Wait a minute, lemme get this straight: You’re in a cave in Uganda, surrounded by Marburg and rabies and black forest cobras, wading through a slurry of dead bats, getting hit in the face by live ones like Tippi Hedren in The Birds, and the walls are alive with thirsty ticks, and you can hardly breathe, and you can hardly see, and . . . you’ve got time to be claustrophobic?

Those data, plus the fragmentary RNA, constituted strong evidence that the Egyptian fruit bat is a reservoir—if not the reservoir—of Marburg virus.

Putting those numbers together with the overall population estimate of a hundred thousand bats at Kitaka, the team could say that about five thousand Marburg-infected bats flew out of the cave every night.

“When again are we going to see pythons and bats in a cave?” she said to me, then caught herself, adding with caustic hindsight: “I can assure you, never.”

What have you been doing for the past four days? Most people seek help before multiple organ failure sets in. I’ve been sucking it up, Barnes answered.

a knowing friend—a journalist she and Rick had met during the Uganda trip—who had just seen a news article about which he thought Michelle should know. In the Netherlands, a woman had died of Marburg after a Uganda vacation during which she had visited a cave full of bats.

The new results went to Fujita, who called Barnes with some left-handed congratulations: “You’re now an honorary infectious disease doctor. You’ve self-diagnosed, and the Marburg test came back positive.”

It wasn’t a vertebra. It was a string of aluminum beads with a number attached. More specifically, it was one of the beaded collars that he and Towner had placed on captured bats at Kitaka Cave, the other Marburg cave, three months earlier and thirty miles away.

Amman’s insane jubilance was in fact just the sane, giddy thrill that a scientist feels when two small bits of hard-won data click together and yield an epiphany.

Marburg is only one instance to which that question applies. Why not more Hendra? Why not more Nipah? Why not more Ebola? Why not more SARS? If bats are so abundant and diverse and mobile, and zoonotic viruses so common within them, why don’t those viruses spill into humans and take hold more frequently? Is there some mystical umbrella that protects us? Or is it fool’s luck?

A virus has geographical distribution. A virus can go extinct. The abundance, survival, and range of a virus all depend upon other organisms and what those do. That’s viral ecology.

An interesting thing about Hendra, Plowright told me, is that it’s one of four new viruses that emerged around the same time from this single group of bats, the pteropids.

“For four viruses to emerge from one host genus within a short period of time is unprecedented,” she said. “So we feel there’s been some change in the ecology of Pteropus species that could precipitate disease emergence.”

If the population is isolated and insufficiently large, then the virus will move through it, infecting the susceptibles and leaving them recovered (and immune to reinfection), until there are virtually no susceptibles left.

metapopulation: a population of populations.

“The east coast of Australia used to be one big contiguous forest,” she told me, “and so you had bat populations pretty evenly dispersed along the coastline.”

There was a continual mixing and a continual reinfection of the smallish groups. This seems to have been the situation—for the little red flying fox, for the other flying foxes, and for Hendra virus—from time immemorial. Then things changed.

They gather now in larger aggregations, traveling shorter distances to feed, living at closer proximity to humans (and to the horses that humans keep).

So those large aggregations—comprising bats that are more sedentary, more urban, less needful of flying long distances in search of wild food—tend to reinfect one another less frequently? And in the interim they accumulate more susceptible individuals? So when the virus does arrive, the spread of new infections is more sudden and intense? The virus is more prevalent and abundant? “Exactly. That’s it,” she said.

Science proceeds by observation and supposition and testing.

virus isolation is still the gold standard for identifying a reservoir.

If the circumstances required for human-to-human transmission hadn’t been met, what were those circumstances?

Human-to-human transmission is the crux. That capacity is what separates a bizarre, awful, localized, intermittent, and mysterious disease (such as Ebola) from a global pandemic.

Which is why it is so important that human to human transmission was not confirmed earlier with SARS-CoV-2

In some zoonotic pathogens, efficient transmissibility among humans seems to be inherent from the start, a sort of accidental preadaptedness for spreading through the human population, despite a long history of residence within some other host. SARS-CoV had it, from the earliest days 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.

Some swabs, both from the wall and the bed frame, tested positive for Nipah RNA. I’ll repeat that: Fragments (at least) of Nipah virus, left from what the patient had spewed out, were still present after five weeks, invisibly decorating the room. To the sanitarian, such spewing represents contamination. To the virus: opportunity.

The Cholera Hospital was founded in 1962, as a clinical adjunct to an earlier Cholera Research Laboratory, both of which were eventually bundled into the ICDDR,B.

Specifically, it was thymus-dependent lymphocytes (T cells, for short) that were “profoundly depressed” in number.

The team of doctors who published these observations saw a “syndrome” that seemed “strikingly similar to the syndrome of immunodeficiency described recently among American homosexuals.”

Gaëtan Dugas, the young Canadian flight attendant who became notorious as “Patient Zero.” You’ve heard of him, probably, if you’ve heard much of anything about the dawning of AIDS. Dugas has been written about as the man who “carried the virus out of Africa and introduced it into the Western gay community.” He wasn’t.

Dugas himself reckoned that in the decade since becoming actively gay he had had at least twenty-five hundred sexual partners.

holy shit

he would have sex with a new acquaintance at the Eighth-and-Howard bathhouse in San Francisco, then turn up the lights—so Randy Shilts claimed—display his lesions, and say: “I’ve got gay cancer. I’m going to die and so are you.”