Streptococcal toxic shock syndrome (STSS) is caused by a highly invasive group A streptococcal infection and is associated with shock and organ failure.

Etiology

he portal of entry of streptococci in STSS cannot be deter mined in at least 50% of cases and can only be presumed in many others. The use of tampons has been associated with acquiring the disorder. In other patients, the use of nonsteroidal antiinflammatory drugs (NSAIDs) may have masked the early symptoms or predisposed the patient to more severe streptococcal infection and shock. Usually, STSS appears after streptococci have invaded areas of injured skin (e.g., cuts, scrapes, surgical wounds).

Immunologic Mechanisms

 Pyrogenic exotoxins cause fever in human beings and animals and also help induce shock by lowering the threshold to exogenous endotoxin. Streptococcal pyrogenic exotoxins A and B induce human mononuclear cells to synthesize not only tumor necrosis factor-α (TNF-α) but also interleukin-1 beta (IL-1β) and interleukin-6 (IL-6), suggesting that TNF could mediate the fever, shock, and tissue injury observed in patients with STSS.

M protein contributes to invasiveness through its ability to impede phagocytosis of streptococci by human PMNs.

Superantigens are capable of binding to alpha and beta T cell receptors (TCRs) and major histocompatibility complex (MHC) class II molecules. Superantigens can directly activate 1% to 2% of T cells and create high levels of cytokines in the blood. These high levels can produce shocklike symptoms.

Cytokine production by less exotic mechanisms also likely contributes to the genesis of shock and organ failure. Exotoxins such as SLO are also potent inducers of TNF-α and IL-1β. Pyrogenic exotoxin B, a proteinase precursor, has the ability to cleave pre–IL-1β to release preformed IL-1. Finally, SLO and pyrogenic exotoxin A together have additive effects in the induction of IL-1β by human mononuclear cells. Regardless of the mechanisms, induction of cytokines in vivo is likely the cause of shock and exotoxins, cell wall components, and other substances are potent inducers of TNF and IL-1.

Epidemiology

The rates of STSS are highest in young children and older adults. More than 50% of patients have an underlying chronic illness. STSS is also associated with a substantial risk of transmission in households and health care institutions. Mortality following an outbreak of S. pyogenes that progresses to toxic shock can be as high as 70%. The illness is classified as a rare infection because it affects only about 300 people annually. STSS almost never follows a simple streptococcal throat infection.

Signs and Symptoms

 The symptoms of STSS include shock; fever; blotchy rash; and a red, swollen, and painful area of infected skin. The average incubation period for STSS is 2 to 3 days, usually after minor nonpenetrating trauma.

Pain, the most common initial symptom of STSS, is abrupt in onset and severe and usually precedes tenderness or physical findings. The pain generally involves an extremity but may also mimic peritonitis, pelvic inflammatory disease, pneumonia, acute myocardial infarction, or pericarditis.

About 20% of STSS patients have an influenza-like syn drome characterized by fever, chills, myalgia, nausea, vomiting, and diarrhea. Fever is the most common early sign, although hypothermia may be present in patients with shock.

About 80% of STSS patients have clinical signs of soft tis sue infection, such as localized swelling and erythema, which in 70% of one group of patients progressed to necrotizing fasciitis or myositis and required surgical débridement, fasciotomy, or amputation. An ominous sign is the progression of soft tissue swelling to the formation of vesicles and then bullae, which appear violaceous or bluish.

Laboratory Data

 The case definition of STSS includes serologic confirmation of group A streptococcal infection by a fourfold rise against SLO and DNAse B. Although initial laboratory studies usually demonstrate only mild leukocytosis, the mean percentage of immature neutrophils can reach 40% to 50%. Blood cultures are positive in 60% of cases.

Renal involvement is indicated by the presence of hemoglobinuria and by serum creatinine values that are, on average, more than 2.5 times normal. Renal impairment precedes hypotension in approximately 40% to 50% of patients. Hypoalbuminemia is associated with hypocalcemia on admission and throughout the hospital course.

Treatment

Streptococcal TSS can be deadly and needs immediate treatment. IV fluids and medications to maintain a normal blood pressure are required in acutely ill patients. Penicillin and other beta-lactam antibiotics are most efficacious against rapidly growing bacteria.

After recovery, the skin may peel as the rash heals. Surgery may be necessary to remove areas of dead skin and muscle around an infected wound.

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