Introduction

  • Description: Toxic shock syndrome (TSS) is caused by toxins produced by an often-asymptomatic infection with Staphylococcus aureus defined by sudden onset of shock, organ failure, and frequently death. Although most commonly associated with prolonged tampon use, approximately 50% of TSS cases are now associated with other conditions.

  • Prevalence: Observed in fewer than 1/100,000 women aged 15–44 years (last active surveillance was conducted in 1987—there are currently approximately 35 cases per month in the United States, and the proportion of cases not associated with menstruation now exceeds 50%).

  • Predominant Age: 30–60 years; nonmenstrual 65 years and older.

  • Genetics: No genetic pattern.

Etiology and Pathogenesis

  • Causes: S. aureus (or less frequently Streptococcus pyogenes ) exotoxins (TSS toxin-1, enterotoxins A, B, and C). For toxic shock to develop, three conditions must be met: there must be colonization by the bacteria, it must produce toxins, and there must be a portal of entry for the toxin. Activation of T cells and massive cytokine cascades contribute to the development of shock or organ failure. The presence of foreign bodies, such as a tampon, is considered to reduce magnesium levels, which promotes the formation of toxins by the bacteria.

  • Risk Factors: Infection by S. aureus or S. pyogenes (also called group A Streptococcus or group A strep), use of super absorbency tampons, prolonged use of regular tampons, use of barrier contraceptive devices, nasal surgery, and postpartum and postoperative staphylococcal wound infections (25% of cases). Chronic illness, diabetes mellitus, and alcohol abuse increase the risk on nonmenstrual TSS. Nonmenstrual TSS can arise in a number of settings, including mastitis, sinusitis, osteomyelitis, arthritis, burns, cutaneous and subcutaneous lesions (extremities, perianal area, and axillae), respiratory infections following influenza, and enterocolitis.

Signs and Symptoms

  • Most common—rapid onset of fever of >38.9°C (102°F), hypotension (BP <90 mm Hg), diffuse rash (commonly absent in places where clothing presses tightly against the skin). Once initial symptoms occur, hypotension generally develops within 24–48 hours. Hypotension may progress to severe and intractable hypotension and multisystem dysfunction. Case fatality rates in nonmenstrual TSS are approximately 5%.

  • Other typical findings—agitation; arthralgias; confusion; diarrhea; erythema of pharynx, vulva, or vagina; conjunctival hyperemia; headache; myalgias; nausea; vomiting.

  • Desquamation, particularly on palms and soles, can occur 1–2 weeks after the onset of the illness.

Diagnostic Approach

Differential Diagnosis

  • Other exanthems (acute rheumatic fever, bullous impetigo, drug reaction, erythema multiforme, Kawasaki disease, leptospirosis, meningococcemia, Rocky Mountain spotted fever, rubella, rubeola, scarlet fever, viral disease)

  • Gastrointestinal illness (appendicitis, dysentery, gastroenteritis, pancreatitis, staphylococcal food poisoning)

  • Acute pyelonephritis

  • Hemolytic uremic syndrome

    Figure 80.1, Etiology, pathogenesis, and clinical features of toxic shock syndrome

  • Legionnaires disease

  • Meningococcemia

  • Pelvic inflammatory disease (PID)

  • Reye syndrome

  • Rocky Mountain spotted fever

  • Rhabdomyolysis

  • Septic shock

  • Stevens-Johnson syndrome

  • Systemic lupus erythematosus

  • Tick typhus

  • Associated Conditions: Other sources—surgical wounds (including dilation and curettage), nonsurgical focal infections, cellulitis, subcutaneous abscesses, mastitis, infected insect bites, postpartum (including transmission to the neonate), nonmenstrual vaginal conditions, vaginal infection, PID, steroid cream use. Even the use of laminaria to dilate the cervix has been reported to be associated with rare cases.

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