Pandemic Read online

  This calculation is a critical one to make in an outbreak, for it immediately predicts its future course. If, on average, each infection results in less than one additional infection—you infect your son and his friend, but each of them infects no one else—then the outbreak will die out on its own, like a population in which each family produces fewer than two children. It doesn’t matter how deadly the infection is. But if, on average, each infection results in one more infection, then the outbreaks can theoretically continue indefinitely. If each infection results in more than one additional infection, then the afflicted population is facing an existential threat that requires immediate and urgent attention. It means that, in the absence of interventions, the outbreak will expand exponentially.

  The basic reproductive number is, in other words, a mathematical expression of the difference between a zoonotic pathogen and one that has crossed the threshold to become a human one. The basic reproductive number of a zoonotic pathogen, which cannot spread from one infected person into another, is always less than 1. But as it refines its attack on humans, its ability to spread among them improves. Once it tips over the number 1, the pathogen has crossed the threshold and broken free of its reservoir animals. It’s a bona fide human pathogen that is self-sustaining in humans.

  There are many mechanisms by which zoonotic pathogens can acquire the ability to spread directly between people, severing the cord that binds them to their reservoir animals. Vibrio cholerae did it by acquiring the ability to produce a toxin.

  The toxin was the vibrio’s pièce de résistance. Normally, the human digestive system sends food, gastric and pancreatic juice, bile, and various intestinal secretions to the intestines, where cells lining the gut extract nutrients and fluid, leaving behind a solid mass of excreta to expel. The vibrio’s toxin altered the biochemistry of the human intestines such that the organ’s normal function reversed. Instead of extracting fluids to nourish the body’s tissues, the vibrio-colonized gut sucked water and electrolytes out of the body’s tissues and flushed them away with the waste.12

  The toxin allowed the vibrio to accomplish two things essential to its success as a human pathogen. First, it helped the vibrio get rid of its competitors: the massive torrent of fluids sloughed off all the other bacteria in the gut, so that the vibrio (clinging to the gut in its tough microcolonies) could colonize the organ undisturbed. Second, it assured the vibrio’s passage from one victim to another. Even tiny drops of that excreta, on unwashed hands or contaminated food or water, could carry the vibrio to new victims. Now, so long as the vibrio could get into a single person and cause disease, it could spread to others, whether or not they exposed themselves to copepods or ingested the vibrio-rich waters of the Sundarbans.

  The first pandemic caused by the new pathogen began in the Sundarbans town of Jessore in August 1817 after a heavy rainfall. Brackish water from the sea flooded the area, allowing salty copepod-rich waters to seep into people’s farms and homes and wells. V. cholerae slipped into the locals’ bodies and colonized their guts. Thanks to the toxin, Vibrio cholerae’s basic reproductive number, according to modern mathematical models, ranged from 2 to 6. A single infected person could infect as many as half a dozen others.13 Within hours, cholera’s first victims were being drained alive, each expelling more than fifteen quarts of milky-white liquid stool a day, filling the Sundarbans’ streams and waste pits with excreta. It leaked into farmers’ wells. Droplets clung to people’s hands and clothes. And in each drop, vibrio bacteria swarmed, ready to infect a new host.14

  The Bengalis called the new disease ola, for “the purge.” It killed people faster than any other disease known to humankind. Ten thousand perished. Within a matter of months, the new plague held nearly two hundred thousand square miles of Bengal in its grip.15

  Cholera had made its debut.

  * * *

  Given the ubiquity of microbes, it would seem that new pathogens could come from anywhere at all, surfacing from their hidden corners to encroach upon humankind from all directions. They could be living inside of us already, becoming pathogenic by exploiting newfound opportunities within, or could emerge from the inanimate environment, like the soil or the pores of rocks and ice cores, or from any number of other microbial niches.

  And yet that’s not how most new pathogens are born, because their entry into our bodies is not random. Microbes become pathogens by following the avenues we pave for them, and these avenues follow particular routes. Even though there are countless repositories of microbes that could become human pathogens, most new human pathogens are like Vibrio cholerae and the SARS virus: they originate in the bodies of other animals. More than 60 percent of our newly emerged pathogens originate in the furred and winged creatures around us. Some of these new pathogens come from domesticated animals, such as pets and livestock. Most—over 70 percent—come from wild animals.16

  Microbes have been crossing between species and turning into new pathogens for as long as humans have lived among other species. Hunting animals and eating them, which exposes people to the internal tissues and fluids of other animals, provides a good opportunity. Being bitten by insects like mosquitoes and ticks, which ferry other animals’ fluids into our bodies, can do the trick, too. These are ancient forms of intimate contact between Homo sapiens and other animals, dating back to our earliest years, and they brought us some of our oldest pathogens, such as malaria, ferried from the bodies of our fellow primates into ours by blood-sucking mosquitoes.

  Because intimate contact between species must be prolonged in order for an animal microbe to turn into a human pathogen, historically we are victim to some animals’ microbes more than others. Many more pathogens come from the bodies of Old World creatures, whom we’ve lived with for millions of years, compared to New World creatures, with whom we’ve been acquainted for just tens of thousands of years. A disproportionate number of human pathogens hail from other primates, who’ve bestowed upon us 20 percent of our most burdensome pathogens (including HIV and malaria), despite comprising just 0.5 percent of all vertebrates. It’s also why so many human pathogens date back to the dawn of agriculture ten thousand years ago, when people started domesticating other species and living in prolonged, intimate contact with them. From cows, we got measles and tuberculosis; from pigs, pertussis; from ducks, influenza.17

  But while animal microbes have been spilling over into humans (and vice versa) for millennia, it’s historically been a rather slow process.

  Not anymore.

  * * *

  Peter Daszak is the scientist who discovered that horseshoe bats were the reservoir of the SARS virus. He directs an interdisciplinary organization that investigates emerging diseases in people and wildlife. I met him one afternoon in his office in New York City. He fell into the business of disease hunting by happenstance, he says. As a kid growing up in Manchester, England, he’d wanted to become a zoologist. “My big thing is lizards,” he says, gesturing toward his pet captive-bred Madagascan day gecko, motionlessly poised in a lighted glass tank next to the front door. At his university, though, all the research projects on the behavior of lizards were filled. Daszak had to settle for one on the diseases of lizards instead. “My God, that’s boring,” he thought at the time.18

  That inquiry, however, turned him into one of the world’s foremost disease hunters. Daszak was working at the Centers for Disease Control in the late 1990s when herpetologists started noticing sudden declines in amphibian populations around the world. Few experts suspected disease. Biologists at the time believed that pathogenic microbes never threatened the survival of their host populations. Such virulence was considered self-defeating: if a pathogen killed too fast or too many of its victims, there’d be none left for it to subsist upon. And so “they were coming up with all these standard theories” to explain the mass mortality in amphibians, Daszak remembers. They thought the culprit might be a pollutant or a sudden change in the climate. But Daszak suspected that a never-before-seen contagion was killing
the amphibians. He had already discovered a disease that had led to the extinction of an entire species of tree snails from the South Pacific.

  In 1998, he published a paper reporting that a fungal pathogen—what turned out to be Batrachochytrium dendrobatidis, or amphibian chytrid fungus for short—had caused the amphibian declines around the world. Most likely, the pathogen had spread thanks to the quickening pace of disruptive human activities, in particular the stepped-up demand for amphibians as pets and in scientific research.19

  And he was struck by something else. Humans, too, were vulnerable to pathogens unleashed by the same accelerated, disruptive forces that brought chytrid fungus to the world’s amphibians. As wetlands were paved over and forests were felled, different species came into novel, prolonged contact with each other, allowing animal microbes to spill over into human bodies. And these developments were proceeding at an unprecedented scale and speed around the world.

  The road from animal microbe to human pathogen was turning into a highway.20

  * * *

  Take the southwest corner of the West African nation of Guinea. One of the world’s most biodiverse forests once covered the region. Large tracts of undeveloped forests, being difficult for people to penetrate, had limited contact between forest animals and humans. Wild animals could live in the forest without encountering humans or human settlements.

  That changed during the 1990s, as the Guinean forest was steadily destroyed. A wave of refugees descended upon the forest to escape a long, bloody, complex conflict between armies and rebel groups from neighboring Sierra Leone and Liberia. (At first they’d tried to settle in refugee camps in the forest area’s central town of Guéckédou, but rebel groups and government soldiers repeatedly attacked their camps.)21

  The refugees cut down trees to plant crops, build huts, and turn into charcoal. Rebel groups started logging the forest, too, selling timber to finance their battles.22 By the end of the 1990s, the transformation of the forest could be seen from space. In satellite images from the mid-1970s, the jungles in Guinea bordering Liberia and Sierra Leone looked like a sea of green splattered with tiny islands of brown, where small clearings had been made for villages. Satellite images from 1999 showed a complete reversal: a sea of treeless brown, with tiny islands of green forest speckled in between. Of the entire region’s original forests, only 15 percent remained.23

  Just how this wide-scale deforestation affected the forest ecosystem has yet to be fully described. Many species that lived in the forest probably just disappeared when humans moved into their habitats. What is known is that some species stayed. They squeezed in, resorting to smaller patches of remaining stands of trees, in increasing proximity to human habitations.

  Bats were among them. It stands to reason: bats are widely distributed and resilient creatures. Of 4,600 species of mammals on earth, 20 percent are bats. And, as a study in Paraguay found, certain bat species thrive in disturbed forests in even higher abundances than in intact ones.24 Unfortunately, bats are also good incubators for microbes that can infect humans. They live in giant colonies of millions of individuals. Some species, like the little brown bat, can survive for as long as thirty-five years. And they have unusual immune systems. For example, because their bones are hollow, like those of birds, they don’t produce immune cells in their bone marrow like the rest of us mammals do. As a result, bats host a wide range of unique microbes that are exotic to other mammals. And they travel around with these microbes over significant distances, because bats can fly. Some even migrate, traveling thousands of miles at a time.25

  As the Guinean forest was chopped down, new kinds of collisions between bats and people likely occurred. Bats were hunted for meat, exposing hunters to microbe-laden bat tissue when the animals were slaughtered. Bats fed on fruit trees near human settlements, exposing local people to their saliva and excreta. (Fruit bats are notoriously messy eaters; their modus operandi is to pick off ripe fruit and suck out the juice, littering the ground below with saliva-covered, half-eaten fruits.)

  At some point—nobody knows just when—a microbe of bats, the filovirus Ebola, started to spill over and infect people. In humans, Ebola causes hemorrhagic fever and can kill 90 percent of those it infects.26 A study of blood samples collected from people in eastern Sierra Leone, Liberia, and Guinea between 2006 and 2008 revealed that nearly 9 percent had been exposed to Ebola: their immune systems had created specific proteins called antibodies in response to the virus.27 A 2010 study of over four thousand people in rural Gabon, where there’d been no outbreaks of Ebola, similarly found that nearly 20 percent had been exposed to the virus.28

  But nobody noticed. The ongoing conflict had severed supply routes and communication networks, leaving the refugees hiding in the jungle bereft of outside help. Even the most stalwart aid organizations such as Médecins Sans Frontières had been forced to withdraw. The isolation coupled with the violence compelled the United Nations to call the West African refugees’ plight “the worst humanitarian crisis in the world.”29

  It wasn’t until the political violence eased, in 2003, and the people hiding in the Guinean forest slowly reconnected with the rest of the world that the virus’s presence became apparent. On December 6, 2013, Ebola virus sickened and killed a two-year-old child in a small forest village outside Guéckédou. Perhaps the toddler had played with a piece of fruit covered with bat saliva, fallen from a nearby tree. Perhaps the parents had been handling a recently slaughtered bat before picking up the child. It was probably not the first time someone in the Guéckédou area had encountered Ebola virus from a local bat. But this time, the people of Guéckédou were no longer as isolated as they’d been in the past. The virus was able to spread.

  By February 2014, a health-care worker had ferried the virus to three other local forest villages. Within a month, at least four clusters of cases had been ignited in Guinea’s forest region, triggering independent chains of transmission.30

  By the time hospital officials and aid workers alerted the Ministry of Health and the World Health Organization to the outbreak in the Guinea forest in March 2014, the virus had already spread into Sierra Leone and Liberia.31 Six months later, the virus had emerged in urban centers throughout the region, and the size of the epidemic was doubling every two to three weeks. According to calculations by modelers, each infected person infected at least one or two others, for a basic reproductive number that ranged from 1.5 to 2.5. In the absence of containment measures, the Ebola outbreak would grow exponentially.32

  Ebola had caused outbreaks on the continent before. Sporadic, contained eruptions in remote villages in Central Africa had occurred since the 1970s, mostly during the transition between rainy and dry seasons, possibly connected to the fruiting of trees, and in the wake of the arrival of large numbers of migratory bats. But never before had the virus caused the devastation that it did in West Africa. The thousands of people infected with Ebola quickly overwhelmed the fragile economies and health-care infrastructures of the three most affected countries. “None of us experienced in containing outbreaks has ever seen, in our lifetimes,” the World Health Organization’s director-general Margaret Chan said, “an emergency on this scale.”33

  In September 2014, the Centers for Disease Control estimated that Ebola might sicken more than a million people across West Africa.34 That estimate proved to be overblown, but many believed it possible at the time. Ebola had already wreaked catastrophic damage on our fellow primates, the gorillas and chimpanzees who feed on the same fruit trees as fruit bats. Over the course of the 1990s and early 2000s, Ebola had killed one-third of the world’s gorilla population and nearly the same proportion of the world’s chimpanzees. By the time the epidemic in Guinea, Sierra Leone, and Liberia finally started to ebb in early 2015, more than ten thousand people had perished.35

  * * *

  Ebola is the most dramatic of the new animal microbes spilling over into people from forest animals in Africa, but it is not the only one.

  Mon
keypox is a virus that lives in Central African rodents. It comes from the same genus of viruses as the now extinct variola, the virus that caused smallpox, which killed between 300 and 500 million people over the course of the twentieth century. In humans, monkeypox causes a disease clinically indistinguishable from smallpox, with characteristic raised lesions, or pox, across the body, particularly on the face and hands. Unlike smallpox, monkeypox is a zoonosis. But according to studies conducted by the University of California epidemiologist Anne Rimoin, it has started to spill over into humans with increasing frequency.36

  Between 2005 and 2007, Rimoin tracked down cases of monkeypox that had occurred in fifteen remote villages in the Democratic Republic of Congo. She took blood samples from those who’d been infected and confirmed that monkeypox was indeed the culprit. When she tallied her numbers, she found that monkeypox infection in humans had grown twentyfold compared to the period between 1981 and 1986.37

  A variety of factors help explain the increase. For one thing, intimate contact between rodents and humans has become more common. Thanks to forest destruction, more people live in and around the monkeypox-infected rodents of Central African forests.38 Because wild game populations and local fisheries have collapsed, many hunt for bushmeat, including the rodents they might have once rebuffed. The cessation of vaccination against smallpox plays an important role, too. A global mass vaccination campaign that stamped out smallpox in the late 1970s had conferred lifelong immunity against smallpox’s entire genus of viruses to its recipients, which included monkeypox. But that campaign had ended in DRC in 1980. Everyone born after that time is as vulnerable to monkeypox as nonvaccinated people were to smallpox centuries ago.39