Affiliation:
1. Departments of Microbiology and Immunology
2. Orthopaedic Surgery
3. Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205
Abstract
ABSTRACT
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.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Reference32 articles.
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4. Blevins, J. S., A. F. Gillaspy, T. M. Rechtin, B. K. Hurlburt, and M. S. Smeltzer. 1999. The staphylococcal accessory regulator (sar) represses transcription of the Staphylococcus aureus collagen adhesin gene (cna) in an agr-independent manner. Mol. Microbiol.33:317-326.
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