The fibronectin-binding protein A gene (<i>fnbpA</i>) was sequenced.Of 2,365 cases of SAB, 92 had IE.After matching, 37 pairs of <i>S. aureus</i> isolates from the IE cases and non-IE controls were compared; <i>fnbpA</i> was detected in 91.9% of the IE isolates and 100% of the non-IE isolates (<i>p</i> = 0.24).
Streptococcus mutans autolysin AtlA is a fibronectin-binding protein and contributes to bacterial survival in the bloodstream and virulence for infective endocarditis.
We thus conclude that (sub)domains of the staphylococcal FnBPA molecule that express Fn-binding modules, alone or in combination, are sufficient to evoke an endothelial proinflammatory as well as a procoagulant response and thus account for IE severity.
The results are consistent with the conclusion that the 63-kDa SmFnB protein of S. mutans is a fibronectin-binding protein that may contribute to the interaction of S. mutans with damaged heart tissue during pathogenesis of infective endocarditis.
The adherence characteristics in vivo and virulence of two isogenic strains of Staphylococcus aureus differing in fibronectin binding were compared in a rat model of catheter-induced infective endocarditis.