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Role of ^B in the Expression of Staphylococcus aureus Cell Wall Adhesins ClfA and FnbA and Contribution to Infectivity in a Rat Model of Experimental Endocarditis

Division of Infection Diseases, Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois,¹ Institute of Fundamental Microbiology, University of Lausanne Lausanne,² Department of Medical Microbiology, University of Zürich, Zürich Switzerland,³ Institute of Molecular Biology, Slovak Academy of Sciences, 84251 Bratislava, Slovak Republic,⁴ Department of Microbiology and Pathology, University of Nebraska Medical Center, Omaha, Nebraska,⁵ Infectious Diseases, Wyeth Research, Pearl River, New York⁶

Received 4 August 2004/ Accepted 18 October 2004

Isogenic Staphylococcus aureus strains with different capacities to produce ^B activity were analyzed for their ability to attach to fibrinogen- or fibronectin-coated surfaces or platelet-fibrin clots and to cause endocarditis in rats. In comparison to the ^B-deficient strain, BB255, which harbors an rsbU mutation, both rsbU-complemented and ^B-overproducing derivatives exhibited at least five times greater attachment to fibrinogen- and fibronectin-coated surfaces and showed increased adherence to platelet-fibrin clots. No differences in adherence were seen between BB255 and a rsbUVWsigB isogen. Northern blotting analyses revealed that transcription of clfA, encoding fibrinogen-binding protein clumping factor A, and fnbA, encoding fibronectin-binding protein A, were positively influenced by ^B. ^B overproduction resulted in a statistically significant increase in positive spleen cultures and enhanced bacterial densities in both the aortic vegetations and spleens at 16 h postinoculation. In contrast, at 72 h postinoculation, tissues infected with the ^B overproducer had lower bacterial densities than did those infected with BB255. These results suggest that although ^B appears to increase the adhesion of S. aureus to various host cell-matrix proteins in vitro, it has limited effect on pathogenesis in the rat endocarditis model. ^B appears to have a transient enhancing effect on bacterial density in the early stages of infection that is lost during progression.

Editor: V. J. DiRita

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