advanced search

<< Back To Home

WHAT'S NEW THIS THURSDAY: ANTICIPATING THE NEXT PANDEMIC

Wednesday, 3rd of October 2012

• ANTICIPATING THE NEXT PANDEMIC

By DAVID QUAMMEN

New York Times, September 22, 2012

BAD news is always interesting, especially when it starts small and threatens to grow large, like the little cloud on the distant horizon, no bigger than “a man’s hand,” that is destined to rise as a thunderhead (1 Kings 18:44). That’s why we read so avidly about the recent outbreaks of Ebola virus disease among villages in Uganda and the Democratic Republic of Congo, and about West Nile fever in the area around Dallas (where 15 have died of it since July). And that’s why, early this month, heads turned toward Yosemite National Park after the announcement of a third death from hantavirus pulmonary syndrome among recent visitors there.

Humans die in large numbers every day, every hour, from heart failure and automobile crashes and the dreary effects of poverty; but strange new infectious diseases, even when the death tolls are low, call up a more urgent sort of attention. Why?

There’s a tangle of reasons, no doubt, but one is obvious: whenever an outbreak occurs, we all ask ourselves whether it might herald the Next Big One.

What I mean by the Next Big One is a pandemic of some newly emerging or re-emerging infectious disease, a global health catastrophe in which millions die. The influenza epidemic of 1918-19 was a big one, killing about 50 million people worldwide. The Hong Kong flu of 1968-69 was biggish, causing at least a million deaths. AIDS has killed some 30 million and counting. Scientists who study this subject — virologists, molecular geneticists, epidemiologists, disease ecologists — stress its complexity but tend to agree on a few points.

Yes, there probably will be a Next Big One, they say. It will most likely be caused by a virus, not by a bacterium or some other kind of bug. More specifically, we should expect an RNA virus (specifically, one that bears its genome as a single molecular strand), as distinct from a DNA virus (carrying its info on the reliable double helix, less prone to mutation, therefore less variable and adaptable). Finally, this RNA virus will almost certainly be zoonotic — a pathogen that emerges from some nonhuman animal to infect, and spread among, human beings.

The influenzas are zoonoses. They emerge from wild aquatic birds, sometimes with a pig as an intermediary host on the way to humanity. AIDS is a zoonosis; the pandemic strain of H.I.V. emerged about a century ago from a single Cameroonian chimpanzee. Ebola is a zoonosis. The Ebola viruses (there are five known species) abide inconspicuously in some as yet unidentified creature or creatures native to Central African forests, spilling over occasionally to kill gorillas and chimps and people. SARS is a zoonosis that emerged from a Chinese bat, fanned out of Hong Kong to the wider world, threatened to be the Next Big One, and then was stopped — barely — by fast and excellent medical science.

And the hantaviruses, of which there are many known species (Andes virus, Black Creek Canal virus, Muleshoe virus, Seoul virus, Puumala virus and dozens more), come out of rodents. The species of hantavirus at large in Yosemite is called Sin Nombre — “nameless” — virus, and is the same one that erupted famously, and lethally, at the Four Corners in 1993. Its primary host is the deer mouse, one of the most widely distributed and abundant vertebrates in North America. The virus makes its way from dried mouse urine or feces into airborne dust, and from airborne dust into human lungs. If that happens to you, you’re in trouble. There’s no treatment, and the fatality rate for hantavirus pulmonary syndrome, the infection in severe form, runs at about 40 percent.

You don’t have to go to Yosemite and sleep in a dusty cabin to put yourself close to a hantavirus. Although one expert, recently quoted by Scientific American, called it a “very rare” kind of virus, that view doesn’t square with the studies I’ve read or the testimony of hantavirus researchers I’ve interviewed. The virus seems to be relatively common, at least among deer mice. A 2008 study done at Tuolumne Meadows in Yosemite found that 24 percent of local deer mice had the antibody for the virus, signaling a past or current infection. One mouse in four is worryingly high. Among these mouse populations nationwide, the prevalence of the antibody seems to vary from as low as zero to as high as 49 percent, or one in two mice.

The question this raises is: Why aren’t more people dying from Sin Nombre virus? The answer seems to be that, although very dangerous when caught, it’s not easy to catch, despite its presence in mouse-infested sheds and trailers and garages and barns across much of America. This is because it doesn’t pass from person to person — only from mouse to mouse, and from mouse excretions to one unlucky person or another, each of whom represents a dead-end host. (The “dead” of that “dead-end” may be figurative or literal.) It’s not a “very rare” virus; it’s a common virus known only rarely to infect humans, and with no ramifying chains of human contagion. So the Next Big One is not likely to be Sin Nombre.

Nor is it likely to be Ebola, which is transmissible from human to human through direct contact with bodily fluids, but can be stopped by preventing such contact. Furthermore, Ebola burns so hotly in its victims, incapacitating and killing so quickly, that it is poorly adapted to achieve global dispersal. Only one human has ever been known to leave Africa with a rampant Ebola virus infection — and that was a Swiss woman, evacuated in 1994 to a hospital in Basel. If you want to be grateful for something today, be grateful for that: Ebola doesn’t fly.

WE should recognize such blessings, and try to focus our deepest concerns on real global dangers. Too often, we’re distracted from good scientific information by yellow journalism and the frisson of melodrama. Ebola is charismatic, the demon that people love to fear. Other lurid candidates, like hantavirus and SARS, also get their share of headlines. When you mention emerging diseases, people’s responses tend to fall at the two ends of a spectrum. Some folks are mesmerized by the dark possibilities and the garish but unrepresentative cases. Others are dismissive, rolling their eyes at the prospect of having to contemplate still another category of dire monition. They want you to cut to the chase. “Are we all gonna die?” they ask. Or they say: “Fine, so what can we do about these bugs?”

Yes, we are all going to die, though most of us not from a strange disease newly emerged from a mouse or a chimp. And there are things we can do: get a flu vaccination; support calls for research; avoid coughing people on airplanes; apply mosquito repellent; wear a mask when you sweep out your old shed; don’t eat any chimpanzee meat from an animal found dead in the forest. But the concrete measures are limited by time, place and circumstance. The broader response is more basic: learn, absorb, understand. Don’t start trying to apply your knowledge until you have some.

Among the other unsettling disease news this summer, you’ve probably seen mention of influenza, that old familiar zoonosis, quite capable of devastation and melodrama all its own. Yes, there’s a new flu bug, a nasty variant of the H1N2 strain, suspected now to be traveling through pigs at state fairs. The influenzas are protean and explosive. Keep your eyes on that one.

Hantavirus in Yosemite is a little cloud that seems likely to stay little. This doesn’t mean that the great dark thunderhead isn’t coming. It just speaks to the need for a bit of informed judgment about which sector of the horizon we should watch.

David Quammen is the author of the forthcoming book “Spillover: Animal Infections and the Next Human Pandemic.”

A version of this op-ed appeared in print on September 23, 2012, on page SR5 of the New York edition with the headline: Anticipating The Next Pandemic.