Pathogenic Mechanisms of Candida auris
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".
Deadline for manuscript submissions: 31 December 2024 | Viewed by 40
Special Issue Editor
Interests: Acinetobacter; Candida; yeasts; resistance genes to antifungals; resistance genes to antibiotics; atmospheric-pressure plasma; biofilm; immune responses
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Invasive candidiasis and, most importantly, candidemia represent major public health problems. The incidence of candidemia has increased during the last few years, and regardless of the ongoing advances in treatment algorithms and the availability of new antifungal agents, candidemia remains associated with high mortality rates.
The recent emergence of novel, multidrug-resistant species, in particular Candida auris, further complicates the management of Candida spp. bloodstream infections.
Increased resistance to fluconazole, both acquired and naturally emerging, threatens the efficacy of azoles, which is the most widely used class of antifungals and the only available oral treatment option. Except for antifungal resistance, persistence in hospital environments and common disinfectants, the ability to biofilm formation and the potential to cause outbreaks represent additional common features of this species. Resistance to azoles in C. auris is mainly caused by amino acid substitutions in the 14α-demethylase ERG11, leading to a reduced azole binding affinity. The most common amino acid substitutions in ERG11 are V125A, F126L, Y132F, and K143R. Other mechanisms contributing to azole resistance involve gain-of-function mutations in the transcriptional factors MRR1 and TAC1b related to the overexpression of respective MDR1 and CDR1 efflux pumps.
In addition to the persistence of C. auris in the hospital environment, the colonization of human skin, and antifungal resistance, it demonstrates unique features that ensure its survival in the human host. Phagocytosed yeast replicate into the phagocytes, avoid host cell lysis, and down-regulate host immune reactions.
The aim of this Special Issue is to elucidate the pathogenic armamentarium of C. auris, including resistance genes, as well as mechanisms for avoiding immune clearance. We welcome studies exploring both aspects—pathogen–yeast infectivity and pathogen–host interactions.
Dr. Anastasia Spiliopoulou
Guest Editor
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Keywords
- C. auris
- antifungal resistance
- immune evasion
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