Giorgia Palladini

Dr. Giorgia Palladini

orcid

Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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12 September 2025 in Mycoses
Verified
Journal Article
Open access
GPGiorgia Palladini
Giorgia Palladini
VLValentina Lepera
Valentina Lepera
STSerena Trubini
Serena Trubini
GTGabriella Tocci
Gabriella Tocci
AZAndrea Zappavigna
Andrea Zappavigna
GCGiuliana Lo Cascio
Giuliana Lo Cascio
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.

2 July 2025 in Microbiology Research
Verified
Journal Article
Open access
PDF file
VLValentina Lepera
Valentina Lepera
NTN/A Tocci
N/A Tocci
GPGiorgia Palladini
Giorgia Palladini
MAMarco Enrico Giovanni Arosio
Marco Enrico Giovanni Arosio
Claudio FarinaClaudio Farina
Claudio Farina
UPUte Panzenboeck
Ute Panzenboeck
Background: Trichophyton indotineae, a new emerging pathogen according to the WHO, is known to cause severe forms of tinea. Given that traditional identification methods rely on morphological characteristics, and the morphological distinctions among T. indotineae, T. mentagrophytes, and T. interdigitale are minimal, the adoption of alternative diagnostic techniques, such as RT-PCR or gene sequencing, has become critically important to prevent misidentification. The purpose of this study was firstly to analyze the local epidemiology of dermatophytes isolated and secondly to investigate the presence of T. indotineae among the isolated strains. Methods: Between January 2021 and June 2024, 1096 samples of skin adnexa were analysed. The isolated strains belonging to the genus Trichophyton were submitted to molecular identification by ITS sequencing, and T. indotineae strains were subjected to squalene epoxidase (SQLE) sequencing analysis. Results: Trichophyton rubrum and Trichophyton interdigitale appear to be the most prevalent pathogenic species. Molecular identification reveals four T. indotineae strains (4/87; 4.61%) from Asian patients, which were also characterized by gene mutations associated with terbinafine resistance. Conclusions: This study has made it clear that there is a need to implement basic mycological diagnostics with molecular methods to avoid misidentifications, ensure the correct identification, and evaluate the presence of mutations associated with antifungal drug resistance.