Excerpt from Toxic Shock Syndrome

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Background

Toxic shock syndrome (TSS) is an acute febrile illness characterized by a generalized erythematous eruption accompanied by systemic involvement. It is due to toxin-producing strains of Staphylococcus aureus, both methicillin-sensitive S aureus (MSSA) and methicillin-resistant S aureus (MRSA). Originally described in 1978 and soon thereafter associated with tampon use,¹ TSS is now recognized to occur in both menstrual and nonmenstrual forms. In the late 1980s, a disease similar in appearance to TSS, but caused by invasive streptococci, was recognized. Also known as toxic strep or streptococcal toxic shocklike syndrome, streptococcal TSS (STSS) was found to share many clinical features with TSS.

The Medscape CME course Invasive Group A Streptococcal Disease in Nursing Homes, Minnesota, 1995-2006 and the Emerging and Reemerging Infectious Diseases Resource Center. Additionally, several other eMedicine Specialty sections have articles on TSS, including Toxic Shock Syndrome from Critical Care.

Pathophysiology

Massive cytokine release as a result of toxin/superantigen activity is postulated to be the mediator of the clinical signs of TSS.² Both menstrual and nonmenstrual forms of TSS have been linked to toxin-producing strains of S aureus. More than 90% of menstrual TSS is mediated by TSS toxin-1 (TSST-1) production, which is associated with massive release of tumor necrosis factor-alpha (TNF-a) and interleukin (IL)–1. These cytokines have been demonstrated to produce fever, rash, hypotension, tissue injury, and shock.

The absence of an antibody to TSST-1 has been shown to be a major risk factor for acquisition of TSS; failure to generate anti-TSST-1 antibody after an episode of TSS predisposes patients to recurrent episodes. Isolates of S aureus from nonmenstrual TSS produce TSST-1 in approximately 50% of cases, whereas the remainder produces staphylococcal enterotoxin B (SEB) and staphylococcal enterotoxin C (SEC). Staphylococcal enterotoxins have been shown to be potent mediators of cytokine production and release in a similar fashion to TSST-1, thereby producing clinically similar diseases.

In most cases of STSS, toxin-producing group A streptococci have been isolated, with streptococcal pyrogenic exotoxin-A (SPE-A) production being most closely linked with invasive disease. However, group A streptococci producing streptococcal pyrogenic exotoxin-B (SPE-B), streptococcal pyrogenic exotoxin-C (SPE-C), streptococcal superantigen and mitogenic factor, as well as non–group-A streptococci, have been found to be causative in individual cases of STSS.

In a similar manner to classic TSS, it is postulated that massive cytokine release (primarily TNF-a, IL-1beta, and IL-6), as a result of toxin/superantigen activity, mediates the clinical signs of STSS. In addition, streptolysin O, produced by 100% of streptococcal strains associated with STSS, has also been shown to cause TNF-a, and IL-1beta production and has been demonstrated to act synergistically with SPE-A. An absence of protective immunity is postulated as a potential risk factor in this population as well.

Frequency

United States

Both TSS and STSS are relatively rare; the incidence of nonmenstrual TSS exceeds that of menstrual TSS.

Mortality/Morbidity

• TSS: The mortality rate is approximately 5-15%, and recurrences have been reported in as many as 30-40% of cases.
• STSS: Mortality rates are more than 5 times higher than in TSS.

Sex

Young adult women are affected more often than men.

Age

The majority of cases of TSS and STSS have occurred in young, otherwise healthy persons aged 20-50 years, despite the fact that very young, elderly, diabetic, or immunocompromised persons are more susceptible to the acquisition of invasive staphylococcal and streptococcal infections.

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