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Abstract
Resistance to fluoroquinolones has increased for bacteriasuchasPseudomonasaeruginosaandEnterococcus spp. In the Stockholm area, 15 to 25% of P. aeruginosa strains in clinical samples are now resistant to quinolones, and the corresponding figure for Enterococcus spp. is 25% (B. Wretlind, unpublished data). Principal mechanisms of bacterial resistance to fluoroquinolones are modifications of the target enzymes topoisomerase II or DNA gyrase (gyrA )a nd topoisomerase IV (parC), or reduction of intracellular drug concentration due to mutations in the regulatory genes for efflux systems. In P. aeruginosa, 3 different efflux systems for quinolones have been identified, MexCD-OprJ, MexAB-OprM, and MexEF-OprN, regulated by NfxB, MexR (NalB), and MexT (NfxC), respectively. [1] For Enterococcus faecium, little is known about resistance mechanisms. The aim of this study was to investigate sites of mutations in clinical strains of these bacteria.
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