Toxic Shock Syndrome and Streptococcal Toxic Shock-Like Syndrome


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Toxic shock syndrome toxin-1 protein from staphylococcus.

Source: By Jawahar Swaminathan and MSD staff at the European Bioinformatics Institute –, displayed on, Public Domain,

OpenStax Microbiology

Toxemia associated with infections caused by Staphylococcus aureus can cause staphylococcal toxic shock syndrome (TSS). Some strains of S. aureus produce a superantigen called toxic shock syndrome toxin-1 (TSST-1). TSS may occur as a complication of other localized or systemic infections such as pneumonia, osteomyelitis, sinusitis, and skin wounds (surgical, traumatic, or burns). Those at highest risk for staphylococcal TSS are women with preexisting S. aureus colonization of the vagina who leave tampons, contraceptive sponges, diaphragms, or other devices in the vagina for longer than the recommended time.

Staphylococcal TSS is characterized by sudden onset of vomiting, diarrhea, myalgia, body temperature higher than 38.9 °C (102.0 °F), and rapid-onset hypotension with a systolic blood pressure less than 90 mm Hg for adults; a diffuse erythematous rash that leads to peeling and shedding skin 1 to 2 weeks after onset; and additional involvement of three or more organ systems. The mortality rate associated with staphylococcal TSS is less than 3% of cases.

Diagnosis of staphylococcal TSS is based on clinical signs, symptoms, serologic tests to confirm bacterial species, and the detection of toxin production from staphylococcal isolates. Cultures of skin and blood are often negative; less than 5% are positive in cases of staphylococcal TSS. Treatment for staphylococcal TSS includes decontamination, debridement, vasopressors to elevate blood pressure, and antibiotic therapy with clindamycin plus vancomycin or daptomycin pending susceptibility results.

A syndrome with signs and symptoms similar to staphylococcal TSS can be caused by Streptococcus pyogenes. This condition, called streptococcal toxic shock-like syndrome (STSS), is characterized by more severe pathophysiology than staphylococcal TSS, with about 50% of patients developing S. pyogenes bacteremia and necrotizing fasciitis. In contrast to staphylococcal TSS, STSS is more likely to cause acute respiratory distress syndrome (ARDS), a rapidly progressive disease characterized by fluid accumulation in the lungs that inhibits breathing and causes hypoxemia (low oxygen levels in the blood). STSS is associated with a higher mortality rate (20%–60%), even with aggressive therapy. STSS usually develops in patients with a streptococcal soft-tissue infection such as bacterial cellulitis, necrotizing fasciitis, pyomyositis (pus formation in muscle caused by infection), a recent influenza A infection, or chickenpox.


Parker, N., Schneegurt, M., Thi Tu, A.-H., Forster, B. M., & Lister, P. (n.d.). Microbiology. Houston, Texas: OpenStax. Access for free at: