A 2-year-old develops HUS (hemolytic uremic syndrome) following bloody diarrhea. Stool culture on sorbitol–MacConkey agar grows colorless colonies (sorbitol non-fermenter). The pathogenic mechanism is:

• A Heat-labile toxin activating adenylate cyclase in enterocytes
• B Intimin-mediated A/E lesion without toxin production
• C Invasion plasmid-mediated intracellular spread mimicking Shigella
• D Shiga toxin 2 produced by EHEC (E. coli O157:H7) inhibiting ribosomal 60S subunit causing endothelial and renal tubular cell death ✓

Explanation

EHEC (O157:H7) is sorbitol non-fermenting; it produces Shiga toxin 2 (Stx2), which binds Gb3 receptors on renal glomerular endothelial cells and ribosomal 60S subunit N-glycosidase activity halts protein synthesis, leading to endothelial death, microangiopathic hemolytic anemia, thrombocytopenia, and renal failure (HUS). Heat-labile toxin (LT) is the mechanism of ETEC causing watery diarrhea. Intimin mediates A/E lesions in EPEC (infantile diarrhea, no HUS). Invasion plasmid characterizes EIEC/Shigella causing dysentery.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.