Abstract

The changing prevalence of drug-resistant community-acquired urinary tract infection (UTI) is often attributed to local antimicrobial drug use or prescribing practices. However, recent molecular epidemiologic studies of community-acquired UTI suggest that other factors may play a greater role. We conducted a multiyear, cross-sectional study to characterize temporal changes in the prevalence of drug-resistant community-acquired UTI at a university community in California. During four 3.5-month sampling periods, urine samples from patients consecutively presenting to the university health service with symptoms of UTI were cultured for Escherichia coli. Antimicrobial susceptibility and genotyping tests of the E. coli isolates were performed. We recovered 780 E. coli isolates from 1667 patients with UTI. The prevalence of trimethoprim-sulfamethoxazole, ciprofloxacin, and nitrofurantoin resistance showed no trend over the 4 periods. The prevalence of ampicillin resistance decreased significantly over the last 2 study periods. A single clonal group accounted for 75% of this decrease. Enterobacterial repetitive intergenic consensus 2 PCR-based genotyping revealed that only 4 large clonal groups accounted for 52% of the UTIs resistant to trimethoprim-sulfamethoxazole, ciprofloxacin, or nitrofurantoin. No initially pansusceptible clonal groups gained resistance over time. This study revealed no obvious trend in the prevalence of drug-resistant community-acquired UTI in a single community. Prevalence at any time was influenced by a small number of E. coli clonal groups. This observation suggests that the introduction of strains that are drug resistant into a community plays a greater role in changing the prevalence of drug-resistant UTI than does the drug use or prescribing habits in that community.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call