Candida auris is an emerging pathogen typically seen in healthcare settings such as ICUs.
The proposed taxonomic description of Candida auris sp. nov. is type strain JCM15448T= CBS10913T= DSM21092T.
So far, no environmental reservoir of C. auris has been identified. A significant percentage of genes in C. auris are devoted to central metabolism, a property that is common to pathogenic Candida spp. and crucial for adaptation in diverse environments.
Four distinct clades of clinical isolates have been identified from separate geographic origins on three continents, suggesting a recent and nearly simultaneous emergence of different clonal populations. Several geographically related clusters have been reported from South Korea, India, South Africa, Pakistan, and hospitals in Latin America. Clonality within C. auris has been shown using AFLP, MLST and MALDI-ToF MS among strains in India, South Africa, and Brazil. Next generation sequencing (NGS) has demonstrated highly-related C. auris isolates in four unrelated and geographically separated Indian hospitals, suggesting that each clade exhibits low diversity.
Candida auris is an emerging pathogen, first reported in 2009 from an ear canal infection in Japan. More recently, it has been associated with life-threatening invasive diseases such as bloodstream and wound infections globally. In a span of only seven years, this yeast which displays clonal inter- and intra-hospital transmission, has become widespread across several countries, causing a broad range of healthcare-associated invasive infections. The increasing isolation of C. auris from various clinical specimens clearly indicates its ability to colonise, invade and cause disease with varying severity.
Candida auris has been reported to cause bloodstream infections, wound infections, and otitis. It has also been cultured from urine and the respiratory tract; however, whether isolation from these sites represents infection versus colonisation in each instance is unknown.
C. auris has been recovered in samples from blood, catheter tips, CSF, bone, ear discharge, pancreatic fluid, pericardial fluid, peritoneal fluid, pleural fluid, respiratory secretions (including sputum and bronchoalveolar lavage), skin and soft tissue samples (both tissue and swab cultures), urine, and vaginal secretions. Clinically, it has been implicated as a causative agent in fungaemia, ventriculitis, osteomyelitis, malignant otitis (including otomastoiditis), complicated intra-abdominal infections, pericarditis, complicated pleural effusions, and vulvovaginitis. Much like other Candida species, there is uncertainty about the ability of C. auris to cause true respiratory, urinary, and skin and soft tissue infections despite being isolated from such samples.
While one study reported no C. auris attributable deaths among nine patients with fungaemia, crude mortality rates for C. auris fungaemia have otherwise ranged from 28-66% across a wide range of healthcare settings and patient populations.
C. auris is indistinguishable from most other Candida species by microscopy . C. auris grows readily at 37–42 °C and forms light pink colonies on chromogenic agars. Differentiation of C. auris from C. haemulonii complex using CHROMagar Candida supplemented with Pal’s medium.
Unlike C. haemulonii, C. auris does not form pseudohyphae however some strains can form rudimentary pseudohyphae on cornmeal agar. C. auris is capable of forming biofilms and adhering to catheter material, although not to the same degree as Candida albicans.
Biosafety level 2
C. auris is phylogenetically related to Candida haemulonii and Candida ruelliae. Previously and currently mis-identified as Candida duobushaemulonii, C. haemulonii, C. famata, C. krusei, C. lusitaniae, C. sake, Saccharomyces spp., Rhodotorula glutinis or Kodamaea ohmeri by commercial identification systems, such as Vitek 2 and bioMérieux Industry API®/ID32.
The CDC recommends further testing for C. auris whenever C. haemulonii is identified or in a number of other scenarios depending on the organism reported and the method of identification. Accurate identification can be performed with VITEK MS and Bruker Biotyper matrix-assisted laser desorption/ionization time-of-flight (MALDI-ToF) devices using their ‘research use only’ databases.
– More information on the CDC website
Molecular sequencing of the D1–D2 domain of the 28S ribosomal DNA can also identify C. auris.
– Download the PCR protocol
In the U.S., all confirmed isolates of C. auris should be reported to local and state public health officials and CDC at firstname.lastname@example.org
Almost all strains of C. auris are resistant to fluconazole and many are resistant to amphotericin B, voriconazole, echinocandins and flucytosine.
There are no Clinical and Laboratory Standards Institute (CLSI) or European Committee for Antimicrobial Susceptibility Testing (EUCAST) defined breakpoints for C. auris susceptibility. Fluconazole (tentative MIC breakpoint ≥32) is associated with high minimum inhibitory concentrations (MICs) with MIC50 results between 64–128 mg/L and MIC90 results between 64–256 mg/L by CLSI microbroth dilution, in four studies. Echinocandins (tentative MIC breakpoint ≥4 for anidulafungin and micafungin, ≥2 for caspofungin) appear to be most active in these studies with favorable results for anidulafungin (MIC50 range 0.125–0.5, MIC90 range 0.5–1), caspofungin (MIC50 0.25–0.5, MIC90 1), and micafungin (MIC50 0.125–0.25, MIC90 0.25–2). Amphotericin B (tentative MIC breakpoint ≥2) susceptibility testing exhibits a wider range of MIC results (MIC50 0.5–1, MIC90 2–4) and is likely less reliable as empiric therapy. In comparison to CLSI microbroth dilution, similar MIC50 and MIC90 results can likely be obtained by the EUCAST method. Caution should be used when interpreting Etest and Vitek antifungal susceptibility testing results.