Antarctic marine microplastics reveals environmental persistence and rapid evolution of Candida auris
Candida ( Candidozyma ) auris is a critical priority fungal pathogen that emerged two decades ago near simultaneously on multiple continents. Since emergence, C. auris resistance to all four classes of antifungal drugs has been described, including pan-drug resistant isolates, sometimes evolving in-patient. Here, we confirm the first isolation of C. auris from Antarctica and show cold-adapted phenotypes and an affinity for binding to nylon. We also provide evidence to suggest mutator phenotypes contribute to the rapid evolution in C. auris and are responsible for the emergence of multiple, distinct genetic clades worldwide. Isolates in clades I, III and IV with a mutator phenotype displayed elevated mutation rates compared to non-auris Candida species. This phenotype had a complex genetic basis and was associated with drug resistance mutations. We postulate that the mutator phenotype has a significant effect on evolutionary potential and is responsible for the emergence and rapid spread of drug-resistance C. auris and novel genetic clades. ### Competing Interest Statement This work was partially support by a Wellcome Trust Institutional Strategic Fung Springboard Fellowship awarded to JR. PH and JR were funded through a JPIAMR IMPACT grant (JPIAMR2024_IMPACT-197 Consortium grant: FuGACI) and the Dutch Organisation for knowledge and innovation in health, healthcare and wellbeing (ZonMw) under project number 10570172410003. NvR is supported by a Wellcome Trust fellowship (226408/Z/22/Z). MCF is a fellow of the Canadian Institute for Advanced Research (CIFAR). RAF is supported by a Wellcome Trust Career Development Award (225303/Z/22/Z). JLS is a Howard Hughes Medical Institute Awardee of the Life Sciences Research Foundation. SD and HG are supported by the MRC Centre for Medical Mycology at the University of Exeter (MR/N006364/2 and MR/V033417/1), and the MRC Doctoral Training Grant (MR/P501955/2), and the NIHR Exeter Biomedical Research Centre. The views expressed are those of the authors and not necessarily those of the NIHR or the Department of Health and Social Care. We also thank the Exeter Sequencing Service facility and support from Wellcome Trust Institutional Strategic Support Fund (WT097835MF), Wellcome Trust Multi User Equipment Awards (WT101650MA and 218247/Z/19/Z), Medical Research Council Clinical Infrastructure Funding (MR/M008924/1) and BBSRC LOLA award (BB/K003240/1), as well as the University of Exeter High-Performance Computing (HPC) facility, funded by the UK MRC Clinical Research Infrastructure Initiative (award number MR/M008924/1). Wellcome Trust, https://ror.org/029chgv08, Strategic Fung Springboard, 226408/Z/22/Z, 225303/Z/22/Z JPI-AMR, JPIAMR2024_IMPACT-197 Consortium grant: FuGACI ZonMw, The Dutch Organisation for knowledge and innovation in health, healthcare and well-being, 10570172410003 CIFAR Howard Hughes Medical Institute Awardee of the Life Sciences Research Foundation MRC Centre for Medical Mycology at the University of Exeter, MR/N006364/2, MR/V033417/1 MRC Doctoral Training Grant, MR/P501955/2 NIHR Exeter Biomedical Research Centre BBSRC, BB/W009625/1 MRC, MR/4002163/1
biorxiv.org
