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.
McNamara
Peter J
PJ
Department of Medical Microbiology & Immunology, 1300 University Avenue, University of Wisconsin, Biochemistry Building, Room 250, Madison, WI 53706, USA. pjmcnamara@facstaff.wisc.edu
Bayer
Arnold S
AS
D000818:Animals; D001426:Bacterial Proteins / Q000502:physiology*; D004697:Endocarditis, Bacterial / Q000209:etiology*; D005260:Female; D009154:Mutation; D011817:Rabbits; D012097:Repressor Proteins / Q000502:physiology*; D013203:Staphylococcal Infections / Q000209:etiology*; D013211:Staphylococcus aureus / Q000472:pathogenicity*; D015534:Trans-Activators / Q000502:physiology*; D014774:Virulence
C095698:Agr protein, Staphylococcus aureus; D001426:Bacterial Proteins; D012097:Repressor Proteins; D015534:Trans-Activators; C408643:rot protein, Staphylococcus aureus