Mycoses · 2025
Inter-Hospital Spread of Fluconazole-Resistant C. parapsilosis in Northern Italy: Insights Into Clonal Distribution, Resistance Mechanisms and Biofilm Production.
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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
Аннотация
BACKGROUND: Starting from 2018 onwards, several outbreaks of fluconazole-resistant C. parapsilosis have been reported in many countries worldwide.
OBJECTIVES: 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.
RESULTS: 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.
CONCLUSIONS: 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.
OBJECTIVES: 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.
RESULTS: 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.
CONCLUSIONS: 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.