Amanloo Saeid, Shams-Ghahfarokhi Masoomeh, Ghahri Mohammad, Razzaghi-Abyaneh Mehdi
Department of Mycology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran 14115-331, Iran.
Department of Mycology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran 14115-331, Iran.
Rev Iberoam Micol. 2018 Apr-Jun;35(2):88-91. doi: 10.1016/j.riam.2018.01.002.
Candida glabrata is a yeast that can cause hazardous fungal infections with high mortality and drug resistance.
The aim of this study was to determine the profile of drug susceptibility in clinical isolates of C. glabrata and review the resistance mechanisms to caspofungin.
A total of 50 C. glabrata clinical isolates from Iran were tested for in vitro susceptibilities to amphotericin B, caspofungin, fluconazole and voriconazole. To investigate the mechanism of resistance to caspofungin, hotspot areas of FKS1 and FKS2 genes were sequenced and gene expression profile was evaluated.
All the isolates were susceptible to amphotericin B and caspofungin. Fluconazole resistance was exhibited in four isolates. In addition, only one isolate was resistant to voriconazole. FKS2 with 12 point mutations showed more mutations compared to FKS1 that had only two mutations. All substitutions were synonymous. FKS genes were expressed at comparable levels (no statistical significance) in caspofungin-treated and non-treated cultures.
The silent mutations in the hotspot areas of FKS genes and inconsiderable changes in gene expression were not associated with increased MIC (0.25μg/ml). Other mechanisms of resistance which include mutations outside the hotspot area of FKS genes could be involved in a slight increase of MIC, and they should be identified through complete FKS gene sequencing.
光滑念珠菌是一种可引发具有高死亡率和耐药性的危险真菌感染的酵母。
本研究的目的是确定光滑念珠菌临床分离株的药敏谱，并综述其对卡泊芬净的耐药机制。
对来自伊朗的50株光滑念珠菌临床分离株进行了体外对两性霉素B、卡泊芬净、氟康唑和伏立康唑的敏感性测试。为研究对卡泊芬净的耐药机制，对FKS1和FKS2基因的热点区域进行了测序，并评估了基因表达谱。
所有分离株对两性霉素B和卡泊芬净敏感。4株分离株表现出对氟康唑耐药。此外，仅1株分离株对伏立康唑耐药。与仅有2个突变的FKS1相比，有12个点突变的FKS2显示出更多突变。所有替换均为同义突变。在卡泊芬净处理和未处理的培养物中，FKS基因以相当的水平表达（无统计学意义）。
FKS基因热点区域的沉默突变和基因表达的微小变化与MIC增加（0.25μg/ml）无关。其他耐药机制，包括FKS基因热点区域以外的突变，可能参与了MIC的轻微增加，应通过完整的FKS基因测序来确定。
