Unlike many pathogenic skin bacteria from the Staphylococcus genus that possess the coagulase enzyme (which binds to and activates prothrombin in the blood, resulting in clotting of plasma or blood), S. epidermidis is coagulase-negative. Many studies have regarded S. epidermidis as a benign or beneficial member of the skin microbiota that is involved in barrier development, maintenance of homeostasis, and control of opportunistic pathogens. For example, the organism produces small α-helical peptides (called phenol-soluble modulins or PSMs) that synergize with host antimicrobial peptides to enhance killing of pathogens [Cogen10], and lipoteichoic acid produced by the organism was shown to attenuate the inflammatory response and accelerate wound healing in a Toll-like receptor (TLR)-3-dependent mechanism [Lai09].

However, it is now well documented that the organism can sometimes cause infections, particularly in people with weakened immune systems or those with implanted medical devices such as catheters, prosthetic joints, and prosthetic heart valves [vonEiff02, Otto09]. The cysteine protease Staphopain A, which is produced by the organism, is a key mediator of S. epidermidis—induced degradation of the skin barrier in atopic dermatitis patients [Hon16, Byrd17, Brown20].

Staphylococcus epidermidis is a facultative anaerobe and possesses complete glycolysis and pentose phosphate pathways, as well as the tricarboxylic acid (TCA) cycle (but not the glyoxylate shunt). It mainly catabolizes carbohydrates through the glycolytic and the pentose phosphate pathways. However, it can use also oxygen, nitrate, and nitrite as terminal electron acceptors, and activity of the TCA cycle and the electron transport chain depends on the availability of these acceptors.

Approximately 80% of the 2.5 Mb S. epidermidis genome is composed of core genes, whereas the remaining 20% are variable [Conlan12]. Native populations are undergoing multiple horizontal gene transfer events via plasmid and phage to adapt to their specific skin niche [Zhou20].

Staphylococcus epidermidis RP62A was isolated in 1979 from a patient with intravascular catheter-associated sepsis during the investigation of an outbreak of coagulase-negative stahpylococcal sepsis that took place at the City of Memphis Hospital and the adjoining University of Tennessee Hospital [Christensen82, Christensen83]. The organism was originally classified as a strain of Staphylococcus hominis, but later reclassified as Staphylococcus epidermidis [Baddour84]. The strain, which is methicillin-resistant, produces a biofilm (originally referred to as slime) [Christensen82a, Christensen85]. Researchers have used Staphylococcus epidermidis RP62A to study the molecular mechanisms underlying biofilm formation, as well as to develop new strategies for preventing and treating biofilm-associated infections. Additionally, the strain has been used as a benchmark strain in genomic studies of S. epidermidis, allowing for comparisons between different strains of the bacterium.

The Staphylococcus epidermidis RP62A genome was sequenced in 2005 [Gill05]. This Pathway/Genome Database (PGDB) was generated by the PathoLogic component of Pathway Tools software version 26.5 [Karp11, Karp16] and MetaCyc version 26.5 [Caspi18] on Aug 24 2022, and improved by limited manual curation.