Abstract
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.
Full Text 
Sign-in/Register to access full text options
Sign-in/Register to access full text options 
Published version (
Free)
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
