Urinary tract infections (UTIs) caused by Escherichia coli remain a major global health burden, particularly among diabetic patients who are prone to recurrent and complicated infections. This article determines the prevalence, antimicrobial resistance patterns, and clinical predictors of extended-spectrum β-lactamase (ESBL) and AmpC β-lactamase coproduction among uropathogenic E. coli isolates. Cross-sectional study was conducted on 300 adult patients with culture-confirmed E. coli UTIs at Misurata Medical Center, including 150 people living with diabetes (PLWD) and 150 nondiabetic participants. Midstream urine specimens were collected and cultured on standard media. Antimicrobial susceptibility testing followed the Clinical and Laboratory Standards Institute 2024 guidelines, while ESBL and AmpC β-lactamases were phenotypically detected using the double-disk synergy and inhibitor-based disk tests. Data were analyzed using SPSS v27 and R v4.3.2. Categorical and continuous variables were compared using chi-square/Fisher's exact and Mann–Whitney U tests, respectively. Predictors of coproduction and its impact on treatment failure were identified via multivariate logistic regression; a p-value of < 0.05 was considered statistically significant. The total prevalence of ESBL, AmpC, and ESBL + AmpC coproduction was 58.3, 14.3, and 14.0%, respectively. While the prevalence of ESBL-only and AmpC-only phenotypes did not differ significantly between PLWD and nondiabetic patients, coproduction was significantly higher in PLWD (22%) compared with nondiabetic patients (6%; p < 0.001) and was associated with extensive multidrug resistance (93%). Diabetes mellitus (adjusted odds ratio OR = 3.64; p = 0.001) and prior antibiotic exposure (adjusted OR = 2.18; p = 0.041) were independent predictors of coproduction. ESBL + AmpC coproduction in uropathogenic E. coli represents an emerging therapeutic and epidemiological concern, particularly among PLWD. Routine AmpC screening and rational antibiotic policies are urgently required to mitigate treatment failure and limit resistance.
Alwashaish et al. (Wed,) studied this question.