The young women are linked by the feminine hygiene products they were using: Four of the five were using super absorbency tampons, and four of the five were using the brand Playtex Sport; there was one case involving U by Kotex. But what exactly is TSS, and why does it matter which tampons the afflicted were using? For women who remember the rise of TSS in the 1970s, the illness and its risk factors may be familiar. But now that the most dangerous tampons have long been off the market, a lack of public awareness could be contributing to the condition's spike.

TSS is a complication arising from infection with certain types of bacteria, a dangerous bodily response to the toxins they produce. And it can kill you: TSS from S. aureus has a mortality rate of between 5 and 15 percent, but for streptococcal TSS, the mortality rate jumps up to 30 to 70 percent.

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TSS, as it relates to menstruation, essentially emerged out of the race to build a better, more commercially viable tampon.

Women have long been absorbing their menses with internal packing materials. The early relatives of what we would recognize as today’s tampons — intravaginal devices featuring absorbent materials tied to a string — date back to the 18th century. However, there are reports of women staunching their flow internally throughout history, from the use of wool in ancient Rome to papyrus in ancient Egypt.

The commercial tampon, however, didn’t come of age until the 20th century, when Tampax hit the shelves in the 1930s. A cotton tampon, it was packaged with a telescoping applicator to allay the fears of those pearl-clutchers concerned about the direct touching of genitals. The tampons were a success, and a new field of commercial feminine hygiene products was born.

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By the 1970s, manufacturers were deeply entrenched in the race to give tampons a competitive edge. To wit, Playtex debuted scented, “deodorant” tampons in 1971, and plastic-domed applicators in 1973. Which made the next frontier, of course, absorbency.

In 1978, Proctor and Gamble began selling American consumers an ultra-absorbent tampon called Rely. What made this tampon special was its composition: instead of the cotton and rayon found in other tampons, Rely was fully synthetic, comprised of a water-loving, hyper-absorbent food-grade thickener called carboxymethylcellulose, also known as cellulose gum. It’s a commonly used substance: It’s in your ice cream, your toothpaste, and, at least in the late 1970s, it was in your tampons.

With a forward-thinking shape that opened into a cup inside the vagina, coupled with the capacity to absorb a significant amount of fluid, the Rely appeared to herald a new era of tampons.

Unfortunately, the product was fraught from the start.

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First, there were issues relating to how the hyperabsorbancy of the Rely tampon could overdry the naturally humid environment of the vagina, desiccating the delicate organ to the point at which the removal of the tampon could tear away some of the vaginal wall, causing ulcerations and easy access to the body for lingering microbes. Then, there was the question of the ol’ bacterial buffet, the fluid in the tampon acting as a surfeit of food available for both native and introduced microbiota.

Enter toxic shock syndrome.

In May 1980, the Centers for Disease Control and Prevention (CDC) reported 55 cases of TSS, an illness characterized by high fever, a sunburn-like rash, low blood pressure, failures or abnormalities in multiple organ systems, and, at the end of the illness, a dramatic desquamation, or peeling, of areas such as the hands and feet. Cases continued to mount. A follow-up report in June identified continuous usage of tampons during the menstrual period as a risk factor for developing TSS, and further study identified a link between the ultra-absorbent Rely tampon and the outbreak of cases. The public was alerted to the dangers posed by using Rely tampons, and in September, Rely was removed from American store shelves, and the sharp spike in TSS cases that started its climb when the products came to market two years earlier dropped as steeply as it’d risen. That year, there were more than 800 cases of TSS reported to the CDC. More broadly, from 1979-1996, there were 5,296 cases of TSS reported; today, the incidence of TSS hovers at around 1 per 100,000 people annually.

But all this begs the question: WTF if TSS?

There are, generally speaking, two routes to developing menstrual TSS: Staphylococcus aureus and Streptococcus pyogenes. The former is a fairly ubiquitous Gram-positive bacteria, commonly found in the nose, respiratory tract and skin; it’s not always pathogenic, but the bacteria gets the name “aureus” thanks to the abundance of gold-colored pus that it is wont to cause in the cases when infection does occur. Streptococcus pyogenes, on the other hand (also known as group A strep or GAS) is an uncommon but usually pathogenic member of the skin’s microbial community. In addition to causing TSS, severe, invasive GAS infections can also lead to necrotizing fasciitis, a condition more commonly known as “flesh-eating disease.”

The role these bacteria can play in the development of TSS begins with simple opportunistic eating. If these bacteria are lucky enough to be blessed with an abundant food source — say, a super-absorbent tampon filled with the nutritive refuse of a womb that has been preparing for baby — they will gladly feast upon it. But the reality of TSS is more complicated than that.

Under normal circumstances, the body’s native immune system does a great job of shutting down bacterial orgies at the meat buffet. Our bodies are warm, delicious havens for many a pathogen looking for a sweet deal, and our immune responses constantly work to keep potentially harmful bacteria from making themselves at home while allowing more peaceful or helpful bacteria to flourish in our bodies.

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But sometimes things go wrong.

In the case of TSS (be it of the menstrual variety or stemming from complications of things like surgical and postpartum wound infections, burns and other types of damage to the protective barrier of the skin) S. aureus and GAS cause trouble because their release can act as "superantigens" inside the body.

"Antigen" is a catch-all term for a molecule that is capable of triggering an immune response from the body, like a cold virus or an allergen. Normally, specialized cells gobble up antigens on site, then said cell wears the surface proteins of the antigen on its own cell membrane like a costume. Kind of like a bacterial war re-enactor, except this re-enactor actually trains a militia. The body learns to recognize and fight the bad guy antigen du-jour and voila, you have an immune system.

Superantigens are sneaky, though: They skip the antigen processing step described above and instead trigger an immediate, exaggerated immune response.

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Conventional antigens activate about 0.01 percent to 0.1 percent of the body’s T-cells, which are immune warriors that work to protect the body from pathogens, both actual and (in the case of allergies) perceived. Soldiers, if you will. Superantigens, however, have the capacity to call 5 to 30 percent of these soldiers to action. For instance, if your body was the U.S. military, reserves and all, antigens would deploy about 200 to 2,000 troops, while superantigens could cause the activation of around 630,000 soldiers. That’s a pretty significant jump in military presence, and one that is not without danger to civilian bystanders.

In TSS, the presence of superantigens triggers what is known as a cytokine storm. Cytokines are small signalling molecules that bark instructions to the cell on a molecular level; they help get things done. One cytokine that is involved in the body’s defense system is called tumor necrosis factor, or TNF; these hardcore regulators can cause fever and cell death, and are primarily involved in the management of other immune cell troops.

When superantigens activate up to a third of the T-cell population, it results in a massive production of cytokines. TNF is one of the signaling molecules involved, but the body’s response to danger also signals many other types of action to stimulate inflammation and healing. To win a biological fight, the cytokine signaling molecules call for assistance at the site(s) of infection, while also instructing immune cells to make more signaling molecules, as they need to make sure that more troops are coming. Normally, the body can keep this in check, but in the case of a cytokine storm, the positive feedback loop of troops calling for troops calling for troops goes off the rails, leading to utter chaos: shock and massive tissue destruction, and possibly even death.

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When a person is colonized with S. aureus or GAS, the toxins they release — the ones acting as superantigens — are absorbed systemically and travel throughout the body, at which point it falls to the immune system to deal with the problem. The good news is that many people carry antibodies to the toxins produced by these bacteria, as they are fairly ubiquitous and likely to be encountered at some point or another. Seventy to 80 percent of people have developed antibodies to TSST-1 (toxic shock syndrome toxin 1, found in TSS caused by S. aureus) by adolescence, with 90 to 95 percent of people expressing the antibody by adulthood. The presence of antibodies indicates that the body has seen a particular threat before and vanquished it; it also means that if TSST-1 shows up in the body thanks to colonization with S. aureus, the body already has at least some kind of defense lined up.

This is interesting, given that most cases of TSS — and certainly those in the Michigan cluster — occur in younger women. But is that really due to the development of antibodies prior to colonization, or is something else going on? After all, young women today might be less educated on the dangers of extended tampon wearing, having missed the outbreak of TSS their mothers likely remember or are at least aware of.

“I don't think anyone really knows why we seem to see more TSS in younger women,” Jen Gunter explained via email. She’s an OB/GYN in the San Francisco Bay area. She's covered the topic of TSS in depth on her blog. “Many people do think that acquiring protective antibodies could be a factor. Women with TSS tend to have lower levels of antibodies to TSST-1 than unaffected women and the presence of these antibodies does increase with age.” Gunter also noted a potential behavioral link. “I think younger women are more likely to use tampons, so that might be a confounder.”

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But even then, it’s difficult to say. “It could also be reporting bias," meaning that young women are more likely to be diagnosed correctly than older women are. "There may also be other ‘host’ factors that make young women more susceptible," Gunter explained.

“Women who have heavier periods are more likely to use more absorbent tampons," Gunter said, explaining that this could mean that the relationship is correlative, not causative. A younger woman may be more likely to have a heavier period, which makes her more likely to use more absorbent tampons.

Gunter also clarified the link between high-absorbency tampons and TSS, noting that it’s not as simple as it may seem. The mere presence of additional nutrition for bacteria might not be enough to cause TSS. “[Rely] had ingredients other than cotton and rayon, so the ingredients may have fostered bacterial growth or somehow affected the body’s ability to contain and kill the toxin," she said. Gunter noted that more absorbent tampons may cause more trauma to the vaginal wall with insertion, further complicating matters.

That's why it's so important to note the kinds of personal hygiene products used by women who suffer from TSS. It's always possible that a particular brand or product is using ingredients that make TSS more likely to develop, or that some kind of contamination is occurring during the production process.

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But even taking tampons off the table entirely doesn't make TSS go away, further muddying the relationship between the product and the disease. “There is a case of TSS associated with the menstrual cup, so that does suggest that it's not all about absorbency," Gunter said. "Also, recurrence after tampon discontinuation has been reported, so there are so many unknowns.”

With all those open questions, the cluster of cases in Michigan becomes even murkier.

“The cause of the increase in cases is unclear,” wrote Jennifer Eisner, a spokesperson for the Michigan Department of Health and Human Services (MDHHS). “[It’s] one reason we issued a public message to promote awareness among health-care providers, other state health departments, and Michigan residents.”

The current goal of the MDHHS is to push for more awareness. “Through heightened awareness, we want to ensure that women seek care sooner if they become ill,” Eisner wrote, also noting the need to gather additional information from clinicians around the country, to see if cases are occurring elsewhere.

As researchers continue to learn more about the relationship between TSS and tampon usage, what can women do to keep themselves safe?

“Always use the lowest absorbency tampon possible and change it at least every 6-8 hours," Eisner wrote. "Know the signs and symptoms of TSS including sudden fever, vomiting, diarrhea, dizziness, muscle aches, low blood pressure and rash. If you develop symptoms, immediately discontinue tampon use and contact your doctor.”

Leigh Cowart is a freelance journalist covering science, sex and sports. She is fully vaccinated for rabies.