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Classification: (1)
Candidiasis can be classified according to the site of infection into:
Localoized mucocutaneous:
Oropharyngeal candidiasis Esophageal candidiasis Candida vulvovaginitis
Invasive Candidiasis: More serious and usually presenting in an immunocompromised host.
Candidaemia Candida endophthalmitis Candida endocarditis Candida osteoarticular disease
Pathophysiology:
Pathogenesis
Candida is a normal commensal of skin and mucous membranes. A competent immune system and an intact regenerating healthy skin prevent inavasion of Candida.
The main virulence factors that mediate the infection: (2) Secreting molecules that mediate adherence into host cells Production of hydrolases which has a lytic effect on tissues and facilitate the invasion by the bacteria. Polymorphism: Candida has the ability to grow either as pseudohyphae (elongated elipsoid form) or in a yeast form (rounded to oval budding form. While the role of polymorphism is not clearly understood in the virulence of Candida, it’s noted that species capable of producing the most severe form of the disease has this ability. Biofilm production: which means the ability to form a thick layer of the organism on the mucosal surfaces or even abiotic surfaces as catheters and dentures.
Patients with invasive candidiasis usually have deficient cell mediated immunity whether specific deficiency against candida or generalized T cell deficiency as in DiGeorge syndrome, Wiscot-Aldrich syndrome and ataxia-telengictasia.
Patients was candida vulvovaginitis were found to have decreased levels of mannose binding lectins (MBL) . Further investigations revealed that 2 genetic mutations in genes responsible for MBL and IL4 production increase the host susceotibility of getting recurrent candidal vulvovaginitis.(3)
Gross picture
In mucocutaneous candidiasis, Candida presents as curdy White lesions.
Microscopic picture
Microscopic examination of the wet mount with 10% KOH or saline demonstrates hyphae, pseudohyphae and blastospores.