Platelet-mediated adhesion of Staphylococcus epidermidis to hydrophobic NHLBI reference polyethylene.

The effects of platelets and plasma proteins on the adhesion of Staphylococcus epidermidis strain RP62A to hydrophobic NHLBI reference polyethylene was quantitatively studied using a rotating disk system to generate well-defined shear conditions simulating the hemodynamics of human blood circulation. Bacterial adhesion was quantified by adhesive coefficient, the percentage of bacteria transported to the surface that becomes adherent. The results showed that surface modification by adsorption of plasma proteins reduced the adhesion of S epidermidis as compared to the bare polymer surface. This surface modification was not sufficient to eliminate completely bacterial adhesion, even at the highest physiologic shear stress level. S epidermidis did adhere strongly to polyethylene surface modified by platelets. This is readily evident as approximately 50% of the adherent S epidermidis were bound to contact-activated platelets which occupied only 4% of the surface area. Adhesive coefficients to platelets were significantly greater than to the protein-adsorbed polyethylene surface by at least one order of magnitude (P < or = .01) across the range of physiological shear conditions investigated. These studies show that it is biologic surface modification by contact-activated platelets, and not plasma proteins, which mediates S epidermidis adhesion to polyethylene.