“Why do faggots have to fuck so fucking much? It’s as if we don’t have anything else to do … all we do is live in our ghetto and dance and drug and fuck,†moaned an exhausted character in Faggots, a play by a gay New York author, Larry Kramer.
Though the emotional price of all this anonymous sexuality was obvious to many participants by the close of the 1970s, its microbial toll was apparent only to those few public health authorities who were paying attention. It was easy to miss.
By 1980 most Americans and Western Europeans were, on average, remarkably healthy compared with their counterparts of a previous generation, or with their contemporaries living in the Southern Hemisphere. Nearly 100 percent of U.S. deaths that year were due to chronic diseases, accidents, suicides, and diseases of old age.4
Reflecting this, only 34 percent of National Institutes of Health resources in the United States were spent on that gamut of problems that included infectious diseases. The agency’s infectious disease prevention and control budget had by 1980 declined 16 percent from 1969–76.5
Given the reported mortality statistics, this resource shift seemed wholly appropriate. Sexually transmitted diseases had declined dramatically all over the industrialized world since the discovery of antibiotic treatments for syphilis and gonorrhea. In the 1920s over 9,000 Americans died each year of syphilis, and 60,000 children were born infected with the spirochete. In 1940, just before the introduction of antibiotics, 13,000 Americans died of syphilis. But by 1949, with the availability of antibiotic treatments, fewer than 6,000 Americans died of syphilis, and all signs pointed toward a continuing decline as physicians improved their use of the drugs and more infected people sought treatment. Nobody, therefore, considered it inappropriate to slash venereal disease control budgets from a 1949 commitment of $18 million down to a 1955 U.S. federal expenditure of barely $3 million.
By 1970 fewer than 0.02 of every 10,000 Americans—or two out of every million—succumbed to syphilis. The gonorrhea death rate had also plummeted and most physicians considered both diseases easily curable and, therefore, controllable.6
But by 1975 the folly of such overconfidence was apparent: gonorrhea reports in the United States tripled between 1965 and 1975, syphilis reports quadrupled. By the early 1980s over 2.5 million people were getting gonorrhea annually, and syphilis ranked behind gonorrhea and chicken pox as the third most common infectious disease in the United States.7
Though few Americans were dying of gonorrhea in the post-antibiotic era, it was not a harmless disease. It clearly contributed to infections in the ovaries and fallopian tubes that comprised pelvic inflammatory disease (PID) in women, with the resultant risks of major surgery and infertility. About 20 percent of the 850,000 women who contracted PID in the United States each year between 1977 and 1980 suffered PID as a result of underlying gonorrhea infection.
A woman who survived a case of PID without obvious lasting effects was ten times more likely to suffer subsequent ectopic pregnancies—which could be life-threatening—due to infectious damage to her reproductive tract. The ectopic pregnancy rate in the United States soared from 19,300 cases in 1971 to 42,000 in 1978. Not only did the numbers of ectopic pregnancies increase, but so did the likelihood that any given pregnancy would be marred by that dangerous complication. In 1970 just over 4 out of every 1,000 U.S. pregnancies was ectopic; a decade later more than 13.5 of every 1,000 pregnancies was ectopic, a fourfold increase.8
Finally, about 15 percent of all women who suffered from PID were rendered sterile either as a result of ovarian infections or hysterectomies necessitated by advanced, life-threatening disease. One out of five PID cases required hospitalization. Estimates of the costs—direct and indirect—of PID by 1978 were already starting to approach the billion-dollar mark in the United States. By the mid-1980s the U.S. direct and indirect medical cost of PID would top $2.6 billion per year, and researchers would predict that, given an apparently out-of-control increase in the incidence of the syndrome and its underlying venereal diseases, societal costs could exceed $3.5 billion by 1990.9
Other microbes could also produce PID, including the Chlamydia trachomatis bacteria, which by 1983 would cause some three million new infections a year among American adults. Like gonorrhea, Chlamydia incidence increased steadily in the United States throughout the 1970s and 1980s. The risk of both infections rose in direct proportion to the number of different sexual partners an individual had over a given amount of time.10
In 1976 there was a dramatic turn of events, further worsening the sexually transmitted disease situation.
On August 27, 1976, the CDC reported that two individuals—one in Maryland, the other in California—had become infected with an apparently new, mutated strain of gonorrhea that defied penicillin treatment. On closer examination the CDC determined that the Neisseria gonorrhoeae made an enzyme that destroyed penicillin; the strain was dubbed Penicillinase-Producing Neisseria gonorrhoeae, or PPNG.11
By October the CDC had identified ten more cases of the penicillin-resistant gonorrhea, and traced all but one of the U.S. cases to recent travel in East Asia, either by the ailing individual or by his/her sex partner. At the same time public health authorities in the port of Liverpool, England, reported that forty cases of PPNG had surfaced in their city during the previous eight months.12
By early 1977, PPNG reports were coming in from all over the United States, and a third of the cases involved U.S. military personnel recently returned from Asia, particularly the Philippines.13 The U.S. Navy and Air Force both had enormous bases in the Philippines, surrounded by a dense urban sprawl of tens of thousands of people eager to earn U.S. dollars. Notably, prostitution thrived around both bases, and black-market penicillin was sold to the brothels and the hookers.
Surveys in the Philippines revealed that some 40 percent of all gonorrhea cases in cities near U.S. military bases were PPNG. And half of all U.S. military personnel stationed in the Philippines who had gonorrhea were infected with PPNG.
“It seems unlikely that efforts to control emergence of penicillinaseproducing gonococci will do more than delay their worldwide spread,†a U.S. National Institutes of Health panel concluded in 1977.14
The same week the CDC reported the Philippines link, it also reported on a Georgia man suffering from a new type of gonorrhea that was resistant to the two other most commonly used treatments for the disease: spectinomycin and ampicillin. The CDC scoured over 9,000 gonorrhea isolates collected nationwide prior to 1976 and found no evidence of the spectinomycin-resistant strain in the United States prior to February 1977. It had existed in Denmark, however, where two cases were discovered in 1976.
By May 1977, the penicillin-resistant PPNG strain had been spotted in seventeen countries, and all the North American and European cases traced back to either the Philippines or West Africa. The United States, by that time, had 150 PPNG cases, most were in New York City, and three of the cases involved microbes with triple resistance—penicillin, ampicillin, and spectinomycin. The CDC warned that physicians had to handle antibiotic use in their gonorrhea patients very carefully or “the probability of PPNG acquiring spectinomycin resistance will increase.â€15
Within four years treatment of gonorrhea would become terribly complicated; not only would there be PPNG and spectinomycin-resistant microbes to worry about but also a strain that was resistant to the entire tetracycline family of antibiotics.16 Soon the microbes were rampant among urban gay men and black and Hispanic heterosexual males in the United States. 17
Herpes simplex Type I, or HSV-I, had been a ubiquitous pediatric disease for as long as anybody had been able to diagnose the distinctive cold sores it produced. Better than 90 percent of elderly residents of North America and Europe in 1980 had antibodies to HSV-I, indicating that they had been infected with the virus sometime during their lives. But the childhood infection rates declined in the industrialized world during
the 1950s and 1960s due to improved personal hygiene standards and an understanding that herpetic sores shed contagious viruses.
As a result of declines in the usually less dangerous HSV-I, herpes simplex Type II (HSV-II) was able to infect a wider range of people. HSV-I offered the infected human an opportunity to make antibodies against it which weakly cross-reacted against HSV-II, offering some protection against the more dangerous virus.
HSV-II was primarily passed sexually between human beings. The virus had several characteristics that allowed its easy passage within a sexually active human population.18 It could infect nerve cells and hide for years on end inside the relatively quiet host. At any time—perhaps decades after infection—the viruses could emerge from those nerve cells, replicate thousands of copies of themselves, and create painful sores around the genitals, mouth, or anus of the infected human. During such times, these areas would be sites where millions of herpes viruses were shed, and the chances of passage to a human sexual partner were extremely high—approaching 100 percent under certain circumstances.
HSV-II was usually found in teenagers and adults, and prior to the 1970s active cases of the disease were primarily seen among prostitutes and their clients.19 But a 1981 survey of middle-class young adults in the city of Toronto found that 15 percent were infected with the genital herpes virus. A Seattle study concluded that nearly half of the city’s homosexual population and a quarter of the women living in the community’s poorer neighborhoods were also infected.
Between 1966 and 1981 the number of Americans treated by their doctors for genital herpes increased ninefold.
A similar escalation was seen in the U.K., Israel, Thailand, New Zealand, and throughout Western Europe, where, overall, visits to clinics for treatment of HSV-II increased at a rate of 12 percent per year from 1975 to 1982.20
Researchers discovered that the virus could lie silently in a woman’s uterine lining for years, causing damage only when she became pregnant. Then it might precipitate an abortion, or be passed to the fetus, producing painful infections all over a neonate’s body.21 Treatment of the neonates required intensive care,22 and, in many cases, the illness was fatal.
Despite public alarm, the incidence of HSV-II infection would continue to rise dramatically, reaching levels in 1986 as high as 60 percent of all adult men living in key U.S. cities.23
During the 1970s, researchers reported similar rises in nearly every other microbe known to be sexually transmitted. Cytomegalovirus, or CMV, was increasingly found in the blood or genital tracts of men and women attending STD clinics in the United States, and by 1980 up to 25 percent of women examined in such clinics had active CMV infections of the cervix.24
Chancroid, a bacterial disease causing ulcerous sores in the rectum and genitals, was less common than the other major sexually transmitted diseases, but the sores served as “portals of entry,†as public health authorities put it, for the passage of other microbes into the human body. Chancroid reached its lowest point in U.S. history during 1975, when fewer than 500 cases would be reported to federal authorities. But almost immediately the trend reversed itself, and outbreaks occurred in Orlando, New York City, Boston, Philadelphia, Dallas, Los Angeles, and other U.S. cities. By 1987 annual U.S. chancroid reports would soar tenfold, topping 5,000 reports a year—the 1950 level.
Like gonorrhea and chlamydia, the chancroid bacterium—Haemophilus ducreyi—mutated around antibiotic treatment. On mobile plasmids that could be passed from one H. ducreyi to another were genes that made the microbes resistant to ampicillin, sulfonamides, chloramphenicol, and tetracyclines. As a result, treatment of chancroid would, by the mid-1980s, be difficult.25
In 1982 H. H. Handsfield focused on why U.S. medicine had been so slow to deal with this rise in all sexually transmitted diseases:
… following World War II and the discovery of penicillin, many doctors and public health authorities believed that syphilis and gonorrhea, then the most important known forms of sexually transmitted diseases in the United States, would shortly be all but abolished. It was widely felt, therefore, that the problem could be safely left to public venereal disease clinics. Many private physicians were quite content with this approach, since it more or less absolved them of having to deal with diseases widely considered “not nice†and which confronted the doctor with the difficult and often delicate problem of contact tracing. The public clinics, however, were relegated to second class status, underfunded and understaffed, even within health departments. Simultaneously, there was a radical de-emphasis of STDs in medical schools: Since the problem was “under control,†there was obviously little point in training physicians to deal with it. Whole academic divisions of “syphilology†disbanded, and venereology became divorced from both medical research and medical training. Most U.S. medical schools now provide no more than a few hours of lectures on STDs, usually during the preclinical training years, and only a small handful provide clinical training of any kind.26
Between the late 1960s and the early 1980s most STDs also climbed in Western European countries, but swift public health action generally prevented U.S.-scale epidemics. In the U.K., for example, syphilis began making a comeback in 1968, but a prompt national control effort brought the incidence down markedly in 1978 among heterosexuals. Homosexual spread of syphilis, however, continued unabated. U.K. control efforts were less successful for gonorrhea, which climbed steadily after 1957 in all sexually active demographic groups.
No country had much luck controlling the spread of genital herpes simplex. Between 1970 and 1984, U.K. herpes cases skyrocketed from 4,000 a year to more than 20,000. On the other hand, chancroid had practically disappeared from most European countries by 1980.27
In developing countries the STD crisis was at least as pronounced as in the United States. Pelvic inflammatory disease cases accounted for an ever-increasing percentage of all gynecological visits, particularly in Africa. By 1980, PID was the reason for 30 percent of all gynecological visits in Ugandan cities; 26.5 percent in Zambia; 30 percent in Ethiopia; Nigeria, 30 percent; Kenya, 40 percent; and Zimbabwe, 44 percent.28 Ectopic pregnancy rates were also rising, and in some countries were responsible for up to a third of all maternal deaths.29
Most PID was due to either gonorrhea or chlamydia, both of which were out of control in the majority of cities in developing countries. Gonorrhea had become so widely antibiotic-resistant by the early 1980s that effective doses had to be a hundred times stronger than doses in 1950. In some Asian countries over half of all cases involved PPNG, and strains resistant to more than one antibiotic were on the rise.
The prevalence of gonorrhea among young adults was high by the early 1980s. The greatest reported incidence was in Uganda, where 40 percent of the women attending family-planning clinics in Entebbe and Kampala were infected. In nearby Nairobi, Kenya, 64 percent of the lower-paid street prostitutes were infected, and a quarter of Nairobi’s high-class prostitutes carried the bacteria.
Syphilis rates varied among women attending family-planning clinics from a low of 1 percent in Saudi Arabia to 35 percent in Khartoum. Among prostitutes, syphilis was extremely prevalent in most developing countries, and rates of 50 to 75 percent were common.
Chlamydia rates among pregnant women were also alarming. In rural South Africa, for example, only 1 percent of women were infected, but in Johannesburg and Cape Town rates of over 12 percent were seen. Kenya reported chlamydia rates of 29 percent; Fiji led the world, with 45 percent of its tested pregnant women found infected with chlamydia.
The numbers were telling a story, issuing a warning that was largely unheeded.
II
In 1978, Dr. Subhash Hira was looking for a change. Ever since he finished his medical training in Baroda, India, and worked in Bombay, the young physician had felt restless. Opportunities for an honest doctor trained in Western medicine were limited in India, unless he had family money
with which to start a private practice. It was particularly hard to find positions that offered a young government physician a chance to escape the Health Ministry’s bureaucratic stranglehold.
He was, therefore, easily recruited by the Zambian government to run a new national program to control syphilis, gonorrhea, and other sexually transmitted ailments—the “shame diseases.â€
When he arrived in Lusaka, Hira immediately noticed that it was overwhelmingly populated by young people who were unmarried or who felt unfettered by their vows on Saturday nights. The city was exploding with new arrivals, and housing was scarce. Men outnumbered women; many were guerrillas fighting to overthrow governments in Rhodesia, South Africa, or Namibia.
In 1978–79 Hira occupied a modest cinder-block office at University Teaching Hospital, Zambia’s premier medical school. He designed an STD control program aimed at keeping case records and planned to replace “shame†with prevention and treatment.
He also surveyed small groups of Lusakans to determine the incidence of STDs, something the old Northern Rhodesia colonial government had never done, and postcolonial Zambian health officials hadn’t considered a priority given the crises of malaria, malnutrition, and other deadly pediatric diseases, like measles.
The Coming Plague Page 41