Spillover: Animal Infections and the Next Human Pandemic (47 page)

“Were you wearing masks?”

“We were.” They had N95 masks, simple and relatively cheap but effective against small particles, standard equipment in this sort of situation. If they had known what to expect in Faridpur, they might have wanted something better, but Gurley’s chief regret was simply that they hadn’t brought more N95s, enough for the local health-care staff as well as themselves. And then, because it was storm season, a heavy squall blew through town and knocked out the electricity. The lights went off, and the staff closed all the windows—“which is not what you want,” Gurley said, laughing grimly. By morning, not just the coughing man but also two other patients in that crowded, stuffy room had died.

Gurley gathered the interview data and, as she started charting an epidemiological curve, realized that “everyone who was in that hospital ward had had very close contact with another person”—one in particular—“who died from this a couple weeks before.” She meant the religious leader. This pattern was quite different from earlier Nipah outbreaks, in which most patients seemed to have gotten infected directly from some environmental source (sick livestock? treetops? the palm-sap hypothesis hadn’t yet arisen), not from human contagion, and in which the symptoms had been mainly neurological, not respiratory. Gurley’s group even doubted, for a while, that Nipah was the cause at Faridpur. But then samples shipped back to Atlanta tested positive for Nipah, at which point the CDC sent a small team of specialists to work alongside Gurley and her colleagues.

The investigation at Faridpur eventually yielded a new understanding of Nipah—as a disease in which person-to-person transmission could be far more important than supposed. Of the thirty-six cases, twenty-two were linked to the religious leader. Those people had gathered closely around him during his final illness. Presumably they had been infected by aerosolized virus, or touch, or spittle, or some other sort of direct transfer. Most cases among the other fourteen also seemed to reflect person-to-person transmission. A rickshaw driver in a nearby village, who worked seasonally as a date-palm-sap collector, fell ill and was nursed by his mother, his son, his aunt, and a neighbor; they all got sick too. The rickshaw driver’s aunt received care from an in-law, a man from Guholaxmipur, who visited her in the hospital; that in-law was the religious leader. One of the sect followers, infected, his condition worsening, was helped to a hospital by another rickshaw driver; that driver fell ill, about ten days later, and died . . . and so on.

Nipah was passing horizontally through the community, like a rumor, not just down from the sky, like a divine curse or a dollop of bat poop. And its seeming ubiquity was confirmed by one other finding of the combined response team. This bit of data was especially spooky. The investigators took swabs from the wall of a hospital room in which one of the patients had been treated, five weeks earlier, and from the soiled frame of a bed in which that patient had lain. None of those surfaces had been cleaned in the meantime; bleach and labor were in short supply. Some swabs, both from the wall and the bed frame, tested positive for Nipah RNA. I’ll repeat that: Fragments (at least) of Nipah virus, left from what the patient had spewed out, were still present after
five weeks
, invisibly decorating the room
.
To the sanitarian, such spewing represents contamination. To the virus: opportunity.

I spoke also with Rasheda Khan, a medical anthropologist just down the hall from Emily Gurley. Khan is a Bangladeshi with dark eyes and a severe, professional manner. Her job was to investigate the cultural and social factors that affect a disease event like the Faridpur outbreak. She had been there in Faridpur, interviewing villagers in their native tongue, Bangla, to collect testimony about behaviors and attitudes as well as to learn who got sick when. She talked about asmani bala (“a curse inflicted by Allah,” was her translation, slightly more blunt than others I’d heard) and how that fateful idea may have dissuaded some victims from seeking hospital care. She helped me understand the sort of little interpersonal intimacies, characteristic of her country, that could be relevant to disease transmission. “In Bangladesh,” she said, “physical contact is very common. We hug, we hold hands all the time.” Even along the road, she said, you see men walking together, holding hands. Such physicality only increased, from a sense of concern, if a person were sick—and more still if the sick person were a venerated figure, like the sect leader in Guholaxmipur. This man was beloved by his followers and seen as close to God. People came as he lay on his deathbed to be favored with a last touch, or to whisper blessings in his ear, or to sponge his body, or to offer him a sip of water or milk or juice. “That is one of the customs here,” Khan explained, “that you give water to the dying person’s mouth.” Many people came to his bedside, bent close, offered him water, she said, “and he was coughing all the time. And the fog was everywhere on people’s—”

I think she was going to say “faces” but like a fool I interrupted her.

“The fog?”

“Yeah, the saliva,” Khan said. “His coughing. So the spit was . . . people told us that he was coughing, and his coughing, the spit, on body, hands . . .” Eliding these thoughts, she left me to fill in the blanks, then mentioned that hand washing, unlike hand holding, is not common practice in Bangladesh. Unlucky followers and family members may have come away from their final audiences lightly glazed with the holy man’s spittle—and then rubbed their eyes, taken food with those hands, or otherwise accepted the virus. You don’t need date-palm sap if you’ve got that.

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O
ver the course of three days I made several trips to the ICDDR,B, which occupies a complex of buildings behind a high wall in the Mohakhali neighborhood of Dhaka. In addition to the talks with Khan and Gurley, I spoke with some high administrators and some bright young researchers, who gave me a wide range of perspectives and insights on Nipah virus. But the most affecting moment occurred when my taxi through the crazed Dhaka traffic pulled up to the wrong gate of the compound, leaving me just disoriented enough to walk in the wrong door. This wasn’t the sleek building that housed Steve Luby’s infectious diseases program. This was the old Cholera Hospital itself.

A solicitous Bangladeshi man, who noticed me looking lost, asked my destination and pointed me along, suggesting I simply cross through the hospital. A guard opened the next door and saluted me. No one asked for a badge. I found myself intruding through an open ward lined with dozens of beds. A few of those beds were empty, sheetless, showing a mattress of red or green vinyl with a bedpan hole in the middle: cold, practical, ready for the next case. Many other beds were filled with the thin, bony bodies of suffering patients, sorrowful brown-skinned people, alone or consoled quietly by relatives. Here came I, a white man with a briefcase, into this hangar of souls eagerly awaiting attention from a doctor. One woman caught my eyes, then whispered to her child, held beside her on the bed, and pointed at me. Out on the street such a gesture would suggest idle curiosity or maybe a prelude to begging, but here it surely indicated hope—deep hope, hope of deliverance, but misplaced. I averted my eyes and walked on, acutely aware that I had no skills, no knowledge, no training, no medicines that could be helpful to this woman and her child, more’s the worse for me. Through further corridors, other doors, more saluting guards, I found my way to the next interview.

The Cholera Hospital was founded in 1962, as a clinical adjunct to an earlier Cholera Research Laboratory, both of which were eventually bundled into the ICDDR,B. The hospital provides free treatment to more than a hundred thousand patients each year, not only for cholera but also for blood dysentery and other diarrheal diseases. Most of its patients are children under the age of six. Eighty percent of those children arrive at the hospital malnourished. I can’t tell you how many survive. I can’t even tell you how many cholera cases occur annually when the flood season in Bangladesh brings infected waters up into villages and slums, because most cases go unreported and there is no systematic national tally. One authoritative guess: a million. What I can tell you is that Bangladesh, wondrous in so many ways, engaging and fascinating as well as horrifying to an affluent visitor, is an especially difficult country in which to be a poor citizen, either urban or rural, because if you’re poor it’s a difficult country in which to remain healthy. Thousands of people, young and old, die of cholera and other diarrheal diseases and pneumonia and tuberculosis and measles. Note that none of those afflictions is newly emergent, mysterious, or zoonotic. Together they dwarf the impact—at least so far—of Nipah virus encephalitis.

Why are zoonotic diseases important? I’ve been asked that question, and have asked it of others, more than a few times during my six years of chasing the subject. (One fellow, a respected historian I met at a conference, suggested that I forget about Ebola and write a book on asthma, which afflicts 22 million Americans. He happened to be asthmatic.) Given the global scorecard of morbidity and mortality caused by old-fashioned and nonzoonotic infectious diseases—such as cholera, typhoid, TB, rotavirus diarrhea, malaria (excepting
Plasmodium knowlesi
), not to mention chronic illnesses such as cancer and heart disease—why divert attention to these boutique infections, these anomalies, that spill out of bats or monkeys or who knows where to claim a few dozen or a few hundred people now and then?
Why?
Isn’t it misguided to summon concern over a few scientifically intriguing diseases, some of them new but of relatively small impact, while boring old diseases continue to punish humanity? After my detour through the Cholera Hospital, after being pinioned by that mother’s expectant stare, I found myself asking the same thing: Why obsess about zoonoses? In the larger balance of miseries, what makes anyone think they should be taken so seriously?

It’s a fair question but there are good answers. Some of those answers are intricate and speculative. Some are subjective. Others are objective and blunt. The bluntest is this: AIDS.

VIII

THE CHIMP AND THE RIVER

85

T
here are many beginnings to what we think we know about the AIDS pandemic, most of which don’t even address the subject of its origin in a single zoonotic spillover.

For instance: In autumn of 1980, a young immunologist named Michael Gottlieb, an assistant professor at the UCLA Medical Center, began noticing a strange pattern of infections among certain male patients. The patients, eventually five of them, were all active homosexuals and all suffering from pneumonia caused by a usually harmless fungus then known as
Pneumocystis carinii.
(Nowadays, after a name change, it’s
Pneumocystis jirovecii.
) The stuff is ubiquitous; it floats around everywhere. Their immune systems should have been able to clear it. But their immune systems evidently weren’t working, and this fungus filled their lungs. Each man also had another sort of fungal infection—oral candidiasis, meaning a mouthful of slimy
Candida
yeast, more often seen in newborn babies, diabetics, and people with compromised immune systems than in healthy adults. Blood tests, done on several of the patients, showed dramatic depletions of certain lymphocytes (white blood cells) that are crucial in regulating immune responses. Specifically, it was thymus-dependent lymphocytes (T cells, for short) that were “
profoundly depressed
” in number. Although Gottlieb noted some other symptoms, those three stood out:
Pneumocystis
pneumonia, oral candidiasis, dearth of T cells. In mid-May of 1981, he and a colleague wrote a brief paper describing their observations. They didn’t speculate about causes. They just saw the pattern as a befuddling, ominous trend and felt they should publish quickly. An editor at
The New England Journal of Medicine
was interested but his lead time would be at least three months.

So Gottlieb turned to the streamlined CDC newsletter,
Morbidity and Mortality Weekly Report.
His barebones text, less than two pages long, appeared in
MMWR
on June 5, 1981, under the dry title “
Pneumocystis
Pneumonia—Los Angeles.” It was the first published medical alert about a syndrome that didn’t yet have a name.

The second alert came a month later, again in the CDC newsletter. While Gottlieb was noticing
Pneumocystis
pneumonia and candidiasis, a New York dermatologist named Alvin E. Friedman-Kien spotted a parallel trend involving a different disease: Kaposi’s sarcoma. A rare form of cancer, not usually too aggressive, Kaposi’s sarcoma was known primarily as an affliction of middle-aged Mediterranean males—the sort of fellows you’d expect to find in an Athens café, drinking coffee and playing dominoes. This cancer often showed itself as purplish nodules in the skin. Within less than three years, Friedman-Kien and his network of colleagues had seen twenty-six cases of Kaposi’s sarcoma in youngish homosexual men. Some of those patients also had
Pneumocystis
pneumonia. Eight of them died. Hmm.
Morbidity and Mortality Weekly Report
carried Friedman-Kien’s communication on July 3, 1981.

Kaposi’s sarcoma also figured prominently in a set of clinical observations made in Miami around the same time. The symptoms among this group of patients were similar; the cultural profile was different. These sick people, twenty of them, hospitalized between early 1980 and June 1982, were all Haitian immigrants. Most had arrived in the United States recently. By their own testimony during medical interviews they were all heterosexuals, with no history of homosexual activity. But their cluster of ailments resembled what Gottlieb had seen among gay men in Los Angeles and Friedman-Kien among gay men in New York:
Pneumocystis
pneumonia, candidiasis in the throat, plus other unusual infections, irregularities in lymphocyte counts, and aggressive Kaposi’s sarcoma. Ten of the Haitians died. The team of doctors who published these observations saw a “syndrome” that seemed “
strikingly similar to the syndrome of immunodeficiency
described recently among American homosexuals.” The early connection to Haitian heterosexuals would later come to seem like a false lead and be largely ignored in discussions of AIDS. It was hard to confirm, based on interview data, and harder still to construe. Calling attention to it even came to seem politically incorrect. Then, later still, its real significance would emerge from work at the level of molecular genetics.

Another perceived starting point was Gaëtan Dugas, the young Canadian flight attendant who became notorious as “Patient Zero.” You’ve heard of him, probably, if you’ve heard much of anything about the dawning of AIDS. Dugas has been written about as the man who “
carried the virus out of Africa
and introduced it into the Western gay community.” He wasn’t. But he seems to have played an oversized and culpably heedless role as a transmitter during the 1970s and early 1980s. As a flight steward, with almost cost-free privileges of personal travel, he flew often between major cities in North America, joining in sybaritic play where he landed, notching up conquests, living the high life of a sexually voracious gay man at the height of the bathhouse era. He was handsome, sandy-haired,
vain but charming, even “gorgeous” in some eyes
. According to Randy Shilts, author of
And the Band Played On
(which includes much heroic research and a fair bit of presumptuous reimagining), Dugas himself reckoned that in the decade since becoming actively gay he had had at least twenty-five hundred sexual partners. Dugas paid a price for his appetite and his daring. He developed Kaposi’s sarcoma, underwent chemotherapy for that, suffered from
Pneumocystis
pneumonia and other AIDS-related infections, and died of kidney failure at age thirty-one. During the brief stretch of years between his Kaposi’s diagnosis and his final invalidism, Gaëtan Dugas didn’t slow down. But he seems to have tipped, in his lonely despair, from hedonism to malice; he would have sex with a new acquaintance at the Eighth-and-Howard bathhouse in San Francisco, then turn up the lights—so Randy Shilts claimed—display his lesions, and say: “
I’ve got gay cancer
. I’m going to die and so are you.”

In the same month as Dugas’s death, March 1984, a team of epidemiologists from the CDC published a landmark study of the role of sexual contact in linking cases of what by then was called AIDS. The world had a label now but not an explanation. “
Although the cause of AIDS is unknown
,” wrote the CDC team, whose lead author was David M. Auerbach, “it may be caused by an infectious agent that is transmissible from person to person in a manner analogous to hepatitis B infection.” Hepatitis B is a blood-borne virus. It moves primarily by sexual contact, intravenous drug use with shared needles, or transfusion of blood products carrying the virus as a contaminant. It seemed like a template for understanding what otherwise was still a bewildering convergence of symptoms. “The existence of a cluster of AIDS cases linked by homosexual contact is consistent with an infectious-agent hypothesis,” the CDC group added. Not a toxic chemical, not an accident of genetics, but some kind of bug, is what they meant.

Auerbach and his colleagues gathered information from nineteen AIDS cases in southern California, interviewing each patient or, if he was dead, his close companions. They spoke with another twenty-one patients in New York and other American cities, and from their forty case histories they created a graphic figure of forty interconnected disks, like a Tinkertoy structure, showing who had been linked sexually with whom. The patients’ identities were coded by location and number, such as “SF 1,” “LA 6,” and “NY 19.” At the center of the network, connected directly to eight disks and indirectly to all the rest, was a disk labeled “0.” Although the researchers didn’t name him, that patient was Gaëtan Dugas. Randy Shilts later transformed the somewhat bland “Patient 0,” as mentioned in this paper,
to the more resonant “Patient Zero” of his book
. But what the word “Zero” belies, what the number “0” ignores, and what the central position of that one disk within the figure fails to acknowledge, is that Gaëtan Dugas didn’t conceive the AIDS virus himself. Everything comes from somewhere, and he got it from someone else. Dugas himself was infected by some other human, presumably during a sexual encounter—and not in Africa, not in Haiti, somewhere closer to home. That was possible because, as evidence now shows, HIV-1 had already arrived in North America when Gaëtan Dugas was a virginal adolescent.

It had also arrived in Europe, though on that continent it hadn’t yet gone far. A Danish doctor named Grethe Rask, who had been working in Africa, departed in 1977 from what was then Zaire and returned to Copenhagen for treatment of a condition that had been dragging her downward for several years. During her time in Zaire, Rask had first run a small hospital in a remote town in the north and then served as chief surgeon at a large Red Cross facility in the capital, Kinshasa. Somewhere along the way, possibly during a surgical procedure done without adequate protective supplies (such as latex gloves), she became infected with something for which no one at the time had a description or a name. She felt ill and fatigued. Drained by persistent diarrhea, she lost weight. Her lymph nodes swelled and stayed swollen. She told a friend: “
I’d better go home to die
.” Back in Denmark, tests revealed a shortage of T cells. Her breath came with such difficulty that she depended on bottled oxygen. She struggled against staph infections.
Candida
fungus glazed her mouth. By the time Grethe Rask died, on December 12, 1977, her lungs were clogged with
Pneumocystis jirovecii
, and that seems to have been what killed her.

It shouldn’t have, according to standard medical wisdom.
Pneumocystis
pneumonia wasn’t normally a fatal condition. There had to be a broader explanation, and there was. Nine years later, a sample of Rask’s blood serum tested positive for HIV-1.

All these unfortunate people—Grethe Rask, Gaëtan Dugas, the five men in Gottlieb’s report from Los Angeles, the Kaposi’s sarcoma patients known to Friedman-Kien, the Haitians in Miami, the cluster of thirty-nine (besides Dugas) identified in David Auerbach’s study—were among the earliest recognized cases of what has retrospectively been identified as AIDS. But they weren’t among the first victims. Not even close. Instead they represent midpoints in the course of the pandemic, marking the stage at which a slowly building, almost unnoticeable phenomenon suddenly rose to a crescendo. Again in the dry terms of the disease mathematicians, whose work is vitally applicable to the story of AIDS:
R
0
for the virus in question had exceeded 1.0, by some margin, and the plague was on. But the real beginning of AIDS lay elsewhere, and more decades passed while a few scientists worked to discover it.

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I
n the early years after its detection, the new illness was a shifting shape that carried several different names and acronyms. GRID was one, standing for Gay-Related Immune Deficiency. That proved too restricted as heterosexual patients began to turn up: needle-sharing addicts, hemophiliacs, other unlucky straights. Some doctors preferred ACIDS, for Acquired Community Immune Deficiency Syndrome. The word “community” was meant to signal that people acquired it
out
there
, not in hospitals. A more precise if clumsier formulation, favored briefly by the CDC’s
Morbidity and Mortality Weekly Report,
was “Kaposi’s sarcoma and opportunistic infections in previously healthy persons,” which didn’t abbreviate neatly. KSOIPHP lacked punch. By September 1982,
MMWR
had switched its terminology to Acquired Immune Deficiency Syndrome (AIDS), and the rest of the world followed.

Naming the syndrome was the least of the early challenges. More urgent was to identify its cause. I just alluded to “the virus in question,” but remember: No one knew, back when those reports from Gottlieb and Friedman-Kien began capturing attention, what sort of pathogen caused this combination of puzzling, lethal symptoms—nor even if there
was
a single pathogen. The virus idea arose as a plausible guess.

One scientist who made the guess was Luc Montagnier, then a little-known molecular biologist at the Institut Pasteur in Paris. Montagnier’s research had focused mainly on cancer-causing viruses, especially the group known as retroviruses, some of which cause tumors in birds and mammals. Retroviruses are fiendish beasts, even more devious and persistent than the average virus. They take their name from the capacity to move backward (retro) against the usual expectations of how a creature translates its genes into working proteins. Instead of using RNA as a template for translating DNA into proteins, the retrovirus converts its RNA into DNA within a host cell; its viral DNA then penetrates the cell nucleus and gets itself integrated into the genome of the host cell, thereby guaranteeing replication of the virus whenever the host cell reproduces itself. Luc Montagnier had studied these things in animals—chickens, mice, primates—and wondered about the possibility of finding them in human tumors too. Another disquieting possibility about retroviruses was that the new disease showing up in America and Europe, AIDS, might be caused by one.

There was still no solid proof that AIDS was caused by a virus at all. But three kinds of evidence pointed that way, and Montagnier recalls them in his memoir, a book titled
Virus
. First, the incidence of AIDS among homosexuals linked by sexual interactions suggested that it was an infectious disease. Second, the incidence among intravenous drug users suggested a blood-borne infectious agent. Third, the cases among hemophiliacs implied a blood-borne agent that escaped detection in processed blood products such as clotting factor. So: It was infinitesimal, contagious, blood-borne. “
AIDS could not be caused by a conventional bacterium
, a fungus, or protozoan,” Montagnier wrote, “since these kinds of germs are blocked by the filters through which the blood products necessary to the survival of hemophiliacs are passed. That left only a smaller organism: the agent responsible for AIDS thus could only be a virus.”