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Inter-Hospital Spread of Fluconazole-Resistant C. parapsilosis in Northern Italy: Insights Into Clonal Distribution,
Giorgia Palladini1, Valentina Lepera1, Serena Trubini2
1Department of Laboratory Medicine, Microbiology Unit, AUSL Piacenza, Piacenza, Italy.
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.
Insights
Fluconazole-resistant Candida parapsilosis (FRCP) strains, often linked to the Y132F mutation, are spreading globally. These resistant strains may produce less biofilm, potentially aiding their survival and spread in healthcare settings.
Area of Science:
- Medical Mycology
- Antimicrobial Resistance
- Molecular Epidemiology
Background:
- Global rise in fluconazole-resistant Candida parapsilosis (FRCP) outbreaks since 2018.
- Need to understand the genetic and phenotypic characteristics of FRCP.
Purpose of the Study:
- Investigate FRCP isolates from Northern Italy (2018-2024).
- Determine the prevalence of antifungal resistance, ERG11 mutations, and genetic relatedness.
- Assess biofilm formation in relation to resistance mechanisms.
Main Methods:
- Retrospective analysis of 169 Candida parapsilosis blood isolates.
- Antifungal susceptibility testing.
- ERG11 gene sequencing.
- Multilocus microsatellite typing.
- Biofilm formation assays.
Main Results:
- 73.4% of isolates were fluconazole-resistant (FRCP).
- The Y132F mutation in ERG11 was prevalent in FRCP (95.2%) and absent in susceptible isolates.
- Microsatellite typing identified distinct clusters, with one cluster (R1) dominated by Y132F-mutated FRCP.
- FRCP with Y132F mutation predominantly formed low biofilms (99.1%).
Conclusions:
- The Y132F mutation is a key driver of azole resistance and inter-hospital spread in Candida parapsilosis.
- FRCP strains causing severe outbreaks exhibit reduced biofilm formation, possibly a survival advantage.
- Understanding resistance mechanisms and biofilm phenotypes is crucial for managing FRCP infections.
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