Whaley Sarah G, Rogers P David
Department of Clinical Pharmacy, Center for Pediatric Pharmacokinetics and Therapeutics, College of Pharmacy, University of Tennessee Health Science Center, 881 Madison Ave., Memphis, TN, 38163, USA.
Curr Infect Dis Rep. 2016 Dec;18(12):41. doi: 10.1007/s11908-016-0554-5.
Candida infections have increased due to the growth and expansion of susceptible patient populations. The azole fluconazole is the most widely prescribed antifungal, but rising rates of clinical resistance among Candida glabrata isolates have greatly limited its utility. A better understanding of the mechanisms of azole antifungal resistance will provide information needed to overcome this clinical problem and reclaim this antifungal class as an option for empiric treatment of Candida infections. By far, the most frequent mechanism of azole resistance in C. glabrata is the overexpression of multidrug transporters due to activating mutations in the gene encoding transcription factor Pdr1. In this review, we will discuss the molecular and genetic basis of azole resistance in C. glabrata with particular attention given to the most recent discoveries in this field.
由于易感患者群体的增长和扩大,念珠菌感染有所增加。唑类药物氟康唑是使用最广泛的抗真菌药物,但光滑念珠菌分离株临床耐药率的上升极大地限制了其效用。更好地了解唑类抗真菌耐药机制将为克服这一临床问题提供所需信息,并使这类抗真菌药物重新成为念珠菌感染经验性治疗的选择。到目前为止,光滑念珠菌对唑类耐药最常见的机制是由于编码转录因子Pdr1的基因发生激活突变,导致多药转运蛋白过度表达。在这篇综述中,我们将讨论光滑念珠菌唑类耐药的分子和遗传基础,特别关注该领域的最新发现。