The Coming Plague

by Laurie Garrett

  In coming months, with no words of comfort from the CDC or the National Institutes of Health, Volberding’s fears sometimes prompted a call to a fellow clinician in Boston to say, “Gee, I’ve got a fever. Do you think I might have it?”

  Volberding was far from alone. Most of the physicians caring for the Kaposi’s/PCP patients in 1981–82 were very worried about their personal safety, as well as the health of their staff. But the majority pushed on, got past the fear, adhered to their Hippocratic oath, and treated the patients. No study to determine the risks to health providers would be funded until 1984. To allay fears, the CDC would issue a list of recommendations for safe practices by health providers and laboratory personnel on November 5, 1982, suggesting that hepatitis B precautions already in place were adequate. But hepatitis B infection rates were soaring among health providers, and few took comfort in the shared “adequacy” of safety measures taken for the two diseases.8

  In Antwerp, Peter Piot closely followed the reports about the new Kaposi’s /PCP syndrome. He had an insight that gave him a cold chill.

  Ever since his rite of passage into global disease research in Yambuku, Piot had maintained close links with Africa and the United States. Unlike most of his Belgian colleagues, Piot didn’t find Americans crude and vulgar—in fact, he rather liked them. And he couldn’t imagine embracing the neocolonialist attitudes toward Africans still so prevalent in 1981 among Belgians. Whenever the money could be found, Piot returned to America for more training and to Africa for research.

  Which was why the CDC’s reports in the summer of 1981 struck him with a sense of unease and recognition. Since 1978 he had been involved in STD research in East Africa, and many Africans came through his Belgian facilities for diagnosis when they suffered from an unusual ailment. Gottlieb’s report of Pneumocystis cases among Los Angeles gay men reminded Piot of the Greek fisherman he had treated in Antwerp in 1978.

  The man had commercially fished Lake Tanganyika, from the Zairian side, during the late 1970s. By the time he had reached Antwerp for treatment, he was just moments from death and could give little medical history. The autopsy was so astonishing that years later Piot would recall performing it in vivid detail.

  The fisherman appeared to be in his late thirties, an outwardly healthy man. But when Piot opened the body the stench and sight of “pure and complete rot” greeted him. Every organ, each bone, all the tissues were covered with some type of mycobacterium. When Piot cultured samples of it in his laboratory neither he nor any of his colleagues could identify the organism. Whatever it was, this strange mycobacterium was not, in test-tube studies, a killer of human cells, and this fisherman shouldn’t have died.

  Having learned in Africa of the possible future value of such mysteries, Piot had carefully labeled and frozen samples of the fisherman’s blood and tissues.

  Piot wondered whether a new, lethal sexually transmitted disease might not be present already in many parts of the world, hidden under layers of neglect, racism, and poverty, and possibly masked by other diseases. He reviewed files on other strange cases that had come through his laboratory since 1978, finding three more bizarre deaths among Africans who sought care in Belgium. Though all three were young adults (one was female), they had, like the fisherman, succumbed to strange fulminant infections of organisms usually known to attack only immunodeficient humans: cryptococcal meningitis, other strange mycobacteria, and Pneumocystis.

  All three patients, as well as the fisherman, had come to Antwerp from Zaire. And they all died before 1980. Could there be a link, Piot wondered, between whatever was killing homosexuals in California and these Zairian deaths?

  By the end of 1981, Michael Callen was feeling lousy. Fatigued, feverish, incontinent, he sought help from a Greenwich Village private practitioner known in gay circles to be a good “clap doctor,” Dr. Joseph Sonnabend.

  The South African-born Sonnabend had been practicing medicine and conducting clinical experiments in New York for years, and was known for his brusque, outspoken style. In December 1981, Sonnabend told Callen that his illnesses were due to an underlying immunodeficiency of some kind. Unable to explain its cause, Sonnabend decided to aggressively treat all the other organisms that were taking advantage of Callen’s beleaguered state, and put him on a prophylactic therapy with trimethoprim to prevent PCP.

  It would be six months before Callen would be officially diagnosed as a GRID case—Gay-Related Immunodeficiency Disease.

  Sonnabend asked Callen to participate in a study to test his hypothesis that the new disease was directly correlated with promiscuity. Having witnessed the steady rise in infectious diseases among New York’s gay men, Sonnabend had a hunch that they had been exposed to ever-greater numbers of microbes, producing a sort of immune system overload, causing it to go haywire and self-destruct.

  To test the hypothesis, Sonnabend divided his gay patients according to three tiers of relative promiscuity: monogamy, fewer than fifty partners a year, and men who, like Callen, had hundreds of sexual encounters a year. He sent the blood samples from the men to the University of Nebraska, where Dr. David Purtilo ran them through a fluorescence-activated cell sorter which separated out and counted specific immune system cells.

  The study found that in some of the men a special class of T cells, called CD4 or T-helper cells, was virtually absent. These cells normally drew the body’s defensive apparatus to the site of an infection and marshaled responses to rid the bloodstream of invading organisms. Without CD4 cells the immune system would be hard pressed to fend off any microbes.

  Purtilo’s data indicated that the most promiscuous men had the lowest CD4 counts, while the monogamous participants in the study had normal numbers of the T-helper cells.

  The finding prompted Sonnabend and Callen to speak out to New York’s gay community, warning that continued promiscuity could be lethal. New York gay playwright Larry Kramer echoed their warnings, issuing pleas for a slowdown on the sexual fast lane. All three men were rewarded with cries of outrage, denounced as “anti-gay faggots,” homophobes, fearmongers, and fools.

  Though vilified, the three were not silenced. Sonnabend flatly told his patients, “You’re fucking yourself to death.” Callen and Kramer tried to cook up ways to awaken their fellow gay liberationists to reality.9 Toward the end of summer of 1981 Kramer called a meeting in Manhattan of like-minded gay activists. A handful of men turned up to hear his plea for health action. Money was raised and a name was selected for their new organization: Gay Men’s Health Crisis (GMHC). The group’s first public approach to their community was via the gay press and brochures distributed on Fire Island, the resort area to which Manhattan’s endless gay party moved during the hot, humid summer.

  They were roundly ignored.

  By fall Bobbi Campbell noticed a few purple blotches on his skin. He had heard of the so-called gay plague. This looked like the ailment about which he had read.

  Campbell went to see University of California at San Francisco physician Marcus Conant, who had been the first local doctor to spot Kaposi’s sarcoma in a young homosexual. In his slight southern drawl Conant confirmed Campbell’s worst suspicions, and soon the youngest member of the Sisters of Perpetual Indulgence had joined Paul Volberding’s expanding clientele at San Francisco General Hospital.

  Almost immediately Campbell went public, declaring himself “The KS Poster Boy,” sporting a canary-yellow “I Will Survive!” button and giving interviews to any and all media interested in the plight that he and a growing pool of San Franciscans shared.

  Like Callen and Kramer in New York, Campbell began preaching caution to fellow gays, though he was less willing to condemn promiscuity, and personally continued visiting the city’s bathhouses. To convince gay men of the danger in their midst, all he thought he had to do was point to his disfi
guring, yet painless, purple tumors, and say, “See this?”

  As the Christmas holidays of 1981 approached, scientists with the CDC and numerous U.S. medical centers reviewed the data on what they had dubbed GRID, Gay-Related Immunodeficiency Disease. It had occurred in 270 known U.S. cases during 1981, most—but not all—of whom were young, homosexual male adults.

  Two leading symptoms marked the GRID syndrome: Kaposi’s sarcoma and Pneumocystis carinii pneumonia. But other odd ailments were also seen: thrush, caused by Candida fungal infections; pronounced herpes simplex-II throughout the body; blood contamination of active cytomegalovirus with unknown effect; mononucleosis due to Epstein-Barr virus; marked lymph node swelling; radical infections of the stomach and gastrointestinal tract with Entamoeba histolytica; diarrhea and gastric problems caused by the Cryptosporidium parasite; similar symptoms caused by, of all things, Mycobacterium avium, a tuberculosis bacteria usually found in chickens; galloping infections in many organs of the Cryptococcus fungus; out-of-control bacterial infections with common organisms, such as Staphylococcus aureus, Escherichia coli, and Klebsiella.

  One or more of these eventually killed many, if not most of the patients. A New York study of gay men with Kaposi’s found that half died within twenty months of diagnosis,10 and there was dire speculation that the strange syndrome might prove almost universally lethal.

  Autopsies revealed that the young victims displayed severe organ damage. Vast expanses of tissue were necrotic. Microbes of all types—bacterial, fungal, and viral—had invaded and it seemed every organ showed signs of having been colonized and damaged. Much of the worst damage was caused by microbes that were usually utterly harmless to humans.11

  The only possible explanation was total collapse of their immune systems.

  Gottlieb’s group at UCLA carefully studied the immune systems of four gay men with PCP, using techniques that were fairly routine in 1981. First, they measured the abilities of their patients’ immune systems to muster antibody responses toward a variety of organisms, and calibrated the levels of antibody-producing B lymphocytes in their bloodstreams. All things considered, the men seemed to have normal antibody and B-cell responses. That meant the arm of the immune system that produced specialized antibody proteins, tailor-made to recognize and attack very specific targets, was intact. But the T-cell side of the men’s immune systems showed total disarray, and the chaos worsened as patients got sicker.

  In 1981 immunologists were just beginning to appreciate the extraordinary complexity of the T-cellular immune response, and techniques for separating out various types of T cells were brand-new. For example, Dr. Len Herzenberg, at Stanford University Medical Center, had just a few years earlier invented the fluorescence-activated cell sorter, or FACS, which sorted different types of blood cells and could be used either to give researchers a pure cell population to study or to count how many of some particular type of cell were present in a blood sample.

  Different types of T cells—which were white blood cells—had various proteins protruding from their surfaces that served to identify their function and form to other components of the body. Every single cell, from those that comprised a heart muscle to the brain’s neurons, had such protein markers on their surfaces, allowing cells to “see” and “recognize” one another. Without such “sight” and “recognition” a collection of billions of cells could not organize itself into the complex entity that is a magnolia, leopard, or human being.

  By the early 1970s immunologists had begun identifying various protein markers found on the surfaces of T cells, and understood that these markers distinguished groups of cells that had different jobs to perform in response to microbial invasion. This could be visualized by making antibodies in the laboratory against a given T-cell marker, attaching a fluorescent molecule to the antibodies, and mixing it all up in a test tube. If cells of a particular type were in a blood sample, the fluorescent antibodies would cluster on their surfaces, and scientists could see and count the cells using a fluorescence microscope. It was a tedious process, and it took days to count the marked cells in a patient’s blood sample.

  The FACS device reduced the counting time to a matter of minutes by dripping the prepared blood sample one drop at a time past a laser beam. The laser bounced off fluorescent cells, deflecting them into a separate test tube and simultaneously taking their count.

  This and other pioneering techniques enabled immunologists to distinguish one population of T cells from another, and by 1981 they had come to appreciate the elegant complexity of the immune system. Hundreds of distinctly different types of cells, ranging from tiny, free-floating lymphocytes to huge, relatively stationary macrophages, were necessary to recognize an incoming microbe, latch on to the foe in order to draw the attention of other components of the immune system, signal secondary and tertiary lines of defense, and eventually consume and destroy the invader. Once the enemy was defeated, other immune system cells had to call off the attack, and dampen the response, lest the entire system overreact and destroy human cells.

  Most of the job of marshaling immune system forces for microbial attack fell to T-helper cells that bore markers designated CD4. The job of calling off the attack and calming the agitated T-helper cells fell to so-called T-suppressor cells, which bore CD8 markers.

  When Gottlieb at UCLA, Henry Masur and his team at New York Hospital in Manhattan, and Frederick Siegal’s group at Manhattan’s Mount Sinai Hospital scrutinized the cellular immune responses of their GRID patients, they discovered that the CD8-to-CD4 ratios were way off: most of the patients had too many CD8s and too few CD4s. Furthermore, it seemed the slow diminution in CD4 cells paralleled the patients’ decline.

  As a result, the patients appeared incapable of responding properly to most secondary infections. They were deficient, overall, in white blood cells and had radically diminished abilities to respond to foreign microbes. In some cases the GRID men’s reactions to such things as Candida or streptococcus toxins were more than 150,000 times below normal. As measured in the laboratory, some patients’ immune systems had no ability to kill any type of invading microbe.

  The discovery of such profound immunodeficiency certainly explained why these men were ravaged by usually rare or benign microorganisms. But the solution to one mystery only deepened another: Why was it happening?

  Several leading researchers were convinced that cytomegalovirus, or CMV, was the culprit. They had witnessed the extraordinarily rapid increase in active CMV cases in the gay population, jumping in less than a decade from less than 10 percent to over 94 percent of the nation’s homosexuals.12 But there was nothing special about the CMV running rampant in the gay community, and the virus was a common pediatric infection that never produced such serious immune system devastation in children. Some theorized that it was CMV superinfection—repeated episodes of sexual exposure to the virus—that resulted in the strange, deadly syndrome.

  Acknowledging that CMV superinfection might have occurred in some of the cases, Masur warned, “In patients with evidence of cytomegalovirus infection, it is unclear whether the viral process was the precipitating cause of the immune depression or the result of reactivation subsequent to the initial immunosuppressive process. We are not aware of previous data suggesting that immunosuppression has been frequent among homosexuals.” 13

  Sonnabend and some other New York physicians favored the multifactorial theory: the notion of microbial overload. They theorized that gay men had simply been exposed to too many microbes, of all kinds.

  In the fall of 1981 Bill Darrow and a team of CDC researchers released a survey study of 4,212 gay men who responded to questionnaires distributed for the federal agency by the National Gay Task Force. The survey could not establish how representative the respondents were of the gay community as a whole (an important drawback), but its findings were striking f
or the STDs about which the men were asked: pediculosis, gonorrhea, urethritis, venereal warts, scabies, herpes, syphilis, and hepatitis B. For all eight diseases, gay men had rates of initial and repeated infections far greater than heterosexual men, and more frequent than had been seen in a CDC study conducted just five years earlier. And when Darrow’s team evaluated what seemed to put gay men at such risk, they found that men who always took the anal-receptive role were at a somewhat greater risk of infection.

  When Darrow’s group charted their findings, a clear picture emerged. For all eight diseases, the incidence shot upward with each increase in the number of reported lifetime sexual partners. For example, a gay man with twelve lifetime sex partners had an 8 percent risk of contracting gonorrhea. But a man with 1,000 gay sex partners in his life ran a 75 percent risk.

  A similar chart showed that chances of contracting one of the STDs increased depending on the population density of the individual’s town. The CDC concluded that this further bolstered the notion that the number of different sexual partners in a lifetime was key, as small-town residents had less opportunity to form new gay liaisons.14

  The lifetime risk factor seemed to imply a cumulative effect, making the men increasingly susceptible to disease as a result of years of microbe overexposure. So, concluded the STD-overload theorists, GRID appeared when a gay man’s lifetime load of disease exceeded some crucial point, beyond which the immune system failed.