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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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