PB0791 - Bacterial biofilms produced by Staphylococcus sp. act as molecular scaffolds for the activation of blood coagulation

Background: Infective endocarditis (IE) is an infection of the cardiac endothelium. It has an annual incidence of 3–10/100,000 of the population with a mortality of up to 30%.(1) Staphylococcus aureus is the most prevalent cause of IE, accounting for approximately 27% of all cases.(2) After an endothelial injury, bacterial colonisation is facilitated, thus triggering additional endothelial injury and thrombus formation. Production of a biofilm, defined as a multicellular community of microorganisms, enclosed in a self-produced extracellular polysaccharide matrix) assists bacterial persistence and contributes to antibiotic tolerance.(3)

Aims: Considered that thrombotic complications are often associated with IE, here we explore the possibility that biofilms produced by Staphylococcus aureus (coagulase +) and Staphylococcus epidermidis (coagulase -), could induce fibrin generation in human plasma in vitro.

Methods: S. aureus and S. epidermidis were cultured each at 37°C in LB broth and after dilution, added to a 96-well microtiter plate and incubated at 37°C for 36h, leading to the formation of bacterial biofilms. Diluted (1:2) human plasma was added to biofilms of each bacterium, and to empty wells as a blank experiment. Fibrin generation was monitored by turbidimetry, along with SDS-PAGE analysis of the ensuing fibrin clot.

Results: The data shown in Figure 1 indicate that both biofilms of Staphylococcus aureus and Staphylococcus epidermidis efficiently and similarly induce fibrin clotting in human plasma.

Conclusion(s): The results of this study point out that bacterial biofilms can trigger blood coagulation, providing the molecular basis for explaining the positive relationship IE, biofilm formation and increased thrombotic risk. Further studies are needed to elucidate the biochemical mechanisms underlying biofilm-induced activation of blood coagulation.

References:
1. Fernández-Hidalgo et al. (2008) CLIN INFECT DIS. 47(10),1287-97. doi:10.1086/592576
2. Selton-Suty et al. (2012) CLIN INFECT DIS. 54(9):1230-9. doi: 10.1093/cid/cis199
3. Cahill et al. (2016) LANCET 387(10021):882-93. doi: 10.1016/S0140-6736(15)00067-7