P47 From commensal to culprit: the genetic diversity driving Staphylococcus epidermidis infections

TL;DR

This study explores how genetic diversity in Staphylococcus epidermidis influences its ability to cause infections, especially in relation to antimicrobial resistance and biofilm formation.

Contribution

The study reveals the complex genotype-phenotype associations in S. epidermidis, highlighting dispersed metal tolerance genes and inconsistent infection-related traits.

Findings

S. epidermidis isolates show significant genetic diversity and distinct phylogenetic groups associated with specific infections like PJI.

Metal tolerance genes are dispersed across all S. epidermidis groups, with some genes like copB, copC, cadA, and ars highly associated with specific groups.

Metal tolerance did not confer cross-tolerance to antimicrobials or influence biofilm formation in tested isolates.

Abstract

Staphylococcus epidermidis is one of the most isolated micro-organisms from clinical samples. Often considered a skin commensal, S. epidermidis infection can be a significant cause of morbidity and mortality, primarily associated with medical device-related infections such as Periprosthetic Joint Infections (PJI), Late Onset Neonatal Sepsis (LOS), both of which are becoming increasingly prevalent. Rising use of prosthetic medical devices and increasing antimicrobial resistance (AMR) complicate treatment. Increased usage of prosthetic medical devices and increased antimicrobial resistance presents significant challenge to treating S. epidermidis infection. There is limited understanding of how a commensal S. epidermidis goes on to cause infection, although we know that the genome of S. epidermidis contains a wide diversity of genes associated with AMR, biofilms and metal tolerance, which are thought to contribute to S. epidermidis ability to persist on medical devices and host evade immune responses.

This research aims to uncover the population structure of S. epidermidis and elucidate its genotype-phenotype associations with regards to AMR, biofilm formation and metal tolerance.

A collection of clinical and non-clinical S. epidermidis isolates (n=378) from UK and Germany were subjected to WGS (Illumina and MinION). A phylogenetic tree of core and pan-genomes constructed using ROARY, distinguished phylogenetic groups with various AMR and Biofilm-associated genes mapped to the tree. The isolates MIC against 5 common antimicrobials were tested. Biofilm formation and metal tolerance against Copper, Zinc and Cobalt, and cross-tolerance between heavy metals and anti-microbials were also investigated.

S. epidermidis is genetically highly diverse group of Staphylococci. A phylogenetic tree based on core gene presence and absences shows various distinct groups of S. epidermidis, of which some were associated with PJI and nosocomial sources. Of these more clinically relevant groups, one was associated with the ica gene, however, were shown to be poorer biofilmers. On testing isolates from across the tree to various metal concentrations did not cause cross tolerance to antimicrobials or affect biofilm formation. Using scoary, it was shown that metal tolerance genes were dispersed across all groups of S. epidermidis, with specific genes more prevalent in particular groups. For resistance genes to copper (copB and copC), cadmium (cadA) and arsenic (ars) were highly associated with specific groups.

This research has uncovered significant diversity in the phylogeny and population structure of S. epidermidis. The findings have emphasized the complex nature of S. epidermidis infection and its phenotype-genotype associations. Mechanisms of biofilm formation, AMR, and metal tolerance are not consistent within the species. Being able to better identify genes associated with infections from S. epidermidis, may allow insights into the development of better diagnostic techniques and novel therapeutic agents.