# The Evolution of Symbiosis in Staphylococcus epidermidis: From a Protective Mutualist to a Parasitic Pathogen

## TL;DR

Staphylococcus epidermidis evolved from a skin protector to a dangerous antibiotic-resistant pathogen through genetic changes and resistance gene transfer.

## Contribution

This paper reviews the genomic evolution and dual role of S. epidermidis as both a commensal and pathogen.

## Key findings

- S. epidermidis has evolved multidrug resistance through mechanisms like biofilm formation and gene transfer.
- Genomic islands and SCCmec elements contribute to its resistance and pathogenicity.
- Antibiotic misuse and hospital exposure have accelerated its genomic remodeling.

## Abstract

Staphylococcus epidermidis is more often known as a human skin commensal, serving as a primary protective bacterium on the skin’s surface. However, more recent literature highlights the role of S. epidermidis as a nosocomial pathogen and a multidrug-resistant organism that poses a global threat. The evolution of S. epidermidis can be owed to its accumulation of resistance mechanisms, including adhesion, biofilm formation, genomic islands, phage elements, integrated plasmids, and quorum sensing. It is suspected that through gene transfer, S. epidermidis is partially responsible for the feared multidrug-resistant Staphylococcus aureus through the mecA gene and many other genomic island transfers. Overall, prolonged nosocomial exposure and misuse of antibiotics have driven dramatic genomic remodeling in S. epidermidis, characterized by many methods of genetic recombination, SCCmec and insertion sequence acquisition, and accumulation of multiple resistance genes. Our review reviews the role of S. epidermidis as both a commensal and a pathogenic bacterium, summarizes the genes responsible for its multidrug resistance, and describes methods of combatting its invasion.