Abstract
Candida glabrata is an opportunistic human fungal pathogen that causes superficial mucosal and life-threatening bloodstream infections in individuals with a compromised immune system. Evolutionarily, it is closer to the non-pathogenic yeast Saccharomyces cerevisiae than to the most prevalent Candida bloodstream pathogen, C. albicans. C. glabrata is a haploid budding yeast that predominantly reproduces clonally. In this review, we summarize interactions of C. glabrata with the host immune, epithelial and endothelial cells, and the ingenious strategies it deploys to acquire iron and phosphate from the external environment. We outline various attributes including cell surface-associated adhesins and aspartyl proteases, biofilm formation and stress response mechanisms, that contribute to the virulence of C. glabrata. We further discuss how, C. glabrata, despite lacking morphological switching and secreted proteolytic activity, is able to disarm macrophage, dampen the host inflammatory immune response and replicate intracellularly.
Highlights
Candida glabrata is an opportunistic human fungal pathogen that accounts for up to 29% of total Candida bloodstream infections [1,2]
While C. glabrata is the second most common bloodstream Candida species after C. albicans in Northern Europe and the USA [1,5,6], it ranks as the third or fourth most prevalent invasive Candida pathogen in Asia [4,6,7]
C. glabrata contains orthologs of 4870 S. cerevisiae genes [https: //yeastmine.yeastgenome.org/], it possesses a set of 337 genes that are absent in S. cerevisiae [23]. Both C. glabrata and S. cerevisiae belong to the Whole Genome Duplication (WGD) group, and are assumed to have arisen from the same tetraploid hybrid ancestor, which existed about 100-200 million years ago [18]
Summary
Candida glabrata is an opportunistic human fungal pathogen that accounts for up to 29% of total Candida bloodstream infections [1,2]. While C. glabrata is the second most common bloodstream Candida species after C. albicans in Northern Europe and the USA [1,5,6], it ranks as the third or fourth most prevalent invasive Candida pathogen in Asia [4,6,7]. Based on molecular evolutionary studies, C. glabrata was later assigned to the genus Nakaseomyces [13]. C. glabrata is primarily diagnosed via culture-based assays viz., colony color (white/pink/purple) on CHROMagar Candida medium and microscopic examination [presence of small-sized (1–4 μm) yeast cells and lack of hyphal structures], and biochemical methods, viz., assimilation of glucose and trehalose sugars [14]. We provide an overview of C. glabrata-host cell interaction mechanisms
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