(228au) S.Epidermidis Alters a Fibrin Clot – Insights into Septic Thromboembolism

Pathological blood clots, for example, venous thromboembolism (VTE), are a leading cause of death and disability worldwide. The 3-fold increased risk of VTE by the presence of bacterial infection motivates work to establish the basis for the high correlation between infection and thrombosis; the specific impacts of bacteria on clot formation, remodeling, and embolization are unclear. Here we demonstrate that the common pathogen and biofilm former Staphylococcus epidermidis RP62A has significant effects on the formation as well as the structural and mechanical properties of an in vitro model of a blood clot (i.e., fibrin clot). By mechanical rheometry, we find that the presence of S.epidermidis cells retards the formation of a fibrin clot. The resultant steady state infectious clot has a bulk elasticity that is about four times larger than a pure fibrin clot. From confocal microscopy images, we observe that the infectious clot has a heterogeneous structure with two characteristic mesh sizes rather than a single one as in a pure fibrin network. We correlate the higher bulk elasticity to this heterogeneous microstructure via fiber motility using multiple-particle tracking microrheology. Finally, we observe that the fibrin network continues to remodel in the presence of S. epidermidis and eventually ruptures. The higher elasticity of the infectious clot may be associated with embolic diseases that have been related to high fibrin rigidity. The rupture of the infectious clots provides insights into the correlation between bacterial infection and embolism.