Objectives Klebsiella pneumoniae is a leading cause of hospital-acquired infections. Its increasing prevalence poses substantial challenges to both hospital and public health systems due to the emergence of multidrug-resistant strains. Understanding the epidemiology of K. pneumoniae and its antimicrobial resistance characteristics may support antimicrobial stewardship and infection control programs. A cross-sectional study was conducted from June to November 2025. Methods: A total of 62 isolates underwent phenotypic identification and antimicrobial susceptibility testing using the BD Phoenix system (Becton Dickinson), followed by molecular detection of K. pneumoniae and efflux pump genes. Sanger sequencing was performed on isolates positive for the tolC gene. Results: Among the isolates, 66.1% were classified as extended-spectrum β-lactamase (ESBL) producers, 6.5% as carbapenem-resistant Enterobacterales (CRE), and 6.5% as both ESBL and CRE producers. Most clinical isolates were resistant to ampicillin, cefazolin, ceftazidime, ceftriaxone, ciprofloxacin, and cefepime. The acrAB and tolC genes were detected in all 62 isolates. One isolate showed a genetic profile similar to that of the K. pneumoniae KP 52.145 strain. Conclusion: This study demonstrated a high prevalence of antibiotic resistance among K. pneumoniae isolates and confirmed the presence of efflux pump genes, including tolC, with observable genetic variability. Further investigation of tolC gene evolution is essential, as these genes play critical roles in antibiotic resistance mechanisms.
Objectives
Enteroaggregative <i>Escherichia coli</i> (EAEC) was recently reported as a major diarrheagenic pathogen in infant and adult travelers, both in developing and developed countries. EAEC strains are known to be highly resistant to antibiotics including quinolones. Therefore in this study we have determined the various mechanisms of quinolone resistance in EAEC strains isolated in Korea. Methods
For 26 EAEC strains highly resistant to fluoroquinolone, minimal inhibitory concentrations for fluoroquinolones were determined, mutations in the quinolone target genes were identified by PCR and sequencing, the presence of transferable quinolone resistance mechanism were identified by PCR, and the contribution of the efflux pump was determined by synergy tests using a proton pump inhibitor. The expression levels of efflux pump-related genes were identified by relative quantification using real-time PCR. Results
Apart from two, all tested isolates had common mutations on GyrA (Ser83Leu and Ser87Gly) and ParC (Ser80Gln). Isolates EACR24 and EACR39 had mutations that have not been reported previously: Ala81Pro in ParC and Arg157Gly in GyrA, respectively. Increased susceptibility of all the tested isolates to ciprofloxacin and norfloxacin in the presence of the pump inhibitor implies that efflux pumps contributed to the resistance against fluoroquinolones. Expression of the efflux pump-related genes, <i>tolC</i>, <i>mdfA</i>, and <i>ydhE</i>, were induced in isolates EACR 07, EACR 29, and EACR 33 in the presence of ciprofloxacin. Conclusion
These results indicate that quinolone resistance of EAEC strains mainly results from the combination of mutations in the target enzyme and an increased expression of efflux pump-related genes. The mutations Ala81Pro in ParC and Arg157Gly in GyrA have not been reported previously the exact influence of these mutations should be investigated further.
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In this study, we measured the drug resistance conferred by <i>mdfA</i> mutations in two <i>Shigella flexneri</i> strains. A mutant in <i>mdfA</i> genes was constructed by polymerase chain reaction–based, one-step inactivation of chromosomal genes. The antimicrobial susceptibility of parent and mutant strains to fluoroquinolones was determined by minimal inhibitory concentration (MICs). The <i>△mdfA</i> mutants were somewhat more susceptible to fluoroquinolones than the parent strains. The low level changes in MICs of the <i>△mdfA</i> mutants suggest that <i>mdfA</i> contributed the fluoroquinolone resistance in <i>S flexneri</i>. This finding found that the increased expression level of an MdfA efflux pump mediated fluoroquinolone resistance, but it is not likely a major effecter of higher resistance levels.
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Objectives
This study investigated the fluoroquinolone-resistant mechanism of 56 clinical cases of <i>A baumannii</i> infection from 23 non-tertiary hospitals, collected between 2004 and 2006. Methods
Susceptibility testing was performed by broth microdilution and Epsilometer test. Analyses of quinolone resistance-determining region (QRDR) were done by sequencing. The activity of the efflux pump was measured using inhibitors. Results
The sequences from selected 56 isolates were divided into seven groups (I-VII) on the basis of mutations in <i>gyrA</i> (S83L), <i>parC</i> (S80L, S80W and S84K) and <i>gyrB</i> (containing the novel mutations E679D, D644Y and A677V). The 27 isolates with triple mutations in <i>gyrA, gyrB</i> and <i>parC</i> (groups IV-VII) showed higher levels of resistance to ciprofloxacin (minimal inhibitory concentration [MIC] of 16-256 μg/mL) than the 26 isolates with double mutations in <i>gyrA</i> and <i>parC</i> (groups II and III, MIC of 8-64 μ g/mL; <i>p</i> < 0.05). Alterations in the efflux pump were observed in four isolates with the <i>parC</i> S80L mutation (group II) or E84K mutation (group VII), but no effect was observed in an isolate with the <i>parC</i> S80 W mutation (group III). Conclusion
These results suggest that triple mutations in clinical isolates of <i>A baumannii</i> contribute to the development of high levels of resistance to fluoroquinolones and that mutations in <i>parC</i> S80L or E84K (groups II and VII) may contribute to alterations in efflux pump activity in <i>A baumannii</i>.
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