Toxic Shock Syndrome

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Basics

Description

  • Toxic shock syndrome (TSS) is a severe, acute life-threatening illness
  • Etiologic organisms:
    • Staphylococcus aureus, more common (TSS)
    • Group A streptococcus (GAS), less common (streptococcal TSS or STSS)
  • Both organisms produce toxins (SAgs) that upregulate immune response
  • S. aureus produces structurally similar toxins:
    • Toxic shock syndrome toxin (TSST-1)
    • Enterotoxins A-E, I (SEA-E, SEI)
  • GAS procedures M-protein, responsible for multiple virulence factors:
    • Produces exotoxins (SPEs) that act as superantigens
    • Creates complexes with fibrinogen that activate neutrophils and induce inflammatory response
    • Interferes with complement pathway and avoids phagocytosis
  • SAgs act as superantigens causing overwhelming immune response:
    • Massive cytokine production (cytokine storm)
    • Induce fever directly at the hypothalamus or indirectly via interleukin-1 (IL-1) and tumor necrosis factor (TNF) production
    • Enhance delayed hypersensitivity
    • Suppress neutrophil migration and immunoglobulin
    • Directly act at tissue sites causing additional local reaction
  • Massive vasodilation occurs
    • Serum protein and fluid shifts leading to hypotension

Etiology

  • Initial cases described in young healthy menstruating females due to highly absorbent tampons
    • Changes made in tampon composition to decrease incidence
  • Approximately one-half of reported TSS cases are nonmenstrual:
    • Surgical wounds
    • Postpartum wound infections
    • Mastitis
    • Septorhinoplasty
    • Sinusitis
    • Osteomyelitis
    • Arthritis
    • Burns
    • Nasal packing (nasal tampons)
    • Cutaneous and subcutaneous lesions
  • Nonmenstrual cases predominantly due to SEB and SEC producing S. aureus
  • 30–50% of healthy adults and children carry S. aureus in the nasal vestibule, vagina, rectum and/or on the skin
  • GAS infection often begin 24–72 hr at the site of monitor trauma, often without visible evidence on the skin site
  • Despite increased incidence of methicillin-resistant S. aureus (MRSA) infections, a recent study reported MRSA only accounting for 7% of cases
  • Association with severe influenza outbreaks and subsequent S. aureus coinfection

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Basics

Description

  • Toxic shock syndrome (TSS) is a severe, acute life-threatening illness
  • Etiologic organisms:
    • Staphylococcus aureus, more common (TSS)
    • Group A streptococcus (GAS), less common (streptococcal TSS or STSS)
  • Both organisms produce toxins (SAgs) that upregulate immune response
  • S. aureus produces structurally similar toxins:
    • Toxic shock syndrome toxin (TSST-1)
    • Enterotoxins A-E, I (SEA-E, SEI)
  • GAS procedures M-protein, responsible for multiple virulence factors:
    • Produces exotoxins (SPEs) that act as superantigens
    • Creates complexes with fibrinogen that activate neutrophils and induce inflammatory response
    • Interferes with complement pathway and avoids phagocytosis
  • SAgs act as superantigens causing overwhelming immune response:
    • Massive cytokine production (cytokine storm)
    • Induce fever directly at the hypothalamus or indirectly via interleukin-1 (IL-1) and tumor necrosis factor (TNF) production
    • Enhance delayed hypersensitivity
    • Suppress neutrophil migration and immunoglobulin
    • Directly act at tissue sites causing additional local reaction
  • Massive vasodilation occurs
    • Serum protein and fluid shifts leading to hypotension

Etiology

  • Initial cases described in young healthy menstruating females due to highly absorbent tampons
    • Changes made in tampon composition to decrease incidence
  • Approximately one-half of reported TSS cases are nonmenstrual:
    • Surgical wounds
    • Postpartum wound infections
    • Mastitis
    • Septorhinoplasty
    • Sinusitis
    • Osteomyelitis
    • Arthritis
    • Burns
    • Nasal packing (nasal tampons)
    • Cutaneous and subcutaneous lesions
  • Nonmenstrual cases predominantly due to SEB and SEC producing S. aureus
  • 30–50% of healthy adults and children carry S. aureus in the nasal vestibule, vagina, rectum and/or on the skin
  • GAS infection often begin 24–72 hr at the site of monitor trauma, often without visible evidence on the skin site
  • Despite increased incidence of methicillin-resistant S. aureus (MRSA) infections, a recent study reported MRSA only accounting for 7% of cases
  • Association with severe influenza outbreaks and subsequent S. aureus coinfection

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