Phenotypic Patterns of Antimicrobial Resistance in Community-Acquired Escherichia Coli Infections
Keywords:
Escherichia Coli, Antimicrobial Resistance, Phenotypic Characteristics, ESBL, Community-Acquired Infection, Surveillance.Abstract
Background: Community-acquired Escherichia coli infections increasingly demonstrate multidrug resistance (MDR), complicating empirical therapeutic strategies. Phenotypic resistance patterns remain poorly characterized in outpatient populations, particularly regarding extended-spectrum β-lactamase (ESBL) production and fluoroquinolone resistance.
Methods: A 24-month cross-sectional study enrolled patients with community-acquired E. coli infections presenting to primary healthcare centers and emergency departments (January 2023 to December 2024). Consecutive urine isolates underwent antimicrobial susceptibility testing using CLSI and EUCAST breakpoints. Phenotypic characteristics including ESBL production, biofilm formation, and virulence factor expression were determined. Statistical associations were evaluated using logistic regression modeling; P < 0.05 denoted significance.
Results: Of 487 community-acquired E. coli isolates, 38.6% exhibited resistance to ≥1 antimicrobial class. ESBL production was documented in 46.2% of isolates; 27.8% demonstrated multidrug resistance. Moderate-to-strong biofilm formation occurred in 69.8% of isolates, with significant correlation to MDR status (P = 0.018). Fluoroquinolone resistance ranged from 12.1% (levofloxacin) to 19.7% (ciprofloxacin), predominantly attributable to gyrA S83L and D87G mutations. Prior fluoroquinolone exposure (OR 3.16, 95% CI 1.11–8.98) and immunosuppressive therapy (OR 10.47, 95% CI 1.07–102.57) were independent risk factors for MDR-ESBL phenotypes. Resistance to trimethoprim-sulfamethoxazole (68.3%), penicillins (71.5%), and nitrofurantoin susceptibility (>98%) were also documented.
Conclusions: Phenotypic resistance in community-acquired E. coli involves multifactorial mechanisms integrating ESBL production, topoisomerase mutations, and virulence factor expression. Prior antimicrobial exposure and immunosuppression are modifiable risk factors. These findings support risk-stratified empirical therapy and antimicrobial stewardship interventions in community populations.
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