Abstract
Infectious endocarditis involves formation of a microbial biofilm in vivo. Enterococcus faecalis Aggregation Substance (Asc10) protein enhances the severity of experimental endocarditis, where it has been implicated in formation of large vegetations and in microbial persistence during infection. In the current study, we developed an ex vivo porcine heart valve adherence model to study the initial interactions between Asc10+ and Asc10− E. faecalis and valve tissue, and to examine formation of E. faecalis biofilms on a relevant tissue surface. Scanning electron microscopy of the infected valve tissue provided evidence for biofilm formation, including growing masses of bacterial cells and the increasing presence of exopolymeric matrix over time; accumulation of adherent biofilm populations on the cardiac valve surfaces during the first 2–4 h of incubation was over 10-fold higher than was observed on abiotic membranes incubated in the same culture medium. Asc10 expression accelerated biofilm formation via aggregation between E. faecalis cells; the results also suggested that in vivo adherence to host tissue and biofilm development by E. faecalis can proceed by Asc10-dependent or Asc10-independent pathways. Mutations in either of two Asc10 subdomains previously implicated in endocarditis virulence reduced levels of adherent bacterial populations in the ex vivo system. Interference with the molecular interactions involved in adherence and initiation of biofilm development in vivo with specific inhibitory compounds could lead to more effective treatment of infectious endocarditis.
Highlights
Enterococcus faecalis is a gram-positive bacterium that normally resides in the gastrointestinal tract of humans
Adherence and biofilm formation on porcine heart valves Endocarditis likely initiates with adherence of bacteria from the bloodstream to the valve surface, followed by their growth as a biofilm
Having confirmed the robust ability of E. faecalis to colonize the heart valves as multicellular microcolonies detectable by fieldemission scanning electron microscopy (FESEM), we examined the specific contribution of Asc10 to this process by comparative examination of isogenic strains where the only genetic difference was whether the strain expressed an intact prgB gene or an in-frame deletion allele
Summary
Enterococcus faecalis is a gram-positive bacterium that normally resides in the gastrointestinal tract of humans This microbe is capable of causing disease, as it is responsible for infections such as infectious endocarditis, urinary tract and wound infections, and bacteremia [1,2]. Valvular damage is inflicted by events such as valvular regurgitation which results in irregularities in blood flow, or scarring on valve tissue due to prolonged intravenous drug use [4]. These lead to damage of the valve tissue, which in turn recruits platelets and fibrin to the damaged site. Once bacteria enter the bloodstream, whether through routes such as during surgical procedures or translocation through the intestinal tract, the sterile vegetation of platelets and fibrin is infected with these bacteria to become the septic vegetation [5]
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