Fungal echinocandin resistance

被引：196

作者：

Walker, Louise A. ^{[1
]}

Gow, Neil A. R. ^{[1
]}

Munro, Carol A. ^{[1
]}

机构：

[1] Univ Aberdeen, Sch Med Sci, Aberdeen AB25 2ZD, Scotland

来源：

FUNGAL GENETICS AND BIOLOGY | 2010年 / 47卷 / 02期

基金：

英国惠康基金;

关键词：

Candida albicans; Aspergillus fumigatus; Antifungals; Fungal cell wall; Glucan; Chitin; CELL-WALL INTEGRITY; EXPERIMENTAL PULMONARY ASPERGILLOSIS; PERSISTENTLY NEUTROPENIC RABBITS; YEAST SACCHAROMYCES-CEREVISIAE; PROSTHETIC VALVE ENDOCARDITIS; ANTIFUNGAL DRUG CASPOFUNGIN; CANDIDA-ALBICANS BIOFILMS; IN-VITRO SUSCEPTIBILITY; AMPHOTERICIN-B; REDUCED SUSCEPTIBILITY;

D O I：

10.1016/j.fgb.2009.09.003

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

The echinocandins are the newest class of antifungal agents in the clinical armory. These secondary metabolites are non-competitive inhibitors of the synthesis of beta-(1,3)-glucan, a major structural component of the fungal cell wall. Recent work has shown that spontaneous mutations can arise in two hot spot regions of Fks1 the target protein of echinocandins that reduce the enzyme's sensitivity to the drug. However, other strains have been isolated in which the sequence of FKS1 is unaltered yet the fungus has decreased sensitivity to echinocandins. In addition it has been shown that echinocandin-treatment can induce cell wall salvage mechanisms that result in the compensatory upregulation of chitin synthesis in the cell wall. This salvage mechanism strengthens cell walls damaged by exposure to echinocandins. Therefore, fungal resistance to echinocandins can arise due to the selection of either stable mutational or reversible physiological alterations that decrease susceptibility to these antifungal agents. (c) 2009 Elsevier Inc. All rights reserved.

引用

页码：117 / 126

页数：10

共 128 条

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