The Coming Plague: Newly Emerging Diseases in a World Out of Balance

In Garrett’s analysis, one of the great “amplifiers” of microbial outbreaks in the twentieth century was sex, specifically, the multiple-partner sex patterns that arose in both industrially-developed and developing nations in the wake of the sexual revolution. Garrett first looks at the culture of gay communities in the 1970s, before the specter of AIDS arose, when a self-described “party atmosphere” prevailed. She also examines the liberation from traditional sexual mores experienced by young adults in developing nations when they emigrated from rural villages to urban centers: “In Europe and North America,” she writes, “it was gay men who took greatest advantage of the new climate; in developing countries, particularly in Africa, it was young heterosexuals” (263). Following the emergence of these social patterns was a corresponding rise in the rates of sexually transmitted diseases, including syphilis, gonorrhea, and herpes simplex viruses, some of which were already showing rapid gains in drug resistance.

Another significant amplifier of disease outbreaks was the rising rates of injected drugs. Microbes could make use of shared syringes and could also take advantage of drug users’ reduced immune systems. Many drug users lived in impoverished conditions with inadequate access to medical care. Because the AIDS epidemic at first appeared to affect only gay men and drug users, who bore a significant stigma in the eyes of society, authorities neglected to address the outbreaks. However, the effects did not remain isolated to those communities. The consequences of microbial transmission began to affect all levels of society, particularly because drug users regularly sold their blood and plasma to blood banks, and their blood carried the agents of disease to new hosts in other social classes.

At the beginning of the 1980s, several doctors around the world began noticing patients with a troubling set of symptoms, wasting away and dying from what appeared to be easily treatable diseases. Among these doctors were Michael Gottlieb and Joel Weisman in Los Angeles, whose studies on affected patients from the gay community showed that their T-cell immune response was practically nonexistent. Similar findings arose at the same time from San Francisco and Western Europe, also linked to gay communities there. The CDC began calling the disease “GRID”—Gay-Related Immunodeficiency Disease—because most known cases (but not all) were in young gay patients. In addition to the gay community, the disease had also begun decimating injecting drug users in several major US cities. The disease, later to be renamed AIDS, caused damage to the human immune system, and over months or years, patients would suffer and die from organ failures and common illnesses that their bodies could no longer fight off.

Initially, scientists struggled to understand the disease. Some thought it was just an immune system collapse caused by repeated behaviors (this perspective was usually set in terms prejudicial to gay culture), while others pointed to its apparent contagiousness and argued that it was likely the result of an unknown microbe. The latter group was proven correct as the spread of AIDS via blood transfusions and heterosexual transmission became apparent, meaning that a contagious agent, not a behavior, was responsible. Research into the disease was frequently held back because of social stigma and political hesitancy, and President Ronald Reagan’s administration was generally unsympathetic to the plight of the gay community and injecting drug users: “[…] [E]very aspect of AIDS research, control, and treatment was highly politicized by 1983” (310).

It became apparent in the early 1980s that AIDS was not isolated to gay communities in Europe and North America; it was widely present and spreading rapidly among heterosexuals in central Africa. Some doctors, particularly those from Western Europe, began postulating an African origin for AIDS, but the specter of racism quickly entered the global public response: “The world was convinced that Africa was witnessing an older, widespread epidemic that originated in monkeys” (353). African officials felt they were being blamed for the epidemic, which sometimes caused them to resist further scientific cooperation. Meanwhile, scientific labs were racing to find the viral microbe that caused the disease, zeroing in on a retrovirus apparently related to some known human retroviruses in the HTLV family; the culprit was eventually isolated and named HIV—human immunodeficiency virus. Unable to determine the precise circumstances of its emergence, the World Health Organization’s official position became that the virus had emerged simultaneously in North America, Europe, and Africa, though most scholars suggest that it had been a low-level endemic virus in rural central Africa that took advantage of global social instability in the early 1970s to adapt and spread.

At the end of the 1970s, just as a few scientists were becoming aware of the first noticeable AIDS cases, a different public health crisis was seizing the headlines: toxic shock syndrome (TSS), a rapidly developing, sometimes fatal condition that struck menstruating women far more frequently than any other group. Public furor centered on a new line of products commonly associated with the syndrome: super-absorbent tampons. The syndrome was believed to be caused by a bacterium, a new penicillin-resistant version of Staphylococcus aureus, which also underlay the appearance of Kawasaki’s syndrome, a worrying new illness that affected children.

Although the microbe in question was quickly identified, the mechanism by which it caused TSS was unknown. Some suggested that tampons created tiny lacerations in the vaginal wall, while others argued that the tampons served as Petri dishes for expanding colonies of the bacterium. The latter position proved correct, but the actual mechanism for how those colonies led to TSS was long debated. Patrick Schlievert of UCLA pinpointed a toxin secreted by this strain of S. aureus, and as the bacteria had access to multiple rounds of accelerating growth thanks to tampon usage, that toxin would eventually reach dangerous levels. The real problem, it turned out, was the development of a new staph strain that had emerged around 1975 and could cause these effects, and tampons served as a passive facilitator of their growth. The sudden appearance of TSS was an indicator of a troubling situation, in which a long-known microbe suddenly changed to become surprisingly lethal, likely because of human interventions on its ecology: “It was tempting to conclude that misuse of penicillin antibiotics was responsible for the event. Because the poison genes and those for antibiotic resistance appeared to be carried together on a plasmid [a gene-bearing molecule], selection pressure imposed by penicillin use could have caused the mutation event” (409).