A 3-year-old child develops hemolytic uremic syndrome (HUS) 7 days after a bloody diarrhea illness. The causal organism produces a toxin that inhibits 60S ribosomal protein synthesis. The blood culture is negative; stool culture grows colonies on sorbitol-MacConkey agar that appear COLOURLESS (sorbitol-non-fermenting). The organism is:

• A Enteroinvasive E. coli (EIEC)
• B Enteropathogenic E. coli (EPEC)
• C Shiga toxin-producing E. coli O157:H7 (STEC) ✓
• D Enteroaggregative E. coli (EAEC)

Explanation

E. coli O157:H7 (STEC) does not ferment sorbitol, producing colourless colonies on sorbitol-MacConkey agar (most E. coli ferment sorbitol and appear pink). STEC produces Shiga toxins (Stx1 and Stx2) that cleave the N-glycosidic bond in 28S rRNA of the 60S ribosomal subunit (same mechanism as Shiga toxin from S. dysenteriae), leading to endothelial cell damage, microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury (HUS). EIEC, EPEC, and EAEC do not produce Shiga toxins and do not cause HUS.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.