Toxic shock syndrome

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Toxic shock syndrome (TSS) is a severe bacterial-toxin mediated condition, characterized by an initial soft tissue infection, which rapidly progresses to systemic disease and circulatory collapse . It is due to a Gram positive infection, most frequently Staphylococcus aureus or Streptococcus pyogenes .

Epidemiology

The staphylococcal toxic shock syndrome is the commonest form, with an annual incidence of 0.5 cases per 100,000 population, with a slightly lower incidence of the second commonest form, streptococcal toxic shock syndrome, estimated at 0.4/100,000 .

Mortality rates vary widely, 5-22% for staphylococcal toxic shock syndrome, and from 30-70% for streptococcal toxic shock syndrome .

Risk factors
Staphylococcal toxic shock syndrome
  • menstruating females (super-absorbent tampons)
  • colonization of surgical wounds
  • burns
  • postpartum infection
  • bacterial pneumonia post-influenza
Streptococcal toxic shock syndrome

Commonly

Less commonly

In these scenarios, additional clinical factors that increase risk further include:

Clinical presentation

The typical signs and symptoms of toxic shock syndrome are non-specific, and it often mimics, and maybe mistaken for sepsis.

  • fever
  • malaise
  • gastrointestinal symptoms
  • myalgia
  • confusion
  • refractory hypotension
Skin manifestations
  • staphylococcal
    • erythematous rash, initially truncal with later extension to the extremities, including the palms and soles
    • desquamation occurs 1–2 weeks after symptoms first appear
    • conjunctival hyperemia
    • strawberry tongue
  • streptococcal
    • scarlatiniform rash, i.e. similar to that seen in scarlet fever

Pathology

Organisms

All cases of toxic shock syndrome are produced by Gram positive bacteria; the most commonly implicated being Staphylococcus aureus or Streptococcus pyogenes (group A streptococci).

However similar presentations have been seen in those with group B (S. agalactiae), C (S. equis), and G (S. dysgalactiae) streptococcal infections. Rarely Clostridium species-related toxic shock syndrome has been reported (e.g. C. perfringens, C. sordellii)  .

Pathogenesis

Toxic shock syndrome occurs primarily due to the release of superantigens:

  • staphylococci: toxic shock syndrome toxin-1 (TSST-1), enterotoxins B and C
  • streptococci: pyrogenic exotoxins A or B

Superantigens sidestep the normal immune system mechanisms of antigen presenting and hyperstimulate clonal T cells by cross-linking major histocompatibility complex (MHC) class II molecules on antigen-presenting cells to T-cell receptors (TCR) . Consequently a massive release of cytokines, including gamma interferon, interleukins and tumor necrosis factors, creating a so-called cytokine storm.

The toxic shock syndrome toxin-1 (TSST-1) also has deleterious effects on the vasculature, with marked capillary leakiness, fluid shifts and hypotension.

Most cases of menstruation-related toxic shock syndrome are secondary to the release of TSST-1. For non-menstrual-related presentations the toxic shock syndrome toxin is only implicated in half the cases, with enterotoxins responsible for the other 50% .

Radiographic features

CT/MRI

In general, cross-sectional imaging is useful to assess for the source of infection. MRI is much more sensitive than CT when diagnosing soft tissue infections but its lack of specificity may be a drawback, increasing risk of false-positives .

Unfortunately, in early disease, the radiological findings may create a false sense of security due to their apparent benign appearances. Soft tissue inflammation may initially be mild, no abscesses might be evident and no gas seen. In fact S. pyogenes is not a gas-forming organism. Indeed in the early phase of fasciitis, there may be a clear lack of concordance between the imaging and surgical presentation of a case .

Ultrasound

Point-of-care ultrasound (POCUS) can provide added value at the bedside in the ICU .

Treatment and prognosis

  • empiric antibiotics initially
    • must include an antimicrobial agent that is known to inhibit superantigen synthesis, e.g. clindamycin or linezolid
  • intravenous immunoglobulins (IVIG) are important as they bind to, and neutralise, the superantigens, thus preventing a potential cytokine storm

Differential diagnosis