Toxic Shock Syndrome (TSS)

Picture of skin loss in toxic shock syndrome (TSS); SOURCE: CDC

Toxic shock syndrome is a severe illness associated with group A Streptococcus (GAS or Streptococcus pyogenes); this bacterium produces a toxin termed TSS toxin-1 (TSST-, or phage-group-1 streptococcal toxic shock syndrome). TSS was first described in 1978 in children, but subsequent reports identified TSS outbreaks in women who use tampons.

Although first thought to be additionally associated with menstruation, over the past years, less than half of TTS cases have been menstruation-related. Although most cases of TTS occur in women who menstruate, about 25% of infections occur in men. TSS is also associated with Staphylococcus infections; some strains of these bacteria produce exotoxins very similar to TSST-1.

Risk factors for TSS include

• a history of using high-absorbency tampons,
• surgical wounds,
• history of using a diaphragm or contraceptive sponge,
• having a localized deep skin infection,
• abortion,
• burns, and
• immunosuppression (for example, as seen with diabetes, chronic lung or heart disease, or in elderly patients).

Not recognizing TTS symptoms while using a tampon can be a serious mistake. For example, Sara Manitoski, a 16-year-old who was on an overnight school trip, complained of stomach cramps before she went to bed. The following morning, she was found unresponsive. She ultimately died, and the autopsy revealed that she died from TTS.

The cause of toxic shock syndrome (TSS) is one of several closely related exotoxins secreted by bacteria that are infecting the person. The toxins (also termed superantigens) activate T cells of the immune system to produce chemicals known as cytokines that subsequently cause shock and tissue damage.

The superantigens have a unique way of interacting with the immune system. Although there are several closely related exotoxins, about 80% of individuals with TSS have an illness caused by TSST-1 or a similar exotoxin. Other exotoxins such as those produced by enterococci A, C, D, E, and H cause most of the remaining 20% of infections.

M protein, a filamentous protein on the cell membrane of group A Streptococcus bacteria enhances the likelihood of the bacterial strain being more likely to cause disease. Bacterial strains that lack M protein are less lethal because M protein can protect bacteria from host immune defenses. In addition, M protein apparently enhances cell damage and inflammation caused by exotoxins.

TSS symptoms and signs a resemble those found in other infections; however, the most common symptoms of TSS are as follows:

• Fever higher than 38.9 C (102 F)
• Low blood pressure (about <90 systolic); lightheadedness
• Decreased kidney function
• Disturbances in blood clotting (platelets less than or equal to 100,000/mm³)
• Liver involvement (twice the upper limit of normal for liver enzyme measurements)
• Acute respiratory distress
• Vomiting
• A sunburn-like red rash that's flat and/or shedding of the skin (erythroderma)
• Damage and death of soft tissues, such as necrotizing fasciitis, myositis, or gangrene due to flesh-eating bacterial infections
• Fatigue
• Headache
• Muscle aches

Skin shedding may occur on the palms and soles of the feet about one or two weeks after the initial infection begins.

Some doctors classify TSS cases by stages -- others do not. However, early symptoms such as a high fever and a falling blood pressure (shock-like symptoms) may occur before later stages of organ damage appear. Early symptoms are flu-like and can be confused with those of other diseases, like norovirus or other viral and bacterial infections, especially in young women.

In general, after the history and physical, if the patient has low blood pressure and multiorgan involvement characterized by two of the above listed symptoms of organ dysfunction (renal, lung, liver, skin, or blood), the clinical diagnosis of TSS is made, according to CDC criteria. A confirmation of the diagnosis is done by isolation of one of the causative bacteria; the bacteria should be identified as capable of producing exotoxin that either is, or functions like, TSST-1.

The treatment for TSS varies from patient to patient; however, the following treatments are fairly common. Patients with TSS usually will be treated with two or more of the following treatments:

• Intravenous fluids to treat shock
• IV antibiotics
• Deep surgical cleaning of any infected wounds
• Cardiac medications to help treat low blood pressure
• Oxygen and/or mechanical ventilation as needed
• Blood products if needed
• Dialysis for patients with kidney failure
• Hospitalization in an intensive-care unit

Patients with TSS who are diagnosed early and given appropriate treatment often have a good prognosis. Early treatment can help prevent life-threatening complications such as renal failure, respiratory failure, and coagulation disorders. However, the mortality (death) rate is about 5%-15%, and patients who develop complications have a poorer prognosis than those who do not. Patients who develop TSS are at risk for reinfection.

It is possible to reduce the chances of developing TSS. Menstruating females should minimize use of items like tampons, diaphragms, and sponges. Women should change tampons frequently and avoid super-absorbent tampons. For example, polyester, carboxymethylcellulose, and polyacrylate rayon, which increase tampon absorbency, have been removed from tampons because they were associated with increased TSS toxin production. Anyone diagnosed with TSS has a higher risk of reinfection. Women diagnosed with TSS should avoid tampon use in the future. Your ob-gyn doctor may provide additional recommendations. Early treatment of wounds, especially deep wounds, can help prevent TSS.