Epidemiology

Etiology

TSS is most commonly caused by toxin-producing strains of Streptococcus pyogenes and Staphylococcus aureus

• Staphylococcal TSS
  • Menstrual factors (∼ 50% of cases)
    • High-absorbency tampons
    • Prolonged placement of tampons, menstrual cups, and vaginal sponges
  • Nonmenstrual factors
    • Burn and wound infections
    • Postpartum or postabortion infections
    • Postsurgical wound packing

Pathophysiology

• Superantigen production: Causative organisms (S. pyogenes and S. aureus) produce superantigens
• Superantigen-mediated T-cell activation
  • Superantigens bypass processing and presentation by antigen-presenting cells.
  • Superantigens directly connect the MHC class II molecule on antigen-presenting cells to the T-cell receptor on T-cells by forming a bridge outside of the normal binding sites → nonspecific T-cell activation → rapid activation of excessive numbers of T cells → massive cytokine release
• SIRS: ↑↑↑ Cytokines → generalized endothelial disruption → capillary leak syndrome → generalized edema → intravascular hypovolemia → organ dysfunction and disseminated intravascular coagulation (DIC)

Clinical features

Prodrome

• Flu-like symptoms: high fever, chills, myalgia, headache, nausea, vomiting, diarrhea
• Dermal rash: more common in menstrual staphylococcal TSS than in nonmenstrual staphylococcal TSS and streptococcal TSS
  • Transient erythematous macular (sunburn-like) rash
  • Commonly involves the palms and soles
  • Typically desquamates 1–2 weeks after onset.

Shock and end-organ dysfunction

• Early: tachycardia, tachypnea, high fever, altered mental status
• Late
  • Hypotension
  • Delayed capillary refill
  • Worsening altered mental status
  • Evidence of organ failure

Diagnostics

Treatment