The Coming Plague (50 page)
Authors: Laurie Garrett
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.
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 disfiguring, 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, mostâbut not allâof 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
.
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.
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 typesâbacterial, fungal, and viralâhad 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
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.
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 cellsâwhich were white blood cellsâhad 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.
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 superinfectionârepeated episodes of sexual exposure to the virusâthat resulted in the strange, deadly syndrome.
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 superinfectionârepeated episodes of sexual exposure to the virusâthat 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
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
for 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.
for 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
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.
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.
A serious problem with this perspective lay in mounting evidence that GRID was transmissible. How could immune system dysfunction be contagious?
“The fact that this illness was first observed in homosexual men is probably not due to coincidence,” Gottlieb wrote. “It suggests that a sexually transmitted infectious agent or exposure to a common environment has a critical role in the pathologies of the immunodeficient state.”
15
15
The only environmental factor under serious consideration was poppersâthe amyl nitrites some gay men used in the bathhouses. Though many in the gay community and in physician circles favored the notion that the well-described, mild immunodepression that could be produced by nitrites explained the profound disturbance seen with GRID, the argument was not considered compelling to most scientists in the field.
There was, of course, a fundamental flaw in trying to solve GRID on the basis of factors unique to the large U.S. gay communities: they weren't the only people suffering and dying from the mysterious new disease.
Frederick Siegal determined from a review of his medical records that his first Mount Sinai GRID patient was a thirty-year-old black woman from the Dominican Republic who died of profound immunodeficiency and related pneumonia in 1979. She, clearly, was not a gay man, nor apparently was her husband. She seemed to be a poor housewife with two children
and no history of prostitution, drug abuse, or anything else to explain the lethal chaos of her T cells.
16
and no history of prostitution, drug abuse, or anything else to explain the lethal chaos of her T cells.
16
In Masur's first New York City pool of eleven GRID patients were three heterosexual heroin or methadone users, one heterosexual cocaine addict, and two homosexual heroin injectors. In other words, for more than half of the men in the first New York group, drug use rather than gay sexual activity might have been the responsible factor. Clearly the phrase “gay-related immunodeficiency” couldn't apply to the four heterosexual drug users; nor could theories of causality that centered on behavior and infections unique to the most promiscuous elements of the gay community.
In Europe a smattering of cases among gay men were also noted in 1981; thirty-six in all, half of them in France. The first French GRID case was spotted by Dr. Willy Rozenbaum of the Claude Bernard Hospital in Paris in July, but Rozenbaum didn't connect the strange symptoms experienced by the man, a gay flight attendant, with those described in the American reports until a month later, when his patient developed PCP.
17
17
By early 1982, GRID had devastated the immune systems of at least 310 men and a handful of women in the United States and Europe since 1978, killing 180 of them, and it appeared to be transmissible. Yet it still had aroused little interest or concern (outside a handful of public health circles), even from the populations at the greatest apparent risk. Total fiscal year 1981 U.S. federal expenditures on GRID research at the CDC and, minimally, at the National Institutes of Health came to less than $200,000.
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