Molecular aspects on pathogenesis of wound and foreign body infections due to staphylococci.

Rapid progress has been made in our understanding how various mucosal bacteria and virus pathogens bind to specific epithelial cell receptors and cause infections in respiratory gastrointestinal and the urogenital tracts, during the last decade. In the present review, I summarize our understanding how pathogens can colonize subepithelial tissues in open wounds and burns by binding to specific subepithelial matrix components such as collagen, laminin, fibronectin and to fibrin in blood clots and cause pyogenic infections. Serum and tissue fibronectin show a high affinity for various surfaces compared to other body fluid proteins. Based on the recent discovery of specific fibronectin binding surface proteins (FNBP) of S. aureus recently cloned and expressed in E. coli a new concept is presented how S. aureus, coagulase-negative staphylococci (CNS) and other wound pathogens bind to wound sutures, intravascular catheters and various prosthesis materials and initiate foreign body infections. Finally, new principles for treating wound infections with hydrophobized and fibronectin substituted wound dressings to decrease the critical bacterial numbers (approx. 10(5) per mg tissue (7] to spead up healing of infected wounds is presented.