A 4-year-old child develops bloody diarrhoea followed 5 days later by pallor, oliguria, and a platelet count of 20,000/µL (normal 1.5–4 lakh). Peripheral smear shows schistocytes. Stool culture grows E. coli that is Sorbitol-MacConkey agar (SMAC) negative (non-sorbitol fermenting). What pathogenic mechanism accounts for the renal injury?

• A Heat-stable enterotoxin (ST-a) activating guanylate cyclase causing cGMP-mediated fluid secretion
• B Lipopolysaccharide (LPS) endotoxin causing DIC and secondary renal failure
• C Shiga toxin 2 (Stx2) of STEC O157:H7 binds Gb3 (globotriaosylceramide) receptors on glomerular endothelial cells and renal tubular cells, inhibiting protein synthesis and causing TMA leading to HUS ✓
• D Intimin (encoded by eae gene) causing attaching-and-effacing lesions in proximal tubules

Explanation

STEC (Shiga toxin-producing E. coli) O157:H7 is identified on SMAC as non-sorbitol fermenting (most E. coli ferment sorbitol). Its Shiga toxin 2 (Stx2) is the primary virulence factor: after absorption into circulation, Stx2 binds its receptor Gb3 (globotriaosylceramide/CD77) on glomerular endothelial cells and podocytes (which have high Gb3 expression), enters cells, and enzymatically cleaves 28S rRNA — halting protein synthesis and triggering apoptosis and microvascular thrombosis (TMA). This results in haemolytic uraemic syndrome (HUS): microangiopathic haemolytic anaemia + thrombocytopenia + AKI.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.