Spillover: Animal Infections and the Next Human Pandemic

The next spillover Quammen investigates occurred in Africa in 1996, in a small village on the Gabon/Congo border called Mayibout 2. Several villagers became ill after eating a chimpanzee. Eventually, 31 people in total became ill and 21 died, with a fatality rate of close to 70%. A disease specialist named Eric Leroy, based at the Centre International de Recherches Médicales de Franceville (CIRMF), determined that the disease was Ebola and that the initial case came from the chimp.

Quammen then turns to his own time in the region shadowing a field biologist named Mike Fay, who was surveying every wild animal within a 2,000-mile radius. Many of Fay’s assistants were from the area, and some had connections to the Mayibout 2 outbreak. They reported that all who became sick had touched the infected chimpanzee. The survivors made it clear that the outbreak had changed their habits: “to this day, he said, no one in Mayibout 2 eats chimpanzee” (58). The men also reported that 13 gorillas had also been found dead nearby, relying on local knowledge and rumor. Fay’s biological expedition relied on more precise counting and tallying of wildlife but ultimately led to the same conclusion: The gorilla population in the area was in rapid decline. Gorillas are “highly susceptible to Ebola” (59).

The Mayibout 2 outbreak was part of a larger pattern of Ebola outbreaks and spillovers since the discovery of the virus in 1976. Mayibout 2 was a “middle episode” (60), in a cluster of three between 1994 and 1996. The first, at a mining camp on the Evindo river, highlights the significance of forest disruption to disease emergence. In all cases, fatality rates were high—above 60%—and there were reports of dead chimps in the area. The outbreaks also spread to traditional healers and hospital workers. Clusters of dead gorillas remained common in the region as late as 2002, with some necropsies showing Ebola antibodies.

In 2006, Quammen returned to Gabon’s Mambili river with another field biologist, Billy Karesh, who was on an expedition to tranquilize gorillas so that their blood could be tested for Ebola antibodies. In stark contrast to Karesh’s early trips in the region, they found only solitary gorillas where there had once been multiple family groups. One of the biologists working on the team, a veterinarian named Alain Ondzie, routinely followed any reports of dead chimps and gorillas and tested the corpses for Ebola. Though the work was dangerous, Ondzie remained dedicated because it might “save some lives” (67). Like Mike Fay, Karesh and his colleagues left without samples due to the absence of gorillas.

Because the search for the reservoir spans multiple decades, Quammen then goes back in time to the early history of Ebola outbreaks in 1976. One occurred in what was then Zaire (now the Democratic Republic of the Congo), and the other in South Sudan. In the Zaire outbreak, which eventually gave the disease its name after the Ebola river, two dozen people at a small Catholic mission hospital became ill. Most of the hospital’s staff and patients died, and the government commissioned a study of the disease. The group conducting the study, says Quammen, “consisting of members from France, Belgium, Canada, Zaire, South Africa, and the United States, including nine from the CDC in Atlanta, became known as the International Commission” (69).

The group’s leader was the American scientist Karl Johnson, head of the CDC’s branch of Special Pathogens. Johnson had initially studied emerging diseases during the Machupo outbreak in Bolivia, when he had identified a native mouse as the reservoir species. He and his colleagues began a similar search for Ebola’s reservoir, after laboratory testing confirmed that the pathogen was a virus, probably related to Marburg virus. Their initial investigations into the reservoir yielded no results when mosquitoes, pigs, cows, rodents, monkeys, and other animals were tested. Three years later, a team tested “over 117 species” and ultimately declared that “no evidence of Ebola virus infection was found” (72).

Finding Ebola’s reservoir is difficult because it “disappears entirely for years at a time,” and outbreaks are relatively infrequent (72). The next cluster did not emerge until the outbreaks in Mayibout 2 and in a large Zairian city called Kikwit. This outbreak in January 1995 was traced to a local man who worked in the forests nearby. He infected much of his family and social network, and they spread the disease into hospitals.

In June 1995, another international team, this one including specialists from the US Army Medical Research Institute of Infectious Diseases (USAMRIID), began searching for the reservoir near the first victim’s worksite. Their efforts were intense and prodigious: “the total yield included 3,066 blood samples and 2,730 spleens, all shipped back to the CDC” (74). Researchers attempted to grow live virus in cultures, in a safety environment that included multiple sealed doors and the use of space suits, called a “biosafety level 4” environment (74). Their efforts to grow the virus were unsuccessful, and the reservoir remained unidentified.

The Kikwit team did reveal some of the key analytical frameworks guiding their search. They posited that the reservoir species was a forest-dwelling mammal and that, due to the “rarity” of outbreaks, the animal either had a small population or rarely encountered humans (75).

Turning from the problem of its animal dwelling to its geographic distribution, Quammen maps and describes major Ebola outbreaks. He notes that the outbreak in Sudan in 1976 was less lethal, and that researchers eventually describe “Sudan virus” as distinct from the more virulent version originally found in Zaire (76). Another outbreak of this virus occurred in 1979.

The next famous Ebola event was the subject of the 1989 narrative nonfiction work The Hot Zone and involved infected Asian lab monkeys at a facility in Reston, Virginia. The Asian macaques living at the Reston Primate Quarantine Unit had originally come from the Philippines. Staff became increasingly concerned when monkeys infected each other, and all the survivors were eventually euthanized. Testing revealed that the virus was similar to Ebola but “different enough to be classified in a new species. It came to be known as Reston virus” (78). However, the disease was clearly Asian in origin, not African, as subsequent research in Luzon found infected monkeys there.

In 1992, an Ebola outbreak in Cote d’Ivoire sickened chimpanzees in a forest refuge. Before the cause was known, necropsies were done with no mask, and a Swiss graduate student became ill. She was flown to Switzerland for treatment and eventually tested for Ebola virus. Only detailed testing proved that the virus was in this family, so the “woman was the world’s first identified victim of what became known as Taï Forest virus” (80). Her case has further ominous portents besides that of a new strain of Ebola, as Quammen points out soberly: “She is the first person known to have carried an ebolavirus infection off the African continent. There is no reason to assume that she will be the last” (80).

Reston virus briefly recurred in the United States in 1996, with no human cases. The next major outbreak Quammen describes was a 2000 outbreak of Sudan virus in Uganda. Data further confirmed that Sudan virus was less lethal than its Ebola counterpart, but it is not clear why. While it may seem easy to attribute this distinction to evolution within humans, “[r]emember, the human body isn’t the primary habitat of ebolaviruses. The reservoir host is” (82). In their reservoirs, viruses flourish with little impact on their hosts. In humans, Ebola dies out quickly, suggesting a role for humans as a “dead-end host”—the spillover was unsuccessful at establishing an enduring human-transmitted lineage for that particular virus (82-83). Though Ebola has not yet succeeded in doing this, other spillovers have, most notably HIV.

Quammen turns to the social and cultural impact of Ebola outbreaks. In Gabon, outbreak survivors told a medical anthropologist that some people got Ebola because of an “evil spirit” (87) that infected them because of their bad behavior. The same anthropologist, Barry Hewlitt, visited Uganda during the 2000 outbreak and discovered a similar set of beliefs. Infection with an evil spirit required quarantining patients, limiting movement of people, and suspending burial practices that involved touching bodies. Many of these practices would be helpful in containing Ebola.

While the effects of Ebola on gorillas can only be inferred from testing corpses, scientists and medical professionals are more familiar with the disease’s effects in humans. Richard Preston’s work in The Hot Zone exaggerates these, shocking readers with descriptions of nearly liquid bodies and uncontrolled bleeding from the eyes. Ebola experts Quammen consulted called many of the book’s claims “bullshit,” noting that many patients do not bleed and that they die of respiratory failure rather than hemorrhaging. Despite this wide range of observational data, experts are not certain exactly “how the virus typically causes death” (94), though many have speculated that it interferes with the immune system’s normal functioning, possibly causing routine bacteria like those in the stomach to become dangerous. Karl Johnson notes that the particularly contagious nature of the virus—and the conditions needed to study it safely—have deterred researchers from doing close observations of infected people or animals.

Other infections outside Africa have transpired due to laboratory accidents. One, in England in 1976, occurred at Britain’s Microbiological Research Establishment. Samples from the initial Ebola outbreak were sent there and to the CDC. A scientist named Geoffrey S. Platt working with samples from lab-infected guinea pigs inadvertently “jabbed himself in the thumb” with a needle (98). Ebola is “not contagious but it is highly infectious” and the small injury was enough to make Platt sick (98). He survived. A Russian researcher working for the Ministry of Defense, Nadezhda Alekseevna Makovetskaya, had a similar accident while working with infected horses. She later died. The same fate befell another researcher in Siberia in 2004. Narratives like these confirm “reflect the inherent perils of doing laboratory research on such a lethal, infectious virus” (100).

Quammen’s next narrative is about American scientist Kelly Warfield, who grew up “not many miles from Fort Detrick, the US Army base devoted to medical research and biodefense within which sits USAMRIID” (100). She developed an early fascination with the research done at the base and eventually earned a PhD in virology at Baylor University, specializing in a lab technique for making vaccines that might be effective against Ebola.

She was eventually hired to work at Fort Detrick and began testing mice to see how they responded to “laboratory created antibodies” that prevent viruses from replicating, and thus halt the disease (102). She treated Ebola-infected mice with the antibodies, using the same syringe 10 times.

Warfield’s fateful accident occurred when one restless mouse “suddenly kicked away the needle, deflecting the point into the base of Kelly Warfield’s left thumb” (104). Unlike others, Warfield had not accidentally injected herself with live virus. Instead, “the needle had gone into ten Ebola-infected mice before going into her. If its point had picked up any particles of Ebola and brought them along, then she might have received a tiny dose” (104), which would have been enough for infection.

Warfield was put in a strictly protected containment area known as “The Slammer,” preparing for the possibility of death. Her blood was tested regularly. Warfield told colleagues: “Please please take something away from this if I die. I want you to learn” (108). Three weeks after her accident, Kelly Warfield returned home, and she eventually resumed work. Quammen asked why she continues to work on such a dangerous virus. Warfield explained her interest in the form of a question: “How can something that is so small and so simple just be so darn dangerous?” (110).

Returning to the question of the reservoir host, Quammen sets up Eric Leroy, one of the doctors who led the response to Mayibout 2, as a leading figure. Leroy devoted his subsequent career to studying Ebola. His first study concluded that outcomes with the disease depended less on the amount of virus and more on the strength of immune systems: Those whose bodies responded quickly were more likely to survive. Leroy later conducted several expeditions to search for the reservoir host and was further interested in the question of how spillovers occur.

On their expeditions, Leroy’s group sampled blood from over a thousand animals. They found antibodies present in one species of bat, while another had evidence of the “genome of Ebola virus” (115). This was not a determinative result, as Quammen indicates when he comments, “The sixteen bats with antibodies contained no Ebola RNA, and vice versa. Furthermore, Leroy and his team did not find live Ebola virus in a single bat—nor in any of the other animals they opened” (115).

Beyond the reservoir debate, scientists ponder whether there is a specific pattern to Ebola outbreaks and what it might mean. Quammen divides the controversy into two schools, calling them the “wave view” and the “particle view” in reference to controversies in physics about whether light is a wave or a particle (117). Leroy sees the virus as a “particle,” arguing that it is, “present all the time, within reservoir species […] And sometimes there is transmission from reservoir species to other species’” (118).

The “wave” view argues that Ebola is a new virus, and its spread is a series of “local events” as the reservoir host gets infected in new places (118). This view is advanced by an ecologist named Peter D. Walsh. Walsh supported his view with a paper pointing out that “all known variants of Ebola virus descended from an ancestor closely resembling the Yambuku virus of 1976” (119). Walsh hypothesized that the virus was newly infecting a reservoir, and its movement through that species was also contributing to the ape deaths, because the reservoir species had “close contact” with apes (122). In the end, the two scientists coauthored a paper and suggested that the virus likely had a new reservoir host, which would explain Leroy’s bat findings, but that an older species may also act as a reservoir.

To conclude his study of Ebola, Quammen takes us back to Billy Karesh and his visit to the village of Mbomo, the site of a 2003 outbreak. One of Karesh’s trackers, a man named Prosper Balo, showed Quammen his village and introduced his wife, who had lost many family members in the outbreak. Because of his scientific knowledge, Balo was able to tell his wife how to protect herself from infection, and she survived. Balo, however, remained marked by his experiences with gorillas, mourning them deeply. This reminds Quammen that humanity’s fate is tied up with the behavior of apes, viruses, and every other being that makes up an ecosystem. He declares, “we’re all in this together” (124).