We examined the capacity of Staphylococcus aureus strains to release Panton-Valentine leukocidin (PVL) in the presence of antibiotics. No PVL was detected when S. aureus was incubated at inhibitory concentrations, while subinhibitory concentrations of oxacillin enhanced the PVL level; clindamycin, linezolid, and fusidic acid were inhibitory; and vancomycin had roughly no effect.Staphylococcus aureus is an important human pathogen. It expresses a variety of exoproteins, including Panton-Valentine leukocidin (PVL) (31). While Voyich et al. could not establish clear differences in virulence between isogenic pairs of PVLpositive/negative strains (29), Labandeira-Rey et al. clearly demonstrated the role of PVL as a major determinant of virulence in an acute pneumonia mouse model using other sets of isogenic strains for PVL (13) and thus confirmed the results of the princeps experiments showing that PVL is a virulence factor (15). The apparent discrepancy between these studies basically comes from the choice of the experimental models and the choice of the strains.

Methicillin-resistant Staphylococcus aureus is increasingly responsible for staphylococcal infections in the community. A large percentage of the community-acquired methicillin-resistant (CA-MRSA) strains in the USA produce Panton–Valentine leukocidin (PVL), which is associated with severe infections. The virulence of the clinical CA-MRSA strain USA300 was compared to that of its isogenic pvl-deleted mutant, and it was shown that PVL contributes to lung and muscle tissue destruction, respectively, in murine necrotizing pneumonia and skin infection models. Mice infected with the USA300 strain developed a dominant anti-PVL response. The PVL subunits were therefore tested as vaccinogens against this isolate, and their vaccine efficacy correlated with both the route of vaccination and infection. These data suggest that PVL is a virulence factor in murine CA-MRSA infections.