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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Format: | Article |
Language: | English |
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MDPI AG
2022-01-01
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Series: | International Journal of Molecular Sciences |
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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. |
first_indexed | 2024-03-10T01:18:02Z |
format | Article |
id | doaj.art-60be2119cae24e2c9e24b8828e914528 |
institution | Directory Open Access Journal |
issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-10T01:18:02Z |
publishDate | 2022-01-01 |
publisher | MDPI AG |
record_format | Article |
series | International Journal of Molecular Sciences |
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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