A child with bloody diarrhoea develops oliguric acute kidney injury with microangiopathic haemolytic anaemia and thrombocytopenia (HUS). Stool culture reveals a sorbitol-negative Gram-negative bacillus on SMAC (sorbitol MacConkey agar). Which virulence factor is directly responsible for glomerular endothelial injury in HUS?
- A Heat-labile toxin (LT) activating adenylyl cyclase in tubular epithelium
- B Shiga toxin 2 (Stx2) binding to Gb3 receptors on endothelial cells ✓
- C Intimin-mediated intimate bacterial adherence causing effacing lesions
- D Verotoxin binding to LPS of co-infecting organisms
Explanation
EHEC O157:H7 produces Shiga toxin 2 (Stx2) which binds with high affinity to globotriaosylceramide (Gb3/CD77) receptors expressed richly on renal glomerular endothelial cells, leading to ribosome inactivation, endothelial apoptosis, thrombotic microangiopathy, and the clinical triad of haemolytic uraemic syndrome. Stx2 is more strongly associated with HUS than Stx1. Heat-labile toxin causes secretory diarrhoea via cAMP in ETEC infections but does not cause HUS. Intimin causes attaching and effacing lesions in the gut but is not responsible for renal injury directly.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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