Oral candidiasis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]


Candida is a normal commensal of the skin and mucous membranes. The balance between the virulence of the fungus and the host immune defense is responsible avoiding opportunistic infection of candida. Deficiency of cell-mediated immunity or poor general status are the main risk factors for having opportunistic candidiasis. Candidiasis is usually localized to skin and mucous membranes. In rare cases, candidiasis can spread causing candidemia and distant infection. These cases are usually associated with deficient immunity . C. albicans is the main species causing infection in humans more than any other candida species.



Candida is a normal commensal of skin and mucous membranes. A competent immune system and an intact regenerating healthy skin prevent the virulence of Candida.

Candida Virulence factors

The main virulence factors that mediate the infection:[1]

Any condition that compromises cell-mediated immunity, worsens the general status of the patient or provide a favorable medium for Candida to form biofilms put the patient at increased risk for having candidiasis.[2]

Candidal gene VPS4 plays an important role in mucosal candidiasis specifically. Moreover, fungi with mutations affecting this gene were found to be less virulent.[3][4]

Gross Pathology

Pseudomembranous candidiasis:

On speculum examination typical curdy white discharge is present. Usually present in newborns or in patients with deficient immunity, administering corticosteroids, etc.

Atrophic candidiasis:

Appears as erythema or edema without the characteristic white plaques. Usually, seen in patients with dental dentures.[5]

Chronic hyperplastic candidiasis (Candidal leukoplakia):

Persistent tough, adherent, white lesions that are indistinguishable from other leukoplakia except through biopsy. Seen more in smokers, patients with iron deficiency anemia or deficient cell-mediated immunity.[6][5]

Chronic mucocutaneous candidiasis (CMCC):

Microscopic pathology:

Candida albicans - By Y tambe - Y tambe's file, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=233284


  • Microscopic examination of the wet mount with 10% KOH or saline demonstrates hyphae, pseudohyphae, and blastospores.




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  2. Pappas PG (2006). "Invasive candidiasis". Infect. Dis. Clin. North Am. 20 (3): 485–506. doi:10.1016/j.idc.2006.07.004. PMID 16984866.
  3. Rane HS, Hardison S, Botelho C, Bernardo SM, Wormley F, Lee SA (2014). "Candida albicans VPS4 contributes differentially to epithelial and mucosal pathogenesis". Virulence. 5 (8): 810–8. doi:10.4161/21505594.2014.956648. PMID 25483774.
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  5. 5.0 5.1 Lynch DP (1994). "Oral candidiasis. History, classification, and clinical presentation". Oral Surg. Oral Med. Oral Pathol. 78 (2): 189–93. PMID 7936588.
  6. "CHRONIC HYPERPLASTTC CANDIDIASIS—CANDIDAL LEUKOPLAKIA - CAWSON - 1968 - British Journal of Dermatology - Wiley Online Library".
  7. Puel A, Cypowyj S, Bustamante J, Wright JF, Liu L, Lim HK, Migaud M, Israel L, Chrabieh M, Audry M, Gumbleton M, Toulon A, Bodemer C, El-Baghdadi J, Whitters M, Paradis T, Brooks J, Collins M, Wolfman NM, Al-Muhsen S, Galicchio M, Abel L, Picard C, Casanova JL (2011). "Chronic mucocutaneous candidiasis in humans with inborn errors of interleukin-17 immunity". Science. 332 (6025): 65–8. doi:10.1126/science.1200439. PMC 3070042. PMID 21350122.
  8. Eyerich K, Foerster S, Rombold S, Seidl HP, Behrendt H, Hofmann H, Ring J, Traidl-Hoffmann C (2008). "Patients with chronic mucocutaneous candidiasis exhibit reduced production of Th17-associated cytokines IL-17 and IL-22". J. Invest. Dermatol. 128 (11): 2640–5. doi:10.1038/jid.2008.139. PMID 18615114.
  9. "Public Health Image Library (PHIL)".

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