Candida parapsilosis

Candida parapsilosis was discovered in Puerto Rico in 1928 by Ashford from a diarrheal stool. It was first named Monilia parapsilosis and considered nonpathogenic.^[1] It was later encountered as a causative agent of sepsis in an intravenous drug user in 1940.^[1] It is now considered an important, emerging nosocomial pathogen.^[2] C. parapsilosis is the most common non-C. albicans species of Candida^[3] and the second most common pathogen in superficial candidiasis after C. albicans.^[4]

Candida parapsilosis does not form true hyphae; it exists in either a yeast phase or pseudohyphal form.^[1] It is white, creamy, and shiny in dextrose agar and its cell shape is oval, round, or cylindrical.^[1] When C. parapsilosis is in yeast form, its phenotype is smooth or cratered. In contrast, the phenotype of the pseudohyphae form is wrinkled or concentric.^[1] Recently found the formation of pseudohyphae is another significant factor that changes the morphology and phenotype of colonies which is related to citrulline.^{[clarification needed][1]} C. parapsilosis is encountered more frequently in nature than other species Candida, likely because it is one of the few species of the genus not restricted to humans.^[1] C. parapsilosis does not need prior colonization and is usually transmitted by external sources.^[1] Invasive infection occurs very often in low-birth weight newborn babies in the United States, and bloodstream infection found in North America.^[1] It is most commonly isolated from human skin^[2] and is most frequently encountered in Asia and Latin America.^[4] C. parapsilosis is considered a killer yeast and fungal antagonist based on its ability to produce chemicals that exert cytotoxic effects on the cells of other organisms.^[5]

Endocarditis can be caused by C. parapsilosis in patients using prosthetic valves (57.4%), intravenous drug (20%), or having intravenous parenteral nutrition (6.9%), abdominal surgery (6.9%), immunosuppression (6.4%), treatment with broad-spectrum antibiotics (5.6%), and previous valvular disease (4.8%). Although the mortality rate is 41.7% to 61%, the treatment is still unknown.^[1] Ocular infection caused by C. parapsilosis has been reported after cataract extraction and with corticosteroid eye drop use.^[1] C. parapsilosis infection of the skin and gastrointestinal tract^[1] can occur, in which the production of pseudohyphae is associated with the elicitation of an inflammatory response.^[3] Candida parapsilosis is occasionally encountered in onychomycosis.^[6][7][8]

Adhesion capacity and biofilm are important for C. parapsilosis, because C. parapilosis infection is mostly due to the use of in-dwelling devices.^[9] Adhesion capacity is the ability of fungus to adhere to other organisms' cells or tissue, especially mucosal surfaces,^[1] which is required for initial colonization.^[10] C. parapsilosis is associated with thin, unstructured biofilms that consist of aggregated blastospores whose membranes contain more carbohydrate than protein.^[10] The existence of the fungus in a biofilm contributes to its ability to resist antifungal treatment.^[1][9] Thus, adhesion to abiotic and biotic surfaces is often a precursor to infection.^[11] The risk of C. parapsilosis infection is increased in the setting of implanted medical devices, prostheses, and therapy with hyperalimentation solutions.^[1] Also, low-birth weight infants are at higher risk of sepsis from this species.^[12]