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Enterococcal Endocarditis: Hiding in Plain Sight
Enterococcus faecalis is a major opportunistic bacterial pathogen of increasing clinical relevance. A substantial body of experimental evidence suggests that early biofilm formation plays a critical role in these infections, as well as in colonization and persistence in the GI tract as a commensal m...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8435889/ https://www.ncbi.nlm.nih.gov/pubmed/34527603 http://dx.doi.org/10.3389/fcimb.2021.722482 |
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author | Barnes, Aaron M. T. Frank, Kristi L. Dunny, Gary M. |
author_facet | Barnes, Aaron M. T. Frank, Kristi L. Dunny, Gary M. |
author_sort | Barnes, Aaron M. T. |
collection | PubMed |
description | Enterococcus faecalis is a major opportunistic bacterial pathogen of increasing clinical relevance. A substantial body of experimental evidence suggests that early biofilm formation plays a critical role in these infections, as well as in colonization and persistence in the GI tract as a commensal member of the microbiome in most terrestrial animals. Animal models of experimental endocarditis generally involve inducing mechanical valve damage by cardiac catheterization prior to infection, and it has long been presumed that endocarditis vegetation formation resulting from bacterial attachment to the endocardial endothelium requires some pre-existing tissue damage. Here we review both historical and contemporary animal model studies demonstrating the robust ability of E. faecalis to directly attach and form stable microcolony biofilms encased within a bacterially-derived extracellular matrix on the undamaged endovascular endothelial surface. We also discuss the morphological similarities when these biofilms form on other host tissues, including when E. faecalis colonizes the GI epithelium as a commensal member of the normal vertebrate microbiome - hiding in plain sight where it can serve as a source for systemic infection via translocation. We propose that these phenotypes may allow the organism to persist as an undetected infection in asymptomatic individuals and thus provide an infectious reservoir for later clinical endocarditis. |
format | Online Article Text |
id | pubmed-8435889 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-84358892021-09-14 Enterococcal Endocarditis: Hiding in Plain Sight Barnes, Aaron M. T. Frank, Kristi L. Dunny, Gary M. Front Cell Infect Microbiol Cellular and Infection Microbiology Enterococcus faecalis is a major opportunistic bacterial pathogen of increasing clinical relevance. A substantial body of experimental evidence suggests that early biofilm formation plays a critical role in these infections, as well as in colonization and persistence in the GI tract as a commensal member of the microbiome in most terrestrial animals. Animal models of experimental endocarditis generally involve inducing mechanical valve damage by cardiac catheterization prior to infection, and it has long been presumed that endocarditis vegetation formation resulting from bacterial attachment to the endocardial endothelium requires some pre-existing tissue damage. Here we review both historical and contemporary animal model studies demonstrating the robust ability of E. faecalis to directly attach and form stable microcolony biofilms encased within a bacterially-derived extracellular matrix on the undamaged endovascular endothelial surface. We also discuss the morphological similarities when these biofilms form on other host tissues, including when E. faecalis colonizes the GI epithelium as a commensal member of the normal vertebrate microbiome - hiding in plain sight where it can serve as a source for systemic infection via translocation. We propose that these phenotypes may allow the organism to persist as an undetected infection in asymptomatic individuals and thus provide an infectious reservoir for later clinical endocarditis. Frontiers Media S.A. 2021-08-30 /pmc/articles/PMC8435889/ /pubmed/34527603 http://dx.doi.org/10.3389/fcimb.2021.722482 Text en Copyright © 2021 Barnes, Frank and Dunny https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Cellular and Infection Microbiology Barnes, Aaron M. T. Frank, Kristi L. Dunny, Gary M. Enterococcal Endocarditis: Hiding in Plain Sight |
title | Enterococcal Endocarditis: Hiding in Plain Sight |
title_full | Enterococcal Endocarditis: Hiding in Plain Sight |
title_fullStr | Enterococcal Endocarditis: Hiding in Plain Sight |
title_full_unstemmed | Enterococcal Endocarditis: Hiding in Plain Sight |
title_short | Enterococcal Endocarditis: Hiding in Plain Sight |
title_sort | enterococcal endocarditis: hiding in plain sight |
topic | Cellular and Infection Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8435889/ https://www.ncbi.nlm.nih.gov/pubmed/34527603 http://dx.doi.org/10.3389/fcimb.2021.722482 |
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