Hira had no way of knowing what sort of trend his STD numbers followed, but even taken alone they were startling. Syphilis was rampant. Responsible for 19 percent of all miscarriages, it infected 32 of every 1,000 babies born in Lusaka, about 16 of whom died immediately before or after birth.30
Fourteen percent of the Lusaka women tested at family-planning or pregnancy clinics had syphilis; some 11 percent had gonorrhea. Chlamydia and chancroid were also rampant, and Hira suspected that the rates of all four STDs would prove even higher in young men.
Outside of Lusaka and the densely populated area around Zambia’s copper mines, these diseases were relatively rare, but Hira noticed that many urban workers returned to their wives in rural villages during holidays. He wondered how long it would be before STDs plagued the villages as well. And how long before the thousands of freedom fighters took Lusaka-acquired microbes to their home countries.
In 1980, Hira set up an STD testing clinic at the University Hospital. It was soon swamped. Men and women, some clutching their children, waited, moved beyond shame to the more familiar ennui of “queuing up.†Some waited for hours, as Hira and his assistants desperately tread water before the tidal wave.
Far away in snowbound Michigan, Dr. June Osborn was reviewing grant applications for National Institutes of Health funding to conduct sexually transmitted disease research. When she had started in her NIH advisory role, Osborn (like most American STD researchers) was focused on heterosexually spread herpes simplex, but by 1979–80 she noticed something troubling: all STDs were increasing, at a rate of about 1 percent a year in the general population, but by an incredible 12 percent annually among gay men.
“I fear we’re looking at a new ecology here,†Osborn told NIH colleagues. Wherever there were large gay communities, there was also a striking disparity in disease rates, particularly for syphilis, gonorrhea, and hepatitis B.
For Osborn one of the most startling findings involved the Entamoeba histolytica parasite. Normally found in the food and water of densely populated areas in developing countries, it was rarely seen in the United States. In the late 1970s, however, it turned up in the bowels of gay men in New York, San Francisco, Los Angeles, and a few other cities. In developing countries where E. histolytica was endemic, the parasites formed bowel cysts, creating ulcerous sores which shed more organisms, some of which might get into the liver, causing severe damage.
As reports of E. histolytica outbreaks among gay men escalated, Osborn and other public health officials became seriously alarmed. By the close of the decade more than 20 percent of the U.S. gay male population was infected with E. histolytica—five years before, no locally acquired cases were reported in the United States. Fortunately, the microbial strain rampant in the United States was not particularly virulent and most men had few or no symptoms.
But things were moving quickly—“too fast,†Osborn said—for the NIH research planners. The all-heterosexual, mostly middle-aged research advisers simply couldn’t fathom what was going on in the U.S. gay community at the time.
“Every time we do an NIH site visit the definition of ‘multiple sex partners’ has changed. First, it was ten to twenty partners per year. That was 1975,†Osborn complained. “Then in 1976 it was fifty partners a year. By 1978 we were talking about a hundred sexual partners a year and now [1980] we’re using the term to describe five hundred sexual partners in a single year.
“I am duly in awe. Perhaps somewhat disbelieving, but duly in awe,†Osborn concluded.
Preliminary 1980 reviews seen only by Osborn’s NIH panel and federal authorities at the CDC revealed that CMV was spreading quickly among gay men. By 1981 the CDC would tell doctors nationwide of another unprecedented new gay male epidemic—of cytomegalovirus. Widespread rectal transmission of CMV among adults had never been seen anywhere before.
Reports of rare diseases among gay men were coming in from public health authorities in Canadian and Western European cities. In Paris, Amsterdam, London, Rome, Madrid, Montreal, Toronto, Copenhagen—wherever researchers looked—the trend was the same.
“We’ve got to pay attention to this ecology,†Osborn warned. “There’s something disturbing going on.â€
To the happy participants in the gay freedom movement, it was the ecology of sexual liberation. A price to pay, so to speak, for newfound freedom.
“I calculated that since becoming sexually active in 1973, I had racked up more than three thousand different sex partners in bathhouses, back rooms, meat racks, and tearooms,†gay pop singer Michael Callen wrote. “As a consequence, I also had the following sexually transmitted diseases, many more than once: hepatitis A, hepatitis B, hepatitis non-A/non-B; herpes simplex Types I and II; venereal warts; amebiasis, including giardia lamblia and entamoeba histolytica; shigella flexneri and salmonella; syphilis; gonorrhea; nonspecific urethritis; chlamydia; cytomegalovirus (CMV), and Epstein-Barr virus (EBV) mononucleosis; and eventually cryptosporidiosis.†31
Another factor in the spread of disease was a change in the culture of homosexuality. In the past, role playing had been a common feature, with some men always being the passive receptors in anal intercourse and others consistently the aggressors.32 But within the culture of gay liberation such role playing was shunned, even taboo, and more men played both roles. That changed the ecology of anal intercourse for the microbes, and allowed a more rapid epidemic spread of disease. If John, for example, played the passive role one week and got rectal gonorrhea from Sam, his chances of passing the microbe to Charlie the following week were greater if John played the aggressive role. If John remained the passive player, however, his partners might not contract his gonorrhea. So if a man had 500 sexual partners in a year, he might receive an extraordinarily rare microbe from just one of his 250 aggressor partners, then pass it on to 250 men with whom he took the aggressive role. The potential for rapid spread was further enhanced by the lack of a strong local immune system in the anal/rectal area. Thus, the one man could amplify a weak microbe signal 250-fold, creating an epidemic din.
None of these details of homosexual behavior were comfortable intellectual terrain for public health scientists in 1980, however. While they charted the upward curves on the STD graphs in the gay communities of North America and Europe, and discussed the trends at meetings, few scientists wanted to discuss the “new ecology.†It was unsettling, and politically volatile.33
Having obtained his Harvard Ph.D. in virology, Don Francis was back working for the CDC in Phoenix, Arizona. The hepatitis B virus remained his greatest concern, and he hadn’t overlooked its alarming rise among gay men. By 1980 he had established a national cohort of gay men who agreed to be tested periodically for hepatitis B. By following these 6,875 men, most of whom were in San Francisco, Francis hoped to establish the dynamics of the microbe’s spread within the homosexual population.
Francis had become one of the world’s experts on hepatitis B. In 1979 he helped investigate an outbreak in India, caused by injections of hepatitiscontaminated human immunoglobulin in 325 people.34 From 1978 to 1983 he participated in three other investigations of nosocomial transmission of the virus: a Baltimore dentist who passed the virus to six patients,35 a Connecticut oral surgeon who infected over a hundred patients during 1978–79,36 and a Mississippi gynecologist who infected three women upon whom he performed surgery during 1979–80. In all three cases, transmission ceased with the routine use of surgical gloves.37
This demonstrated to Francis that the hepatitis B virus, unlike the food-borne hepatitis A, was primarily transmitted through blood-to-blood contact. And that contact could be entirely prevented by a layer of latex.
To Francis this seemed to be ample reason to recommend that gay men start using condoms, but such proclamations were uncomfortable for the CDC, which still adhered to the old venereal di
sease paradigm of identifying cases, contacting all their partners, and treating everyone with antibiotics.
But hepatitis B was a virus; it couldn’t be effectively treated with any drug. And contact tracing was clearly impossible if an individual had multiple, anonymous sex partners. Francis saw no alternative but prevention to block transmission of the virus, by creating either a physical barrier (condoms) or immunity (vaccination). By 1980 he was actively pushing both angles and, in his usual gruff but earnest manner, making enemies among the more traditional bureaucrats and venereologists at the CDC. Francis, however, was a man with a mission. Prone to impatience and maverick action, he became increasingly outspoken about hepatitis B prevention. On the basis of lab work he had done with Max Essex, and studies he made of Native Alaskans and their parallel epidemics of liver cancer and hepatitis B infections,38 Francis was convinced that the escalating hepatitis epidemic among gay men presaged a plague of gay liver cancer. He showed that spread could be blocked with condom use.39 And it was well known that one out of ten adults newly infected with hepatitis B went on to become chronic carriers of the virus, potentially infecting others for decades and putting themselves at risk for liver cancer.40
In 1978, federal researchers estimated there were approximately 200,000 hepatitis B carriers in the United States, but as the gay epidemic struck San Francisco, New York, Washington, D.C., Los Angeles, Miami, Paris, London, and other key cities, it became clear that the numbers were mere guesses.41 By late 1981, San Francisco Health Department officials would estimate that 73 percent of gay men in the city “either have or have had†hepatitis B, and physician Pat McGraw would reckon that at least 1,000 gay men were carriers, or roughly one in fifty of the city’s openly gay citizens.42
At CDC headquarters Drs. Harold Jaffe and Jim Curran read the field reports coming in on hepatitis B and recognized that all young sexually active Americans—particularly homosexuals—seemed to stand a far greater chance of acquiring a sexually transmitted disease in 1980 than did their counterparts just a decade earlier. The trends, they felt, augured for loss of what little control public health authorities still claimed over the STD microbes, and they tried to argue that case both inside the CDC and at medical conventions.
Jaffe always returned from such meetings sizzling mad. Few physicians or scientists shared his concerns, and many publicly retorted as late as 1980 that “there’s really no further need for an infectious disease specialty†in medicine.
Jaffe, thirty-four, answered to Curran, who was just thirty-six. Jaffe had a bit of Northeast passion; Curran was a classic case of Midwest cool. In late 1978 Curran had come to the CDC from Ohio University College of Medicine, where he’d been a professor of preventive medicine. He headed the CDC’s research branch for the Venereal Disease Control Division.
Curran’s low-key style and extremely fastidious presence led many people to mistakenly conclude that he was a conservative straitlaced sort. But well before he joined the CDC, Curran had concluded that the old-fashioned approaches to venereal disease control—indeed, the very word “venerealâ€â€”were outmoded. He favored new approaches to a problem he readily acknowledged was out of control.
Like Jaffe, Francis, and Osborn, Curran recognized that something unique was occurring among gay male residents of some cities with large homosexual populations. He tried to warn the physicians Michael Callen called “the clap doctors,†their patients, and gay organizations. But everybody was enjoying the party too much. Besides, after so many decades of maltreatment by every imaginable government agency and medical organization, including officially being labeled mentally ill during the 1950s by the American Psychiatric Association, gay men weren’t about to let another bureaucrat tell them to slow down.
III
By 1980 thirty-year-old Greggory Howard had been carrying a heroin addiction for thirteen years. Cut off from his family, Howard was a member of a community of heroin addicts who lived amidst the extraordinary squalor of Newark’s burned-out tenements.
It was shortly after the 1967 riots that Greggory Howard, then a high school junior, first shot heroin into his veins. His warm personality and good grades held promise that he might escape New Jersey’s notorious slum to a better life.
“Life was good to Greggory,†Howard said, always referring to himself in the third person. “Yes, it was. It really was. My parents did everything right, they were very good to me. But Greggory just had … just had to drift away.â€
In 1967 racial tensions in the United States were as high as anyone could remember. The civil rights movement had passed from polite sit-down demonstrations and peaceful marches to unfettered rage when its leaders shifted their foci from the Deep South to the industrialized North. By the mid-1960s racial tensions had reached a tinderbox level.
Newark ignited in 1967; block after block went up in flames amid riots between residents of the city’s slums and the police and National Guard. Tanks patrolled the streets.
Frightened, Greggory stayed out of the fray, but it left him with a sense of tragedy and hopelessness. Afterward, he took to walking along Prince Street and Hamilton, staring at the charred structures that had once housed his friends, teachers, and relatives, and he tried heroin for the first time. One of his ex-girlfriends was already shooting up, and she seemed to like getting high. Why not try?
Now it was 1980. Howard’s nose was broken, a nasty scar zigzagged across his left cheek, and he walked with a jerk, all thanks to beatings by dealers, crooks, and hoodlums. Those veins that hadn’t disappeared were on the verge of collapse or embolism from the thousands of needles he’d jammed into his arms, neck, and thighs. Howard’s liver was shot, because of hepatitis.
To avoid being arrested for carrying drug paraphernalia43 Howard rarely had on his person either heroin or the gear—the cooker, tourniquet, syringe, and needles—that was needed to prepare and inject the drug. Like most street-savvy addicts, Howard always had on hand a supply of minor street drugs, possession of which did not constitute a major crime: Valium, marijuana, a variety of “downers†that could help him stay relatively steady between heroin highs. And when he had the cash, Howard went to dealers at any of a number of apartments, abandoned buildings, alleys, parked cars, or parks and shot up, using works supplied by the dealer or another junkie.
KEY GAY COMMUNITIES AND CENTERS
OF INJECTING DRUG USE, 1980s
“Someday I’m going to detox my ass,†Howard would say, staring off on a high at Newark’s hundreds of empty lots—the legacy of 1967.
Heroin, cocaine, amphetamines, and the host of other drugs easily purchased in the full glare of sunlight in most large American and European cities hadn’t always been public health disasters. But they clearly did pose a crisis for urban health by 1980—an opportunity, a new ecology, for the microbes.
The anonymity of cities provided cover for illegal activity. The density of the population offered a steady flow of consumers, even for self-destructive products. And the alienation ensured that there would always be people willing to trade their health, wealth, and esteem for something that would take their minds to another place, be it alcohol, Valium, or heroin.
Once it reached Newark, a two-pound bag of pure heroin might be “cut†or “stepped on†with some other chemical by 90 or 95 percent, giving the wholesaler nearly 200 pounds (90 kilos) of street-quality heroin to sell to a retailer. The retailer might further cut the drug to increase his profit potential, so that Greggory Howard’s daily high might be on a solution ranging from 2 to 15 percent heroin. In 1974, by the time it reached Newark, one acre’s opium could yield more than $40 million.44
Profits in the opium/morphine/heroin network were greatest when the risks of police interdiction or interference from competitors was low. Large cities with slums afforded ideal
environments, particularly if they were near ports or international airports. If hefty sales could be maintained in the crime-ridden inner-city areas there was no need to risk law enforcement’s attention in small towns or tight-knit suburban communities. In slum neighborhoods where most people were hostile to the police, retailers could operate with near-impunity. If kids in the suburbs wanted heroin—and by 1980 many of them very much did—they could come into the city to obtain supplies.45
Despite expenditures of billions of federal law enforcement dollars since 1969, when the U.S. Congress voted for a “full-scale attack†on the heroin problem, the number of heroin addicts in the United States would rise from 55,000 in 1955 to 1.5 million in 1987 and they could be found, regardless of race, in any community that offered a steady supply of the drug.46 In Greggory Howard’s state, New Jersey, by 1980 heroin users were of all races, ages, and economic backgrounds, though the majority were white men between twenty-five and thirty-five years of age. About 40 percent of the state’s heroin users were holding down jobs. Most had sought treatment several times—and failed several times.47
The urban heroin environment was ideal for dozens of different microbes. The drug user generally had an impaired immune system due to the narcotics’ effects, to the constant injection of other people’s blood cells carried on shared syringes, and to the numerous compounds used to cut the product. On the one hand, they had overexcited antibody responses provoked by all the immune system stimulators, such as other people’s cells. Many therefore tested positive for rheumatoid factor and other markers of a system so overstimulated that it might be producing antibodies against itself. This autoimmunity could lead to the body’s inability to distinguish genuine microbial threats from vital human cells.48
On the other hand, the large phagocytic cells of the immune systems of injecting drug users, which usually bore the responsibility of ingesting and destroying bacteria and other invaders, were alarmingly nonresponsive. And the T-cell system, comprised of cells that usually tipped the rest of the immune system off to the presence of potential threats, was seriously dysfunctional, in part because some lymphocytes bore receptors for opiates, and were dampened directly by heroin.49
The Coming Plague Page 42