A rot mutation restores parental virulence to an agr-null Staphylococcus aureus strain in a rabbit model of endocarditis

Mutations in rot restore in vitro toxin production to agr-negative strains of Staphylococcus aureus. We show that a rot mutation returns wild-type virulence to an agr mutant, as measured in experimental endocarditis infections by target organ bacterial counts. Implications of our data are discussed in terms of agr antagonist strategies.