2026/02/18 by Charlie J. D. Holt, Catrin C. Wiliams, Jane Usher · 1 voice
Agricultural and Biological Sciences · Immunology and Microbiology · Medicine · #Antifungal resistance and susceptibility #Coccidia and coccidiosis research #Parasitic Infections and Diagnostics
paper · doi:10.1099/jmm.0.002127
openalex publication_date 2026/02/18 · openalex created_date 2026/02/19 · openalex updated_date 2026/07/22
Candida glabrata is an opportunistic fungal pathogen and a leading cause of invasive candidiasis, particularly in immunocompromised patients, where treatment is increasingly compromised by intrinsic and acquired antifungal resistance. Despite lacking morphological plasticity, C. glabrata employs distinct virulence strategies, including adhesin-mediated host colonization, intracellular survival within phagocytes, stress tolerance, iron acquisition and biofilm formation. This review synthesizes current knowledge of C. glabrata virulence and antifungal resistance mechanisms, with a particular focus on azole and echinocandin resistance driven by efflux pump regulation and FKS mutations. We critically evaluate the greater wax moth larva, Galleria mellonella , as a non-mammalian in vivo model for studying C. glabrata pathogenesis, host–pathogen interactions and antifungal efficacy. Evidence demonstrating concordance between G. mellonella , murine models and clinical outcomes is discussed, alongside the model’s limitations, including the absence of adaptive immunity. Collectively, this review highlights G. mellonella as a robust, cost-effective platform for dissecting C. glabrata virulence traits and for preclinical screening of antifungal therapies, supporting its growing role in translational fungal research.