Clinical isolates of Enterococcus faecalis aggregate human platelets

Abstract

Many endocarditis pathogens activate human platelets and this has been proposed to contribute to virulence. Here we report for the first time that many clinical isolates of Enterococcus faecalis, a common pathogen in infective endocarditis, aggregate human platelets. 84 isolates from human blood and urine were screened for their ability to aggregate platelets from four different donors. Platelet aggregation occurred for between 11 and 65 % of isolates depending on the donor. In one donor, a significantly larger proportion of isolates from blood than from urine caused platelet aggregation. Median time to aggregation was 11 minutes and had a tendency to be shorter for blood isolates as compared to urine isolates.Immunoglobulin G (IgG) was shown to be essential in mediating activation and aggregation. Platelet aggregation could be abolished by an IgG-specific proteinase (IdeS), by an antibody blocking FcRIIa on platelets, or by preabsorption of plasma with an E. faecalis isolate. Fibrinogen binding to bacteria or platelets does not contribute to platelet activation or aggregation under our experimental conditions. These results indicate that platelet activation and aggregation by E. faecalis is dependent on both host and bacterial factors and that it may be involved in the pathogenesis of invasive disease with this organism.

Transcriptional Regulator PerA Influences Biofilm-Associated, Platelet Binding, and Metabolic Gene Expression in Enterococcus faecalis

“…E. faecalis is known to aggregate platelets [57] a phenotype mediated, at least in part, by the Ebp pilus [58]. When comparing the ability of DBS01 and E99 to bind human platelets, DBS01 was found to adhere to platelets significantly (∼5 fold) better than E99 (Fig.…”

“…The lysin protein serves a dual purpose: permeablizing the bacterial cell wall, thus permitting release of PblA and PblB, and binding to platelets through interaction with fibrinogen and fibrinogen receptors [55], [56]. E. faecalis is known to aggregate human platelets, yet the molecular mechanisms coordinating this process have not been discovered [57]. The repression of pblA , pblB and lysin in DBS01 suggests that PerA influences the expression of genes putatively involved in platelet binding and cell wall permeability residing on a temperature bacteriophage in E99.…”

The genus Enterococcus as probiotic: safety concerns

“…Enterococci have long been presented in numerous fermented products, but their applications as probiotic are still debated due to the genus containing species and strains etiologically involved in diseases (Shankar et al 1999(Shankar et al , 2002Conde-Esteves et al 2010;Rasmussen et al 2010, Tan et al 2010Heikens et al 2011) and in the risks of transfer of antimicrobial resistance and virulence genes to human strains. The rapid acquisition of antimicrobial among enterococci and other species probably contributes to their emergence as prominent nosocomial pathogens.…”

Platelet Activation and Biofilm Formation by Aerococcus urinae , an Endocarditis-Causing Pathogen

“…Direct interactions between bacteria and platelets can also lead to platelet activation (5,17,21). In addition, Streptococcus sanguis, S. aureus, and Enterococcus faecalis can activate platelets in the absence of bacterial bound fibrinogen through an IgG-and sometimes complement-dependent mechanism with a longer lag time (13,19,20,24). Upon activation, platelets release antibacterial peptides, and resistance to such substances has been linked to the capacity of S. aureus to cause IE (4,32).…”