In vitro selection of fluoroquinolone resistance in Brucella melitensis
Résumé
Moxifloxacin-resistant mutants of 16M [moxifloxacin minimum inhibitory concentration (MIC)=1mg/L] were selected in order to characterise fluoroquinolone resistance mechanisms in this species. Eight independent mutants were obtained, with moxifloxacin MICs of 16–32mg/L. The mutants displayed variable cross-resistance levels to other fluoroquinolone compounds, but no increased resistance to aminoglycosides, tetracycline, rifampicin, macrolides or co-trimoxazole. Sequencing of type II topoisomerase-encoding genes (, , and ), which are natural targets for fluoroquinolones, revealed a mutation leading to the amino acid substitution Ala83Val ( numbering system) in five mutants with a moxifloxacin MIC of 32mg/L, whereas no mutation was found in the remaining three mutants with an MIC of 16mg/L. Phenylalanine-arginine-β-naphthylamide dihydrochloride, an efflux pump inhibitor, reduced moxifloxacin MICs by a factor of two to eight in all resistant mutants. In , fluoroquinolone resistance may arise from mutation and efflux pump overexpression mechanisms.
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PEER_stage2_10.1016%2Fj.ijantimicag.2009.01.002.pdf (373.52 Ko)
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