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Staphylococcus epidermidis

Staphylococcus epidermidis is a Gram-positive, coagulase-negative coccus that forms clusters and is a ubiquitous commensal bacterium colonizing the skin and mucous membranes of humans.^[1] As a facultative anaerobe and catalase-positive organism, it is one of the most abundant members of the coagulase-negative staphylococci group, with a genome consisting of approximately 2.5 million base pairs, including a core set of genes shared across strains and variable elements contributing to its adaptability.^[2] Typically harmless and even beneficial in healthy individuals, it plays a key role in the skin microbiome by promoting immune homeostasis, enhancing barrier function through ceramide production, and inhibiting pathogenic bacteria like Staphylococcus aureus via colonization resistance and antimicrobial peptides.^[3] In its commensal state, S. epidermidis interacts positively with the host immune system, priming regulatory T cells and mucosal-associated invariant T cells while modulating inflammatory responses to maintain skin integrity.^[3] It produces metabolites such as trace amines that accelerate wound healing and molecules like 6-N-hydroxyaminopurine (6-HAP), which exhibit anti-cancer properties by inhibiting tumor growth.^[3] These beneficial activities underscore its role as a "skin friend," particularly in moist areas like the antecubital fossa where it is most prevalent, with strain diversity enabling tailored adaptations to different skin sites.^[2] However, S. epidermidis can transition to an opportunistic pathogen, especially in immunocompromised patients or those with indwelling medical devices, where it causes nosocomial infections through biofilm formation on surfaces like catheters and prosthetic implants.^[1] It is the leading cause of catheter-related bloodstream infections and contributes to up to 40% of prosthetic valve endocarditis cases, as well as infections in cardiac devices, joints, and cerebrospinal fluid shunts.^[1] Virulence factors such as adhesins (e.g., accumulation-associated protein) and extracellular proteases (e.g., EcpA) facilitate adherence and tissue invasion, while its frequent multidrug resistance, including to methicillin, complicates treatment.^[2] In conditions like atopic dermatitis, certain strains exacerbate inflammation by disrupting the skin barrier.^[3]

Etymology and History

Etymology

The genus name Staphylococcus derives from the Greek words staphýlē (σταφυλή), meaning "bunch of grapes," and kókkos (κόκκος), meaning "berry" or "grain," reflecting the characteristic grape-like clusters formed by the spherical (cocci) cells of these bacteria under microscopic observation.^[4] This descriptive nomenclature was coined in 1880 by Scottish surgeon Sir Alexander Ogston, who first observed such clusters in pus from a surgical abscess.^[4] The species epithet epidermidis originates from the Greek epidermis (ἐπιδερμίς), denoting the outermost layer of the skin, combined with the Latin genitive neuter ending -idis to indicate "of the epidermis."^[5] This name highlights the bacterium's frequent isolation from human skin surfaces, where it is a common commensal.^[4] Historically, the organism was initially described in 1884 by German physician Friedrich Julius Rosenbach as Staphylococcus albus (Latin for "white"), distinguishing it from the golden-pigmented S. aureus based on colony color on agar media.^[4] The name S. albus was later revised; Winslow and Winslow proposed Albococcus epidermidis in 1908, and in 1916, Arthur C. Evans formally transferred it to the genus Staphylococcus as S. epidermidis to better reflect its skin association.^[6]^[5]

Discovery

Staphylococcus epidermidis was first isolated in 1884 by the German physician Friedrich Julius Rosenbach from purulent material in human skin abscesses.^[7] Initially, Rosenbach distinguished it from Staphylococcus aureus based on its white-pigmented colonies on agar plates and named it Staphylococcus albus, grouping it among other non-pathogenic staphylococci commonly found on the skin.^[8] This early isolation highlighted its presence as a commensal organism on human skin, though it was not yet recognized as a distinct species.^[7] In the early 20th century, further differentiation of staphylococci relied on biochemical properties, with the coagulase test emerging as a pivotal method. The slide coagulase test, developed by F. Berger in 1943, detected bound coagulase (clumping factor) in plasma, allowing rapid distinction of coagulase-positive S. aureus from coagulase-negative strains like S. epidermidis.^[9] This test became essential for classifying staphylococci, confirming S. epidermidis as a coagulase-negative staphylococcus (CoNS) and shifting focus toward its potential clinical relevance beyond commensalism.^[10] During the 1950s and 1960s, key studies solidified the taxonomic status of CoNS, including S. epidermidis, through comprehensive biochemical and physiological analyses. Baird-Parker's 1965 classification scheme, based on over 600 strains from global sources, divided staphylococci into groups using criteria such as lipase production, nitrate reduction, and pigmentation, firmly establishing S. epidermidis as a distinct CoNS species prevalent on human skin.^[11] These investigations, building on earlier work, emphasized the heterogeneity of CoNS and their ecological roles, laying groundwork for recognizing their opportunistic pathogenic potential.^[10] The recognition of S. epidermidis as a significant pathogen accelerated in the 1970s and 1980s, driven by rising implant-related infections amid the proliferation of indwelling medical devices like catheters and prosthetic valves. Studies during this period, such as Archer and Tenenbaum's 1980 report on antibiotic-resistant S. epidermidis isolates from cardiac surgery patients, documented its role in nosocomial bacteremia and device-associated outbreaks, often linked to biofilm formation.^[12] This era marked a paradigm shift, transforming S. epidermidis from a dismissed contaminant to a major cause of healthcare-associated infections, particularly in immunocompromised individuals with foreign bodies.^[8]

Taxonomy and Genomics

Classification

Staphylococcus epidermidis belongs to the phylum Bacillota, class Bacilli, order Bacillales, family Staphylococcaceae, and genus Staphylococcus.^[13] This Gram-positive coccus is one of over 40 recognized species in the genus Staphylococcus, which comprises primarily skin and mucosal commensals as well as opportunistic pathogens.^[5] The species was formally described in 1884 and has since been delineated through phenotypic and genotypic characteristics that distinguish it from other staphylococci.^[14] As a coagulase-negative staphylococcus (CoNS), S. epidermidis is differentiated from the coagulase-positive Staphylococcus aureus by the lack of coagulase enzyme production, a key virulence factor in S. aureus that promotes clotting and abscess formation.^[7] This absence of coagulase is a hallmark trait shared among CoNS, which include over 30 species, but S. epidermidis is the most frequently isolated from human skin and medical devices. No formal subspecies are recognized for S. epidermidis; taxonomic classification remains at the species level, with intraspecies diversity captured through multilocus sequence typing (MLST).^[5] Strains of S. epidermidis are grouped into clonal complexes (CCs) via MLST, which analyzes allelic variations in seven housekeeping genes to infer population structure. Clonal complex 2 (CC2) dominates, encompassing the majority of clinical isolates and exhibiting enhanced biofilm-forming capabilities.^[15] Other complexes, such as CC5 and CC9, represent less prevalent lineages often associated with commensal carriage. This clonal framework highlights the species' genetic diversity without necessitating subspecies delineation. Phylogenetically, S. epidermidis clusters within the "Epidermidis-Aureus" group alongside S. aureus, S. haemolyticus, S. warneri, and S. lugdunensis, based on multilocus sequence data including 16S rRNA, dnaJ, rpoB, and tuf.^[16] It shares particularly close evolutionary ties with other human skin-associated CoNS like S. hominis and S. capitis, forming a subclade adapted to commensal lifestyles on epithelial surfaces.^[17] This positioning reflects a divergence within the genus Staphylococcus that underscores adaptations to host-associated niches.^[16]

Genome Structure

The genome of Staphylococcus epidermidis typically consists of a single circular chromosome ranging from 2.0 to 2.5 million base pairs in size, with a GC content of approximately 32%, and encodes roughly 2,000 to 2,500 protein-coding genes.^[18]^[19] This compact structure supports the bacterium's commensal lifestyle on human skin while enabling opportunistic adaptations. The chromosome includes essential housekeeping genes for basic cellular functions, such as DNA replication and metabolism, which are highly conserved across strains.^[20] The core genome of S. epidermidis comprises about 80% of its genetic content, encompassing genes vital for fundamental processes like replication, transcription, and core metabolic pathways, while the accessory genome accounts for the remaining 20% and includes variable elements acquired through horizontal gene transfer.^[20] The accessory portion features mobile genetic elements, such as plasmids that confer antimicrobial resistance—for instance, small plasmids carrying tetL genes for tetracycline resistance—and insertion sequences like IS256, which promote genomic rearrangements and strain diversity.^[21]^[22] Key genomic features include the icaADBC operon, responsible for synthesizing polysaccharide intercellular adhesin, and type III-A CRISPR-Cas systems that provide defense against phages by integrating spacers from invading nucleic acids, particularly at chromosomal termini and rRNA loci.^[23]^[24] These elements contribute to the open pan-genome architecture, allowing ongoing gene acquisition and variability among isolates.^[20] Sequencing efforts have illuminated the genomic diversity of S. epidermidis, with the first complete genome assembly of strain ATCC 12228 published in 2003, revealing a 2.5 Mb chromosome with 2,298 protein-coding genes and highlighting initial insights into virulence gene distribution. More recent high-quality assemblies from 2024 and 2025, including those of multidrug-resistant ST215 and nasal isolate B273, have uncovered strain-specific prophages and hotspots for horizontal gene transfer, such as integrons and transposons, underscoring the role of mobile elements in evolutionary adaptation.^[25]^[26] These advancements, achieved through long-read technologies like PacBio, have expanded the reference dataset to thousands of genomes available in public databases such as NCBI, facilitating comparative analyses of commensal versus pathogenic lineages.^[27]

Microbiology

Morphology and Growth

Staphylococcus epidermidis is a Gram-positive coccus measuring 0.5–1.5 μm in diameter, typically appearing in irregular grape-like clusters, pairs, tetrads, or short chains due to successive divisions in multiple planes.^[28] The bacterium is non-motile and non-spore-forming, with cells that are usually unencapsulated, though some strains may produce a thin capsule-like polysaccharide layer under specific conditions.^[28] Its cell wall features a thick peptidoglycan layer characteristic of the A3α type, consisting of long, highly cross-linked peptide chains with pentaglycine interpeptide bridges and amidated D-glutamic acid residues, conferring resistance to lysozyme through diacetylated muramic acid derivatives.^[28] Teichoic acids, composed of glycerol phosphate polymers, are covalently linked to the peptidoglycan and play roles in cell wall integrity and interactions with the environment.^[29] As a facultative anaerobe, S. epidermidis exhibits optimal growth at 35–37°C and pH 7.0–7.5, with more rapid proliferation under aerobic conditions compared to anaerobic ones, where it ferments glucose to lactate.^[28] On blood agar, it forms small, white to cream-colored, opaque colonies measuring 1–2 mm in diameter after 18–24 hours of incubation, typically non-hemolytic.^[30] The organism is halotolerant, capable of growth in media containing up to 10% NaCl; on mannitol salt agar (7.5% NaCl), it produces small colonies without fermenting mannitol, leaving the medium pink.^[30]^[31] Nutritionally, S. epidermidis requires several amino acids, including arginine, isoleucine, valine, and proline, and grows slowly in minimal media without supplementation, reflecting its adaptation to nutrient-limited skin environments.^[32] Some strains also depend on vitamins such as nicotinic acid, thiamine, biotin, and pantothenic acid for robust growth.^[32] This auxotrophy underscores its commensal lifestyle, where it thrives on host-derived nutrients while tolerating osmotic stress from skin salts.^[3]

Biochemical Properties

Staphylococcus epidermidis is a Gram-positive coccus characterized by distinct biochemical properties that reflect its metabolic versatility and adaptation to skin environments. These properties include specific enzyme activities, sugar fermentation patterns, and metabolic pathways that support its commensal lifestyle while contributing to opportunistic pathogenicity. The bacterium is catalase-positive, enabling it to decompose hydrogen peroxide and protect against oxidative stress generated by host immune responses.^[33] It is oxidase-negative, lacking the terminal oxidase in its respiratory chain that would reduce tetramethyl-p-phenylenediamine.^[34] S. epidermidis is coagulase-negative, distinguishing it from S. aureus by its inability to clot plasma through fibrin formation.^[34] Urease activity is positive in some strains, hydrolyzing urea to produce ammonia, which may aid in nutrient acquisition on the skin.^[33] DNase production is variable among strains, with some exhibiting thermostable nuclease activity that degrades extracellular DNA. Additionally, S. epidermidis is sensitive to novobiocin, an inhibitor of bacterial DNA replication, unlike certain other coagulase-negative staphylococci.^[28] Fermentation profiles further define its carbohydrate metabolism. S. epidermidis produces acid from glucose, lactose, and sucrose under anaerobic conditions, supporting energy production via glycolysis.^[28] It does not ferment mannitol or xylose, which helps differentiate it from species like S. saprophyticus.^[33] Metabolically, S. epidermidis primarily relies on aerobic respiration through an electron transport chain involving cytochromes (such as bo and aa3) and menaquinones (MK-7 to MK-9), facilitating efficient ATP generation in oxygenated skin niches.^[34] Under anaerobic conditions, it shifts to fermentation, primarily producing lactate from glucose.^[28] The organism produces lipases (e.g., GehC, GehD) and esterases that hydrolyze skin lipids, providing carbon sources for growth and contributing to its colonization persistence.^[34] Other notable traits include slime production, detectable on Congo red agar where biofilm-forming strains appear black or dark crystalline, indicating polysaccharide intercellular adhesin (PIA) synthesis and potential for surface adherence.^[35]

Identification Methods

Identification of Staphylococcus epidermidis in clinical and research settings typically begins with traditional microbiological techniques that leverage its characteristic phenotypic traits. The bacterium appears as gram-positive cocci arranged in clusters under Gram staining, distinguishing it from gram-negative organisms and other gram-positive morphologies.^[1] It tests positive for catalase, producing bubbles in the presence of hydrogen peroxide, which differentiates it from streptococci.^[36] Coagulase tests, including both slide and tube methods, yield negative results, confirming its classification as a coagulase-negative staphylococcus (CoNS), unlike S. aureus.^[1] Additionally, latex agglutination assays for protein A and clumping factor are negative, further ruling out S. aureus.^[30] Commercial identification systems provide automated biochemical profiling for more precise species-level confirmation. The API Staph panel, a strip-based system, identifies S. epidermidis with high accuracy by analyzing carbohydrate fermentation and enzymatic reactions, achieving correct identification in approximately 94% of isolates.^[37] Similarly, the VITEK 2 system uses fluorogenic substrates in cards like the GP or ID-GP for rapid analysis, reporting species-level identification for S. epidermidis and other CoNS at rates of 88-95%.^[38] These systems streamline workflows in clinical labs, with overall accuracy for CoNS exceeding 90% when combined with preliminary tests.^[39] Molecular methods offer enhanced specificity for definitive identification and strain differentiation. Polymerase chain reaction (PCR) targeting the 16S rRNA gene amplifies conserved sequences for genus confirmation, while species-specific primers enable S. epidermidis detection.^[40] Sequencing the tuf gene provides superior discriminatory power over 16S rRNA for distinguishing CoNS species, resolving ambiguities in clinical isolates.^[41] Multilocus sequence typing (MLST) amplifies and sequences seven housekeeping genes (e.g., arcC, aroE) to assign sequence types, facilitating epidemiological tracking of strains.^[42] Matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry rapidly profiles protein spectra, with log scores above 2.0 indicating secure species-level identification of S. epidermidis.^[43] Recent advances incorporate whole-genome sequencing (WGS) for comprehensive outbreak investigation and resistance profiling. WGS assembles full genomes to trace clonal relationships via single-nucleotide polymorphisms, as demonstrated in a 2024 hospital protocol analyzing linezolid-resistant S. epidermidis outbreaks through core-genome MLST.^[44] This approach has been integrated into clinical diagnostics for real-time surveillance, enhancing resolution beyond traditional MLST.^[45] As of 2025, emerging techniques include micropore devices combined with machine learning for distinguishing S. epidermidis from S. aureus with high accuracy, and long-read whole-genome sequencing for detailed intra-species diversity analysis.^[46]^[47]

Ecology

Habitats

Staphylococcus epidermidis is primarily a commensal bacterium inhabiting the human skin, where it colonizes at densities typically ranging from 10³ to 10⁵ colony-forming units per square centimeter (CFU/cm²).^[48] This colonization is particularly prominent in moist areas such as the axillae, groin, and toe webs, where environmental conditions favor bacterial persistence.^[49] Additionally, it is commonly found on mucous membranes, including those of the nasal cavity and conjunctiva, contributing to its role as a normal part of the human microbiota.^[50] Beyond human hosts, S. epidermidis has been isolated from various non-human sources, including animals like cattle udders, where it can be associated with subclinical mastitis in dairy herds.^[51] It is also detected in food products such as dairy items and raw meat, often originating from processing environments or animal reservoirs.^[52] Environmental isolates include hospital surfaces and water bodies, such as marine environments contaminated through human activity.^[53] The bacterium exhibits notable survival traits that enable its persistence in diverse niches, including tolerance to desiccation, which allows it to endure dry conditions similar to those faced by related staphylococci.^[54] It also shows relative resilience to UV exposure, though it is ultimately inactivated by sufficient doses, facilitating survival on exposed surfaces.^[55] On fomites like hospital equipment, S. epidermidis can persist for weeks to months, underscoring its environmental adaptability.^[56] Globally, S. epidermidis is ubiquitous in areas populated by humans, with no specific geographic restrictions, reflecting its close association with human activity and migration.^[3]

Microbiome Role

Staphylococcus epidermidis plays a central role as a commensal bacterium in the human skin microbiome, where it dominates among coagulase-negative staphylococci (CoNS). On healthy skin, it accounts for up to 90% of the staphylococcal population within the aerobic resident flora, exhibiting site-specific variations in abundance—typically higher in moist regions such as the antecubital fossa (up to 50% relative abundance) compared to dry sites like the volar forearm. This distribution reflects adaptations to local environmental cues, including moisture and pH, contributing to overall microbial equilibrium.^[57]^[3]^[58] In community dynamics, S. epidermidis maintains balance by competing for essential nutrients and adhesion sites with co-colonizing microbes, thereby limiting pathogen invasion. It actively produces antimicrobial peptides, such as epidermin-like lantibiotics and bacteriocins (e.g., epidermicin and nukacin IVK45), which selectively inhibit Gram-positive competitors like Staphylococcus aureus while sparing beneficial species. These mechanisms, mediated partly through quorum sensing via the accessory gene regulator (Agr) system, foster a protective niche and enhance community resilience against dysbiosis.^[3]^[59]^[60] Dysbiosis in skin conditions often involves shifts in S. epidermidis abundance, underscoring its commensal importance. In atopic dermatitis, S. epidermidis populations are typically reduced in lesional areas, where S. aureus overgrowth dominates and correlates with decreased microbial diversity. In contrast, certain strains proliferate in dry skin disorders like dandruff and seborrheic dermatitis, potentially exacerbating inflammation through biofilm formation in sebaceous regions. These imbalances highlight S. epidermidis's role in barrier homeostasis.^[3]^[61]^[62] Metagenomic analyses from 2025 studies have elucidated the long-term dynamics of S. epidermidis colonization, revealing apparent species-level stability over years despite intraspecies turnover. Using over 4,000 isolate genomes and 350 metagenomes from facial skin, researchers found that individual strains persist for an average of two years, with multi-lineage coexistence (median of six lineages per person) driving functional diversity and resilience. This strain-specific pattern supports sustained commensalism while allowing adaptation to host changes across life stages.^[63]^[64]

Microbial Interactions

Staphylococcus epidermidis exhibits antagonistic interactions with Staphylococcus aureus, a common skin pathogen, primarily through the production of bacteriocins and competition for nutrients. Bacteriocins such as epidermin and Pep5, produced by certain strains of S. epidermidis, inhibit the growth of multiple S. aureus strains by disrupting cell membranes.^[65] More recent discoveries include epilancin A37, which specifically targets corynebacterial competitors, such as Corynebacterium accolens, in competitive environments, enhancing S. epidermidis dominance.^[66] Additionally, the short-lived antimicrobial peptide epifadin enables S. epidermidis to eliminate S. aureus from shared habitats, as demonstrated in both laboratory and skin models.^[67] Nutrient competition further contributes to this antagonism, with S. epidermidis limiting S. aureus access to essential resources on the skin surface.^[3] Studies indicate that early colonization by S. epidermidis can reduce S. aureus-induced cytotoxicity and potentially limit pathogen adherence over time, though effects vary by environmental conditions such as humidity.^[68] In contrast, S. epidermidis forms synergistic relationships with Cutibacterium acnes, particularly in sebaceous-rich areas of the skin. These two commensals co-occur in lipid-abundant environments, where C. acnes metabolizes sebum into short-chain fatty acids that may support S. epidermidis growth and persistence.^[69] This shared lipid metabolism fosters mutual benefits, as S. epidermidis can enable C. acnes biofilm formation under anaerobic conditions typical of deeper skin layers, promoting community stability. Such interactions highlight S. epidermidis's role in balanced microbial consortia that maintain skin homeostasis without favoring pathogenic overgrowth.^[70] Recent research has illuminated phage-mediated interactions shaping S. epidermidis strain diversity. A 2024 study revealed that phage susceptibility, governed by host receptors like wall teichoic acids, influences strain competition and coexistence within skin microbiomes, with certain phages exhibiting broad host ranges that restrict less resistant variants.^[71] These findings underscore how bacteriophages contribute to intraspecies dynamics, potentially driving evolutionary adaptations in S. epidermidis populations.^[72]

Pathogenicity

Virulence Factors

Staphylococcus epidermidis possesses a repertoire of virulence factors that facilitate adhesion to host tissues and medical devices, toxin-mediated damage, immune evasion, and coordinated gene expression, enabling it to transition from commensal to opportunistic pathogen. These factors, distinct from biofilm matrix components, contribute to infections such as sepsis and device-related bacteremia. Key adhesins, toxins, immune modulators, and regulatory systems underpin its pathogenicity, as highlighted in recent reviews.^[73] Adhesins play a critical role in the initial attachment of S. epidermidis to host extracellular matrix proteins and abiotic surfaces. The autolysin AtlE, a bifunctional enzyme with amidase and glucosaminidase domains, promotes primary adhesion by cleaving peptidoglycan in the cell wall, exposing binding sites, and directly interacting with host proteins such as heat shock cognate protein 70 (Hsc70) and the α5β1 integrin via fibronectin. This mechanism is essential for colonization of polymer surfaces like catheters, with mutants lacking AtlE showing reduced attachment in infection models. Similarly, SdrG, a serine-aspartate repeat-containing surface protein, binds fibrinogen through a "dock, lock, and latch" mechanism involving the C-terminus of fibrinogen's β-chain, facilitating adherence to fibrinogen-coated surfaces and enhancing bacterial persistence in vivo; antibodies targeting SdrG impair this binding and promote phagocytosis.^[74]^[75]^[73] Toxins produced by S. epidermidis contribute to cytolysis, inflammation, and systemic effects during infection. Phenol-soluble modulins (PSMs), a family of amphipathic α-helical peptides including PSMα, PSMβ1/β2, PSMγ (δ-toxin), PSMδ, and PSMε, exhibit potent cytolytic activity against host cells such as neutrophils and erythrocytes, while also recruiting immune cells to amplify inflammatory responses via chemokine induction. These modulins are secreted in high amounts during quorum sensing and are key to skin inflammation and dissemination in device infections. Enterotoxins, such as SEC and SEL, are superantigens present in up to 95% of clinical blood isolates from septic patients; they hyperstimulate T-cells, leading to massive cytokine release (e.g., TNF-α, IL-6) that exacerbates sepsis, toxic shock-like syndromes, and even foodborne illness in rare cases.^[76]^[77]^[73] Immune evasion strategies allow S. epidermidis to subvert host defenses, particularly complement and phagocytosis. The extracellular fibrinogen-binding protein Efb, a homolog of Protein A in S. aureus, binds the α-chain of complement C3 to inhibit the alternative pathway, thereby blocking opsonization and reducing bacterial uptake by macrophages and neutrophils. Capsular polysaccharides, including poly-N-acetylglucosamine (PNAG) variants, form a protective glycocalyx that masks pathogen-associated molecular patterns (PAMPs) like lipoteichoic acids, impeding recognition by pattern recognition receptors and limiting opsonophagocytosis; this shielding enhances survival in bloodstream infections.^[73] The expression of these virulence factors is tightly regulated by the accessory gene regulator (Agr) quorum-sensing system, which senses bacterial population density via autoinducing peptides to activate RNAIII, a key effector that upregulates toxin genes like those for PSMs while repressing surface adhesins in stationary phase. This density-dependent control coordinates virulence during infection progression, with Agr mutants exhibiting reduced PSM production and attenuated skin colonization in animal models. Recent 2024 analyses emphasize non-biofilm contributors to sepsis, such as lipoteichoic acid (LTA), a cell wall-anchored polymer that activates Toll-like receptor 2 (TLR2) on immune cells, triggering proinflammatory cytokines (IL-6, IL-1β, TNF-α) and antibody responses that drive systemic inflammation in device-associated bacteremia. LTA's role in sepsis severity is evident from studies showing elevated cytokine levels in LTA-exposed models, independent of biofilm formation.^[78]^[73]

Biofilm Formation

Staphylococcus epidermidis forms biofilms as a key survival strategy, particularly on abiotic surfaces like medical implants, enabling persistence in hostile environments. This process involves a structured sequence of events that culminates in a protective community encased in an extracellular matrix, conferring tolerance to host defenses and antimicrobials. Biofilm development is primarily mediated by the polysaccharide intercellular adhesin (PIA), alongside proteinaceous factors, and is tightly regulated by environmental cues and genetic switches.^[79] The biofilm formation process unfolds in distinct stages. Initial attachment occurs through nonspecific hydrophobic interactions or specific adhesins such as the autolysin AtlE and the autolysin/adhesin Aae, which facilitate adhesion to host proteins or synthetic surfaces and promote the release of extracellular DNA (eDNA) to anchor cells.^[79] Subsequent multiplication involves cell proliferation and the onset of intercellular aggregation, driven by PIA or alternative protein adhesins. Maturation follows, where the biofilm architecture develops into three-dimensional structures with channels and towers, supported by an extracellular matrix comprising polysaccharides, proteins, and eDNA; this stage often includes metabolic adaptations, such as enhanced arginine catabolism via the ADI operon, to sustain the community.^[80] Finally, dispersal is triggered by the accessory gene regulator (Agr) system, releasing subpopulations via phenol-soluble modulins (PSMs) and proteases, allowing colonization of new sites.^[80] Central to biofilm integrity are key matrix components. The ica operon (icaADBC) encodes enzymes for synthesizing PIA, also known as poly-N-acetylglucosamine (PNAG), a linear β-1,6-linked N-acetylglucosamine polymer that promotes cell-to-cell adhesion and matrix stability; IcaA and IcaD form the core synthase, while IcaC exports the polymer and IcaB modifies it through de-N-acetylation and succinylation to enhance antiphagocytic properties.^[81] In ica-negative strains, protein-based mechanisms predominate, including the accumulation-associated protein (Aap), a 220-kDa surface protein present in ~90% of clinical isolates that, after proteolytic cleavage, mediates intercellular bridging under flow conditions.^[82] Other proteins like the biofilm-associated homologous protein (Bhp) and extracellular matrix-binding protein (Embp) contribute in select strains, with eDNA further reinforcing the matrix by trapping cells and modulating structural integrity.^[79] Regulation of biofilm formation is multifaceted, ensuring adaptability. The IcaR protein acts as a transcriptional repressor of the ica operon, with its activity downregulated by glucose or other environmental signals like ethanol and salt stress, thereby inducing PIA expression during nutrient limitation or quorum sensing activation.^[80] Phase variation introduces heterogeneity, occurring at high frequencies (10⁻³ to 10⁻⁴) through insertion sequence IS256-mediated inversion or excision in the ica locus, or tandem repeat variations in icaC, allowing subpopulations to switch between biofilm-proficient and -deficient states for survival optimization.^[79] Additional regulators, such as the global stress sigma factor SigB and the SarA protein, fine-tune expression in response to shear stress or iron availability, promoting PIA-dependent biofilms under dynamic conditions.^[83] Clinically, S. epidermidis biofilms significantly enhance persistence in implant-associated infections by providing structural protection, increasing antibiotic tolerance up to 1,000-fold through reduced metabolic activity, limited drug penetration, and persister cell formation.^[84] Recent studies highlight their role in modulating host immunity; for instance, biofilm-derived eDNA activates Toll-like receptor 9 (TLR9) in macrophages, suppressing pro-inflammatory cytokines (e.g., IL-1β, TNF-α) while elevating anti-inflammatory IL-10, and promoting an M2-like polarization that impairs phagocytosis—evidenced by only 16.2 bacteria internalized per macrophage with wild-type biofilms versus 43.8 in matrix mutants.^[85] This immune evasion contributes to chronic, low-grade infections, often necessitating device removal for resolution.^[85]

Infections Caused

Staphylococcus epidermidis primarily causes nosocomial infections, particularly those associated with indwelling medical devices such as intravascular catheters, prosthetic joints, cardiac pacemakers, and cerebrospinal fluid shunts. These device-related infections often manifest as localized inflammation with erythema, pain, and purulence at the insertion site, potentially progressing to systemic involvement if untreated. As a coagulase-negative staphylococcus (CoNS), S. epidermidis is the predominant species, accounting for approximately 70-80% of nosocomial bloodstream infections caused by CoNS, making it a leading pathogen in hospital settings.^[86]^[1]^[87] Systemic infections include endocarditis, especially on prosthetic heart valves where S. epidermidis is responsible for up to 40% of cases, presenting with fever, chills, malaise, new or changing cardiac murmurs, and embolic phenomena like petechiae. Sepsis due to S. epidermidis is common in vulnerable populations, such as neonates, the elderly, and immunocompromised individuals, often linked to central line-associated bloodstream infections and characterized by fever, hypotension, and organ dysfunction. In neonatal intensive care units, S. epidermidis causes approximately 73% of bacteremias and is a leading etiology of late-onset sepsis, with an incidence of 1 to 2 cases per 1,000 live births among very low birth weight infants.^[1]^[86]^[88] Other infections encompass wound infections at surgical sites or device insertion points, catheter-associated urinary tract infections with symptoms of dysuria and hematuria, and rare community-acquired cases such as peritonitis in patients undergoing peritoneal dialysis. Mortality rates for S. epidermidis bacteremia range from 5% to 28%, rising to 36% in endocarditis and 20% to 30% when complicated by septic shock; in neonates, sepsis mortality is 4.8% to 9.4% among low birth weight infants.^[1]^[89] Recent studies as of 2025 underscore the ongoing significant burden of S. epidermidis infections in intensive care units, driven by aging populations, increased use of invasive devices, and higher rates of immunosuppression, with neonates, elderly patients, and immunocompromised individuals at greatest risk for nosocomial bloodstream infections. A 2025 study suggests that skin decolonization efforts in ICUs may contribute to higher rates of resistant S. epidermidis bloodstream infections, with the bacterium identified in 45% of cases.^[88]^[90]

Antibiotic Resistance

Staphylococcus epidermidis exhibits high levels of resistance to methicillin, primarily mediated by the mecA gene, which encodes a penicillin-binding protein 2a (PBP2a) that confers resistance to beta-lactam antibiotics. Methicillin-resistant S. epidermidis (MRSE) accounts for 70-90% of clinical isolates, with prevalence rates reported as high as 75-90% in nosocomial infections. This organism also demonstrates multidrug resistance, including to aminoglycosides such as gentamicin (up to 63% resistance in some cohorts) and fluoroquinolones like ciprofloxacin (moderate to high resistance, often exceeding 50% in clinical samples). These patterns contribute to challenges in treating device-related infections. Key resistance mechanisms in S. epidermidis include beta-lactamase production, which hydrolyzes beta-lactam antibiotics, and efflux pumps such as QacA, which expel antiseptics, quaternary ammonium compounds, and certain antibiotics like fluoroquinolones. Efflux systems like QacA/B and NorA further enhance multidrug resistance by actively transporting antimicrobial agents out of the cell. Biofilms formed by S. epidermidis augment tolerance to antibiotics by limiting penetration and creating a protected microenvironment, though this physical barrier is distinct from genetic resistance. Emerging resistance concerns include vancomycin-intermediate S. epidermidis (VISA) strains, characterized by heterogeneous resistance and cell wall thickening that traps vancomycin molecules, reducing its efficacy; such strains have been documented in clinical outbreaks with minimum inhibitory concentrations (MICs) of 4-8 μg/mL. Additionally, linezolid resistance has been reported in recent cases, with the cfr gene detected in approximately 2.5% of resistant isolates as of 2025, often conferring cross-resistance to other protein synthesis inhibitors. For MRSE infections, vancomycin remains the first-line treatment due to its reliable activity against most strains, typically administered intravenously at 15-20 mg/kg every 8-12 hours with therapeutic monitoring. Alternative therapies include daptomycin (8-10 mg/kg daily) or combinations such as rifampin with vancomycin or daptomycin, which show synergistic effects against biofilms and persistent infections in prosthetic device cases. Prevention strategies focus on antimicrobial coatings for medical devices, such as chitosan-based or polymer brush layers, which reduce S. epidermidis adhesion and biofilm formation by up to 90% in vitro.

Beneficial Roles

Skin Health Maintenance

Staphylococcus epidermidis reinforces the skin's physical barrier by secreting lipases that hydrolyze sebum triglycerides into free fatty acids, thereby maintaining the lipid composition necessary for stratum corneum integrity and preventing excessive dryness.^[91] As a dominant commensal, it occupies surface niches through competitive exclusion, limiting adhesion sites and resources available to invasive pathogens like Staphylococcus aureus and thereby reducing the risk of opportunistic infections.^[3] The bacterium also contributes to chemical barrier maintenance by metabolizing sebum components via lipases and fermentation pathways, generating acidic byproducts such as acetic acid and lactic acid that lower skin surface pH to approximately 5.0, an environment that selectively favors commensal proliferation while inhibiting pathogen growth.^[92]^[93] This pH modulation enhances overall microbial homeostasis on the skin. During early colonization of wounds, S. epidermidis promotes epithelial cell repair and re-epithelialization, accelerating barrier restoration post-injury.^[94] Recent investigations, building on seminal work, demonstrate that specific strains increase host ceramide synthesis through secretion of sphingomyelinase, elevating stratum corneum ceramide levels and significantly reducing transepidermal water loss to preserve hydration and barrier function.^[95]

Immune System Interactions

Staphylococcus epidermidis interacts with the host immune system primarily through mechanisms that promote tolerance and balanced responses, facilitating its role as a commensal organism on the skin. One key aspect of this interaction involves the induction of immune tolerance via lipoteichoic acid (LTA), a cell wall component of the bacterium. LTA from S. epidermidis stimulates the production of the anti-inflammatory cytokine interleukin-10 (IL-10) in immune cells, such as dendritic cells and keratinocytes, while modulating Toll-like receptor 2 (TLR2) signaling to prevent excessive pro-inflammatory activation. This balanced IL-10 to IL-12 cytokine profile helps maintain homeostasis by dampening potential overreactions to commensal presence, reducing the risk of unnecessary inflammation on the skin surface.^[96]^[97] In addition to tolerance, S. epidermidis primes defensive immune responses that enhance host protection without causing overt inflammation. Colonization by the bacterium promotes the accumulation and activation of Th17 cells, a subset of CD4+ T helper cells that drive the production of antimicrobial peptides such as human β-defensin-2 (hBD-2) and cathelicidin (LL-37) in keratinocytes. This process is mediated by commensal-specific T cell responses, where S. epidermidis antigens elicit non-inflammatory T cell populations that bolster innate defenses against pathogens like Staphylococcus aureus. For instance, exposure to S. epidermidis-derived molecules activates TLR2 in a controlled manner, leading to increased expression of these peptides and supporting a protective barrier against invading microbes.^[98]^[99] Recent research highlights the influence of S. epidermidis on macrophage function, particularly in modulating polarization to favor anti-inflammatory states. A 2024 study demonstrated that S. epidermidis, especially in biofilm forms releasing extracellular DNA (eDNA), polarizes human monocyte-derived macrophages toward an M2-like phenotype (e.g., expressing CD163 and CD200R1), which promotes IL-10 secretion and suppresses pro-inflammatory cytokines like TNF-α and IL-1β. This shift reduces chronic inflammation in skin tissues by enhancing tissue repair and limiting excessive immune activation, thereby aiding in the resolution of minor skin perturbations while allowing bacterial persistence as a commensal. The eDNA component interacts with TLR9 to drive this polarization, underscoring a mechanism for sustained low-level immune modulation.^[85] However, in the context of infections, dysregulation of these interactions can occur, particularly with biofilm formation. Biofilms of S. epidermidis overstimulate immune cells through persistent release of eDNA and other components, leading to a state of chronic low-grade immunity characterized by subdued but ongoing macrophage activation and cytokine production. This results in prolonged inflammation that hinders complete clearance, contributing to persistent infections such as those on indwelling medical devices, where the anti-inflammatory M2 bias paradoxically supports bacterial survival and subtle tissue damage over time.^[85]^[100]

Emerging Applications

Staphylococcus epidermidis has shown promise as a probiotic agent through engineered strains designed for topical skin applications to inhibit Staphylococcus aureus colonization. Researchers have developed genetically modified S. epidermidis variants that express antimicrobials, such as lysostaphin, under the control of a S. aureus quorum-sensing promoter, enabling targeted killing of pathogenic S. aureus while sparing commensal bacteria.^[101] These engineered probiotics demonstrate selective antimicrobial activity in skin models, reducing S. aureus burdens without disrupting the overall microbiome.^[101] A phase 1 randomized clinical trial in 2021 evaluated a live biotherapeutic based on S. epidermidis for atopic dermatitis, showing safety and potential to restore skin microbiota balance.^[102] In biotechnology, S. epidermidis biofilms serve as valuable models for testing anti-infective drugs due to their structural similarity to those causing implant-related infections. Three-dimensional bioprinted S. epidermidis biofilms provide a clinically relevant platform for assessing antimicrobial penetration and efficacy, outperforming traditional two-dimensional cultures in predicting in vivo outcomes.^[103] Additionally, S. epidermidis produces biosurfactants with emulsifying and antimicrobial properties suitable for cosmetic formulations. These glycolipid biosurfactants enhance skin moisturization and inhibit pathogen adhesion, offering a sustainable alternative to synthetic surfactants in skincare products.^[104]^[105] Studies confirm their low toxicity and compatibility with skin microbiota, supporting applications in anti-aging and barrier-repair creams.^[106] Therapeutically, phage therapy targeting antibiotic-resistant S. epidermidis strains has emerged as a precision approach for biofilm-associated infections. Patient-derived bacteriophages effectively disrupt S. epidermidis biofilms on medical devices, restoring susceptibility to standard antibiotics and reducing bacterial loads in chronic wound models.^[107] Systematic reviews highlight phages' efficacy against multidrug-resistant staphylococcal biofilms, with lytic activity persisting in vivo for up to 72 hours post-application.^[108] Furthermore, recombinant AtlE, the major autolysin/adhesin of S. epidermidis, is being explored for anti-adhesive coatings on implants to prevent initial bacterial attachment. By incorporating AtlE-derived peptides or inhibitors into polymer surfaces, adhesion of S. epidermidis to biomaterials like polystyrene is reduced by over 80% in vitro, potentially lowering infection rates in orthopedic and cardiovascular devices.^[74]^[109] Recent advances in synthetic biology have engineered S. epidermidis to express tumor antigens, inducing antitumor T-cell responses that infiltrate and reduce the growth of localized and metastatic melanoma in murine models.^[110] In December 2024, researchers developed a topical vaccine using engineered S. epidermidis expressing tetanus toxin fragments, applied to mouse skin to elicit protective antibody responses against tetanus without needles or inflammation.^[111] These platforms incorporate quorum-sensing circuits to control antigen expression, enabling safe and targeted immune activation.^[110]

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