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Review
. 2022 Jan 13;23(2):860.
doi: 10.3390/ijms23020860.

Look Who's Talking: Host and Pathogen Drivers of Staphylococcus epidermidis Virulence in Neonatal Sepsis

Isabella A Joubert  1   2   3 , Michael Otto  4 , Tobias Strunk  3   5 , Andrew J Currie  1   2   3
Affiliations
Review

Look Who's Talking: Host and Pathogen Drivers of Staphylococcus epidermidis Virulence in Neonatal Sepsis

Isabella A Joubert et al. Int J Mol Sci. .

Abstract

Preterm infants are at increased risk for invasive neonatal bacterial infections. S. epidermidis, 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 S. epidermidis strains. Furthermore, comparative genomics studies have yielded insights into the emergence and spread of nosocomial S. epidermidis strains, and their genetic and functional characteristics implicated in invasive disease in neonates. These studies have highlighted the multifactorial nature of S. epidermidis traits relating to pathogenicity and commensalism. In this review, we discuss the known host and pathogen drivers of S. epidermidis virulence in neonatal sepsis and provide future perspectives to close the gap in our understanding of S. epidermidis as a cause of neonatal morbidity and mortality.

Keywords: S. epidermidis; commensalism; host–pathogen interactions; neonatal sepsis; pathogenesis; virulence.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Summary of potential mechanisms underlying the establishment of neonatal tolerance to commensal S. epidermidis and its contribution to neonatal host defense. Antimicrobial peptides (AMPs), Phenol-soluble modulins (PSMs), Peforin-2 (P2), Toll-like receptor (TLR), Regulatory T cells (Tregs). Created with BioRender.com.
Figure 2
Figure 2
Risk factors associated with skin-derived and gut-derived S. epidermidis late-onset sepsis (LOS) in the preterm neonate. Created with BioRender.com.
Figure 3
Figure 3
S. epidermidis functional and genetic determinants with potential role in late-onset sepsis (LOS pathogenicity). Created with BioRender.com.
See this image and copyright information in PMC

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