Look Who’s Talking: Host and Pathogen Drivers of <i>Staphylococcus epidermidis</i> Virulence in Neonatal Sepsis

Preterm infants are at increased risk for invasive neonatal bacterial infections. <i>S. epidermidis</i>, a ubiquitous skin commensal, is a major cause of late-onset neonatal sepsis, particularly in high-resource settings. The vulnerability of preterm infants to serious bacterial infectio...

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Main Authors: Isabella A. Joubert, Michael Otto, Tobias Strunk, Andrew J. Currie
Format: Article
Language:English
Published: MDPI AG 2022-01-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/2/860
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author Isabella A. Joubert
Michael Otto
Tobias Strunk
Andrew J. Currie
author_facet Isabella A. Joubert
Michael Otto
Tobias Strunk
Andrew J. Currie
author_sort Isabella A. Joubert
collection DOAJ
description Preterm infants are at increased risk for invasive neonatal bacterial infections. <i>S. epidermidis</i>, a ubiquitous skin commensal, is a major cause of late-onset neonatal sepsis, particularly in high-resource settings. The vulnerability of preterm infants to serious bacterial infections is commonly attributed to their distinct and developing immune system. While developmentally immature immune defences play a large role in facilitating bacterial invasion, this fails to explain why only a subset of infants develop infections with low-virulence organisms when exposed to similar risk factors in the neonatal ICU. Experimental research has explored potential virulence mechanisms contributing to the pathogenic shift of commensal <i>S. epidermidis</i> strains. Furthermore, comparative genomics studies have yielded insights into the emergence and spread of nosocomial <i>S. epidermidis</i> strains, and their genetic and functional characteristics implicated in invasive disease in neonates. These studies have highlighted the multifactorial nature of <i>S. epidermidis</i> traits relating to pathogenicity and commensalism. In this review, we discuss the known host and pathogen drivers of <i>S. epidermidis</i> virulence in neonatal sepsis and provide future perspectives to close the gap in our understanding of <i>S. epidermidis</i> as a cause of neonatal morbidity and mortality.
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spelling doaj.art-60be2119cae24e2c9e24b8828e9145282023-11-23T14:05:29ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-01-0123286010.3390/ijms23020860Look Who’s Talking: Host and Pathogen Drivers of <i>Staphylococcus epidermidis</i> Virulence in Neonatal SepsisIsabella A. Joubert0Michael Otto1Tobias Strunk2Andrew J. Currie3Centre for Molecular Medicine & Innovative Therapeutics, Murdoch University, Murdoch, WA 6150, AustraliaPathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health, Bethesda, MD 20892, USAWesfarmers Centre of Vaccines and Infectious Diseases, Telethon Kids Institute, Nedlands, WA 6009, AustraliaCentre for Molecular Medicine & Innovative Therapeutics, Murdoch University, Murdoch, WA 6150, AustraliaPreterm infants are at increased risk for invasive neonatal bacterial infections. <i>S. epidermidis</i>, a ubiquitous skin commensal, is a major cause of late-onset neonatal sepsis, particularly in high-resource settings. The vulnerability of preterm infants to serious bacterial infections is commonly attributed to their distinct and developing immune system. While developmentally immature immune defences play a large role in facilitating bacterial invasion, this fails to explain why only a subset of infants develop infections with low-virulence organisms when exposed to similar risk factors in the neonatal ICU. Experimental research has explored potential virulence mechanisms contributing to the pathogenic shift of commensal <i>S. epidermidis</i> strains. Furthermore, comparative genomics studies have yielded insights into the emergence and spread of nosocomial <i>S. epidermidis</i> strains, and their genetic and functional characteristics implicated in invasive disease in neonates. These studies have highlighted the multifactorial nature of <i>S. epidermidis</i> traits relating to pathogenicity and commensalism. In this review, we discuss the known host and pathogen drivers of <i>S. epidermidis</i> virulence in neonatal sepsis and provide future perspectives to close the gap in our understanding of <i>S. epidermidis</i> as a cause of neonatal morbidity and mortality.https://www.mdpi.com/1422-0067/23/2/860host–pathogen interactionsneonatal sepsis<i>S. epidermidis</i>commensalismpathogenesisvirulence
spellingShingle Isabella A. Joubert
Michael Otto
Tobias Strunk
Andrew J. Currie
Look Who’s Talking: Host and Pathogen Drivers of <i>Staphylococcus epidermidis</i> Virulence in Neonatal Sepsis
International Journal of Molecular Sciences
host–pathogen interactions
neonatal sepsis
<i>S. epidermidis</i>
commensalism
pathogenesis
virulence
title Look Who’s Talking: Host and Pathogen Drivers of <i>Staphylococcus epidermidis</i> Virulence in Neonatal Sepsis
title_full Look Who’s Talking: Host and Pathogen Drivers of <i>Staphylococcus epidermidis</i> Virulence in Neonatal Sepsis
title_fullStr Look Who’s Talking: Host and Pathogen Drivers of <i>Staphylococcus epidermidis</i> Virulence in Neonatal Sepsis
title_full_unstemmed Look Who’s Talking: Host and Pathogen Drivers of <i>Staphylococcus epidermidis</i> Virulence in Neonatal Sepsis
title_short Look Who’s Talking: Host and Pathogen Drivers of <i>Staphylococcus epidermidis</i> Virulence in Neonatal Sepsis
title_sort look who s talking host and pathogen drivers of i staphylococcus epidermidis i virulence in neonatal sepsis
topic host–pathogen interactions
neonatal sepsis
<i>S. epidermidis</i>
commensalism
pathogenesis
virulence
url https://www.mdpi.com/1422-0067/23/2/860
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AT tobiasstrunk lookwhostalkinghostandpathogendriversofistaphylococcusepidermidisivirulenceinneonatalsepsis
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