Toxic shock syndromes

Introduction

  • Classical: Staph aureus or Group A strep
  • Difficult to differentiate from sepsis

Differences


Toxic shock syndromeStrep toxic shock syndrome
OrganismS. AureusGroup A strep
ToxinToxic shock syndrome toxin-1 (TSST-1) Staphylococcal enterotoxinsStreptococcal pyrogenic exotoxins (A and B)
Risk factorsRetained tampon or female barrier contraceptives OR nasal packing Skin and soft tissue infections Varicella Surgery Trauma Childbirth Influenza (secondary staph pneumonia)Necrotising soft tissue infections Varicella Surgery Trauma Childbirth  Influenza
PainUncommonCommon
RashCommonUncommon
BC positive5%60%
Mortality<5%20-45%

Pathophysiology – Staph

  • Superantigen-mediated
  • Bind to histocompatibility complex class II and T-cell receptors on APC’s with massive T cell and cytokine release leading to SIRS response
  • 9% of women are vaginally colonised with Staph, only 1% of whom are toxigenic
  • Almost all menstrual TSS is due to TSST-1 toxin vs. only half of non-menstrual cases
  • Wounds harbouring toxigenic S. aureus may not even appear infected
  • Wound swabs often positive for S. aureus (despite BC + in only 5%)

Case definition (Staph)

  • Probable case = 4 or more clinical criteria + lab criteria met
  • Confirmed = 5 clinical criteria + lab criteria met including desquamation (unless dies before this)
  • Clinical criteria
    • Fever >38.9
    • Diffuse macular erythroderma (like sunburn)
    • Desquamation 1-2 weeks after rash
    • Hypotension
    • Multiorgan failure (3 or more organ systems): GI, CK, mucous membrane hyperaemia, renal, hepatic, Plt <100, CNS
  • Lab criteria
    • Negative BC or CSF culture (BC can be positive for Staph. Aureus)
    • Negative serology for lepto, measles and rocky mountain spotted fever

Differential diagnosis

  • Streptococcal toxic shock syndrome
  • Myonecrosis due to Clostridium perfringens
  • Toxic shock syndrome due to Clostridium sordellii associated with gynaecological surgery, childbirth, miscarriage and abortions (often without fever)
  • Staphylococcal scalded skin syndrome (lacks hypotension or organ dysfunction)
  • Sepsis or septic shock of any cause (erythroderma is distinguishing factor)
  • Rocky mountain spotted fever
  • Leptospirosis
  • Meningococcaemia
  • SJS
  • TEN
  • Kawasaki’s disease

Treatment

  • Treat as for sepsis
  • Remove any nidus of infection (including tampon/nasal packing)
  • Consider coverage of MRSA
    • Options:
      • Vancomycin 25-30mg/kg load then 15mg/kg BD
      • Linezolid 600mg IV BD
        • May directly suppress TSST-1 production
  • If low risk of MRSA
    • Flucloxacillin 2g q4h +- Clindamycin 900mg IV q8h
      • Clindamycin can be added to inhibit protein synthesis and TSST-1 production but should not be used as monotherapy
  • IVIG
    • Reserved for failure to improve over 6 hours despite above
    • 1-2g/kg
    • Contraindicated in IgA deficiency
  • High-dose corticosteroids not recommended

Streptococcal TSS

  • Mostly in older patients and those under 1 year old with necrotising fasciitis
  • Around 3.4% of invasive Group A strep infections (S. pyogenes) suffer this
  • Pathophysiology
    • Streptococcal pyrogenic exotoxins A and B
    • Act in same way as staph toxins
    • BC positive in 60% and wound swabs almost always positive

Streptococcal TSS

  • Probable case: All clinical criteria met + absence of other cause + isolation of GAS from non-sterile site
  • Confirmed case: All clinical criteria met + Isolation of GAS from sterile site
  • Clinical criteria
    • Hypotension
    • Multiorgan dysfunction (2 or more): Renal, Plt <100 or DIC, hepatic, ARDS, generalised erythematous macular rash, soft tissue necrosis

Treatment

  • PipTaz 4.5 q8h or meropenem 1g IV q8h + clindamycin 900mg IV q8h
  • If MRSA prevalent – add vancomycin
  • Once GAS confirmed, narrow spectrum to Pen G 4 million units IV q4h + clindamycin
  • IVIG may play a role

Last Updated on October 2, 2020 by Andrew Crofton