Candidiasis and the mechanism of action for anti-Candida compounds

Candidiasis is a fungal infection caused by yeast belonging to the genus Candida and results in both superficial and systemic infections. The most common type of candidiasis is a superficial infection of the vagina, skin, or mouth presenting with red or white patches, irritation, and itching. Superficial infections of the skin or mucous membranes may enter the bloodstream and cause systemic Candida infections. Infections can evolve into disseminated candidiasis by spreading to other organs, including the central nervous system, liver, eyes, kidneys, and bones. Candida albicans is the most common pathogen of cutaneous and oropharyngeal candidiasis. For candidiasis treatment, various antimicrobial agents are used, such as polyenes and azoles, as well as novel antimicrobial compounds including natural products or antimicrobial peptides. These compounds have been reported to target the cytoplasmic membrane, RNA, DNA, proteins and cell wall synthesis. Apart from targeting cell constituents, the formation of hydroxyl radicals and disruption of ion homeostasis leads to fungal cell death via apoptosis. In C. albicans, apoptotic mechanisms are valuable as major strategies with several characteristics such as phosphatidylserine exposure, DNA fragmentation, and activation of metacaspase. Studying antifungal agents with varying mechanisms of action can be effective in appropriately treating potentially fatal candidiasis.