Spillover: Animal Infections and the Next Human Pandemic (2 page)

“That’s it,” Reid said. “That’s the bloody tree.” That’s where the bats gathered, he meant.

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I
nfectious disease is all around us. Infectious disease is a kind of natural mortar binding one creature to another, one species to another, within the elaborate biophysical edifices we call ecosystems. It’s one of the basic processes that ecologists study, including also predation, competition, decomposition, and photosynthesis. Predators are relatively big beasts that eat their prey from outside. Pathogens (disease-causing agents, such as viruses) are relatively small beasts that eat their prey from within. Although infectious disease can seem grisly and dreadful, under ordinary conditions it’s every bit as natural as what lions do to wildebeests and zebras, or what owls do to mice.

But conditions aren’t always ordinary.

Just as predators have their accustomed prey, their favored targets, so do pathogens. And just as a lion might occasionally depart from its normal behavior—to kill a cow instead of a wildebeest, a human instead of a zebra—so can a pathogen shift to a new target. Accidents happen. Aberrations occur. Circumstances change and, with them, exigencies and opportunities change too. When a pathogen leaps from some nonhuman animal into a person, and succeeds there in establishing itself as an infectious presence, sometimes causing illness or death, the result is a zoonosis.

It’s a mildly technical term, zoonosis, unfamiliar to most people, but it helps clarify the biological complexities behind the ominous headlines about swine flu, bird flu, SARS, emerging diseases in general, and the threat of a global pandemic. It helps us comprehend why medical science and public health campaigns have been able to conquer some horrific diseases, such as smallpox and polio, but unable to conquer other horrific diseases, such as dengue and yellow fever. It says something essential about the origins of AIDS. It’s a word of the future, destined for heavy use in the twenty-first century.

Ebola is a zoonosis. So is bubonic plague. So was the so-called Spanish influenza of 1918–1919, which had its ultimate source in a wild aquatic bird and, after passing through some combination of domesticated animals (a duck in southern China, a sow in Iowa?) emerged to kill as many as 50 million people before receding into obscurity. All of the human influenzas are zoonoses. So are monkeypox, bovine tuberculosis, Lyme disease, West Nile fever, Marburg virus disease, rabies, hantavirus pulmonary syndrome, anthrax, Lassa fever, Rift Valley fever, ocular larva migrans, scrub typhus, Bolivian hemorrhagic fever, Kyasanur forest disease, and a strange new affliction called Nipah encephalitis, which has killed pigs and pig farmers in Malaysia. Each of them reflects the action of a pathogen that can cross into people from other animals. AIDS is a disease of zoonotic origin caused by a virus that, having reached humans through just a few accidental events in western and central Africa, now passes human-to-human by the millions. This form of interspecies leap is common, not rare; about 60 percent of all human infectious diseases currently known either cross routinely or have recently crossed between other animals and us. Some of those—notably rabies—are familiar, widespread, and still horrendously lethal, killing humans by the thousands despite centuries of efforts at coping with their effects, concerted international attempts to eradicate or control them, and a pretty clear scientific understanding of how they work. Others are new and inexplicably sporadic, claiming a few victims (as Hendra does) or a few hundred (Ebola) in this place or that, and then disappearing for years.

Smallpox, to take one counterexample, is not a zoonosis. It’s caused by variola virus, which under natural conditions infects only humans. (Laboratory conditions are another matter; the virus has sometimes been inflicted experimentally on nonhuman primates or other animals, usually for vaccine research.) That helps explain why a global campaign mounted by the World Health Organization (WHO) to eradicate smallpox was, as of 1980, successful. Smallpox could be eradicated because that virus, lacking ability to reside and reproduce anywhere but in a human body (or a carefully watched lab animal), couldn’t hide. Likewise poliomyelitis, a viral disease that has afflicted humans for millennia but that (for counterintuitive reasons involving improved hygiene and delayed exposure of children to the virus) became a fearsome epidemic threat during the first half of the twentieth century, especially in Europe and North America. In the United States, the polio problem peaked in 1952 with an outbreak that killed more than three thousand victims, many of them children, and left twenty-one thousand at least partially paralyzed. Soon afterward, vaccines developed by Jonas Salk, Albert Sabin, and a virologist named Hilary Koprowski (about whose controversial career, more later) came into wide use, eventually eliminating poliomyelitis throughout most of the world. In 1988, WHO and several partner institutions launched an international effort toward eradication, which has succeeded so far in reducing polio case numbers by 99 percent. The Americas have been declared polio-free, as have Europe and Australia. Only five countries, as of latest reports in 2011, still seemed to have a minor, sputtering presence of polio: Nigeria, India, Pakistan, Afghanistan, and China. The eradication campaign for poliomyelitis, unlike other well-meant and expensive global health initiatives, may succeed. Why? Because vaccinating humans by the millions is inexpensive, easy, and permanently effective, and because apart from infecting humans, the poliovirus has nowhere to hide. It’s not zoonotic.

Zoonotic pathogens can hide. That’s what makes them so interesting, so complicated, and so problematic.

Monkeypox is a disease similar to smallpox, caused by a virus closely related to variola. It’s a continuing threat to people in central and western Africa. Monkeypox differs from smallpox in one crucial way: the ability of its virus to infect nonhuman primates (hence the name) and some mammals of other sorts, including rats, mice, squirrels, rabbits, and American prairie dogs. Yellow fever, also infectious to both monkeys and humans, results from a virus that passes from victim to victim, and sometimes from monkey to human, in the bite of certain mosquitoes. This is a more complex situation. One result of the complexity is that yellow fever will probably continue to occur in humans—unless WHO kills every mosquito vector or every susceptible monkey in tropical Africa and South America. The Lyme disease agent, a type of bacterium, hides effectively in white-footed mice and other small mammals. These pathogens aren’t
consciously
hiding, of course. They reside where they do and transmit as they do because those happenstance options have worked for them in the past, yielding opportunities for survival and reproduction. By the cold Darwinian logic of natural selection, evolution codifies happenstance into strategy.

The least conspicuous strategy of all is to lurk within what’s called a reservoir host. A reservoir host (some scientists prefer “natural host”) is a living organism that carries the pathogen, harbors it chronically, while suffering little or no illness. When a disease seems to disappear between outbreaks (again, as Hendra did after 1994), its causative agent has got to be
somewhere
, yes? Well, maybe it vanished entirely from planet Earth—but probably not. Maybe it died off throughout the region and will only reappear when the winds and the fates bring it back from elsewhere. Or maybe it’s still lingering nearby, all around, within some reservoir host. A rodent? A bird? A butterfly? A bat? To reside undetected within a reservoir host is probably easiest wherever biological diversity is high and the ecosystem is relatively undisturbed. The converse is also true: Ecological disturbance causes diseases to emerge. Shake a tree, and things fall out.

Nearly all zoonotic diseases result from infection by one of six kinds of pathogen: viruses, bacteria, fungi, protists (a group of small, complex creatures such as amoebae, formerly but misleadingly known as protozoans), prions, and worms. Mad cow disease is caused by a prion, a weirdly folded protein molecule that triggers weird folding in other molecules, like Kurt Vonnegut’s infectious form of water, ice-nine, in his great early novel
Cat’s Cradle
. Sleeping sickness results from infection by a protist called
Trypanosoma brucei
, carried by tsetse flies among wild mammals, livestock, and people in sub-Saharan Africa. Anthrax is caused by a bacterium that can live dormant in soil for years and then, when scuffed out, infect humans by way of their grazing animals. Toxocariasis is a mild zoonosis caused by roundworms; you can get it from your dog. But fortunately, like your dog, you can be wormed.

Viruses are the most problematic. They evolve quickly, they are unaffected by antibiotics, they can be elusive, they can be versatile, they can inflict extremely high rates of fatality, and they are fiendishly simple, at least relative to other living or quasi-living creatures. Ebola, West Nile, Marburg, the SARS bug, monkeypox, rabies, Machupo, dengue, the yellow fever agent, Nipah, Hendra, Hantaan (the namesake of the hantaviruses, first identified in Korea), chikungunya, Junin, Borna, the influenzas, and the HIVs (HIV-1, which mainly accounts for the AIDS pandemic, and HIV-2, which is less widespread) are all viruses. The full list is much longer. There is a thing known by the vivid name “simian foamy virus” (SFV) that infects monkeys and humans in Asia, crossing between them by way of the venues (such as Buddhist and Hindu temples) where people and half-tame macaques come into close contact. Among the people visiting those temples, feeding handouts to those macaques, exposing themselves to SFV, are international tourists. Some carry away more than photos and memories. “
Viruses have no locomotion
,” according to the eminent virologist Stephen S. Morse, “yet many of them have traveled around the world.” They can’t run, they can’t walk, they can’t swim, they can’t crawl. They ride.

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I
solating the Hendra bug had been a task for virologists, working in their high-security labs down at AAHL. “Isolating,” in this sense of the word, means finding some of the virus and growing more. The isolate becomes a live, captive population of virus, potentially dangerous if any were to escape but useful for ongoing research. Virus particles are so tiny they can’t be seen, except by electron microscopy, which involves killing them, so their presence during isolation must be detected indirectly. You start with a small bit of tissue, a drop of blood, or some other sample from an infected victim. Your hope is that it contains the virus. You add that inoculum, like a dash of yeast, to a culture of living cells in a nutrient medium. Then you incubate, you wait, you watch. Often, nothing happens. If you’re lucky, something does. You know you’ve succeeded when the virus replicates abundantly and asserts itself sufficiently to cause visible damage to the cultured cells. Ideally it forms plaques, large holes in the culture, each hole representing a locus of virus-caused devastation. The process demands patience, experience, expensively exact bench tools, plus meticulous precautions against contamination (which can falsify results) or accidental release (which can infect you, endanger your co-workers, and maybe panic a town). Laboratory virologists are not generally knockabout people. You don’t meet them in bars, waving their arms and bragging lustily about the perils of their métier. They tend to be focused, neat, and still, like nuclear engineers.

Discovering where a virus lives in the wild is work of a very different sort. It’s an outdoor job that entails a somewhat less controllable level of risk, like trapping grizzly bears for relocation. Now, the people who look for wild viruses aren’t rowdy and careless, no more so than the lab specialists; they can’t afford to be. But they labor in a noisier, more cluttered, more unpredictable environment: the world. If there is reason to suspect that a certain new virus infecting humans is zoonotic (as most such viruses are), the search may lead into forests, swamps, crop fields, old buildings, sewers, caves, or the occasional horse paddock. The virus hunter is a field biologist, possibly with advanced training in human medicine, veterinary medicine, ecology, or some combination of those three—a person who finds fascination in questions that must be answered by catching and handling animals. That profile fits a lanky, soft-spoken man named Hume Field, midthirtyish at the time he became involved with Hendra.

Field grew up in the provincial towns of coastal Queensland, from Cairns to Rockhampton, a nature-loving kid who climbed trees, hiked in the bush, and spent school holidays on his uncle’s dairy farm. His father was a police detective, which seems only too prefigurative of the son’s later role as a viral sleuth. Young Field earned an undergraduate degree in veterinary science at the University of Queensland, in greater Brisbane, and volunteered at an animal refuge on the side, helping to rehabilitate injured wildlife. After graduation in 1976, he worked in a mixed veterinary practice in Brisbane for some years and then as a temporary fill-in (the Australians call it “doing locums”) all over the state. During that time, he doctored a lot of horses. But he became increasingly aware that his deepest interest was wildlife, not livestock and pets, so in the early 1990s Field returned to the University of Queensland, this time for a doctorate in ecology.

He focused on wildlife conservation and, in due time, needed a dissertation project. Because feral cats (domestic cats gone wild on the landscape) cause considerable damage to native Australian wildlife, killing small marsupials and birds and acting as a source of disease, he undertook a study of feral cat populations and their impact. He was trapping cats, fitting them with radio collars to track how they lived, when the outbreak occurred at Vic Rail’s stable. One of Field’s doctoral mentors, a scientist who worked with the Department of Primary Industries, asked Field whether he would be interested in changing projects. The department needed someone to investigate the ecological side of this new disease. “So I forgot my feral cats,” Field told me, when I visited him long afterward at the Animal Research Institute, a DPI facility near Brisbane, “and started off looking for wildlife reservoirs of Hendra virus.”