The interactions are from bacterial adhesins, FnBPA and FnBPB, and host ligands explain the pathogenesis of clumping and adhesion during device infection sustained by the CoNS strain of S. aureus. Studies using the combination of seven different strains of S. aureus and Lactococcus lactis, a Gram-positive surrogate that naturally lacks adhesins to mammalian ligands, suggest that, in the absence of soluble ligands (i.e., fn or fg), both FnBPA and FnBPB are able to interact with adjacent FnBPs of neighboring bacteria to mediate aggregation. Here, FN1 is linked to infection.