Toxic Shock Syndrome
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Direct answer
Toxic shock syndrome is a severe multisystem illness caused by superantigen toxins from Staphylococcus aureus or group A streptococci, producing fever, hypotension and organ dysfunction. The staphylococcal and streptococcal forms have different diagnostic criteria, and a definite streptococcal case requires isolation of the organism from a sterile site. Treatment combines source control, fluids, vasopressors and antibiotics, with clindamycin added because it suppresses toxin synthesis.
What you must remember
- Mechanism: superantigens such as toxic shock syndrome toxin 1 activate large numbers of T cells, producing a cytokine storm.
- Staphylococcal criteria: fever of 38.9 degrees Celsius or more, diffuse macular erythema, desquamation after one to two weeks, hypotension and involvement of three or more organ systems.
- Streptococcal criteria: isolation of group A streptococcus from a normally sterile site, with hypotension and at least two features such as renal impairment, coagulopathy, liver involvement or ARDS.
- Soft-tissue clue: necrotising fasciitis or gangrene is an important feature of streptococcal disease and points to an extensive source.
- Sources: abscesses, deep wounds, burns, packing material and surgical sites, with tampons a historical source in adults.
- Antibiotic cover: an anti-staphylococcal beta-lactam (penicillin for confirmed streptococcal disease), with vancomycin where MRSA is prevalent, plus clindamycin to suppress toxin production.
- Source control and support: drain abscesses, remove packing or foreign material, give fluids and vasopressors, and monitor renal, coagulation and liver function.
A stepwise approach to a child with a deep abscess and shock
A 9-year-old with a thigh abscess develops fever, vomiting, a diffuse red rash and hypotension within hours. The sequence below treats the shock and the source together.
- Resuscitate at once. Give rapid isotonic fluid boluses, monitor perfusion closely and add vasopressors if hypotension persists.
- Culture and find the focus. Draw blood and site cultures before antibiotics, and look carefully for abscess, wound or packing.
- Control the source. Drain the abscess, remove any packing or foreign material and debride necrotic tissue.
- Start combination antibiotics. Give an anti-staphylococcal beta-lactam, with vancomycin if MRSA is likely, plus clindamycin to suppress toxin production.
- Consider immunoglobulin. Intravenous immunoglobulin is added in severe streptococcal disease where local practice supports it.
- Watch the organs. Track renal function, coagulation, liver enzymes, respiratory status and the skin over the coming days.
Clindamycin and the anti-staphylococcal beta-lactam are used together, so the regimen covers both the organism and its toxin. Fluid and vasopressor support run in parallel with source control, and neither replaces the other.
Where the exam tries to catch you
Three errors recur on this topic.
- Trap: choosing a beta-lactam alone Correct: clindamycin is added because it inhibits toxin synthesis, which a beta-lactam does not.
- Trap: expecting desquamation at presentation Correct: palm and sole peeling appears one to two weeks later, so it aids recall rather than early diagnosis.
- Trap: giving antibiotics without source control Correct: an undrained focus keeps toxin production going, so drainage and debridement are essential.
Frequently asked questions
Why is clindamycin added in toxic shock syndrome?
Clindamycin is added in toxic shock syndrome because it inhibits bacterial protein synthesis and so suppresses toxin production, including toxic shock syndrome toxin 1 and streptococcal exotoxins. Beta-lactam antibiotics alone do not switch off toxin synthesis.
What are the staphylococcal criteria for toxic shock syndrome?
Staphylococcal toxic shock syndrome criteria include fever of 38.9 degrees Celsius or more, diffuse macular erythema, desquamation after one to two weeks, hypotension and involvement of three or more organ systems. The diagnosis is made clinically, supported by laboratory findings.
What distinguishes streptococcal toxic shock syndrome?
Streptococcal toxic shock syndrome requires isolation of group A streptococcus from a normally sterile site, together with hypotension and at least two organ features. It is often linked to soft-tissue infection such as necrotising fasciitis.
Is immunoglobulin recommended in toxic shock syndrome?
Intravenous immunoglobulin is considered as adjunctive therapy in severe streptococcal toxic shock syndrome, but evidence of benefit is mixed. It does not replace source control, antibiotics and organ support.