Abstract
We studied the molecular epidemiology and mechanism of azole resistance of 164 C. guilliermondii isolates from a nationwide multi-center surveillance program. The isolates were identified by ITS gene sequencing, and the in vitro susceptibility to fluconazole and voriconazole was determined by broth microdilution method. The 14-α-demethylase gene ERG11 was amplified and sequenced, and microsatellite analysis was performed to study the genetic relatedness of the isolates. Amongst the 164 C. guilliermondii isolates, 15 (9.1%) and 17 (10.4%) isolates were assigned to be non-wild type (non-WT) to fluconazole and voriconazole, respectively. Sixteen sequence types (STs) were detected by comparing the amino acid sequence polymorphisms of the ERG11 gene. Fifteen isolates of STs 9, 10, 12, 13, 14, 15 and 16, were all assigned to be non-WT to fluconazole and voriconazole. By microsatellite analysis, 40 different genotypes were identified. Thirty-seven isolates from one hospital (Z1) shared the same ERG11 sequence type (ST 2), microsatellite genotype (PU40) and drug resistance pattern. In conclusion, this is the first molecular epidemiology study of C. guilliermondii in China. The rate of non-WT isolates to azoles was high and the accurate contribution of ERG11 gene mutations to azole resistance need be confirmed by further studies.
Highlights
C. guilliermondii is usually regarded as an opportunistic pathogen that is widely distributed in the natural environment, and the human skin and mucosal microflora[8]
The majority (64.5%; 106 of 164) of the C. guilliermondii isolates was acquired from blood cultures, which is similar to other studies[6], and may lead to unfavourable outcomes especially for compromised cancer hosts
The geographical distribution of the isolates varied widely, with the majority of the isolates derived from the east (36%, 59 isolates) and northeast (36%, 59 isolates) of China (Fig. 1)
Summary
C. guilliermondii is usually regarded as an opportunistic pathogen that is widely distributed in the natural environment, and the human skin and mucosal microflora[8] This organism has been reported to be an important pathogen causing a variety of deep-seated infections in immunocompromised patients[8,9,10]. Accurate identification of this organism and determination of antifungal susceptibility profiles, is important in clinical decision making. The drug resistance mechanism of this organism is important for clinical therapy decision making and infection control strategies. In the current study, we investigated one azole resistance mechanism by sequencing the ERG11 gene of 164 C. guilliermondii isolates collected from a nationwide multi-center surveillance program called China Hospital Invasive Fungal Surveillance Net (CHIF-NET)[4]. We performed microsatellite analysis to determine whether isolates with shared mutations originated from a shared lineage
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