Toxic shock syndrome

Overview

•Life-threatening toxin-mediated emergency caused by Staphylococcus aureus (MSSA/MRSA) or Group A Streptococcus

•Mechanism: bacterial superantigens bypass normal antigen presentation, activating up to 20% of T cells simultaneously → massive cytokine storm (TNF-alpha, IL-1) → vasodilation, capillary leak, multiorgan failure

•Mortality approximately 8%; streptococcal TSS carries higher mortality than staphylococcal TSS

Presentation

•Fever - typically >38.9°C; early and consistent

•Erythrodermic rash - widespread sunburn-like erythema (>90% BSA including mucosae), macular and blanching

•Desquamation - peeling of palms and soles; classic late feature

•Hypotension - systolic BP <90 mmHg; vasodilation and capillary leak (not primary cardiac failure)

•Myalgia, confusion/encephalopathy, nausea/vomiting/diarrhoea

•Severe localised limb pain - particularly characteristic of streptococcal TSS, often the first complaint

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Fever + sunburn rash + hypotension = TSS until proven otherwise. Do not wait for desquamation to make the diagnosis.

Investigations

•Blood cultures - before antibiotics if possible; identifies organism and guides therapy

•Wound/throat/vaginal swabs - swab suspected source

•FBC - leucocytosis/leucopenia; thrombocytopaenia if DIC developing

•Serum lactate - elevated indicates tissue hypoperfusion/shock

•CK - markedly elevated in rhabdomyolysis

•U&Es/creatinine - AKI common; LFTs - hepatic involvement; coagulation screen - DIC; CRP - typically markedly elevated

Differential diagnosis

•Meningococcal septicaemia - petechial, non-blanching rash; meningism; no desquamation

•Stevens-Johnson syndrome - drug-triggered; targetoid lesions and mucosal blistering; less acute haemodynamic compromise

•Kawasaki disease - children <5; fever >5 days; cervical lymphadenopathy, red cracked lips

•Severe cellulitis - suspect TSS if systemic compromise is out of proportion to local skin findings

Management

•Three simultaneous pillars: resuscitation + source control + antibiotics - all in parallel; HDU/ICU admission

•Resuscitation: IV fluids for hypotension; initiate Sepsis Six within 1 hour of suspicion

•Source control: surgical exploration, debridement, and removal of any foreign body/tampon - critical as toxin continues to be produced while source remains

•Antibiotics: broad-spectrum cover plus clindamycin in every regimen

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Clindamycin is added not just for antibacterial cover but because it inhibits ribosomal protein synthesis, directly halting superantigen production. A beta-lactam alone kills bacteria but does not stop toxin already being made - this distinction is high-yield.

Complications

•AKI - hypoperfusion and direct cytotoxic effects

•Rhabdomyolysis - markedly elevated CK; worsens AKI

•ARDS - capillary leak and cytokine-mediated lung injury

•DIC - coagulopathy from inflammatory cascade

•Cardiomyopathy, encephalopathy, recurrence (staphylococcal TSS if antibody immunity not established)

Causes and risk factors

Staphylococcal vs streptococcal TSS
FeatureStaphylococcal TSSStreptococcal TSS
OrganismS. aureus (MSSA/MRSA)Group A Streptococcus (S. pyogenes)
Key toxinsTSST-1 (menstrual TSS), enterotoxins A, B, CStreptococcal pyrogenic exotoxins (SPEs)
Classic associationTampon use; wounds; post-surgicalSkin/soft tissue infection; severe limb pain as first symptom
MortalityLowerHigher

Feature	Staphylococcal TSS	Streptococcal TSS
Organism	S. aureus (MSSA/MRSA)	Group A Streptococcus (S. pyogenes)
Key toxins	TSST-1 (menstrual TSS), enterotoxins A, B, C	Streptococcal pyrogenic exotoxins (SPEs)
Classic association	Tampon use; wounds; post-surgical	Skin/soft tissue infection; severe limb pain as first symptom
Mortality	Lower	Higher

•Risk factors: tampon use (extended/highly absorbent), skin wounds/burns, post-surgical (foreign body/prosthesis), cellulitis, immunosuppression, IVDU, post-partum, lack of antibodies to toxins (younger adults most at risk)