Mechanisms of quinolone resistance in<i>Escherichia coli</i>isolated from companion animals, pet-owners, and non-pet-owners

Abstract

The present study investigated the prevalence and mechanisms of fluoroquinolone (FQ)/quinolone (Q) resistance in <i>Escherichia</i> (<i>E</i>.) <i>coli</i> isolates from companion animals, pet-owners, and non-pet-owners. A total of 63 <i>E. coli</i> isolates were collected from 104 anal swab samples, and 27 nalidixic acid (NA)-resistant isolates were identified. Of those, 10 showed ciprofloxacin (CIP) resistance. A plasmid-mediated Q resistance gene was detected in one isolate. Increased efflux pump activity, as measured by organic solvent tolerance assay, was detected in 18 NA-resistant isolates (66.7%), but was not correlated with an increase in minimum inhibitory concentration (MIC). Target gene mutations in Q resistance-determining regions (QRDRs) were the main cause of (FQ)Q resistance in <i>E. coli.</i> Point mutations in QRDRs were detected in all NA-resistant isolates, and the number of mutations was strongly correlated with increased MIC (<i>R</i> = 0.878 for NA and 0.954 for CIP). All CIP-resistant isolates (n = 10) had double mutations in the <i>gyrA</i> gene, with additional mutations in <i>parC</i> and <i>parE</i>. Interestingly, (FQ)Q resistance mechanisms in isolates from companion animals were the same as those in humans. Therefore, prudent use of (FQ)Q in veterinary medicine is warranted to prevent the dissemination of (FQ)Q-resistant bacteria from animals to humans.