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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Bacterial Proteins / physiology*
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Endocarditis, Bacterial / etiology*
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Female
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Mutation
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Rabbits
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Repressor Proteins / physiology*
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Staphylococcal Infections / etiology*
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Staphylococcus aureus / pathogenicity*
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Trans-Activators / physiology*
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Virulence
Substances
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Agr protein, Staphylococcus aureus
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Bacterial Proteins
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Repressor Proteins
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Trans-Activators
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rot protein, Staphylococcus aureus