Spillover: Animal Infections and the Next Human Pandemic (60 page)

Inviting me to a chair at her big double-viewer Olympus microscope, Karen Terio brought out the same slides she had shared with Hahn and Lonsdorf. From her place at the scope she could manipulate a cursor, a little red arrow, moving it over the field to point out what we were seeing. First she showed me a thin-slice section from a lymph node of a normal, SIV-negative chimpanzee. This was for comparison. It looked like a peat bog as viewed on Google Earth, bulging and rife with sphagnum and huckleberry, thick, rich, and riddled just slightly with narrow spaces resembling small sloughs and creeks. The tissue was stained magenta and heavily speckled with darker blue dots. The dots, Terio explained, were lymphocytes in their healthy abundance. In an area where they’re especially dense, they pack together into a follicle, like a bag full of jellybeans. She jabbed her red arrow at a follicle.

Then she placed another slide into viewing position. The slide held a slice from one of Yolanda’s lymph nodes. Instead of a peat bog, it looked like scrub desert slashed by a large drywash, many days since the last rain.

“Mmmm,” I said.

“This is essentially the connective tissue,” Terio said. She meant that it was supportive structure only, minus the working innards. Sere and empty. “We’ve got very, very few lymphocytes left in this animal.”

“Yeah.”

“And it’s collapsed. You see, this whole thing has just sort of collapsed on itself, ’cause there’s nothing in there to hold it up.” Her little red arrow wandered forlorn through the desert. No sphagnum, no follicles, no little blue dots. I imagined Karen Terio, back in April 2008, examining these slides on her lonesome—and encountering such evidence, before anyone else, at a time when the illusion of nonpathogenic SIV
cpz
was embraced by researchers everywhere.

“So you sat there, and looked at this . . .”

“And went, ‘Oh, no,’ ” she said.

106

T
erio’s findings, plus the field data from Gombe, plus the molecular analyses from Hahn’s lab—these all came together in a paper published by
Nature
during the summer of 2009. Brandon Keele was first author; Beatrice Hahn was last. “Increased Mortality and AIDS-like Immunopathology in Wild Chimpanzees Infected with SIV
cpz
” was the catchy title. I think of it—and I’m not alone—as “the Gombe paper.” Among the long list of coauthors were Karen Terio, Terio’s boss, Elizabeth Lonsdorf, Jane Raphael, two of Hahn’s senior colleagues, the expert on primate cell pathology, the chief scientist at Gombe, and Jane Goodall herself.

“Well, I sort of had to be. But I had these long talks with Beatrice first,” Jane told me. “She was going to publish it anyway.” In the sweep of inevitability and the name of science, Dr. Goodall signed on.

The paper’s salient conclusion was that, contrary to Keele’s earlier draft abstract, there is indeed a death hazard for SIV-positive chimps at Gombe. Of the eighteen individuals that died during the study period, seven were SIV-positive. Given that less than 20 percent of the population was SIV-positive, and adjusted for normal mortality at a given age, this reflected a risk of death ten times to sixteen times higher for SIV-positive chimps than for SIV-negatives. Repeat: ten to sixteen times higher. The total numbers were small but the margin was significant. Infected animals were falling away. Furthermore, SIV-positive females had lower birth rates and greater infant mortality. Further still, three necropsied individuals (including Yolanda, though her name wasn’t mentioned) showed signs of lymphocyte loss and other damage resembling end-stage AIDS.

The authors suggested, cautiously but firmly, “
that SIV
cpz
has a substantial negative impact
on the health, reproduction and lifespan of chimpanzees in the wild.” So it’s not a harmless passenger. It’s a hominoid killer, their problem as well as ours.

107

H
ere’s what you have come to understand. That 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.

Spread how? Once it reached Léopoldville, the group M virus seems to have entered a vortex of circumstances unlike anything at the headwaters of the Sangha. It differed from HIV-2 biologically (having adapted to chimpanzee hosts) and it differed from groups N and O by chance and opportunity (having found itself in an urban environment). Whatever happened to it in Léopoldville during the first half of the twentieth century can only be conjectured. Population density of potential human hosts, a high ratio of males to females, sexual mores different from what prevailed in the villages, and prostitution—these were all parts of the mix. But sex plus crowding may not be a sufficient explanation. A fuller chain of conjecture, and maybe a better one, has been offered by Jacques Pepin, a Canadian professor of microbiology who, during the 1980s, worked for four years at a bush hospital in Zaire. Pepin coauthored several journal papers on the subject and, in 2011, published a book titled
The Origins of AIDS.
Having added some deep historical research to his own field experience and microbiological expertise, he proposed that the crucial factor intermediating between the Cut Hunter and the global pandemic was the hypodermic syringe.

Pepin wasn’t referring to recreational drugs and the works shared by addicts at shooting galleries. In a paper titled “Noble Goals, Unforeseen Consequences,” and then at greater length in his book, he pointed instead to a series of well-intended campaigns by colonial health authorities, between 1921 and 1959, aimed at treating certain tropical diseases with injectable medicines. There was a massive effort, for instance, against trypanosomiasis (sleeping sickness) in Cameroon. Trypanosomiasis is caused by a persistent little protist (
Trypanosoma brucei
)
,
transmitted in the bite of tsetse flies. The treatment in those years entailed injections of arsenical drugs such as tryparsamide—and a patient didn’t get just one shot but a series. In Gabon and Moyen-Congo (the French colonial name for what’s now the Republic of the Congo), the regimen for trypanosomiasis sometimes entailed thirty-six injections over three years. And there were similar efforts to control syphilis and yaws. Malaria was treated with injectable forms of quinine. Leprosy patients, in that era before oral antibiotics, underwent a course of injections with extract of chaulmoogra (an Indian medicinal plant), two or three shots per week for a year. In the Belgian Congo, mobile teams of
injecteurs,
people with no formal education but a small bit of technical training, visited trypanosomiasis patients in their villages to give weekly shots. It was a period of mania for the latest medical wonder: needle-delivered cures. Everyone was getting jabbed.

Of course, this was long before the era of the disposable syringe.
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. A famous 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. This sort of production-line delivery of injectable medicines didn’t allow time for boiling a syringe and needle between uses. It’s difficult now, based on skimpy sources and laconic testimony, to know exactly what sort of sanitary precautions were taken. But according to one Belgian doctor, writing in 1953: “
The Congo contains various health institutions
(maternity centres, hospitals, dispensaries, etc.) where every day local nurses give dozens, even hundreds, of injections in conditions such that sterilisation of the needle or the syringe is impossible.” This man was writing about the risk of accidental transmission of hepatitis B during treatment for venereal diseases, but Pepin quoted his report at length, for its potential relevance to AIDS:

The large number of patients and the small quantity of syringes
available to the nursing staff preclude sterilisation by autoclave after each use. Used syringes are simply rinsed, first with water, then with alcohol and ether, and are ready for a new patient. The same type of procedure exists in all health institutions where a small number of nurses have to provide care to a large number of patients, with very scarce supplies. The syringe is used from one patient to the next, occasionally retaining small quantities of infectious blood, which are large enough to transmit the disease.

How much of this went on? Very much. Pepin’s diligent search through old colonial archives turned up some big numbers. In 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.

All those injections, according to Pepin, might account for boosting the incidence of HIV infection beyond a critical threshold. Once the reusable needles and syringes put the virus into enough people—say, several hundred—it wouldn’t come to a dead end, it wouldn’t burn out, and sexual transmission could do the rest. Some experts, including Michael Worobey and Beatrice Hahn, doubt that needles were necessary in any such way to the establishment of HIV in humans—that is, to its early transmission from one person to another. But even they agree that injection campaigns could have played a role later, spreading the virus in Africa once it was established.

This needle theory didn’t originate with Jacques Pepin. It dates back more than a decade to work by an earlier team of researchers, including Preston Marx of the Rockefeller University, who proposed it in 2000 at the same Royal Society meeting on AIDS origins at which Edward Hooper spoke for his oral polio vaccine theory. Marx’s group even argued that serial passage of HIV through people, by means of such injection campaigns, might have accelerated the evolution of the virus and its adaptation to humans as a host, just as passaging malarial parasites through 170 syphilis patients (remember the crazed Romanian researcher, Mihai Ciuca?) could increase the virulence of
Plasmodium knowlesi
. Jacques Pepin picked up where Preston Marx left off, though with less emphasis on the evolutionary effect of serial passage. Pepin’s main point was simply that dirty needles, used so widely, must have increased the prevalence of the virus among people in Central Africa. Unlike the OPV theory, this one hasn’t been discredited by further research, and Pepin’s new archival evidence suggests that it’s highly plausible, if unprovable.

Most of those injections for trypanosomiasis occurred in the countryside. City dwellers were less exposed to trypanosomiasis, partly because the tsetse fly doesn’t thrive in urban jungles as well as it does in green ones. One question that needed answering, therefore, was whether any such mania for injecting had also gripped Léopoldville, where HIV met its most crucial test. Pepin’s answer is unexpected, interesting, and persuasive. Never mind trypanosomiasis. He discovered a different but equally aggressive campaign of injections, aimed at limiting syphilis and gonorrhea in the city’s population.

In 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, near the river, it was a private facility providing a public service. Male migrants, arriving to seek work, were required by city regulations to report to the Dispensaire for an exam. Anyone experiencing symptoms could visit the place voluntarily, and there was no charge for treatment. But the bulk of the caseload, according to Pepin, “
consisted of thousands of asymptomatic free women
who came for screening because they were required to do so by law, in theory every month.” The colonial government accepted prostitution as an ineradicable fact but evidently hoped to keep the trade hygienic—so
les
femmes libres
were obliged to get checked.

If a person tested positive for syphilis or gonorrhea, he or she would be treated. But the diagnostic testing was imprecise. Any free woman or male migrant who had once been exposed to yaws (caused by a bacterium very similar to the syphilis bacterium, but not sexually transmissible) might flunk the blood test, be classed as syphilitic, and receive a long course of drugs containing arsenic or bismuth. Harmless vaginal flora could be mistaken for gonococcus, the agent of gonorrhea. A woman diagnosed gonorrheic might be injected with typhoid vaccine, or a drug called Gono-yatren, or (even Jacques Pepin seems puzzled by this one) milk. 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.