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Infection and Immunity, June 2005, p. 3806-3809, Vol. 73, No. 6
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.6.3806-3809.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

A rot Mutation Restores Parental Virulence to an agr-Null Staphylococcus aureus Strain in a Rabbit Model of Endocarditis

Peter J. McNamara1* and Arnold S. Bayer2,3

Department of Medical Microbiology & Immunology, University of Wisconsin Medical School, Madison, Wisconsin 53706,1 LA Biomedical Research Institute at Harbor-UCLA, Torrance, California 90502,2 Geffen School of Medicine at UCLA, Los Angeles, California 900243

Received 2 September 2004/ Returned for modification 29 November 2004/ Accepted 27 January 2005

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.

* Corresponding author. Mailing address: Department of Medical Microbiology & Immunology, 1300 University Avenue, University of Wisconsin, Biochemistry Building, Room 250, Madison, WI 53706. Phone: (608) 263-5591. Fax: (608) 262-8418. E-mail: pjmcnamara{at}facstaff.wisc.edu.

Editor: V. J. DiRita

Infection and Immunity, June 2005, p. 3806-3809, Vol. 73, No. 6
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.6.3806-3809.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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  • Oscarsson, J., Kanth, A., Tegmark-Wisell, K., Arvidson, S. (2006). SarA Is a Repressor of hla ({alpha}-Hemolysin) Transcription in Staphylococcus aureus: Its Apparent Role as an Activator of hla in the Prototype Strain NCTC 8325 Depends on Reduced Expression of sarS. J. Bacteriol. 188: 8526-8533 [Abstract] [Full Text]  


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