Epidemiology and Pathogenesis of Staphylococcus epidermidis

Staphylococcus epidermidis is a ubiquitous commensal of human skin and mucous membranes that has emerged as a leading cause of device-associated and nosocomial infections worldwide. Carriage rates in healthy individuals often exceed 90 %, yet particular lineages have adapted to hospital settings, acquiring multidrug resistance and enhanced virulence traits. Epidemiological surveillance has revealed the global dissemination of methicillin-resistant S. epidermidis (MRSE) lineages, many carrying the mecA resistance gene and diverse mobile genetic elements that confer resistance to β-lactams, glycopeptides and other antibiotic classes. Pathogenesis is driven primarily by biofilm formation on indwelling materials, facilitated by polysaccharide intercellular adhesin and surface adhesins, while immune-evasion strategies include alteration of wall teichoic acid glycosylation, secretion of proteases and modulation of host coagulation pathways. Genomic studies have uncovered an open pan-genome with frequent horizontal gene transfer events, enabling rapid acquisition of antibiotic resistance genes and virulence islands. Within-host evolution during chronic infections further refines phenotypes towards increased antibiotic tolerance, augmented biofilm capacity and altered growth kinetics. These multifactorial adaptations underpin the clinical challenge posed by S. epidermidis and highlight the need for novel therapeutic strategies and stringent infection control measures.

Research from Nature Portfolio

Recent studies have uncovered cryptic susceptibilities in hospital-adapted MRSE lineages. Despite carriage of mecA, many isolates display in vitro susceptibility to penicillin combined with β-lactamase inhibitors. In vivo murine models confirmed that single-dose amoxicillin/clavulanic acid can markedly reduce bacterial loads without immediate resistance emergence, offering a potential therapeutic avenue conditional on monitoring for adaptive resistance under prolonged exposure. Foundational genomic analyses of global strain collections have also delineated infection-associated genotypes: pangenome-wide association studies identified specific k-mers linked to increased biofilm formation, cell toxicity and interleukin-8 induction. These genetic signatures, dispersed across diverse lineages by horizontal transfer, enabled prediction of invasive versus commensal status with high accuracy, illustrating the power of genome-based risk stratification. Furthermore, clinical investigation of a pacemaker-associated endocarditis case revealed in-host evolution over a 16-week infection. Sequential isolates exhibited increased antibiotic tolerance due to extended lag phases and reduced growth rates, accompanied by genetic diversification and enhanced biofilm production, underscoring the dynamic adaptation of S. epidermidis during persistent device-related infections.

Epidemiology and Pathogenesis of Staphylococcus epidermidis publication trend

The graph below shows the total number of articles in epidemiology and pathogenesis of staphylococcus epidermidis across all publications each year (not limited to Nature Index journals).

Technical terms

Biofilm: A structured community of bacteria encased in a self-produced extracellular matrix, adherent to surfaces and highly tolerant to antibiotics.

mecA gene: A gene encoding a penicillin-binding protein (PBP2a) with low β-lactam affinity, conferring methicillin resistance.

Wall teichoic acid (WTA): An anionic glycopolymer in the Gram-positive cell wall that influences adhesion, autolysis and immune recognition.

Mobile genetic element (MGE): A DNA segment, such as plasmids, transposons or integrated conjugative elements, capable of horizontal transfer between bacteria.

Pan-genome: The full complement of genes within a species, comprising a core genome shared by all strains and an accessory genome variable between strains.

References

1. Cryptic susceptibility to penicillin/β-lactamase inhibitor combinations in emerging multidrug-resistant, hospital-adapted Staphylococcus epidermidis lineages. Nature Communications (2023).
2. Invasive Staphylococcus epidermidis uses a unique processive wall teichoic acid glycosyltransferase to evade immune recognition. Science Advances (2023).
3. Staphylococcus epidermidis ST2 strains associated with bloodstream infections contain a unique mobile genetic element encoding a plasmin inhibitor. mBio (2024).
4. Comprehensive genomic landscape of antibiotic resistance in Staphylococcus epidermidis. mSystems (2024).
5. Staphylococcus epidermidis—Skin friend or foe?. PLOS Pathogens (2020).
6. Disease-associated genotypes of the commensal skin bacterium Staphylococcus epidermidis. Nature Communications (2018).
7. Staphylococcus epidermidis pan-genome sequence analysis reveals diversity of skin commensal and hospital infection-associated isolates. Genome Biology (2012).
8. In-host evolution of Staphylococcus epidermidis in a pacemaker-associated endocarditis resulting in increased antibiotic tolerance. Nature Communications (2019).