Palladini Giorgia, Lepera Valentina, Trubini Serena, Tocci Gabriella, Zappavigna Andrea, Iskandar Elizabeth, Ferrari Guglielmo, Prigitano Anna, Ferraro Nicola, Schiavo Roberta, Baldanti Fausto, Cavanna Caterina, Lo Cascio Giuliana
Department of Laboratory Medicine, Microbiology Unit, AUSL Piacenza, Piacenza, Italy.
Department of Oncology-Hematology, AUSL Piacenza, Piacenza, Italy.
Mycoses. 2025 Sep;68(9):e70111. doi: 10.1111/myc.70111.
Starting from 2018 onwards, several outbreaks of fluconazole-resistant C. parapsilosis have been reported in many countries worldwide.
Here we report a retrospective study on C. parapsilosis blood isolates collected over 7 years (2018-2024) in two hospitals in Northern Italy.
PATIENTS/METHODS: The study involved 169 C. parapsilosis isolates collected from individual hospitalised patients. We assessed the antifungal susceptibility of the isolates, evaluated the presence of mutations in the ERG11 gene and performed multilocus microsatellite typing to highlight the genetic relatedness of the strains. All isolates were also tested for their ability to produce biofilm.
Among the 169 clinical isolates, 124 (73.4%) were classified as fluconazole-resistant C. parapsilosis (FRCP) and 45 (26.6%) as fluconazole-susceptible (FSCP). ERG11 sequencing highlighted that the most frequent mutation in FRCP is the Y132F (118/124, 95.2%). None of the FSCP carried the Y132F. Microsatellite genotyping showed five major clusters and 13 sub-clusters, formed by isolates sharing identical genotypes. Sub-cluster R1 included 96 FRCP carrying the Y132F substitution, isolated from 2018 to 2024 in both hospitals. Interestingly, 99.1% of the FRCP carrying the Y132F mutation were categorised as low biofilm formers, while FRCP carrying other ERG11 mutations were categorised as medium or high biofilm formers.
Our results confirmed that Y132F may be mainly responsible for azole resistance in C. parapsilosis and inter-hospital spread. As we found, recent clinical studies indicate that FRCP isolates responsible for severe outbreaks produce thin biofilms. Mutated and therefore resistant strains may exhibit reduced biofilm production as a protective mechanism.
自2018年起，全球多个国家报告了几起耐氟康唑的近平滑念珠菌疫情。
在此，我们报告一项对意大利北部两家医院在7年（2018 - 2024年）期间收集的近平滑念珠菌血液分离株的回顾性研究。
患者/方法：该研究涉及从169名住院患者中分离出的近平滑念珠菌菌株。我们评估了这些分离株的抗真菌药敏性，检测了ERG11基因中的突变情况，并进行多位点微卫星分型以突出菌株间的遗传相关性。所有分离株还进行了生物膜形成能力测试。
在169株临床分离株中，124株（73.4%）被归类为耐氟康唑的近平滑念珠菌（FRCP），45株（26.6%）为氟康唑敏感株（FSCP）。ERG11测序表明，FRCP中最常见的突变是Y132F（118/124，95.2%）。FSCP中均未携带Y132F突变。微卫星基因分型显示有五个主要簇和13个子簇，由具有相同基因型的分离株组成。子簇R1包含96株携带Y132F替代的FRCP，于2018年至2024年在两家医院分离得到。有趣的是，携带Y132F突变的FRCP中有99.1%被归类为低生物膜形成者，而携带其他ERG11突变的FRCP则被归类为中等或高生物膜形成者。
我们的结果证实Y132F可能是近平滑念珠菌对唑类耐药及医院间传播的主要原因。如我们所发现的，近期临床研究表明，导致严重疫情的FRCP分离株产生的生物膜较薄。发生突变因而具有耐药性的菌株可能会减少生物膜的产生作为一种保护机制。
