Skin Candida Auris: Traits, Variation, and Transmission

Candida auris is an emerging fungal pathogen that has raised global concern due to its resistance to multiple antifungal drugs and persistence in healthcare environments. While it can cause life-threatening infections, it also colonizes the skin asymptomatically, contributing to its spread among vulnerable populations.

Understanding how C. auris interacts with human skin is essential for controlling its transmission and preventing outbreaks.

Biological Traits And Skin Colonization

Candida auris exhibits unique characteristics that enable it to persist on human skin, distinguishing it from other Candida species. Unlike Candida albicans, which primarily colonizes mucosal surfaces, C. auris has a strong affinity for the stratum corneum, the outermost epidermal layer. This affinity is supported by its ability to form biofilms, which enhance its resistance to desiccation and antimicrobial agents. Studies have shown that C. auris biofilms contain a dense extracellular matrix composed of β-glucans, mannans, and chitin, aiding its persistence on skin and in healthcare environments (Kean et al., 2018, mSphere). These biofilms not only protect the fungus from external stressors but also promote adherence to keratinized surfaces, making skin an effective reservoir.

The lipid composition of C. auris cell membranes further supports its survival. Unlike other Candida species, C. auris has an altered ergosterol biosynthesis pathway that increases its tolerance to azole antifungals. Additionally, its membrane contains a higher proportion of long-chain fatty acids, which may enhance its ability to withstand the dry conditions of the epidermis (Zamith-Miranda et al., 2019, mBio). The ability of C. auris to persist on intact skin for months has been documented in longitudinal studies, even in the absence of active infection (Schelenz et al., 2016, Clinical Microbiology and Infection).

Environmental factors also influence C. auris colonization. Its optimal growth temperature of 37–42°C exceeds that of many other fungal species, allowing it to thrive on febrile patients and persist in warm, humid hospital conditions. Additionally, its ability to survive on dry surfaces for weeks suggests that colonization is not solely dependent on direct host interactions but also on environmental contamination. Studies have shown that C. auris remains viable on inanimate surfaces for extended periods, increasing the risk of re-colonization following transient skin contact (Piedrahita et al., 2017, Journal of Clinical Microbiology).

Phenotypic Variation Among Skin Isolates

Candida auris exhibits considerable phenotypic variation among skin isolates, complicating clinical detection and eradication efforts. Differences in colony morphology, antifungal susceptibility, biofilm formation, and metabolic adaptability influence its persistence on human skin. Some isolates form smooth, cream-colored colonies, while others display a wrinkled or dry appearance when cultured on agar media (Borman et al., 2017, Journal of Clinical Microbiology). These morphological differences often correlate with genetic variations that impact virulence and environmental resilience.

Antifungal resistance among C. auris isolates varies significantly across geographic regions and even within the same patient. Whole-genome sequencing has revealed that mutations in the ERG11 and FKS1 genes, which confer resistance to azoles and echinocandins, are not uniformly distributed among skin-colonizing strains (Lockhart et al., 2017, Emerging Infectious Diseases). Some isolates exhibit high-level fluconazole resistance but remain susceptible to amphotericin B, whereas others display pan-resistance, severely limiting treatment options. Skin colonization may serve as a reservoir for more resistant subpopulations, particularly in patients undergoing prolonged antifungal therapy.

Biofilm production further distinguishes skin isolates. Some strains produce significantly greater biofilm biomass and extracellular matrix, increasing their resistance to desiccation and disinfectants. High-biofilm-forming isolates tend to persist longer on skin and hospital surfaces. Comparative studies have shown that certain isolates produce thicker biofilms with enhanced metabolic activity, leading to increased tolerance to common antiseptics like chlorhexidine and hydrogen peroxide (Kean et al., 2018, mSphere). This may explain why some patients remain colonized despite decolonization efforts.

Metabolic flexibility also contributes to phenotypic differences. Some strains exhibit enhanced growth at elevated temperatures or in nutrient-limited environments, aiding their persistence in different anatomical sites. Proteomic analyses have identified variations in stress response proteins and lipid metabolism enzymes among isolates, suggesting that some strains are better equipped to survive fluctuating skin conditions (Zamith-Miranda et al., 2019, mBio).

Transmission Pathways In Clinical Environments

Candida auris spreads efficiently in healthcare settings, where its persistence on surfaces and medical equipment facilitates ongoing transmission. Unlike airborne fungal pathogens, C. auris is primarily transferred through direct contact, making contaminated hands, gloves, and patient-care devices significant vectors. Healthcare workers unknowingly contribute to its spread, as even brief interactions with colonized patients can facilitate transfer to new hosts. Genomic sequencing studies have shown that hospital outbreaks often stem from a single introduction event, followed by rapid person-to-person transmission (Chow et al., 2020, Clinical Infectious Diseases).

C. auris survives on both porous and nonporous surfaces for weeks, exacerbating its persistence in clinical environments. High-touch objects such as bed rails, infusion pumps, and blood pressure cuffs frequently harbor viable fungal cells, even after routine cleaning. Environmental sampling in outbreak settings has detected C. auris on hospital furniture, computer keyboards, and disposable medical supplies (Piedrahita et al., 2017, Journal of Clinical Microbiology). Its resistance to standard disinfectants, particularly quaternary ammonium compounds, allows it to persist in patient rooms long after discharge, increasing the risk of recolonization and cross-contamination.

Biofilm formation on medical equipment presents another challenge. C. auris readily adheres to catheters, ventilators, and dialysis machines, forming structured communities that resist antifungal treatment and mechanical removal. Biofilm-embedded populations exhibit heightened disinfectant tolerance, necessitating more aggressive sterilization measures such as hydrogen peroxide vapor or ultraviolet-C light (de Groot et al., 2021, Antimicrobial Resistance & Infection Control). The difficulty in eradicating these biofilms has been highlighted in case reports documenting persistent colonization of intensive care unit surfaces despite repeated cleaning efforts. Even a small number of residual cells can repopulate a clinical environment.

Laboratory Methods For Identification

Accurately identifying Candida auris in clinical laboratories presents challenges due to its phenotypic similarities with other yeast species. Traditional biochemical identification systems, such as those based on carbohydrate assimilation patterns, often misidentify C. auris as Candida haemulonii or Rhodotorula glutinis, leading to diagnostic delays. To improve accuracy, laboratories now rely on advanced methods like matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and molecular techniques. However, MALDI-TOF MS depends on the availability of C. auris reference spectra in the database.

Molecular diagnostics, particularly polymerase chain reaction (PCR)-based assays and whole-genome sequencing, provide high sensitivity and specificity. PCR assays targeting species-specific regions of the ITS or D1/D2 rRNA genes enable rapid identification directly from clinical samples, reducing turnaround time compared to culture-based methods. Whole-genome sequencing not only confirms species identity but also provides insights into antifungal resistance mechanisms and outbreak tracking. Next-generation sequencing has revealed distinct genetic clusters of C. auris across different regions, highlighting its independent emergence on multiple continents.