Introduction: Since the nalidixic acid, the first quinolone, was introduced in 1962 it has been using widely. Quinolone is a synthetic antimicrobial effecting on most Enterobacteriaceae at clinical use. (Fluoro) Quinolone have been extensively used in animal industry, as feed additives, as well as in veterinary and human medicine. Recently, it has been increasing the resistance against quinolone in bacteria isolated from animals. Bacteria acquire the resistance against (fluoro) quinolone by chromosomal mutations in quinolone resistance determining regions (QRDR) oracquisition of plasmidshaving quinolone resistance (PMQR) genes. In Korea, there were few papers that reported prevalence of PMQR genes but lack of study investigating the mechanisms of quinolone resistance. The aim of this study is to investigate the mechanism of fluoroquinolone resistance in E. coli isolates from swine feces. Methods: Total 237 swine fecal samples were collected. E. coli isolation and confirmation were conducted following our lab protocol. Ciprofloxacin (CIP) resistant E. coliisolates were selected by antimicrobial susceptibility test as recommended by Clinical and Laboratory Standards Institute (CLSI). Among CIP resistant isolates, extended-spectrum beta-lactamases (ESBLs)-producing isolates were confirmed by the double disk diffusion method which compares the diameters of inhibition zone of CTX, CTX/CL and CAZ, CAZ/CL. Minimum inhibitory concentrations (MICs) against nalidixic acid (NA), CIP and ofloxacin (OFL) were determined by the broth microdilution method according to CLSI recommendation. PCR and sequence analysis were performed to confirm chromosomal mutations in QRDRs including gyrA, gyrB, parC and parE genes and to detect PMQR genes including qnrA, qnrB, qnrS, and qepA genes. Results: Among 171 E. coli isolates, 59 isolates (34.5%)were resistant to CIP. These CIP resistant isolates showed a wide range of MICs against CIP from 4 μg/ml to 256 μg/ml and OFL from 8 μg/ml to 64 μg/ml. All of these CIP resistant isolates were phenotypically resistant to NA.The MICs of those resistant isolates against NA were above 1024μg/ml except for one isolate (256 μg/ml). Most isolates (57/59; 96.6%) had mutations at both codons 83 and 87 of gyrA gene. However, two isolates only had a single codon mutation at codon 83 and the other one isolate had no mutations. None of isolates harbored qnrA or qnrB gene. However, qepA andqnr Sgenes were found in 1(1/59; 1.6%) and 7 isolates(7/59; 11.9%), respectively. In addition, 11of CIP resistant isolates (18.6%) were confirmed as ESBLs-producing isolates. Conclusion: Among the 171 isolates from swine fecal samples, 59 isolates (59/171; 34.5%) had ciprofloxacin resistance which indicates a high prevalence of (fluoro) quinolone resistance in animal industry in Korea. According to previous studies, it was well known that specific amino acid substitutions in gyrA gene boost the high resistance to (fluoro) quinolone. Likewise, most of CIP resistant isolates in this study had mutants in gyrA gene. In addition 11 of those CIP resistant isolates were ESBLs-producing E.coli . ESBLs producing Enterobacteriaceaeis an increasing problem in veterinary and human medicine. Therefore, further characterization of these CIP resistant E.coli on additional (fluoro) quinolone resistant mechanisms, such as efflux pump, and the ability of ESBLs production should be informative.