REVIEW ARTICLE
Virulence Factors Associated with Enterococcus Faecalis Infective Endocarditis: A Mini Review
Kristian T. Madsen1, *, Marianne N. Skov1, Sabine Gill2, Michael Kemp1
Article Information
Identifiers and Pagination:
Year: 2017Volume: 11
First Page: 1
Last Page: 11
Publisher ID: TOMICROJ-11-1
DOI: 10.2174/1874285801711010001
Article History:
Received Date: 02/09/2016Revision Received Date: 16/01/2017
Acceptance Date: 28/01/2017
Electronic publication date: 31/03/2017
Collection year: 2017

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Introduction:
The enterococci are accountable for up to 20% of all cases of infective endocarditis, with Enterococcus faecalis being the primary causative isolate. Infective endocarditis is a life-threatening infection of the endocardium that results in the formation of vegetations. Based on a literature review, this paper provides an overview of the virulence factors associated with E. faecalis infective endocarditis. Furthermore, it reports the effects of active or passive immunization against some of these involved factors.
Individual virulence factors:
Nine virulence factors have in particular been associated with E. faecalis infective endocarditis. Absence of these factors entailed attenuation of strains in both mixed- and mono-bacterial infection endocarditis models as well as in in vitro and ex vivo assays when compared to their virulence factor expressing parental strains.
Pathogenesis:
The virulence factors promote a broad spectrum of events that together allow for disease development and progression. The infection is initiated through bacterial binding to ligands present at the site of infection after which the colonization can be accelerated through inter-bacterial attachment and modulation of the host immune response. The formation and growth of the vegetation provide protection and promote growth. Controlled degeneration of the vegetation appears to increase the likelihood of embolization and dissemination, without exposing protected bacteria.
Prophylactic immunization:
In most cases, active and passive immunization against associated virulence factors provided partial protection.
Future prospects:
There is a need for further evaluation of the known virulence factors. Immunization against two or more virulence factors might be an effective prophylactic tool.