Zoonotic Disease Discussion on National Geographic

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Zoonotic Disease Discussion on National Geographic

By David Quammen 2007

When zoonotic diseases pass from animals to humans, pandemics can result. Scientists are tracking lethal new viruses.

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

In September 1994, a violent disease erupted among racehorses in a suburb of Brisbane, Australia. The place, called Hendra, was a quiet old neighborhood filled with racecourses, stables, newsstands that sell tip sheets, corner cafés with names like The Feed Bin, and racing people. The first victim was a pregnant mare named Drama Series, who started showing symptoms in an outlying pasture and was brought back to her trainer’s stable for doctoring, where she only got worse. Three people worked to save her—the trainer himself, his stable foreman, and a veterinarian. Within two days Drama Series died, leaving the cause of her trouble uncertain. Had she been bitten by a snake? Had she eaten some poisonous weeds out in that scrubby, derelict meadow? Those hypotheses were eliminated two weeks later, when most of her stablemates fell ill. This wasn’t snakebite or toxic fodder. It was something contagious.

The other horses suffered fever, respiratory distress, facial swelling, and clumsiness; in some, bloody froth came from the nostrils and mouth. Despite heroic efforts by the veterinarian, 12 more animals died within days. Meanwhile the trainer himself got sick; so did the stable foreman. The vet, who was following cautionary procedures but working amid the same mad circumstances, stayed healthy. After a few days in a hospital, the trainer died. His kidneys had failed and he couldn’t breathe. The stable foreman, a bighearted man named Ray Unwin, who had merely gone home to endure his fever in private, survived. He and the veterinarian told me their stories when I found them in Hendra last year. Ray Unwin is a middle-aged working bloke with a sandy red ponytail and a weary sadness in his eyes, who professed that he wasn’t a “whinger” (complainer) but said his health has been “crook” (not right) since it happened.

Laboratory analysis revealed that the horses and the men were infected by a previously unknown virus. At first the lab people called it equine morbillivirus, meaning a horse virus closely related to measles. Later, as its uniqueness became better appreciated, it was renamed after the place itself: Hendra. The veterinarian, a tall, gentle fellow named Peter Reid, told me that “the speed with which it went through those horses was unbelievable.” At the height of the crisis, seven animals had succumbed to ugly deaths or required euthanasia within just 12 hours. One of them died thrashing and gasping so desperately that Reid couldn’t get close enough to give it the merciful needle. “I’d never seen a virus do anything like that before,” he said. A man of understatement, he recalled it as “a pretty traumatic time.”

Identifying the new virus was only step one in solving the immediate mystery of Hendra, let alone understanding the case in a wider context. Step two involved tracking that virus to its hiding place. Where did the thing exist when it wasn’t killing horses and people? Step three entailed asking a further cluster of questions: How did it emerge from its secret refuge, and why here, and why now?

After our first conversation, Peter Reid drove me out to the site where Drama Series took sick. Tract houses on prim lanes have been built over the original pasture. Not much of the old landscape remains. But toward the end of one street is a circle, called Calliope Circuit, in the middle of which stands a single mature tree, a native fig, beneath which the mare would have found shelter from eastern Australia’s fierce subtropical sun.

Infectious 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 edifices we call ecosystems. It’s one of the basic processes that ecologists study, including also predation, competition, 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, zebras, and gazelles.

But conditions aren’t always ordinary.

Just as predators have their accustomed prey species, 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, opportunities and exigencies also change. When a pathogen leaps from some nonhuman animal into a person, and succeeds there in making trouble, the result is what’s known as a zoonosis.

The word zoonosis is unfamiliar to most people. But it helps clarify the biological reality behind the scary headlines about bird flu, SARS, other forms of nasty new disease, and the threat of a coming pandemic. It says something essential about the origin of HIV. It’s a word of the future, destined for heavy use in the 21st century.

Ebola is a zoonosis. So is bubonic plague. So are yellow fever, monkeypox, bovine tuberculosis, Lyme disease, West Nile fever, Marburg, many strains of influenza, rabies, hantavirus pulmonary syndrome, and a strange new affliction called Nipah, which kills pigs and pig farmers in Malaysia. Each of them reflects the action of a pathogen that can cross to people from other species. This form of interspecies leap is common, not rare; about 60 percent of all human infectious diseases currently known are shared between animals and humans. Some of those—notably rabies—are widespread and famously lethal, still killing humans by the thousands despite centuries of effort at coping with their effects, concerted international attempts to eradicate or control them, and a clear scientific understanding of how they work. Others are new and inexplicably sporadic, claiming a few victims (as Hendra did) or a few hundred in this place or that, and then disappearing for years.

Smallpox, to take one counterexample, is not a zoonosis. It’s caused by a virus that infects Homo sapiens and, in very exceptional cases, certain nonhuman primates, but not horses or rats or other species. That helps explain why the World Health Organization’s global campaign to eradicate the disease was, as of 1979, successful. Smallpox could be eradicated because its virus, lacking ability to reside virtually anywhere other than in humans, couldn’t hide. Zoonotic pathogens can hide.

Monkeypox, though closely related to smallpox, differs in two crucial ways—its propensity to afflict monkeys as well as humans, and the ability of its virus to exist in still other species, some of which are so far unidentified. Yellow fever, also infectious to both monkeys and humans, and caused by a virus that hides in several species of mosquito, will probably never be eradicated. The Lyme disease perpetrator, a type of bacterium, hides effectively in white-footed mice and other small mammals. These pathogens aren’t consciously hiding, of course. For their purposes, such behavior merely constitutes a strategy of indirect transmission or inconspicuous survival.

The least conspicuous strategy of all is to lurk within what’s called a reservoir host, a species that carries the pathogen while suffering little or no symptomatic illness. When a disease seems to disappear between outbreaks (again, as Hendra did after the 1994 carnage), its causal pathogen may indeed have died out, at least from the region—but then again, maybe not. Maybe its still lingering nearby, all around, within some reservoir host. A rodent? A bird? A butterfly? Possibly 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.

Some months after the deaths in Australia, a scientific sleuth named Hume Field started looking for Hendra’s reservoir host. Field was a veterinarian who, having practiced privately for years, had decided to pursue a doctorate in veterinary epidemiology. The search for the reservoir became his dissertation project. He gathered blood samples from 16 different species, a whole menagerie of suspects, including marsupials, birds, rodents, amphibians, and insects. He sent the samples to a laboratory for screening, which yielded no evidence whatsoever of Hendra.

Then he took blood from Pteropus alecto, a species of fruit bat, big as a crow and commonly known as the black flying fox. Bingo: The lab team found molecular traces left by Hendra virus. Further sampling produced similar evidence from three other species of flying foxes, all native to the forests of Queensland (the state encompassing Brisbane) and other wooded regions of Australia. Field and his collaborators had established that bats were the reservoir. Detecting molecular traces is less definitive than finding particles of live virus, but within one female bat they did find that form of evidence also.

The lab work suggested that Hendra was an old virus, having probably existed within its reservoir host for thousands of years. Despite its age, it had never before—so far as historical records and human memory could say, anyway—caused disease in humans. What accounts for its emergence in 1994? Well, bad luck for Drama Series and those who knew her. Bats came to eat the figs in that solitary tree, and the poor mare, seeking shade, grazing too carelessly, evidently swallowed not just grass but also something of what they dropped, such as fruit pulp, feces, urine, afterbirth, and virus.

But there had to be a broader answer, too. Why did Hendra emerge in 1994, not decades or centuries earlier? Something was different. Some sort of change, or combination of changes, must have caused the virus to be transferred from its reservoir host into other species.

The fancy name for such transfer is spillover. Maybe the virus needed horses (which only reached Australia with European colonists), as distinct from kangaroos (which have been eating grass beneath Australian fig trees for millennia), to mediate its spillover from the reservoir. Maybe bats, figs, horses, and humans had simply never been brought so closely together. Hume Field is currently a research scientist at the Animal Research Institute of Queensland’s Department of Primary Industries, in Brisbane. When I spoke with him at his office there, he raised the issue of “what might be happening now that hasn’t happened before.” Part of the answer is that human destruction of eucalyptus forests has disrupted the customary feeding and roosting habits of some flying foxes, forcing them toward shady suburbs, orchards, botanical gardens, city parks, and closer proximity to people.

But proximity is one thing; spilling virus into horses is another. “How does transmission occur?” Field wondered aloud, at the end of our long conversation. “Well, we still don’t know.”

Nearly all zoonotic diseases result from infection by one of six kinds of pathogen: viruses, bacteria, protozoans, prions, fungi, 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 is a protozoan infection, carried by tsetse flies between wild and domestic mammals and people on the landscapes of sub-Saharan Africa. Anthrax is a bacterium that can live dormant in soil for years and then, when scuffed out, infect humans by way of cattle. 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 mortality, and they are fiendishly simple, at least relative to other living or quasi-living creatures. Hanta, SARS, monkeypox, rabies, Ebola, West Nile, Machupo, dengue, yellow fever, Junin, Nipah, Hendra, influenza, and HIV 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 by way of venues (such as Buddhist and Hindu temples) where people and half-tame macaques come into close contact. Some of the people visiting those temples, feeding handouts to those macaques, exposing themselves to SFV, are international tourists. “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.

About the same time as the Hendra outbreak near Brisbane, another spillover occurred, this one in central Africa. Along the upper Ivindo River in northeastern Gabon, near the border with the Republic of the Congo, lies a small village called Mayibout II. In early February 1996, 18 people there became suddenly sick after they participated in the butchering and eating of a chimpanzee. Their symptoms included fever, headache, vomiting, bleeding in the eyes, bleeding from the gums, hiccuping, and bloody diarrhea. All 18 were evacuated downriver to a regional hospital, where four soon died. The bodies were returned to Mayibout II and buried, with no special precautions; a fifth victim escaped from the hospital, went back to the village, and died there. Secondary cases occurred among people infected by loved ones or friends, or in handling the dead bodies. Eventually 31 people got sick, of whom 21 died—a mortality rate of 68 percent.

Those facts and numbers were collected by a team of medical researchers, some Gabonese, some French, who reached Mayibout II during the outbreak. Among them was a Frenchman named Eric M. Leroy, based at the Centre International de Recherches Médicales de Franceville (CIRMF), in Franceville, Gabon. Leroy and his colleagues identified the disease as Ebola hemorrhagic fever and deduced that the butchered chimpanzee had been infected with Ebola virus. Their investigation also revealed that the chimp hadn’t been killed by village hunters; it had been found dead in the forest and scavenged.

Four years later, I sat at a campfire near the upper Ivindo River with a group of local men working as forest crew for a long overland trek. (See “The Green Abyss: Megatransect, Part II,” March 2001.) The men, mostly Bantu, had been walking for weeks before I joined them on the march. Their job involved carrying heavy bags through the jungle and building a new camp every night for the Wildlife Conservation Society biologist J. Michael Fay, whose extraordinary grit and sense of mission drove the enterprise forward. This particular day had been a relatively easy one—no swamps crossed, no charging elephants—which allowed for a relaxed, confiding atmosphere at the evening fire. I learned that two of the men, Thony M’Both and Sophiano Etouck, had been present in Mayibout II when Ebola struck the village. M’Both, slim in build, older, and more voluble than the others, was willing to talk about it. He spoke in French while Etouck, a shy man with wide shoulders, an earnest scowl, and a goatee, sat silent. Etouck’s own family had been devastated by the disease. He had held one of his dying nieces in his arms, while an IV drip in her wrist became clogged, swelled her hand, and exploded, covering him with her blood. Yet Etouck himself never got sick. Nor did I, said M’Both. The cause of the illnesses was a matter of confusion and fearful rumor. M’Both suspected that French soldiers, visiting nearby, had killed the chimpanzee with some sort of chemical weapon and carelessly left it to poison unsuspecting people. But whatever the cause, whatever the contaminant, his fellow villagers had learned their lesson. To this day, he said, no one in Mayibout II eats chimpanzee.

Amid the chaos and sorrow of the outbreak, M’Both told me, he and Etouck had seen something bizarre: 13 gorillas, all dead, lying in the forest. That image, of 13 gorilla carcasses strewn on the leaf litter, is lurid but plausible. Subsequent research has confirmed that gorillas are susceptible to Ebola. Being social creatures, they could easily pass the infection among group members by mutual grooming, infant care, or trying to rouse their sick or their dead.

In the years since 1996, other outbreaks of Ebola have struck both people and great apes (chimps as well as gorillas) within the region surrounding Mayibout II. One area hit hard lies along the Mambili River, just over the border in northwestern Congo, another zone of dense forest encompassing several villages, a national park, and a gorilla sanctuary known as Lossi. Mike Fay and I walked through that area also, in March 2000, during one of my earlier stints with his expedition. At the time, gorillas were abundant within the Mambili drainage. But in 2002 a team of researchers at Lossi began finding gorilla carcasses, some of which tested positive for Ebola. Within a few months, 91 percent of the individual gorillas they’d been studying (130 of 143 animals) had vanished, and most of those were presumably dead. Extrapolating from confirmed deaths and disappearances to overall toll throughout their study area, the researchers published a paper in Science under the headline: “Ebola Outbreak Killed 5000 Gorillas.”

Last autumn I returned to the Mambili River with a team led by William B. (Billy) Karesh, director of the Wildlife Conservation Society’s Field Veterinary Program and an authority on zoonotic diseases. Karesh’s goal was to tranquilize a few surviving gorillas, take blood samples, and see whether those animals showed exposure to Ebola. Along with an expert tracker named Prosper Balo, plus other veterinarians and guides, we spent eight days searching the forest. Prosper Balo had worked at Lossi. With his guidance, we staked out a bai (a natural clearing) full of succulent vegetation, previously known for the dozens of gorillas that came there daily to eat and relax. Billy Karesh himself had visited the same area in 2000, before Ebola struck, to gather baseline data on gorilla health. “Every day,” he told me, “every bai had at least a family group.” He’d been successful on that trip—the only person ever to tranquilize-dart lowland gorillas. This time things were different. So far as we could see, there were scarcely any survivors. We caught glimpses of just two gorillas. The others had either dispersed to parts unknown, or they were . . . dead? Anyway, once gorillas had been abundant hereabouts, and now they were gone.

The virus seemed to be gone, too. But we knew it was only hiding.

Hiding where? For a decade, the identity of Ebola’s reservoir host was one of the darkest mysteries in the world of disease science. Several sets of researchers were trying to solve it. Then, two years ago, Eric Leroy and some colleagues announced in the journal Nature: “We find evidence of asymptomatic infection by Ebola virus in three species of fruit bat, indicating that these animals may be acting as a reservoir for this deadly virus.” Leroy’s group hadn’t captured any live virus, but they had established—with positive results from several kinds of molecular tests—that Ebola had passed through at least a few of the bats examined.

Leroy himself wants stronger evidence. “We continue to catch bats—to try to isolate virus from their organs,” he said late last year, when I visited him in Franceville. Identifying the reservoir host with certitude, though, would still leave other questions unanswered.

For instance, how does Ebola emerge from that reservoir? “We don’t know if there’s direct transmission from bats to humans,” Leroy said. “We only know there is direct transmission from dead great apes to humans.” And how has the virus evolved, producing four distinct strains? Why is the Ebola-Zaire strain, the one found in Gabon and Congo, so highly lethal (about 80 percent mortality) to people? What is its natural life cycle? What’s the spillover mechanism into gorillas and chimps? How does the virus affect the human immune system? How does it find its way into humans at all? Ebola is difficult to study, Leroy explained, because of the character of the disease. It strikes rarely, it progresses quickly, it kills or it doesn’t kill within just a few days, it affects relatively few people in each outbreak, and those people generally live in remote, forested areas, far from research hospitals or medical institutes; then it exhausts itself locally or is successfully stanched, and disappears back into the forest, like a hit-and-run force of guerrilla warriors. “There is nothing to do,” Leroy said, with the perplexity of a patient man. He meant, nothing to do except keep trying, keep working in the lab, keep responding to outbreaks when they occur. No one can predict where Ebola might next appear. “The virus seems to decide for itself.”

Hendra and Ebola are part of a much larger pattern: the recent emergence of new zoonotic diseases, variously lethal and horrific, more than a few of which seem to be associated with bats. Another part of the pattern is human-caused disruption of wild landscape. Nipah came next.

In September 1998, a pork seller in peninsular Malaysia checked into a hospital with some sort of brain inflammation and died. Around the same time, a number of pig-farm workers came down with similar symptoms, bad fever leading to coma; several of them also died. Pigs in the area meanwhile suffered an illness of their own (or what seemed their own), coughing and wheezing, keeling over dead. The pig disease was taken to be classical swine fever. The human deaths were attributed to Japanese encephalitis. But within a few months, scientists showed that both the pigs and the people had been infected with the same virus, a new one, first isolated from a patient whose home village was called Sungai Nipah. The virus was highly contagious from pig to pig, but not from person to person. It spread elsewhere in Malaysia, and even to Singapore, with shipments of live pigs, infecting people who came in contact with the sick animals or their meat. Within seven months, the outbreak had caused 265 human cases, 105 human deaths, and led to the culling of 1.1 million pigs.

The molecular profile of this new virus suggested a close kinship with Hendra. That provided a clue. Not long afterward, researchers found Nipah living sedately in a reservoir host: Pteropus hypomelanus, another species of fruit bat. They also noted that fruit bats, deprived of habitat elsewhere, had been congregating in orchards near the pig farms.

And then there was SARS. It came out of southeastern China in early 2003, spreading readily from person to person, traveling as fast as airplanes, killing 774 humans in nine countries and scaring people all over the world. A quick bit of research pointed suspicion at the masked palm civet, a medium-size mammal often sold in Chinese markets for its meat, as the reservoir of SARS. That suspicion was discounted, though, after experiments showed that masked palm civets themselves suffer symptomatic SARS. Then a group of scientists led by Wendong Li, of the Chinese Academy of Sciences, announced that they had found reservoirs hosting a virus very similar to the one that caused the SARS outbreak: horseshoe bats of the genus Rhinolophus.

There’s more. Australian bat lyssavirus, a newly identified virus closely related to rabies, has killed at least two people with rabies-like symptoms after the victims were bitten by bats. Menangle and Tioman are also bat-carried viruses, of the same family as Hendra, that scientists are watching carefully. Rabies itself and rabies-like viruses, found in bat reservoirs around the world, are still probably the most lethal of all viral pathogens if untreated—with nearly 100 percent mortality among humans. In northern Peru, last autumn, 11 children from native communities along the Amazon headwaters died from rabies contracted when they were nipped by vampire bats.

At this point, you’re entitled to ask: Damn, what is it about bats?

I asked that myself, in conversation with Charles Rupprecht, a virologist and veterinarian who leads the rabies section at the Centers for Disease Control and Prevention, in Atlanta. Rupprecht recited a list of factors that make this order of mammals, the Chiroptera, ideal candidates to host a variety of dangerous viruses. Some bats roost in huge colonies, snuggled intimately together; they give birth to only a few young, and therefore nurture those young dotingly; they have long life spans, especially for small mammals; they are old, too, in evolutionary terms; they encompass a great diversity of species, roughly 20 percent of all mammals; they fly, and therefore they get around the world nicely, finding places and ways to sustain themselves on nearly every landmass except Antarctica. Add to those traits the fact that, being nocturnal and airborne, they’re hard to study. “Bats really are the undiscovered country,” Rupprecht said. His point—the point of a rabies biologist who happens to like bats—is that they aren’t sinister and, if they seem to harbor an undue variety of nightmare diseases, it’s probably because they are so various and so poorly known.

Another informed view came from Xavier Pourrut, a research veterinarian based at CIRMF in Gabon. His job involves capturing and taking blood samples from bats near Ebola out-breaks so that Eric Leroy can study their serum for evidence of the virus. “Bats represent an ancient lineage of mammals,” Pourrut told me, and like Rupprecht he sees them with a biologist’s appreciation. The thing to remember, he said, is that their flight powers give them great range of access, not just horizontally to places around the world, but vertically within the forest. That potentially puts them in contact not just with the fruits or the insects on which they feed, and the treetops from which they dangle, but also with an inordinate number of other species, from the canopy to the ground, including rodents, monkeys, carnivores, birds, snakes, chimpanzees, gorillas, and people.

Contact is crucial. Close contact between two species represents an opportunity for a pathogen to expand its horizons and possibilities. The pathogen may be well adapted to its quiet, secure life within a reservoir host; spilling over into a new species presents a chance, at some risk, of vastly increasing its abundance and its geographic reach. The risk is that, by killing the new host too quickly, before getting itself transmitted onward, the pathogen will come to a dead end. But evolutionary theory suggests that some pathogens, on some occasions, will accept that risk in exchange for the chance of a big payoff. Long-term survival is only one form of evolutionary success. Gross abundance and broad distribution is another.

Think of tortoises and rats. Tortoises tend to live by a conservative strategy, remaining within their preferred habitat and reproducing slowly. Rats tend to be opportunists, fanning out, traveling across land and sea as stowaways, arriving in new places and reproducing fast. Similarly, pathogens may differ in their degree of adventurousness. Spillover from a reservoir host isn’t necessarily an accident, always leading to the dead end. It may be a strategy, leading to evolutionary success. Simian immunodeficiency virus (SIV) achieved that sort of success when it spilled over from one subspecies of chimpanzee into humans, probably in west-central Africa, and became HIV-1.

Close contact between humans and other species can occur in various ways: through killing and eating of wild animals (as in Mayibout II), through caregiving to domestic animals (as in Hendra), through fondling of pets (as with monkeypox, brought into the American pet trade by way of imported African rodents), through taming enticements (feeding bananas to the monkeys at a Balinese temple), through intensive animal husbandry combined with habitat destruction (as on Malaysian pig farms), and through any other sort of disruptive penetration of humans into wild landscape—of which, needless to say, there’s plenty happening around the world. Once the contact has occurred and the pathogen has crossed over, two other factors contribute to the possibility of cataclysmic consequences: the sheer abundance of humans on Earth, all available for infection, and the speed of our travel from one place to another. When a bad new disease catches hold, one that manages to be transmissible from person to person by a handshake, a kiss, or a sneeze, it might easily circle the world and kill millions of people before medical science can find a way to control it.

But our safety, our health, isn’t the only issue. Another thing worth remembering is that disease can go both ways: from humans to other species as well as from them to us. Measles, polio, scabies, influenza, tuberculosis, and other human diseases are considered threats to non-human primates. The label for those infections is anthropozoonotic. Any of them might be carried by a tourist, a researcher, or a local person, with potentially devastating impacts on a tiny, isolated population of great apes with a relatively small gene pool, such as the mountain gorillas of Rwanda or the chimps of Gombe.

That’s why Billy Karesh and his colleagues at the Wildlife Conservation Society label their program with the slogan “One World, One Health.” The guiding principles come from ecology, of which human and veterinarian medicine are merely subdisciplines. “It’s not about wildlife health or about human health or about livestock health,” he told me. “There’s really just one health”—the health and balance of ecosystems throughout the planet.

After our fruitless stakeout along the Mambili River, in northwestern Congo, Karesh and I and Prosper Balo, along with other members of the team, traveled three hours downstream by pirogue. From there we drove a dirt road to a town called Mbomo, center point of an area where Ebola had killed 128 people during the same outbreak that struck gorillas at Lossi. We stopped at a little hospital, beside which stood a sign, painted in stark red letters:






(Don’t ever touch dead animals found in the forest.)

Mbomo was Balo’s hometown. Visiting his house, we met his wife, Estelle, and some of his many children. We learned that Estelle’s sister, two brothers, and another close relative all died of Ebola in 2003, and that Estelle herself was shunned by townspeople because of her association with the disease. No one would sell food to her. No one would touch her money. She had to hide in the forest. She would have died herself, Balo said, if he hadn’t taught her the precautions he’d learned from Eric Leroy and the other scientists for whom he’d worked during the outbreak—sterilize everything with bleach, wash your hands, and don’t touch corpses. But now the bad time was past and, with Balo’s arm around her, Estelle was a smiling, healthy young woman.

Balo remembered the outbreak in his own way, mourning Estelle’s losses and some of a different sort. He showed us a book, a botanical field guide, on the endpapers of which he had written a list of names: Apollo, Cassandra, Afrodita, and almost 20 others. They were gorillas, an entire group that he had known well, that he had tracked daily and observed lovingly at Lossi. Cassandra was his favorite, Balo said. Apollo was the silverback. “Sont tous disparus en deux-mille trois,” he said. All of them, gone in the 2003 outbreak. He’d lost his gorilla family, and also members of his own family. It was very hard, Balo said.

For a long time he stood holding the book, opened for us to see those names. He comprehended emotionally what the scientists know from their data: That we—people and gorillas, horses and pigs and bats, monkeys and rats and mosquitoes and viruses—are all in this together.


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