A 6-year-old child in Kolkata develops sudden onset bloody diarrhoea followed by oliguria, haematuria and anaemia on day 7. Peripheral smear shows schistocytes. Stool culture reveals E. coli O157:H7. What is the pathogenesis linking the diarrhoea to the renal failure?
- A Systemic invasion by E. coli O157 causes direct glomerulonephritis
- B LPS (endotoxin) of O157 triggers systemic complement activation causing platelet consumption
- C Shiga toxin (Stx1/Stx2) produced in the colon is absorbed into the bloodstream and binds Gb3 receptors on renal endothelium, inhibiting protein synthesis and causing endothelial damage, microangiopathic haemolytic anaemia and renal cortical necrosis (HUS) ✓
- D Haemolysin (hemolysin A) directly lyses erythrocytes causing haemolytic anaemia and haemoglobinuria
Explanation
Haemolytic uraemic syndrome (HUS) from STEC (O157:H7) is the classic triad of microangiopathic haemolytic anaemia, thrombocytopenia and acute kidney injury. Shiga toxin (especially Stx2) is absorbed from the gut, circulates bound to neutrophils and platelets, and binds glycolipid receptor Gb3 (globotriaosylceramide) richly expressed on glomerular endothelium. Inside cells it cleaves 28S rRNA, halting protein synthesis and causing endothelial apoptosis, fibrin thrombi in glomerular capillaries, microangiopathic haemolysis (schistocytes) and acute cortical necrosis. Antibiotics are generally avoided as they may increase Stx release.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
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Written and medically reviewed by the StethoPrep medical team.