耳念珠菌耐药机制的研究进展

Research progress in antifungal resistance mechanisms in Candida auris

耳念珠菌是近年来新发现的病原体,不仅鉴别困难、致死率高、易导致院内传播,还可对多种抗真菌药物产生耐药性。但其耐药机制尚不十分明确。本文综述了ERG11的错义突变或过表达、外排泵、TAC1B突变、额外的5号染色体的获得、Hsp90及生物膜形成在耳念珠菌对唑类药物的耐药性产生中所起的作用,以及耳念珠菌对其他药物包括棘白菌素类、多烯类、核苷类似物及丙烯胺类的耐药机制。

Candida auris(C.auris)is a recently emerged multidrug-resistant fungal pathogen,featured by difficulty in identification,high mortality and easy spread in hospital environments.Furthermore,C.auris is resistant to various frontline antifungals.However,the mechanisms governing drug resistance remain unclear.This review summarized the mechanisms of triazole resistance in C.auris,including ERG11 missense mutations or overexpression,the activity of efflux pumps,missense mutations in TAC1B,the gain of an extra copy of chromosomeⅤ,the role of Hsp90 and biofilm formation.In addition,the factors associated with the resistance to other drugs including echinocandins,polyenes,nucleoside analogues and acrylamide were also reviewed.