Abstract
Candida krusei is a notable pathogenic fungus that causes invasive candidiasis, mainly due to its natural resistance to fluconazole. However, to date, there is limited research on the genetic population features of C. krusei. We developed a set of microsatellite markers for this organism, with a cumulative discriminatory power of 1,000. Using these microsatellite loci, 48 independent C. krusei strains of clearly known the sources, were analyzed. Furthermore, susceptibility to 9 antifungal agents was determined for each strain, by the Clinical and Laboratory Standards Institute broth microdilution method. Population structure analyses revealed that C. krusei could be separated into two clusters. The cluster with the higher genetic diversity had wider MIC ranges for six antifungal agents. Furthermore, the highest MIC values of the six antifungal agents belonged to the cluster with higher genetic diversity. The higher genetic diversity cluster might have a better adaptive capacity when C. krusei is under selection pressure from antifungal agents, and thus is more likely to develop drug resistance.
Highlights
Invasive candidiasis is the most common fungal disease among hospitalized patients, and affects more than 250,000 people worldwide annually, with more than 50,000 deaths reported (Kullberg and Arendrup, 2015)
The correlation between genetic diversity and adaptive capacity of the population has long been studied in the field of molecular ecology
It was found that the Arabidopsis thaliana population with higher genetic diversity had better colonization success (Crawford and Whitney, 2010)
Summary
Invasive candidiasis is the most common fungal disease among hospitalized patients, and affects more than 250,000 people worldwide annually, with more than 50,000 deaths reported (Kullberg and Arendrup, 2015). C. krusei exhibits resistance to other antifungal drugs such as voriconazole, echinocandins, and amphotericin B (Fukuoka et al, 2003; Hakki et al, 2006; Pfaller et al, 2008). It has been known for some time that mutations in ERG11 and FKS 1 genes are the major mechanisms responsible for azole- and echinocandin-resistance in Candida species, including C. krusei (Jensen et al, 2014; Forastiero et al, 2015; Feng et al, 2016; Perlin et al, 2017). There have been some C. krusei antifungal resistant phenotypes, including resistance to azoles other than fluconazole and to enchinocandins e.g., caspofungin, that cannot be explained by currently known mechanisms of resistance (Hakki et al, 2006; Whaley et al, 2017)
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