Candida parapsilosis (C. parapsilosis)

Candida parapsilosis is a significant opportunistic fungal pathogen and a leading cause of invasive candidiasis worldwide, particularly affecting neonates, transplant recipients, and individuals with indwelling medical devices [4, 12]. As a member of the non-albicans Candida (NAC) group, it is characterized by its high capacity for biofilm formation on catheters and its frequent transmission via the hands of healthcare workers [2, 9]. Pathologically, it causes conditions ranging from superficial skin infections to life-threatening fungemia, endocarditis, and sepsis [4, 9, 13]. Unlike Candida albicans, C. parapsilosis often exhibits a naturally reduced susceptibility to echinocandin antifungals due to polymorphisms in the FKS1 gene [1, 5]. Therapeutic management typically involves the use of azoles, echinocandins, or polyenes, which target essential fungal components like the cell wall and the ergosterol biosynthetic pathway [2, 6, 7]. The emergence of drug-resistant strains, particularly those with ERG11 and acquired FKS1 mutations, poses a significant challenge in clinical settings [1, 6, 12]. Research into its unique virulence factors, such as secreted aspartic proteases and phospholipases, continues to provide insights for novel drug development [9, 14].

Other names

Monilia parapsilosisCandida parapsilosis sensu stricto

Antifungal drugs used to treat this organism act via several distinct mechanisms: (1) azoles (e.g., fluconazole, voriconazole) inhibit the fungal enzyme lanosterol 14-alpha-demethylase (CYP51), disrupting ergosterol synthesis; (2) echinocandins (e.g., micafungin, caspofungin) inhibit 1,3-beta-D-glucan synthase, compromising cell wall integrity; and (3) polyenes (e.g., amphotericin B) bind directly to ergosterol in the fungal cell membrane, creating pores that lead to cell death [1, 2, 6, 7].