Background: Stenotrophomonas maltophilia is an opportunistic human pathogen causing nosocomial infections worldwide. S. maltophilia infection is of particular concern due to its inherent resistance to currently used antibiotics. Proton motive force-driven transporters of the major facilitator superfamily frequently contribute to the efflux of substances, including antibiotics, across cell membranes.
Methods: An mfsA expression plasmid (pMfsA) was constructed and transferred into bacterial strains by electroporation. The antibiotic susceptibility levels of S. maltophilia strains were determined using standard methods.
Results and conclusions: S. maltophilia MfsA is an efflux pump associated with paraquat resistance. We show here that plasmid-mediated overexpression of mfsA in WT S. maltophilia K279a increased resistance not only to paraquat but also to second-generation fluoroquinolone antibiotics, i.e. ciprofloxacin, norfloxacin, levofloxacin and ofloxacin. Ciprofloxacin was used as a representative drug. Addition of the proton motive force inhibitor carbonyl cyanide-m-chlorophenylhydrazone increases susceptibility to ciprofloxacin. Taken together these results suggest that MsfA is a novel fluoroquinolone efflux pump of S. maltophilia. Moreover, heterologous expression of mfsA in other Gram-negative pathogenic bacteria conferred resistance to paraquat as well as to fluoroquinolones. Thus, if this determinant was horizontally transferred, it could cause the spread of fluoroquinolone resistance among bacterial species.