| Summary: | Since <i>Candida auris</i> integrates strains resistant to multiple antifungals, research has been conducted focused on knowing which molecular mechanisms are involved. This review aims to summarize the results obtained in some of these studies. A search was carried out by consulting websites and online databases. The analysis indicates that most <i>C. auris</i> strains show higher resistance to fluconazole, followed by amphotericin B, and less resistance to 5-fluorocytosine and caspofungin. In <i>C. auris,</i> antifungal resistance to amphotericin B has been linked to an overexpression of several mutated <i>ERG</i> genes that lead to reduced ergosterol levels; fluconazole resistance is mostly explained by mutations identified in the <i>ERG11</i> gene, as well as a higher number of copies of this gene and the overexpression of efflux pumps. For 5-fluorocytosine, it is hypothesized that the resistance is due to mutations in the <i>FCY2</i>, <i>FCY1,</i> and <i>FUR1</i> genes. Resistance to caspofungin has been associated with a mutation in the <i>FKS1</i> gene. Finally, resistance to each antifungal is closely related to the type of clade to which the strain belongs.
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