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Infection and Immunity, June 2001, p. 3791-3799, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3791-3799.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Variance in Fibronectin Binding and fnb Locus Polymorphisms in Staphylococcus aureus: Identification of Antigenic Variation in a Fibronectin Binding Protein Adhesin of the Epidemic CMRSA-1 Strain of Methicillin-Resistant S. aureus

Kelly Rice, Mario Huesca, Dareyl Vaz, and Martin J. McGavin*

University of Toronto, Department of Laboratory Medicine and Pathobiology, and Sunnybrook and Women's College Health Science Center, Department of Microbiology, Toronto, Ontario M4N 3M5, Canada

Received 6 October 2000/Returned for modification 2 January 2001/Accepted 14 March 2001

The fnbA and fnbB genes of Staphylococcus aureus 8325-4 encode fibronectin (Fn) binding proteins FnBPA and FnBPB, which promote adherence to host tissues. Each adhesin contains three copies of a repeated D motif that binds Fn and is a target for vaccine development. In this study, we assess variability within the Fn-binding domain of the FnBP adhesins and evaluate factors that promote variance in Fn binding among clinical isolates. Based on variation in the number of fnb genes or the number of D motifs, we identified five polymorphism groups. S. aureus 8325-4 and 91% of methicillin-resistant S. aureus (MRSA) isolates belong to polymorphism group I, with two fnb genes and three copies of the D motif. Polymorphism group II contained one fnb gene with only two D motifs and was associated with the epidemic CMRSA-4 strain, which exhibited high protease activity and low Fn binding. Polymorphism group III was unique to the epidemic CMRSA-1 strain, defined by the presence of a fourth D motif that exhibited antigenic variation within a conserved sequence that is essential for Fn binding. However, the sequence of the D motifs was otherwise highly conserved among the other polymorphism groups. Variation in Fn binding among MRSA isolates was inversely related to protease activity but not to the number of fnb genes or the number of D motifs. Therefore, the fnb locus is polymorphic in a small number of strains, but this does not contribute to variation in Fn binding. The antigenic variation that was observed only in the epidemic CMRSA-1 strain may have evolved in response to a host immune response encountered during successive cycles of colonization, transmission, and infection in the nosocomial environment.

* Corresponding author. Mailing address: S-112 Department of Microbiology, Sunnybrook and Women's College Health Science Center, 2075 Bayview Ave., Toronto, Ontario M4N 3M5, Canada. Phone: (416) 480-5831. Fax: (416) 480-5737. E-mail: martin.mcgavin{at}swchsc.on.ca.

Infection and Immunity, June 2001, p. 3791-3799, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3791-3799.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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Copyright © 2001 by the American Society for Microbiology. All rights reserved.