Enterohemorrhagic E. coli (EHEC O157:H7) produces Shiga toxin (Stx). After intestinal infection, which mechanism leads to hemolytic uremic syndrome (HUS)?
- A Stx binds Gb3 (globotriaosylceramide) receptor on renal tubular and endothelial cells, inhibits 28S rRNA and protein synthesis causing endothelial apoptosis and microangiopathic hemolytic anemia ✓
- B Stx activates complement alternative pathway causing platelet consumption
- C Stx activates neutrophil elastase which damages glomerular basement membrane
- D E. coli lipopolysaccharide directly activates coagulation cascade in renal vessels
Explanation
Shiga toxin (Stx1 and Stx2) consists of one A subunit and five B subunits (AB5 toxin). The B pentamer binds to Gb3 (globotriaosylceramide) receptors, which are abundant on renal cortical endothelial cells and glomerular cells. The A subunit is an N-glycosidase that cleaves the 28S rRNA of 60S ribosomal subunit, halting protein synthesis and causing endothelial cell apoptosis, platelet aggregation, fibrin thrombi in glomerular microvasculature, microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure — classic HUS triad. Antibiotics are avoided in EHEC as they induce Stx phage and increase toxin release.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.