Azole resistance among Aspergillus fumigatus isolates, which is mainly related to mutations in the cyp51A gene, is a concern because it is rising, worldwide disseminated, and associated with treatment failure and death. Data on azole resistance of aspergillus from Latin American countries is very scarce and do not exist for Peru. Two hundred and seven Aspergillus clinical isolates collected prospectively underwent mycology and molecular testing for specie identification, and 143 isolates were confirmed as A. fumigatus sensu stricto (AFSS). All AFSS were tested for in vitro azole susceptibility, and resistant isolates underwent PCR amplification and sequencing of the whole cyp51A gene and its promoter. The in vitro susceptibility showed a minimal inhibitory concentration (MIC) range, MIC50 and MIC90 of 0.125 to >16, 0.25, and 0.5 μg/ml for itraconazole; 0.25 to 2, 0.5, and 0.5 μg/ml for voriconazole; and 0.003 to 1, 0.06, and 0.125 μg/ml for posaconazole. Three isolates (2%) showed resistance to itraconazole and exhibited different mutations of the cyp51A gene. One isolate harbored the mutation M220K, while a second one exhibited the G54 mutation plus a modification in the cyp51A gene promoter. The third isolate, from an azole naive patient, presented an integration of a 34-bp tandem repeat (TR34) in the promoter region of the gene and a substitution of leucine 98 by histidine (L98H). The three source patients had a diagnosis or suspicion of chronic pulmonary aspergillosis.

中文翻译：

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利马-秘鲁烟曲霉临床分离株之间的偶氮抗性。

烟曲霉菌株之间的偶氮抗药性主要与cyp51A基因的突变有关，这是一个令人担忧的问题，因为它正在上升，在全球范围内传播并与治疗失败和死亡有关。来自拉丁美洲国家的曲霉对唑类的抗药性数据非常稀少，秘鲁则不存在。前瞻性收集的207株曲霉临床分离株进行了真菌学和分子检测以鉴定菌种，并确认了143株分离出的严格烟曲霉（AFSS）。测试了所有AFSS的体外唑敏感性，并对耐药菌株进行了整个cyp51A基因及其启动子的PCR扩增和测序。体外药敏显示最小抑菌浓度（MIC）范围，MIC50和MIC90为0.125至> 16、0.25和0。伊曲康唑5μg/ ml; 伏立康唑为0.25至2、0.5和0.5μg/ ml; 泊沙康唑为0.003至1,0.06和0.125μg/ ml。三个分离株（占2％）显示出对伊曲康唑的耐药性，并显示出cyp51A基因的不同突变。一个分离株带有突变M220K，而第二个分离株则具有G54突变以及cyp51A基因启动子的修饰。来自未接受过唑治疗的患者的第三个分离株在基因的启动子区域中整合了一个34 bp的串联重复序列（TR34），并被组氨酸取代了亮氨酸98（L98H）。这三例患者诊断或怀疑患有慢性肺曲霉病。三个分离株（占2％）显示出对伊曲康唑的耐药性，并显示出cyp51A基因的不同突变。一个分离株带有突变M220K，而第二个分离株则具有G54突变以及cyp51A基因启动子的修饰。来自未接受过唑治疗的患者的第三个分离株在基因的启动子区域中整合了一个34 bp的串联重复序列（TR34），并被组氨酸取代了亮氨酸98（L98H）。这三例患者诊断或怀疑患有慢性肺曲霉病。三个分离株（占2％）显示出对伊曲康唑的耐药性，并显示出cyp51A基因的不同突变。一个分离株带有突变M220K，而第二个分离株则具有G54突变以及cyp51A基因启动子的修饰。来自未接受过唑治疗的患者的第三个分离株在基因的启动子区域中整合了一个34 bp的串联重复序列（TR34），并被组氨酸取代了亮氨酸98（L98H）。这三例患者诊断或怀疑患有慢性肺曲霉病。提出了在基因的启动子区域中34bp串联重复序列（TR34）的整合和组氨酸（L98H）取代亮氨酸98。这三例患者诊断或怀疑患有慢性肺曲霉病。提出了在基因的启动子区域中34bp串联重复序列（TR34）的整合和组氨酸（L98H）取代亮氨酸98。这三例患者诊断或怀疑患有慢性肺曲霉病。