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Authors: Laurie Garrett

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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.”
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.
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.”
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.
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.”
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 disease 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 “venereal”—were outmoded. He favored new approaches to a problem he readily acknowledged was out of control.

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