Multidrug-resistant Pseudomonas aeruginosa poses a serious problem due to hospital- and
healthcare-associated infections. A major drug resistance mechanism of P. aeruginosa involves active efflux via resistance nodulation cell division (RND)-type multidrug efflux pumps of which MexXY is increasingly recognized as a primary determinant of
aminoglycoside resistance in P. aeruginosa. MexXY overexpression is often observed in
drug-resistant P. aeruginosa clinical isolates. MexXY deficiency increased
pyoverdine production in all four P. aeruginosa strains we tested. MexXY-overproducing multidrug-resistant P. aeruginosa PA7 exhibited the greatest effect among the strains. Complementation with a MexXY-expressing plasmid restored low-level
pyoverdine production in a MexXY-deficient P. aeruginosa mutant from PA7, indicating that MexXY expression decreases
pyoverdine production. Because P. aeruginosa produces
pyoverdine to acquire
iron, MexXY-deficient mutants might be more susceptible to
iron deficiency than MexXY-producing strains or might require extra
iron. High-risk clones of multidrug-resistant P. aeruginosa reportedly tend to be MexXY overproducers but defective
pyoverdine producers. This study suggests that P. aeruginosa reduces production of a
virulence factor after acquiring a drug resistance factor.