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. 2025 Sep;68(9):e70111.
doi: 10.1111/myc.70111.

Inter-Hospital Spread of Fluconazole-Resistant C. parapsilosis in Northern Italy: Insights Into Clonal Distribution, Resistance Mechanisms and Biofilm Production

Giorgia Palladini  1 , Valentina Lepera  1 , Serena Trubini  2 , Gabriella Tocci  1 , Andrea Zappavigna  1 , Elizabeth Iskandar  3   4 , Guglielmo Ferrari  3   4 , Anna Prigitano  5 , Nicola Ferraro  3 , Roberta Schiavo  1 , Fausto Baldanti  3   6 , Caterina Cavanna  3 , Giuliana Lo Cascio  1   7
Affiliations

Inter-Hospital Spread of Fluconazole-Resistant C. parapsilosis in Northern Italy: Insights Into Clonal Distribution, Resistance Mechanisms and Biofilm Production

Giorgia Palladini et al. Mycoses. 2025 Sep.

Abstract

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.

Keywords: C. parapsilosis; ERG11; Italy; Y132F; biofilm; fluconazole resistance.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
UPGMA (unweighted pair group method with arithmetic mean) dendrogram based on microsatellite genotyping of 169 Candida parapsilosis isolates collected from two hospitals (Pavia and Piacenza). The dendrogram illustrates the distribution of isolates into five major clusters (I–V) and 13 sub‐clusters, comprising isolates with identical multilocus genotypes. R1–R5 (in red) represent sub‐clusters of fluconazole‐resistant isolates; S1–S8 (in green) represent sub‐clusters of fluconazole‐susceptible isolates. Isolates from Pavia are labelled with the prefix ‘PV’, whereas those from Piacenza are identified by sequential numbers only. Fluconazole‐resistant isolates (n = 124) are identified with the final letter ‘R’ and fluconazole‐susceptible isolates (n = 45) with ‘S’.
See this image and copyright information in PMC

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