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Pathophysiology
Vaginal Defensive mechanisms aganist Candida
Innate Mechanisms
| Defense | Mechanism of protection | Evidence of protection |
|---|---|---|
| Epithelial cells | ||
| Mannose-binding lectin |
|
|
| Vaginal bacterial flora |
|
|
| Phagocytic systems/polymononuclear leukocytes, mononuclear cells, complement |
|
|
Adaptive Mechanisms
| Defense | Mechanism | Role in Protection |
|---|---|---|
| Immunoglobulin mediated immunity | Systemic IgM, IgG, and local IgA antibodies are produced in response to the infection[5] | |
| Cell Mediated Immunity |
Interleukin 4 (Th2) inhibits anti-Candida activity of nitric oxide and protective pro-inflammatory Th1 cytokines.[7] |
|
Candida Virulence Factors
- C. albicans exists as blastospores, germ tubes, pseudomycelia, true mycelia and chlamydospores on special culture media. C. glabrata exists exclusively in blastospores.
- All strains of Candida species possess a yeast surface mannoprotein which helps in adhering to epithelial cells of the vagina.[9][10]
- Germination of the spores helps in colonizing the vagina.[11]
- Proteolytic enzymes, toxins and phospholipase destroy the proteins that normally impair fungal invasion, enhancing the ability of Candida to colonize the vagina.[9][10][12][13]
- Phenotypic switching of Candida is described in patients with recurrent vaginitis.[14]
- C. albicans can form biofilms on the intrauterine devices or sponges, causing disease recurrence.[15]
Pathogenesis
- Candida vulvovaginitis is a microbial disease and not all patients with detectable pathogen are symptomatic. Multiple risk factors and the imbalance in the protective vaginal defenses predispose patients to develop active disease.
- Candida vaginal infections are more common in the reproductive age group because of the high concentration of estrogen as it increases the amount of glycogen in the vagina providing a carbon source for Candida organisms to colonize. It also increases the adherence of Candida to the vaginal epithelial cells.[16]
- The most common source of the infection is from the perianal area. Other less common source is sexual transmission and persistence of organisms in the vagina after treatment which is responsible for recurrence.[17]
- The initial step of infection is colonization and symptoms appear with the invasion of the blastospores or pseudohyphae of the vaginal wall.[18]
- The understanding of the transition from asymptomatic vaginal colonization with Candida to symptomatic vulvovaginitis is not clear.[10][12]
References
- ↑ Barousse MM, Espinosa T, Dunlap K, Fidel PL (2005). "Vaginal epithelial cell anti-Candida albicans activity is associated with protection against symptomatic vaginal candidiasis". Infect Immun. 73 (11): 7765–7. doi:10.1128/IAI.73.11.7765-7767.2005. PMC 1273905. PMID 16239581.
- ↑
- ↑ Ip WK, Lau YL (2004). "Role of mannose-binding lectin in the innate defense against Candida albicans: enhancement of complement activation, but lack of opsonic function, in [[phagocytosis]] by human dendritic cells". J Infect Dis. 190 (3): 632–40. doi:10.1086/422397. PMID 15243942. URL–wikilink conflict (help)
- ↑ Diamond RD, Krzesicki R, Jao W (1978). "Damage to pseudohyphal forms of Candida albicans by neutrophils in the absence of serum in vitro". J Clin Invest. 61 (2): 349–59. doi:10.1172/JCI108945. PMC 372545. PMID 340470.
- ↑ Waldman RH, Cruz JM, Rowe DS (1972). "Immunoglobulin levels and antibody to Candida albicans in human cervicovaginal secretions". Clin Exp Immunol. 10 (3): 427–34. PMC 1713147. PMID 4556009.
- ↑ Fidel PL, Sobel JD (1996). "Immunopathogenesis of recurrent vulvovaginal candidiasis". Clin Microbiol Rev. 9 (3): 335–48. PMC 172897. PMID 8809464.
- ↑ Fidel PL (2005). "Immunity in vaginal candidiasis". Curr Opin Infect Dis. 18 (2): 107–11. PMID 15735412.
- ↑ Fidel PL, Barousse M, Espinosa T, Ficarra M, Sturtevant J, Martin DH; et al. (2004). "An intravaginal live Candida challenge in humans leads to new hypotheses for the immunopathogenesis of vulvovaginal candidiasis". Infect Immun. 72 (5): 2939–46. PMC 387876. PMID 15102806.
- ↑ 9.0 9.1 Sobel JD (2007). "Vulvovaginal candidosis". Lancet. 369 (9577): 1961–71. doi:10.1016/S0140-6736(07)60917-9. PMID 17560449.
- ↑ 10.0 10.1 10.2 Sobel JD (1985). "Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis". Am. J. Obstet. Gynecol. 152 (7 Pt 2): 924–35. PMID 3895958.
- ↑ Sobel JD, Muller G, Buckley HR (1984). "Critical role of germ tube formation in the pathogenesis of candidal vaginitis". Infect Immun. 44 (3): 576–80. PMC 263631. PMID 6327527.
- ↑ 12.0 12.1 Sobel JD (1989). "Pathogenesis of Candida vulvovaginitis". Curr Top Med Mycol. 3: 86–108. PMID 2688924.
- ↑ Schaller M, Bein M, Korting HC, Baur S, Hamm G, Monod M; et al. (2003). "The secreted aspartyl proteinases Sap1 and Sap2 cause tissue damage in an in vitro model of vaginal candidiasis based on reconstituted human vaginal epithelium". Infect Immun. 71 (6): 3227–34. PMC 155757. PMID 12761103.
- ↑ Soll DR (1988). "High-frequency switching in Candida albicans and its relations to vaginal candidiasis". Am J Obstet Gynecol. 158 (4): 997–1001. PMID 3284370.
- ↑ Muzny CA, Schwebke JR (2015). "Biofilms: An Underappreciated Mechanism of Treatment Failure and Recurrence in Vaginal Infections". Clin Infect Dis. 61 (4): 601–6. doi:10.1093/cid/civ353. PMC 4607736. PMID 25935553.
- ↑ Dennerstein GJ, Ellis DH (2001). "Oestrogen, glycogen and vaginal candidiasis". Aust N Z J Obstet Gynaecol. 41 (3): 326–8. PMID 11592551.
- ↑ Miles MR, Olsen L, Rogers A (1977). "Recurrent vaginal candidiasis. Importance of an intestinal reservoir". JAMA. 238 (17): 1836–7. PMID 333134.
- ↑ Fidel PL, Vazquez JA, Sobel JD (1999). "Candida glabrata: review of epidemiology, pathogenesis, and clinical disease with comparison to C. albicans". Clin Microbiol Rev. 12 (1): 80–96. PMC 88907. PMID 9880475.