1075. In vitro Activity of Gepotidacin against Escherichia coli Causing Urinary Tract Infections in the United States, Including Molecularly Characterized Fluoroquinolone Resistant Subsets
Abstract
Abstract Background Gepotidacin (GEP) is a novel bacterial type II topoisomerase inhibitor in Phase 3 clinical trials for the treatment of gonorrhea and uncomplicated urinary tract infections (UTI). This study characterized fluoroquinolone (FQ)-not susceptible (not S) E. coli causing UTI in U.S. patients and evaluated the in vitro activity of GEP and comparators against various drug resistance (R) subsets. Methods 1,035 E. coli collected from 38 U.S. sites were included as part of the GEP Global UTI Surveillance Program (2019). Isolates were tested for susceptibility by broth microdilution. E. coli with MICs ≥0.5 mg/L for ciprofloxacin (not S) and/or ≥1 mg/L for levofloxacin (not S) were selected for screening of FQ-R mechanisms, and subjected to genome sequencing, followed by screening of FQ-R genes and QRDR mutations in GyrA, GyrB, ParC and ParE. Results A total of 26.8% (277/1,035) E. coli met the screening criteria for FQ-not S (Table). Overall, GEP had MIC90 values of 2 mg/L and 4 mg/L against FQ-S and FQ-not S isolates, respectively. Nitrofurantoin had activity against the FQ-S and FQ-not S subsets (98.8% and 94.2%S, respectively), whereas amoxicillin-clavulanate (86.5% and 59.6%S) and trimethoprim-sulfamethoxazole (75.8% and 37.0%S) had limited activity. Most FQ-not S isolates (52.7%; 146/277) had double mutations in GyrA and ParC, followed by those isolates (20.6%; 57/277) with double mutations in GyrA and single mutations in ParC and ParE. The third most common…
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