A 58-year-old man on empirical ceftriaxone for biliary sepsis caused by Enterobacter cloacae improves initially, then fever recurs on day 7. Repeat culture grows the same organism now resistant to ceftriaxone and cefotaxime but still susceptible to cefoxitin and carbapenems. ESBL screening is negative. The most likely mechanism is:

• A Acquisition of a plasmid-borne CTX-M gene under selection
• B Stable derepression of chromosomal AmpC beta-lactamase following mutations in ampD ✓
• C Emergence of porin loss combined with SHV hyperproduction
• D Induction of Klebsiella pneumoniae carbapenemase by cephalosporin exposure

Explanation

Enterobacter cloacae carries a chromosomal inducible AmpC cephalosporinase normally repressed by AmpD. Mutations in ampD cause stable derepressed hyperproduction, producing resistance to third-generation cephalosporins during therapy, a well-known clinical pitfall. AmpC hydrolyses cephamycins poorly compared with true ESBL patterns, so cefoxitin susceptibility can be preserved early, and carbapenems remain active. Plasmid CTX-M would typically give a positive ESBL screen, and KPC is not induced by cephalosporins.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.