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

<i>Staphylococcus epidermidis</i> 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 <i>S. epidermidis</i> as a nosocomial pathogen and a multidrug-resistant organism that poses a global threat. The evolution of <i>S. epidermidis</i> 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, <i>S. epidermidis</i> is partially responsible for the feared multidrug-resistant <i>Staphylococcus aureus</i> through the <i>mecA</i> gene and many other genomic island transfers. Overall, prolonged nosocomial exposure and misuse of antibiotics have driven dramatic genomic remodeling in <i>S. epidermidis</i>, characterized by many methods of genetic recombination, <i>SCCmec</i> and insertion sequence acquisition, and accumulation of multiple resistance genes. Our review reviews the role of <i>S. epidermidis</i> as both a commensal and a pathogenic bacterium, summarizes the genes responsible for its multidrug resistance, and describes methods of combatting its invasion.