Mechanisms of quinolone resistance in Escherichia coli isolated from companion animals, pet-owners, and non-pet-owners.

The present study investigated the prevalence and mechanisms of fluoroquinolone (FQ)/quinolone (Q) resistance in Escherichia (E.) coli isolates from companion animals, pet-owners, and non-pet-owners. A total of 63 E. coli 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 E. coli. Point mutations in QRDRs were detected in all NA-resistant isolates, and the number of mutations was strongly correlated with increased MIC (R = 0.878 for NA and 0.954 for CIP). All CIP-resistant isolates (n = 10) had double mutations in the gyrA gene, with additional mutations in parC and parE. 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.