Spillover: Animal Infections and the Next Human Pandemic

by David Quammen

Until recently, the Bakweles have been using chimps for this ritual. They claim two chimps could be used for circumcision of as many as 36 people. They amputate the arms of the chimps. This part of the animal is eaten by elders of the village. Of late, however, due to the scarcity of chimps, Bakweles go for gorillas. Eight gorilla arms had lately been seized when a poacher fled from game rangers, leaving the meat behind in a bag. The arms were intended for an impending beka. “We cannot do without these animals,” the Bakwele chief complained, “if we must perform this important traditional rite.”

The park’s population of great apes (chimps and gorillas combined) had fallen abruptly since 2002, he told me: from about sixty-three hundred animals to about twenty-seven hundred.

Bands of well-armed poachers come across the river, mow down elephants and anything else they see, whack out the ivory and the elephant meat, lop off the heads and limbs of the apes, take the smaller creatures whole, and escape back across the water.

Throughout the rest of the world you see AIDS-education materials crying out: Practice safe sex! Wear a condom! Don’t reuse needles! Here the message was: Don’t eat apes!

It did what a retrovirus does: penetrated cells, converted its RNA genome into double-stranded DNA, then penetrated further, into the cells’ nuclei, and inserted itself as DNA in the DNA genome of those host cells. Its primary targets were T cells of the immune system. A certain protein receptor (CD4) on the surface of those cells, in the Cut Hunter, was not very different from the equivalent receptor (another CD4) on the T cells of the butchered chimpanzee. The virus attached, entered the human cells, and made itself at home. Once integrated into the cellular genome, it was there for good. It was part of the program. It could proliferate in two ways: by cell replication (each time an infected T cell copied itself, the retroviral genome was copied also) and by activating its little subgenome to print off new virions, which then escaped from the T cell and floated off to attack other cells.

Spillovers of SIVcpz into humans had almost certainly occurred in the past (plenty of chimps were butchered, plenty of hunters were cut) and resulted in previous chains of infection, but those chains had been localized and short. The smoldering outbreak had always come to a cold end. This time it didn’t.

SIV is highly diverse and broadly distributed, found as a naturally occurring infection in members of more than forty different species of African monkey and ape.

For nine years the study continued. Fieldworkers at Gombe collected fecal samples from ninety-four different chimpanzees, each of which was known by name and, in most cases, by its individual character and family history. Beatrice Hahn’s people did the analyses, finding that seventeen of those ninety-four chimps were SIV-positive. As time passed, some chimps died. Others disappeared in the forest and were presumed dead when they failed to reappear. Death is often a private matter for wild creatures, including chimpanzees, especially when it comes upon them by slow and painful degrees. They tend to go absent from the social group, if there is a social group, and meet the end alone. Gimble last showed himself to trackers on January 23, 2007. His body was never found.

the AIDS pandemic is traceable to a single contingent event. That this event involved a bloody interaction between one chimpanzee and one human. That it occurred in southeastern Cameroon, around the year 1908, give or take. That it led to the proliferation of one strain of virus, now known as HIV-1 group M. That this virus was probably lethal in chimpanzees before the spillover occurred, and that it was certainly lethal in humans afterward. That from southeastern Cameroon it must have traveled downriver, along the Sangha and then the Congo, to Brazzaville and Léopoldville. That from those entrepôts it spread to the world.

Hypodermic syringes, for injecting medicines into muscles or veins, were invented in 1848 and, until after World War I, were handmade of glass and metal by skilled craftsmen. They were expensive, delicate, and meant to be reused like any other precision medical instrument. During the 1920s their manufacture became mechanized, to the point where 2 million syringes were produced globally in 1930, making them more available but not more expendable. To the medical officers working in Central Africa at that time, they seemed invaluable but were in short supply.

French colonial doctor named Eugène Jamot, working just east of the upper Sangha River (in a portion of French Equatorial Africa then known as Oubangui-Chari) during 1917–1919, treated 5,347 trypanosomiasis cases using only six syringes.

the period 1927–1928, Eugène Jamot’s team in Cameroon performed 207,089 injections of tryparsamide, plus about 1 million injections of something called atoxyl, another arsenical drug for treating trypanosomiasis. During just the year 1937, throughout French Equatorial Africa, the army of doctors and nurses and semipro jabbers delivered 588,086 injections aimed at trypanosomiasis, not to mention countless more for other diseases. Pepin’s arithmetic totaled up 3.9 million injections just against trypanosomiasis, of which 74 percent were intravenous (right into a vein, not just a muscle), the most direct method of drug delivery and also the best for unintentionally transmitting a blood-borne virus.

1929, the Congolese Red Cross established a clinic known as the Dispensaire Antivénérien, open to women and men for the treatment of what we used to call venereal diseases. Located in a neighborhood on the east side of Léopoldville,

During the 1930s and 1940s, the Dispensaire Antivénérien administered more than forty-seven thousand injections annually. Most were intravenous. Straight into the blood. With increased migration to the city following World War II, the numbers rose. In the early 1950s, the quackier remedies (intravenous milk?) and the metallic poisons gave way to penicillin and streptomycin, which had longer-lasting effects and therefore meant fewer shots. The campaign peaked in 1953, at about 146,800 injections, or roughly 400 per day. Many if not most of those injections were administered to femme libres, sex workers, ladies of hospitality, however you want to describe them, who had multiple male clients. They came and went. The syringes were rinsed and reused. This in a city where HIV-1 had arrived. Six years later came the blood sample that yielded the HIV-1 sequence now known as ZR59. One year after that, DRC60. The virus had spread

a plasmapheresis machine, gargling your blood and the blood of many other donors over the course of days, can infect you with a blood-borne virus.

From the time of our beginning as a species (about 200,000 years ago) until the year 1804, human population rose to a billion; between 1804 and 1927, it rose by another billion; we reached 3 billion in 1960; and each net addition of a billion people, since then, has taken only about thirteen years. In October 2011, we came to the 7-billion mark

eminent biologist (and ant expert) Edward O. Wilson felt compelled to do some knowledgeable noodling on the matter. Wilson came up with this: “When Homo sapiens passed the six-billion mark we had already exceeded by perhaps as much as 100 times the biomass of any large animal species that ever existed on the land.”

In ecological terms, we are almost paradoxical: large-bodied and long-lived but grotesquely abundant. We are an outbreak.

Although wild aquatic birds are now known to be the ultimate origin of all influenzas, the viruses reassort themselves in pigs and elsewhere (quail also serve as mixing bowls), and by the time they get into humans, they have generally been assembled from H1, H2, or H3 plus the ten other necessary proteins, some of those in forms borrowed from this or that bird flu or pig flu virus.

A three-year-old boy died in Hong Kong of influenza, in May 1997, and a swab sample from his windpipe yielded virus. The lab scientists in Hong Kong didn’t recognize that virus. Some of the boy’s sample went to the CDC, but no one there got around to characterizing it. Then a Dutch scientist on a visit to Hong Kong was given a bit of the virus, and he went home and worked on it immediately. Hmm, mijn God. The Dutchman informed his international colleagues that it looked like an H5. A bird flu.

this was the first documented case of a purely avian influenza virus—containing no human-flu genes brought in by reassortment—to cause killer respiratory illness in a person.

The toll in Egypt is high enough: 151 confirmed as of August 2011, of which 52 were fatal. Those numbers represent more than a quarter of all the world’s known human cases of bird flu, and more than a third of all fatalities, since H5N1 emerged in 1997.

(1) Will a new disease emerge, in the near future, sufficiently virulent and transmissible to cause a pandemic on the scale of AIDS or the 1918 flu, killing tens of millions of people? and (2) If so, what does it look like and whence does it come? Their answers to the first part have ranged from Maybe to Probably. Their answers to the second have focused on RNA viruses, especially those for which the reservoir host is some kind of primate. None of them has disputed the premise, by the way, that if there is a Next Big One it will be zoonotic.

these recent outbreaks of new zoonotic diseases, as well as the recurrence and spread of old ones, are part of a larger pattern, and that humanity is responsible for generating that pattern. We should recognize that they reflect things that we’re doing, not just things that are happening to us. We should understand that, although some of the human-caused factors may seem virtually inexorable, others are within our control.

Medical people of the earlier eras might guess that bubonic plague was somehow related to rodents, yes, but they didn’t know how or why until Alexandre Yersin, during an 1894 epidemic in Hong Kong, found the plague bacterium in rats. Even that didn’t illuminate the path to human infection until Paul-Louis Simond, several years later, showed that the bacterium is transmitted by rat fleas.

During the early twentieth century, disease scientists from the Rockefeller Foundation and other institutions conceived the ambitious goal of eradicating some infectious diseases entirely. They tried hard with yellow fever, spending millions of dollars and many years of effort, and failed. They tried with malaria, and failed. They tried later with smallpox, and succeeded. Why? The differences among those three diseases are many and complex, but probably the most crucial one is that smallpox resided neither in a reservoir host nor in a vector. Its ecology was simple. It existed in humans—in humans only—and was therefore much easier to eradicate.