The Coming Plague

by Laurie Garrett

  All in all, it was a clever design that caught on immediately, despite a widespread hue and cry about the immorality of such a device. It was said that tampon insertion stimulated the female excitatory nerves, prompting wanton masturbation. It was also asserted that tampons would puncture the hymen, thus destroying a girl’s premarital proof of virginity.

  But Haas had no trouble selling his patent to Tampax Incorporated of Palmer, Massachusetts, which promptly proceeded to manufacture the devices. It was a sensation: within a generation most menstruating females in North America used tampons, and 90 percent of all tampon users relied on a single brand—Tampax. A smattering of smaller manufacturers competed for market shares in the United States, Canada, and post-World War II Europe. By the 1960s tampons were in widespread use wherever in the world women could afford to buy them.

  Hundreds of millions of women used billions of tampons throughout their reproductive lives. And though history showed that other approaches to the bleeding problem had been associated with elevated risks of some infectious diseases, commercial tampons were sold without any more regulation than hammers or soap. In the United States no federal or state health agencies oversaw tampon production, and the products were never submitted to any required set of safety tests.

  During the early 1970s Tampax encountered serious competition as four multinational corporations launched tampon products aimed at grabbing a share of the huge baby boomer market of young women born during the post-World War II American population explosion. The Kimberly-Clark Corporation, Procter & Gamble, Playtex, and Johnson & Johnson entered the market, offering a variety of modifications on Haas’s old cardboard-and-cotton design.

  The competition turned to a feeding frenzy when the National Association of Broadcasters lifted their long-standing ban on radio and television advertising of tampons, and newsmagazines followed suit, accepting explicit menstrual product ads. By 1975 all five tampon manufacturers were spending millions of dollars on advertising each year. And the key pitches made to women centered on two things: comfort and security. There were few ways companies found to improve upon the relative comfort of the old cardboard tampon design, though some offered plastic tube applicators as an alternative.

  Security was Tampax’s vulnerable point, for no matter how careful a woman might be, there were those humiliating occasions when the old tampon failed to do its job. Playtex targeted this issue by offering perfumed tampons and the ad slogan: “When you’re wearing a tampon you don’t worry about odor. But should you?”—implying that small, unseen leaks could still be detected by the sharp olfactory senses of co-workers, friends, and dates.

  These new products were allowed on the market without any demonstrated prior proof of safety for either the plastic inserter designs or the perfumes. Following an outcry from Planned Parenthood, Playtex put labels on their perfumed tampon boxes, warning that some women might experience discomfort or irritation from the chemicals.2

  Meanwhile, competition in the tampon industry escalated radically.

  Recent entrants into the field turned to their marketing analysts to determine how better to exploit weaknesses in Tampax’s long-standing monopoly, and the unanimous answer was “absorbency.” Thanks to feminist challenges to male workplace dominions, American women were filling jobs never, or rarely, before open to their gender. No woman who was among the first of her gender to work as a police detective, firefighter, bank executive, or television news anchor could afford the embarrassment of the bleeding problem.

  The first breakthrough in absorbency came in 1974 out of the Procter & Gamble laboratory, where engineers concocted a product based not on cotton and cardboard but on polyester fibers and plastic. Dozens of different types of natural stabilizing fibers had previously been mixed in with cotton to increase absorbency and maintain the tampon’s shape inside the vagina. Reportedly among them in the 1950s was asbestos.3

  Procter & Gamble’s use of synthetic fibers, however, changed the entire picture because it allowed engineers an almost unlimited number of ways to vary the shape and relative absorbency of tampons. They could manufacture what amounted to small sponges that ranged from low-density polyester to a very high-density, superabsorbent synthetic.

  As was the case with Playtex’s introduction of perfumes and plastic inserters into the vaginal ecology, no regulatory agency or medical organization questioned the insertion of petrochemical by-products into the nutrient-rich environment. Again, no safety tests were required. Indeed, with all five competitors quickly putting similar synthetic products on the market, the entire industry declared tampon content to be a matter of trade secrecy.

  Among the synthetic materials used in marketed superabsorbent tampons in 1979–81 were polyurethane, polyester, collagen, polyvinyl alcohol, acetyl cellulose, and carboxymethyl cellulose.

  In 1979 Procter & Gamble released a tampon comprised of highly compressed beads of, alternately, polyester and carboxymethyl cellulose. The product was, as its name implied, something a woman could Rely upon to prevent embarrassing bleeding accidents, as the synthetic composite was capable of absorbing nearly twenty times its own weight in fluids, and would expand to take the shape of, and fill, the vagina.

  With a huge advertising kickoff, Rely hit the North American market and quickly gained enough popularity to radically alter the balance of power among tampon manufacturers. The notion that a tampon could be left in for hours—all night long—without any fear of unsightly failures was extremely attractive to young consumers. Other manufacturers retaliated immediately, marketing Assure!, MaxiSorb, SuperPlus, and other new synthetic superabsorbent products.

  The impact on female genital ecology was immediately obvious, as the new tampons were capable of absorbing more fluid than most women actually had in their vaginas at a given time.4 As the tampons swelled, expanding to touch the vaginal walls, dryness made the usually mucus-coated areas vulnerable. If one of the new tampons was left in the vagina long enough —say, five or six hours—it might adhere to the vaginal walls, and removal would leave behind a residue of synthetic pieces.5 Some women experienced pain as they removed the new tampons, resulting from the adherent sections of the devices actually tearing cells off the vaginal wall. And still other women required medical assistance to withdraw tampons that had expanded so much that they were too big to come out of the vagina in one piece.

  Though nobody officially questioned the introduction of Rely and its competing synthetic products, there were studies that might have served as warnings about the vaginal ecological impact of the new tampons. Tests on rabbits, for example, showed that sterilized tampons made from collagen, polyurethane, polyvinyl alcohol, or acetyl cellulose produced lesions and ulcerations in the vagina’s epithelial tissue. In addition, cell regrowth in the epithelium plummeted markedly: by 18–29 percent with collagen and 84–100 percent with other fibers.6 Another 1979 study, not intended as tampon research, found that carboxymethyl cellulose (CMC) served as an ideal filter for bacterial toxins. In particular, the researchers noted that CMC did a wonderful job of filtering toxins made by Staphylococcus bacteria. 7

  From the moment superabsorbent tampons hit the market there were published accounts of vaginal ulcerations, lesions, and lacerations.8

  In January 1980, Dr. Jeffrey Davis, of the Wisconsin Division of Health, notified the Centers for Disease Control in Atlanta that something potentially dangerous was afoot: he had spotted a sudden surge in Toxic Shock Syndrome cases in the state.9 On July 15, 1979, a young menstruating woman was admitted to the emergency room of a Madison, Wisconsin, hospital, suffering from shock. Over the subsequent months of 1979, six more TSS victims were admitted to Madison hospitals. All but one of them were menstruating females: the exception was a thirty-six-year-old man. Madison was the state’s big college town, heavily populated by postadolescents. All the TSS patients were white, otherwise healthy, and oddly in
fected with Staphylococcus aureus.

  Back in 1977, a Denver pediatrician, James Todd, reported having treated seven children, aged eight to seventeen, for an acute life-threatening ailment he called Toxic Shock Syndrome. The children were infected between 1975 and 1977 with bacteria S. aureus, which had taken hold in their bodies in an unusual manner, secreting a poison into the youngsters’ bloodstreams. 10 The unidentified toxin produced a host of symptoms in the children: fevers of over 102°F, diffuse red rashes all over their bodies, the death and subsequent shedding of skin cells, a marked and dangerous drop in blood pressure, vomiting, diarrhea, muscle aches, kidney dysfunction, liver failure, elevated blood clotting and platelet formation, mental confusion, and loss of consciousness.

  One of Todd’s patients was a fifteen-year-old girl who had a heavy vaginal discharge and was in a state of shock for two days. Though she eventually survived, the teenager was at death’s door for eight days, periodically losing consciousness, and she lost two toes to gangrene. Her vaginal discharge contained a strain of S. aureus bacteria that was remarkable for two features: it was genetically resistant to the entire penicillin class of antibiotics, and it appeared to secrete some unique toxin.

  Two of Todd’s patients were less fortunate than the teenager: one boy died, and another developed “shock lung” that required a laparotomy and resuscitation.

  “We suggest that the toxic-shock syndrome is a new staphylococcaltoxin-related disease,” Todd’s group wrote, adding that “the acute illness which we have described and called the toxic-shock syndrome seems to affect older children.”

  Todd scoured the medical literature for clues, hoping to find evidence that somebody had previously noted such a severe reaction to Staphylococcus infection. He discovered the strange account of a twelve-year-old girl in New York City who developed what looked like scarlet fever in 1927. But it wasn’t scarlet fever; it couldn’t have been, because the girl was infected with staph bacteria, not the streptococci that caused the bright crimson rashes that were the hallmark of The Fever.11 Back then, Dr. Franklin Stevens, at the Columbia University College of Medicine and Surgery in Manhattan, treated that ailing girl, whose fever topped 105°F. Her body was covered with “raspberry-like reddened spots,” Stevens wrote, and the child complained of pain in her thigh: the result of an unknown injury. When pus was drained from the wound, it was found to be full of staph bacteria.

  The New York physician soon saw two more strange Staphylococcus-caused scarlet fever cases, in a pair of eight-year-old boys. Much as Todd would do in 1978, Stevens puzzled over the occurrences and marched off to Columbia’s medical library in search of clues. He happened upon the 1899 account of rabbit experiments conducted by a German physician, Von Lingelscheim. The German scientist produced scarlet fever in the animals by injecting them with S. aureus.

  Fourteen years later, in 1941, in Baltimore, Drs. Henry Aranow and W. Barry Wood spent three months struggling to save a fifteen-year-old girl who also suffered from scarlet fever, due, again, to S. aureus. The Baltimore girl’s symptoms seemed to be a perfect blend of those seen in Stevens’s twelve-year-old in New York and Todd’s fifteen-year-old Denver case. Like the New York girl in 1927, the Baltimore teenager complained of pain in her thigh, ran a 105°F fever for days, and had “raspberry” formations all over her skin. And as was the case with Todd’s ailing teen, the Baltimore girl had discharges from her vagina that were found in the laboratory to be filled with Staphylococcus.12

  During the mid-1970s Japanese pediatrician Tomisaku Kawasaki noticed another odd syndrome in children, involving Staphylococcus infection that produced skin shedding and loss of fingers and toes.13 Todd had no idea whether Kawasaki syndrome, as it was subsequently called, was a manifestation of the same illness he was seeing among Denver children. Certainly, there were differences. The Japanese children were far more likely to suffer heart infections, while Todd’s kids seemed to go into shock. In addition, the Japanese children seemed to be much younger than Todd’s. On the other hand, Kawasaki syndrome surfaced in Japan at about the same time Todd first noted TSS cases in Denver. 14

  Meanwhile, Minnesota state epidemiologist Dr. Andrew Dean reported finding five TSS cases during 1979. Both the Wisconsin and Minnesota cases involved teens and adults, about 95 percent of whom were female.

  Following the 1980 New Year, the CDC issued an alert to physicians, noting that an apparently new syndrome was surfacing, involving an ancient organism—S. aureus.

  As calls poured in from around the country during February 1980, the CDC decided to form a task force to investigate the phenomenon, led by the agency’s Drs. Bruce Dan, George Schmid, and Kathryn Shands. Dan was in charge of the epidemiological detective work, Shands of laboratory analysis of the staph stains collected from TSS victims. Schmid oversaw group operations.

  By May 1980 the federal agency had confirmed forty-three more cases of Toxic Shock Syndrome, and some commonalities were beginning to emerge. 15 The most striking of these were that 95 percent of the cases were female, and 95 percent of the females were menstruating at the time they developed TSS. In most instances, TSS struck on the second or third day of their periods.

  The race was on to solve the Toxic Shock mystery, and from the outset the investigation was fraught with scientific backstabbing, rivalries, name-calling, and controversy—most played out in the bright glare of television lights and news photographers’ flash bulbs. There would be little interestfree information for public digestion.

  One of the first controversies concerned the CDC’s definition of Toxic Shock Syndrome, which was drafted by Shands and Todd in February 1980. Though it underwent revisions during the year, the basic case definition remained that of an acute syndrome involving a high fever, scarlet fever-like rash, skin peeling, radically lowered blood pressure, and at least three of the following systemic symptoms: diarrhea and vomiting; muscle aches; vaginal or throat infection; kidney malfunction; liver failure; disorientation or confusion.16 By focusing on such acute cases, critics charged, the CDC was missing a large pool of people who suffered a milder form of the ailment, and thus underestimating the full extent of the emergence of what might be a new strain of Staphylococcus.

  “We’re using a case definition that is epidemiological, not clinical,” Minnesota state epidemiologist Dr. Michael Osterholm said diplomatically. “That means we miss a lot of cases. But it also means that all the cases we name are genuine. The trade-off is that there is no way to answer basic science questions about why these people developed acute shock syndrome, while others who were infected with Staphylococcus developed mild or even no symptoms.”

  Among the first 100 cases reported to the CDC, the agency selected 43 that met the stringent definition of TSS. That meant 57 cases went unexplored—at least some of which might have proven to be milder manifestations of staph infection. As publicity increased, so did the number of ostensible TSS cases that fell outside of the CDC definition.

  Throughout the summer of 1980 the number of reported TSS cases rose steadily, reaching 408 reports between January 1975 and October 1980. Of those 408, 14 were in men. The men, of course, had contracted the disease through means other than tampon exposure. They were the anomalies. In five years, 394 cases had occurred in women, 40 of whom had died. Some 95 percent of those women had been menstruating at the time, and 100 percent were tampon users.

  The news coverage was terrifying. “Teenager dies of tampon use. Details at eleven!” “Toxic Shock Syndrome survivor tells her story tonight on Eyewitness News.” “Centers for Disease Control warning women to beware of tampons. Stay tuned for more!”

  Most American women reacted with a sense of helplessness: how could something which had become such an essential part of women’s lives turn out to be potentially deadly?

  The staphylococcal strain respon
sible for TSS was genetically resistant to all penicillin-class antibiotics. Many of the acute cases had suffered previous, milder forms of the disease, suggesting that there was some sort of cumulative effect. To the degree that the Minnesota, Wisconsin, and CDC laboratories could be certain, on the basis of currently available technology, the recent TSS sufferers were all infected with the same staph strain. There was absolutely no evidence of person-to-person transmission of the microbes. The outbreaks seemed to cluster in distinct geographic areas of the United States, notably the midwestern states of Wisconsin and Minnesota.

  And, according to the CDC, most of the female TSS cases involved superabsorbent tampons. In September 1980 the CDC released its third report,17 pointing the finger at Rely tampons. In a controlled study of forty-two TSS victims and another pool of non-TSS tampon users, the CDC found that 71 percent of the TSS victims used Rely brand tampons. Other brands came in with markedly lower incidences of TSS: Playtex was used by 19 percent of the cases, Tampax 5 percent, Kotex 2 percent, and OB 2 percent. The CDC pointed out that “consumer use of Rely tampons has increased as the apparent incidence of TSS has increased.”18

  The CDC’s investigation also found that a third of the TSS sufferers had had a previous episode of milder menstrually associated symptoms. And the agency suggested that “tampons play a contributing role, perhaps by carrying the organism from the fingers or the introitus into the vagina in the process of insertion, by providing a favorable environment for growth of the organism or elaboration of toxin regardless of the manner in which the organism is introduced, or by traumatizing the vaginal mucosa and thus facilitating local infection with S. aureus or absorption of toxin from the vagina.”

  Though the CDC was convinced that Rely was the bad actor in TSS—and had so informed Procter & Gamble prior to the September 19 release of the agency’s findings—the federal scientists were aware that state epidemiologists in Minnesota and Wisconsin had evidence that weakened their case. Osterholm’s group surveyed all female TSS cases that had occurred in Minnesota since early 1979, finding that only 35 percent used Rely. Though more TSS sufferers had used Rely compared with matched non-TSS women (35 percent versus 18 percent), the rates were markedly lower than those reported by the CDC.