A 5-year-old child develops bloody diarrhea followed by oliguric renal failure and thrombocytopenia (platelet 35,000/μL). Peripheral smear shows fragmented RBCs (schistocytes). Stool culture reveals a sorbitol-negative E. coli colony on SMAC (Sorbitol MacConkey agar). The toxin responsible for the renal damage primarily acts by:

• A Heat-stable enterotoxin (STa) — activating guanylate cyclase C, increasing cGMP in renal tubular cells
• B LT-I enterotoxin — ADP-ribosylating Gsα protein, increasing cAMP in renal mesangial cells
• C Hemolysin (HlyA) — forming pores in renal tubular cell membranes causing osmotic lysis
• D Shiga toxin (Stx1/Stx2) — N-glycosidase cleaving 28S rRNA of 60S ribosomes, inhibiting protein synthesis in glomerular endothelial cells ✓

Explanation

This is hemolytic uremic syndrome (HUS) caused by Shiga toxin-producing E. coli (STEC), most commonly O157:H7. STEC is sorbitol-negative on SMAC agar (other E. coli are sorbitol-positive, appearing pink). Shiga toxins (Stx1 and especially Stx2) are AB5 toxins that bind via B subunit to globotriaosylceramide (Gb3) receptor on glomerular endothelial cells. The A subunit is an N-glycosidase that cleaves a specific adenine from the 28S rRNA of the 60S ribosomal subunit — this halts protein synthesis, causing endothelial cell death, microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and acute renal failure — the triad of HUS. Antibiotics are contraindicated in STEC-HUS as they trigger 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.