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The emergence of multidrug-resistant  Pseudomonas aeruginosa  has become a serious problem in medical settings.  P. aeruginosa  clinical isolate PA7 is resistant to fluoroquinolones, aminoglycosides, and most β-lactams but not imipenem. In this study, enhanced efflux-mediated fluoroquinolone resistance of PA7 was shown to reflect increased expression of two resistance nodulation cell division (RND) -type multidrug efflux operons,  mexEF-oprN  and  mexXY-oprA . Such a clinical isolate has rarely been reported because MexEF-OprN-overproducing mutants often increase susceptibility to aminoglycosides apparently owing to impairment of the MexXY system. A mutant of PA7 lacking three RND-type multidrug efflux operons ( mexAB-oprM ,  mexEF-oprN , and  mexXY-oprA)  was susceptible to all anti-pseudomonas agents we tested, supporting an idea that these RND-type multidrug efflux transporters are molecular targets to overcome multidrug resistance in  P. aeruginosa .  mexEF-oprN -upregulation in  P. aeruginosa  PA7 was shown due to a MexS variant harboring the Valine-155 amino acid residue. This is the first genetic evidence shown that a MexS variant causes  mexEF-oprN -upregulation in  P. aeruginosa  clinical isolates.

frontiers in microbiology

Efflux-mediated fluoroquinolone resistance in the multidrug-resistant Pseudomonas aeruginosa clinical isolate PA7: identification of a novel MexS variant involved in upregulation of the mexEF-oprN multidrug efflux operon