(104c) Invited Speaker: Structure, Stability, and Mechanics of Bacterial Communities Colocalized with Fibrin Network

Bacterial communities – biofilms – are a determinant of bacterial virulence in human infection. For example, biofilms that form on implanted medical devices are recalcitrant to treatment, including antibiotic regimens. Most experimental models of medical device infection have focused on biofilms that are monoculture; however, any such infection would be expected to be colocalized with host clot. Here we study the common blood borne pathogen and biofilm former Staphylococcus epidermidis in the presence of a host protein network comprised of fibrin, which is the primary structural component of clot. We report structure and mechanics on both microscopic and macroscopic scales. Bacteria present during fibrin network formation produce a visibly disorganized microstructure differing from the structure of a pure fibrin network. These structural changes corelate with fibrin network stiffness; they furthermore trigger mechanical instability over time. We also discuss the role of the staphylococcal exopolysaccharide, polysaccharide intercellular adhesin (PIA), on the stability of fibrin networks. Specifically, we use an icaB deletion mutant, which changes the charge state of PIA, to manipulate the degree of colocalization of fibrin and bacteria. These changes in colocalization affect mechanics and network structure. The results have potential implications for the persistence of surface adherent bacterial communities in the human circulatory system.