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Infection and Immunity, January 2003, p. 516-523, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.516-523.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Role of sarA in the Pathogenesis of Staphylococcus aureus Musculoskeletal Infection

Jon S. Blevins,1 Mohamed O. Elasri,1 Scott D. Allmendinger,1 Karen E. Beenken,1 Robert A. Skinner,2 J. Roby Thomas,3 and Mark S. Smeltzer1*

Departments of Microbiology and Immunology,1 Orthopaedic Surgery,2 Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 722053

Received 9 July 2002/ Returned for modification 29 August 2002/ Accepted 3 October 2002

We recently demonstrated that mutation of sarA in clinical isolates of Staphylococcus aureus results in a phenotype that is distinct by comparison to sarA mutants generated in the laboratory strain RN6390 (J. S. Blevins, K. E. Beenken, M. O. Elasri, B. K. Hurlburt, and M. S. Smeltzer, Infect. Immun. 70:470-480, 2002). This raises the possibility that studies demonstrating that RN6390 sarA mutants are attenuated do not accurately reflect the role of sarA in the pathogenesis of staphylococcal disease. To test this hypothesis, we used a murine model of musculoskeletal infection to assess the virulence of sarA and agr mutants generated in a clinical isolate of S. aureus (UAMS-1). By using this model, we confirmed that mutation of sarA and/or agr results in a reduced capacity to cause both septic arthritis and osteomyelitis.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Mail Slot 511, University of Arkansas for Medical Sciences, 4301 W. Markham, Little Rock, AR 72205. Phone: (501) 686-7958. Fax: (501) 686-5359. E-mail: smeltzermarks{at}uams.edu.

Editor: A. D. O'Brien

Infection and Immunity, January 2003, p. 516-523, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.516-523.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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