A urine culture from a 28-year-old woman with recurrent UTI grows E. coli: >10⁵ CFU/mL. Disc diffusion shows resistance to ampicillin, co-trimoxazole, ciprofloxacin, and cefotaxime. Double disc synergy test (DDST) is positive. The carbapenem sensitivity disc shows full sensitivity. What is the most likely resistance mechanism and appropriate empirical treatment?
- A Carbapenem-producing Klebsiella (KPC); treat with ceftazidime-avibactam
- B AmpC beta-lactamase overproduction; no reliable phenotypic test; treat with cefepime
- C Metallo-beta-lactamase (MBL); treat with fosfomycin since MBLs also hydrolyse carbapenems
- D Extended-spectrum beta-lactamase (ESBL) producing E. coli; confirm phenotypically by combined disc method; treat with a carbapenem (ertapenem or meropenem) ✓
Explanation
A positive DDST (double disc synergy test) with clavulanate-containing discs (e.g., amoxicillin-clavulanate) placed near extended-spectrum cephalosporin discs showing enhanced zones ('keyhole' or enhanced inhibition) confirms ESBL production. ESBL-producing Enterobacteriaceae (commonly E. coli and K. pneumoniae) hydrolyse all penicillins, extended-spectrum cephalosporins, and aztreonam but are inhibited by beta-lactamase inhibitors (clavulanate) — hence the synergy. They remain carbapenem-sensitive. Current guidelines recommend carbapenems (ertapenem for uncomplicated UTI, meropenem for invasive infections) as the treatment of choice for ESBL-producing E. coli. AmpC beta-lactamases are not inhibited by clavulanate and do not produce synergy.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
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Written and medically reviewed by the StethoPrep medical team.