Abstract
Fluoroquinolone resistance in pneumococci is known to be associated with the efflux pump, PmrA. However, there may be other efflux systems that also cause drug resistance. Two types of mutants were studied. The efflux phenotype from mutants selected by sub-MIC levofloxacin or gemifloxacin was transformed into R6. These transformants did not show increased pmrA transcripts in Northern blots; insertional inactivation of pmrA in the transformants did not abolish the efflux phenotype. A second set of efflux phenotype mutants was selected in R6:cat by ethidium bromide but not by norfloxacin; accumulation of ethidium bromide in the one among these mutants studied was reduced in comparison to its parent. This evidence suggests that systems other than PmrA can contribute to efflux-mediated resistance in pneumococci.
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