Candida glabrata (C. glabrata)

Candida glabrata is a haploid, nondimorphic yeast (existing only as blastoconidia) that acts as an opportunistic fungal pathogen, ranking as the second most common cause of candidiasis after Candida albicans, particularly in immunocompromised patients such as those with AIDS, cancer, diabetes, or undergoing immunosuppressive therapy. It colonizes mucosal surfaces (mouth, gastrointestinal tract, vagina, skin) as a commensal but can cause superficial (oropharyngeal, esophageal, vaginal, urinary) or invasive bloodstream infections (candidemia) with high mortality. Key virulence factors include strong adherence via adhesins (EPA and GPI proteins), biofilm formation, secretion of hydrolytic enzymes (phospholipases, proteases, haemolysins, yapsins), cell wall hydrophobicity, chitin synthesis for structural integrity, and immune evasion through macrophage survival and neutrophil resistance. It exhibits intrinsic resistance to azoles due to ergosterol pathway modifications (e.g., ERG2, ERG6, ERG11 mutations), efflux pumps, and mitochondrial adaptations, complicating therapy; guidelines recommend echinocandins or amphotericin B initially, with step-down to high-dose fluconazole or voriconazole for susceptible strains.[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15]

Other names

Nakaseomyces glabrataC. glabrata

Ergosterol biosynthesis inhibition (azoles targeting ERG11, ERG6, ERG2), Cell wall beta-glucan synthesis inhibition (echinocandins), Membrane disruption (amphotericin B), DNA/RNA synthesis inhibition (flucytosine)