Characterization of the molecular mechanisms of quinolone resistance in Yersinia enterocolitica O:3 clinical isolates

• Published in: Journal of antimicrobial chemotherapy Vol. 53; no. 6; pp. 1068 - 1071
• Main Authors: Capilla, S., Ruiz, J., Goñi, P., Castillo, J., Rubio, M. C., Jiménez de Anta, M. T., Gómez-Lus, R., Vila, J.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01-06-2004; Oxford Publishing Limited (England)
• Subjects: Anti-Infective Agents - pharmacology; Antibiotics. Antiinfectious agents. Antiparasitic agents; Biological and medical sciences; Ciprofloxacin - pharmacology; Dipeptides - pharmacology; DNA Gyrase - genetics; DNA Topoisomerase IV - genetics; Drug Resistance, Bacterial; Humans; Medical sciences; Microbial Sensitivity Tests; Mutation - genetics; Nalidixic Acid - pharmacology; Pharmacology. Drug treatments; Phe-Arg-β-naphthylamide; quinolones; Quinolones - pharmacology; Spain; Y. enterocolitica; Yersinia enterocolitica; Yersinia enterocolitica - drug effects; Yersinia enterocolitica - genetics; Yersinia Infections - microbiology; Spain; Characterization; Resistance; Yersinia enterocolitica; Bacteria; Antibacterial agent; Mechanism of action; Clinical isolate; Quinolone derivatives; Enterobacteriaceae
• DOI: 10.1093/jac/dkh225
• EISSN: 1460-2091
• ISSN: 0305-7453; 1460-2091

Objectives: The aim of this study was to determine the roles of mutations in the gyrA and parC genes and the overexpression of efflux pump(s) as mechanisms of resistance to quinolones. Forty-five Yersinia enterocolitica O:3 clinical isolates (41 nalidixic acid-resistant, three nalidixic acid-susceptible and one nalidixic acid-resistant strain obtained in vitro) were analysed. Results: All the nalidixic acid-resistant strains showed mutations in the gyrA gene and none in the parC gene. The presence of the inhibitor produced decreases in the MIC values of nalidixic acid by two to six serial dilution steps in 37 of the 41 nalidixic acid-resistant strains. Meanwhile, the MIC value of ciprofloxacin was affected in two strains whose values diminished three serial dilution steps. The nalidixic acid-resistant mutant obtained in vitro was also affected by the inhibitor decreasing the MIC value of nalidixic acid three serial dilutions steps whereas the MICs for the nalidixic acid-susceptible strains were not affected. Conclusions: Our results show that the high level of resistance to nalidixic acid is likely due to an overexpression of an efflux pump plus a mutation in the gyrA gene, whereas decreased susceptibility to ciprofloxacin is only associated with the presence of a mutation in the gyrA gene.