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The epidemiology data for candidiasis indicate an increase in Candida glabrata infections. Moreover, several reports have shown an increasing number of drug-resistant cases of these infections. The source of drug resistance can often be traced to genetic mutations in genes related to a drug's mechanism of action. Therefore, we conducted whole genome sequencing of several drug-resistant isolates of Candida glabrata collected from patients hospitalized in Eastern Poland to assess whether mutations in selected genes correlated with susceptibility analysis results. The fungal species from patient samples were identified, and the isolated Candida glabrata were subjected to antifungal drug susceptibility testing. The results were interpreted according to the EUCAST and CLSI recommendations. Susceptibility to 5-flucytosine was assessed using the ATB FUNGUS kit. Libraries were prepared according to the NEXTERA XT DNA Library Prep and subsequently sequenced. The outcomes indicated common resistance to two of the three analyzed echinocandins, as well as two cases of simultaneous resistance to echinocandins and selected azole-based drugs. We detected several previously reported mutations in selected resistance-related genes, as well as five that are first described here: ERG5 (M267I), ERG6 (R57K), PDH1 (K438Q, V434I, F600V, V1192S), FCY1 (M129T), and FCY2 (I384F). Neither of the identified nonsynonymous mutations was correlated with the drug resistance demonstrated in the susceptibility testing. Furthermore, we can exclude the possibility of acquired drug resistance, thereby raising questions about the possibility of unknown mechanisms of resistance to azole-based and echinocandin drugs.
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http://dx.doi.org/10.1007/s12223-025-01298-w | DOI Listing |
mBio
September 2025
Department of Biology, Laboratory of Molecular Cell Biology, KU Leuven, Leuven, Flanders, Belgium.
Echinocandins, which target the fungal β-1,3-glucan synthase (Fks), are essential for treating invasive fungal infections, yet resistance is increasingly reported. While resistance typically arises through mutations in Fks hotspots, emerging evidence suggests a contributing role of changes in membrane sterol composition due to mutations. Here, we present a clinical case of () in which combined mutations in and , but not alone, appear to confer echinocandin resistance.
View Article and Find Full Text PDFCurr Pharm Des
August 2025
Department of Pharmaceutics, Noida Institute of Engineering and Technology (Pharmacy Institute), Greater Noida-Uttar Pradesh, 201306, India.
The main culprit behind cutaneous candidiasis, a fungal infection that can lead to major dermatological and systemic health problems, is Candida albicans. Over the past 20 years, cutaneous candidiasis has become more prevalent, especially in hospitalized or immunocompromised patients. Conventional treatment methods employ antifungal drugs like azoles and polyenes, which are effective but have drawbacks because of their high recurrence rates, negative side effects, and growing antifungal resistance.
View Article and Find Full Text PDFObjectives: (formerly ) is a leading cause of invasive candidiasis and rapidly develops antifungal drug resistance during treatment. An increasing number of clinical isolates shows reduced susceptibility to echinocandins and azoles, leaving amphotericin B (AMB) as a last therapeutic option. Resistance of to this drug is rare and its underlying mechanisms are still not fully understood.
View Article and Find Full Text PDFIndian J Med Microbiol
September 2025
Department of Microbiology, All India Institute of Medical Sciences, Raipur, C.G, India. Electronic address:
Purpose: Pemphigus vulgaris (PV) is a chronic immunobullous disorder treated with high doses of immunosuppressants. Oral candidiasis (OC) is the most common opportunistic infection reported in PV. Previous studies have shown variability in species distribution and the emergence of multidrug-resistant Candida species in PV.
View Article and Find Full Text PDFClin Microbiol Rev
September 2025
Division of Infectious Diseases, Escola Paulista de Medicina-Universidade Federal de São Paulo, São Paulo, Brazil.
SUMMARYMany yeast species causing life-threatening invasive infections that were formerly classified in the genus have been reclassified due to their evolutionary and phylogenetic relationships elucidated by DNA sequencing methods that are increasingly using whole genomes. This review explores the evolving taxonomy, epidemiology, and clinical implications of clinically relevant, rare, emerging and Saccharomycotina yeasts that have recently been reclassified from . This article highlights the urgent need for intensified research efforts to enhance knowledge and improve outcomes in the management of infections caused by these yeasts.
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