by Sonia Shah
For now, monkeypox is still tethered to the rodents—probably rope squirrels, Rimoin says, but it’s unclear—that carry it. It’s only occasionally able to spread directly from human to human. According to Rimoin’s colleague, the ecologist James Lloyd-Smith, monkeypox’s basic reproductive number in humans is somewhere between 0.57 and 0.96, just shy of the 1 required to graduate from a zoonotic to a human pathogen. The Central African populations it infects, after all, are relatively remote and spread out. There aren’t that many people around for monkeypox to jump into.40
Fortunately, even if monkeypox does complete the journey from animal microbe to human pathogen, it’s unlikely that it would have the impact that smallpox did. The vaccines and drugs developed to fight smallpox would likely also help contain human-adapted monkeypox outbreaks. But monkeypox, Rimoin says, is the devil we know. Being similar to smallpox, and manifesting itself in a distinctive disease that’s hard not to notice, monkeypox is a spillover microbe that’s relatively easy to track. Microbes that cause less immediately noticeable symptoms could easily travel the same spillover pathways, undetected. Some probably already have.
* * *
The emergence of the SARS virus is similarly the result of an abrupt expansion, in this case in the size of wet markets and the diversity of the strange panoply of animals they sell.
The SARS virus was not new. Nor were the practices that brought bats into proximity with people in southern China. The SARS virus “was probably there in bats for centuries,” says the University of Hong Kong virologist Malik Peiris, whose team first isolated the virus.41 And the yewei cuisine and wet markets that brought bats together with people in southern China were long-standing, too.
Yewei cuisine is part of a range of traditional cultural practices in China that draw wild animals closer so that people can tap into the animals’ power, strength, and longevity. People keep wild animals as pets (or, for the aspirational, dye their domesticated dogs’ fur to look like tigers and pandas) and mimic their postures in practices such as kung fu. Traditional medicine practitioners administer their body parts as remedies: tiger whiskers for toothaches, bear bile for liver disease, bat skeletons for kidney stones.42 For people who consider wild animals precious natural resources—the rarer, wilder, and more exotic the more precious—consuming them is bu, restorative and stimulating for the body, endowing the consumer with a whiff of the animal’s natural energy.43
But for many years, economic and geographic barriers limited the consumption of yewei cuisine in China, and with it the size of wet markets. China had troubled political relations with neighboring countries such as Thailand and Laos and Vietnam, where many of the most desirable exotic animals roamed, so their supply for consumption was thin and prices high. While the elites could afford to dine on braised bear paw with carp tongue, gorilla lips and pig brain in wine sauce, and leopard placenta steamed with camel hump and garnished with pear, ordinary folk made do with more ordinary fare, or hunted for their own wild game.44
Then, in the early 1990s, the Chinese economy started growing by 10 percent or more every year. Suddenly, a new class of young, aspiring, prosperous Chinese in booming cities had more money than they knew what to do with. Along with stocking up on Western luxury goods—Louis Vuitton sold more bags in China than anywhere else in 2011—they started demanding more yewei cuisine. New restaurants serving peacock, swan geese, and sea cucumber, along with other exotic creatures, sprang up across the region.45 China reestablished trade with many of its Southeast Asian neighbors, allowing poachers and traders to plunge ever deeper into the countryside to meet the rising demand. They crammed their stocks of wild animals into ever larger wet markets, stacking cages of live animals from increasingly disparate locales across Asia next to each other, awaiting sale to yewei-hungry shoppers.46
It was only then, after the size and scale of wet markets grew, that a serendipitous sequence of events that could turn a virus of horseshoe bats into a human pathogen became probable.
The growing size of pig farms in Malaysia had similarly allowed a bat virus called Nipah to spill over into people. As pig farms in Malaysia have grown, they’ve increasingly abutted the forests where bats roost. This allows bats and pigs to come into novel, intimate contact. The pigs’ troughs are situated near the fruit trees where bats roost. When bat excreta drop into those troughs, the pigs are exposed to bat microbes. At one particularly large pig farm, Nipah virus sickened so many pigs that it was able to spill over into the local farmers, killing 40 percent of those infected. Nipah virus also struck in South Asia and now erupts in Bangladesh nearly every year, killing 70 percent of the afflicted.47
These spillovers are happening not only in distant societies and in impoverished, tropical locales. They’re also happening in cities at the center of the global economy such as New York and in the prosperous suburbs of the northeastern United States.
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West Nile virus is a flavivirus of migratory birds named after the district in Uganda where it was first isolated in 1937. Migratory birds have probably been introducing the virus into the United States for decades, especially into New York City, which lies on the Atlantic flyway, one of the four primary migratory routes in North America. The virus can spill over from birds’ bodies into ours when mosquitoes bite infected birds and then bite people.
But despite the repeated introduction of the virus and the enduring phenomenon of mosquito biting, West Nile virus did not break out in the United States until 1999, more than fifty years after it was identified.
That’s because the diversity of the local bird population limited our exposure to it. Different bird species vary in their vulnerability to the virus. Robins and crows are especially susceptible. Woodpeckers and rails are not. Their feathery bodies act like a barrier. So long as the local bird population was diverse, including plenty of virus-repelling woodpeckers and rails, there wasn’t much virus around. The chances that the virus would spill over from birds into humans were slim.
But avian biodiversity, like the biodiversity of other species, has plummeted, in the United States as elsewhere. Urban sprawl, industrial agriculture, and climate change, among other disruptions caused by human activity, steadily destroy bird habitats, reducing the number of species among us. But habitat destruction doesn’t affect all species equally. Some species—the so-called specialist species—get hit especially hard. They’re the ones, like monarch butterflies, salamanders, and woodpeckers and rails, that rely on exacting conditions and can’t easily survive when those conditions change. When trees are felled and nesting grounds paved over, they’re the ones that tend to disappear first. That means there’s more food and territory around for the “generalist” species like robins and crows—the opportunistic, sharp-elbowed types that can live anywhere and eat anything. Their numbers skyrocket in the vacuum.
As avian diversity declined in the United States, specialist species like woodpeckers and rails disappeared, while generalist species like American robins and crows boomed. (Populations of American robins have grown by 50 to 100 percent over the past twenty-five years.)48 This reordering of the composition of the local bird population steadily increased the chances that the virus would reach a high enough concentration to spill over into humans. At some point, a threshold was crossed. In the summer of 1999, West Nile infected over 2 percent of the population of Queens, more than eight thousand people, in New York City.49 Once it took hold, it spread inexorably. Within five years, the virus had emerged in all forty-eight contiguous states. By 2010, an estimated 1.8 million people in North America had been infected from New York to Texas and California. Experts agree that West Nile is here to stay.50
The loss of species diversity in northeastern forests of the United States similarly allowed tickborne pathogens to spill over into humans. In the original, intact northeastern forests, a diversity of woodland animals such as chipmunks, weasels, and opossums abounded. These creatures imposed a limit on the local tick population, for a single oposs
um, through grooming, destroyed nearly six thousand ticks a week. But as the suburbs grew in the Northeast, the forest was fragmented into little wooded plots crisscrossed by roads and highways. Specialist species like opossums, chipmunks, and weasels vanished. Meanwhile, generalist species like deer and white-footed mice took over. But deer and white-footed mice, unlike opossums and chipmunks, don’t control local tick populations. When the opossums and the chipmunks disappeared, tick populations exploded.51
As a result, tickborne microbes increasingly spill over into humans. The tickborne bacteria Borrelia burgdorferi first emerged in humans in an outbreak in Old Lyme, Connecticut, in the late 1970s. If left untreated, the disease it caused—Lyme disease—can lead to paralysis and arthritis among other woes. Between 1975 and 1995, cases increased twenty-five-fold. Today, three hundred thousand Americans are diagnosed with Lyme every year, according to estimates from the Centers for Disease Control. Other tickborne microbes are spilling over as well. Between 2001 and 2008, cases of tickborne Babesia microti, which causes a malaria-like illness, increased twentyfold.52
Neither West Nile virus nor Borrelia burgdorferi and its kin can spread directly from one person to another, yet. But they continue to change and adapt. And elsewhere, the reordering of wildlife species that precipitated their spillover into humans proceeds. Globally, 12 percent of bird species, 23 percent of mammals, and 32 percent of amphibians are at risk of extinction. Since 1970, global populations of these creatures have declined by nearly 30 percent. Just how these losses will shift the distribution of microbes between and across species, pushing some over the threshold, remains to be seen.53
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Strains of my family’s emerging pathogen, MRSA, come from animals. Pigs harbor MRSA. They pass it on to their handlers, and the bacteria appear in their slaughtered flesh sold at the supermarket, although whether people get infected from eating it is still an open question. A University of Iowa study found that 3 percent of meat samples collected from Iowa grocery stores carried MRSA. In the Netherlands, the strain of MRSA commonly found among pigs causes 20 percent of MRSA infections in humans.54
I’ve never lived near a pig farm. But I have been known to eat the flesh of pigs. It’s not something I’m particularly proud of. I grew up in a strictly vegetarian household. My parents were both raised as Jains, a religion that preaches an extreme form of nonviolence. Its cardinal rule is not to harm any other living thing, not even by stepping on grass (you might smash an insect) or breathing in germs, which is why while praying, my Jain grandmothers tied white cotton masks over their mouths. My Jain aunt wouldn’t even accept my youthful offer of a goldfish cracker, because of the sinful implication of its fishy shape. No, Jains are supposed to be kind and gentle to our fellow animals, by doing things like spooning sugar on anthills, or, as my grandfather used to do, visiting Jain-run animal sanctuaries to hand-feed the cows and sheep rescued from the slaughterhouse. Shamefully, my only nod to these admirable traditions is a reluctance to visit zoos, or to kill the confused flies and spiders and ants that end up in my kitchen.
A true Jain, of course, would never be complicit in the usurpation of wild habitat or the business of herding animals onto giant farms and markets, which drive animal microbes into human populations. That’s not me. So perhaps there was a certain logic in what happened the year after MRSA infected my son: a visceral display of an emerging pathogen’s ability to spread from person to person, the first, necessary prerequisite to becoming a pandemic pathogen.
My son’s second bout of MRSA arrived a few months after the first, requiring another round of semitoxic antibiotics. He spiked a fever while on the meds and had to be sent home from school. I was out of town with the family car, so he had to walk home, while I spent the rest of the day rushing back, fretting about the fever. Was he reacting to the antibiotics, or had his MRSA grown impervious to them? How could we tell the difference? If he was reacting to the antibiotics, would there be any other effective medications he could use? One whole class of the drugs had already been ruled out when they had caused an angry rash. If, on the other hand, MRSA had broken through the antibiotics, did that mean it would now lodge deeper into his body, into his tissues and organs? I’d read about the cases of healthy young people, like a twenty-one-year-old college student in Minnesota who’d developed a MRSA infection in the lungs, and a seven-year-old whose MRSA infection in her right hip had spread to her lungs. They both died.55
A third MRSA infection appeared on the inside of his elbow after another few months. By this time, there was no doubt: MRSA lived inside his body. There was no fissure in this protected bit of skin that would have allowed an external invader to creep in. The infection appeared from within. My husband squeezed five tablespoons of pus from the swollen lesions.
We had not regularly bathed in diluted bleach, as advised. I tried it a few times. After my skin turned reptilian, I gave it up. But we had devised other, equally elaborate hygiene measures to contain the bug. We washed. We laundered. We maintained a sterile box with hand sanitizers, disposable gauzes, and antiseptic sprays. A set of cast-off pots lived on the stove, for boiling bandages and compresses, which we did religiously.
It didn’t matter. Six months after my son’s boils had healed, a burning spot appeared on the back of my thigh.
With the help of a small hand mirror and some contortions—at last, I thought, a practical application for years of yoga classes—I could see a small spider bite, one that felt as if a torch were being held to my skin. It soon turned swollen and hard. I stopped wearing jeans, and then pants, to avoid any inadvertent tug or millibar of pressure. Five days passed before I limped into my doctor’s office, where she took her scalpel to it and started to dig. Half an hour later, I staggered home in tears, with a giant wad of gauze to soak up the MRSA-infested pus that poured out for days.
MRSA had expressed an ability critical to its effectiveness as a human pathogen: despite our awareness of its presence, and our admittedly halfhearted attempts at controlling it, it had successfully spread from one human body into another. Its basic reproductive number, in our little population, had crossed the critical threshold of 1.
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The toll of pathogens like MRSA, SARS, West Nile virus, and even Ebola are relatively minor in the grander scheme of things. More people die in car accidents in the United States every year than these new pathogens have managed to fell during their collective tenures on Earth. The reason to pay attention to them regardless is that they’ve begun a journey that pathogens such as cholera completed. And we can see where that road leads.
The transformations that had birthed Vibrio cholerae in the wetlands of the Sundarbans were momentous, to be sure. The vibrio had come a long way from its origins as a placid marine bacterium, floating in the sea. But as a pathogen, it still faced an uncertain future. In order to cause a pandemic, a pathogen must infect a large proportion of the human population. The trouble is that human populations are spread out over wide distances. To do it, cholera would have to become ubiquitous, crossing oceans and traversing continents, snaking thousands of miles across desert and tundra. And yet pathogens themselves are microscopic and immobile. They have no wings or legs or any other independent means of locomotion. On their own, they are as isolated as island castaways, marooned in their obscure birthplaces.
To progress to the next stage in the journey to pandemicity, cholera would have to rely almost entirely upon us.
TWO
LOCOMOTION
I first heard about Chewy, a pet prairie dog, from the microbiologist Mark Slifka outside a banquet room in a Westin hotel in Boston, one chilly November morning. Slifka, one of the world’s foremost experts on poxviruses, had just delivered a plenary address to a small group of infectious-disease specialists gathered for a conference about the dynamics of epidemics.
Chewy was a newly acquired pet, Slifka told me, who had been brought to a veterinarian’s office by its owners in 2003. They were concerned about their pet�
��s sneezing and coughing. The veterinarian decided to nebulize Chewy with oxygen, encasing him in a hamster ball, a hollow sphere made of plastic, while forcing a jet of oxygen into the ball through a vent.
What the veterinarian didn’t know is that Chewy, though a native species (prairie dogs are a kind of North American ground squirrel), had been exposed to killer pathogens from half a world away. The animal had been housed in a pet distribution center alongside a crate of creatures destined for the pet trade that had arrived on a commercial flight from Ghana.1 That crate included two Gambian giant pouched rats, nine dormice, and three rope squirrels, which had been trapped near the town of Sogakofe, Ghana, where 40 percent of the local rope squirrels, and more than a third of local people, have been exposed to poxviruses.2
Little Chewy’s sneezes and coughs, along with those of a few dozen other prairie dogs who’d been housed at the same distribution center, were the result of infection with monkeypox. The virus had created pox lesions under Chewy’s fur, which seeped the virus, and in his lungs, which spewed the virus in his exhales. Chewy’s vet, by nebulizing him in a hamster ball, had just filled the sphere with aerosolized virus. In other words, Slifka said, the vet had created a poxvirus bomb.
When the vet cracked open the ball to let Chewy out, the bomb detonated. A cloud of monkeypox virions wafted into the room. The virus infected ten people who were in the room or who happened to walk through it sometime later. Ultimately, Chewy and other prairie dogs infected by the Ghanaian pets spread monkeypox to seventy-two people in six U.S. states. Luckily, the introduced monkeypox was of the less virulent West African subtype, rather than the more deadly Central African subtype. Only nineteen victims had to be hospitalized.3
