A 4-year-old child presents with bloody diarrhoea, and 5 days later develops oliguria and elevated creatinine. Peripheral blood smear shows schistocytes and thrombocytopenia. Stool culture grows an organism that ferments sorbitol slowly and is O157:H7 serotype. The toxin responsible for the haemolytic uremic syndrome (HUS) acts by:
- A Activating adenylyl cyclase, increasing cAMP and causing secretory diarrhoea
- B Disrupting tight junctions in intestinal epithelium via ZOT (zonula occludens toxin)
- C Superantigen activity causing systemic cytokine release
- D N-glycosidase cleavage of 28S rRNA of 60S ribosomal subunit, inhibiting protein synthesis in endothelial cells ✓
Explanation
Haemolytic uremic syndrome (HUS) is caused by Shiga toxin-producing E. coli (STEC) O157:H7. Shiga toxin (Stx1 and Stx2) has an AB5 structure — the B pentamer binds to Gb3 (globotriaosylceramide) on endothelial cells (especially in glomeruli), and the A subunit cleaves the N-glycosidic bond of adenine in 28S rRNA of the 60S ribosomal subunit, halting protein synthesis and causing endothelial cell death. Microvascular injury in glomeruli leads to thrombotic microangiopathy, microangiopathic haemolytic anaemia, thrombocytopenia, and acute kidney injury — the HUS triad. ZOT is a Vibrio cholerae toxin; adenylyl cyclase activation is by cholera toxin/ETEC.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.