Candida vulvovaginitis pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
Line 16: Line 16:
<gallery>
<gallery>
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
Image:speculum_vagina.jpg|left|thumb|350px|This photograph is a speculum examination of the vagina with Candida infection and the typical thick, curdy vaginal discharge.


Image:Renal candidiasis 001.jpg|left|thumb|350px|This autopsy photograph of the kidneys demonstrates the multifocal punctate lesions visible on the serosal surface (arrows). Don't confuse these small yellow punctate lesions with the fat that is adherent to the renal capsule.
Image:Renal candidiasis 001.jpg|left|thumb|350px|This autopsy photograph of the kidneys demonstrates the multifocal punctate lesions visible on the serosal surface (arrows). Don't confuse these small yellow punctate lesions with the fat that is adherent to the renal capsule.

Revision as of 16:41, 20 October 2016

Candidiasis Main page

Patient Information

Overview

Causes

Classification

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]

Overview

Pathophysiology

Pathogenesis

  • All strains of C. albicans possess a yeast surface mannoprotein. This allows the various strains to adhere to both the exfoliated and buccal epithelial cells of the vagina.[1][2]
  • Several virulence factors of Candida are implicated in vulvovaginitis. These include proteolytic enzymes, toxins and phospholipase. Proteolytic enzymes destroy the proteins that normally impair fungal invasion, allowing for Candida to colonize the vagina.[1][2][3]
  • The understanding of the transition from asymptomatic vaginal colonization with Candida to symptomatic vulvovaginitis is not clear.[2][3]

Genetics

Genetic factors could be involved in the pathophysiology of Candida vulvovaginitis. Supporting evidence is that many cases were found to be more common in African-American women, run in families, as well as being associated with ABO-Lewis non-secretor phenotype, a rare blood group. In addition, women with Candida vulvovaginitis were found to have decreased concentrations of mannose binding lectin (MBL), hence, the variant (MBL) gene is thought to be a contributing factor in the development of Candida vulvovaginitis.[1][4][5]

Gross Pathology

  • This photograph is a speculum examination of the vagina with Candida infection and the typical thick, curdy vaginal discharge.

    This photograph is a speculum examination of the vagina with Candida infection and the typical thick, curdy vaginal discharge.

  • This autopsy photograph of the kidneys demonstrates the multifocal punctate lesions visible on the serosal surface (arrows). Don't confuse these small yellow punctate lesions with the fat that is adherent to the renal capsule.

    This autopsy photograph of the kidneys demonstrates the multifocal punctate lesions visible on the serosal surface (arrows). Don't confuse these small yellow punctate lesions with the fat that is adherent to the renal capsule.

  • This photograph of the cut surface of these kidneys shows that these multifocal punctate lesions are primarily in the cortex (arrows).

    This photograph of the cut surface of these kidneys shows that these multifocal punctate lesions are primarily in the cortex (arrows).

Microscopic Pathology

  • This is a low-power photomicrograph of lymph node with three prominent areas of Candida colonies (arrows). Even at this low magnification, the purple-staining yeast and pseudohyphae can be easily seen. This section was stained with Periodic Acid-Schiff Hematoxylin (PASH), which stains the cell wall of fungi to make them more easily visible.]]

    This is a low-power photomicrograph of lymph node with three prominent areas of Candida colonies (arrows). Even at this low magnification, the purple-staining yeast and pseudohyphae can be easily seen. This section was stained with Periodic Acid-Schiff Hematoxylin (PASH), which stains the cell wall of fungi to make them more easily visible.]]

  • This high-power photomicrograph shows the yeasts (1) and pseudohyphae (2).

    This high-power photomicrograph shows the yeasts (1) and pseudohyphae (2).

  • This is a low-power photomicrograph of the kidney from this same case. Note the Candida colonies (arrows). The pseudohyphae are evident around the periphery of these colonies even at this low magnification.

    This is a low-power photomicrograph of the kidney from this same case. Note the Candida colonies (arrows). The pseudohyphae are evident around the periphery of these colonies even at this low magnification.

  • This is a higher-power photomicrograph of a Candida colony in the kidney. Note the pseudohyphae of the Candida organisms.

    This is a higher-power photomicrograph of a Candida colony in the kidney. Note the pseudohyphae of the Candida organisms.

Associated Conditions

  • Candida vulvovaginitis may be associated with other pathogens that cause vulvovaginitis. These include Trichomonas vaginalis and Gardnerella vaginalis. The association may be a mixed infection, where 2 or more pathogens are symptomatic, or a co-infection, in which there are 2 or more pathogens but some are not symptomatic.[6][7]

References

  1. ↑ 1.0 1.1 1.2 Sobel JD (2007). "Vulvovaginal candidosis". Lancet. 369 (9577): 1961–71. doi:10.1016/S0140-6736(07)60917-9. PMID 17560449.
  2. ↑ 2.0 2.1 2.2 Sobel JD (1985). "Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis". Am. J. Obstet. Gynecol. 152 (7 Pt 2): 924–35. PMID 3895958.
  3. ↑ 3.0 3.1 Sobel JD (1989). "Pathogenesis of Candida vulvovaginitis". Curr Top Med Mycol. 3: 86–108. PMID 2688924.
  4. ↑ Liu F, Liao Q, Liu Z (2006). "Mannose-binding lectin and vulvovaginal candidiasis". Int J Gynaecol Obstet. 92 (1): 43–7. doi:10.1016/j.ijgo.2005.08.024. PMID 16256117.
  5. ↑ Donders GG, Babula O, Bellen G, Linhares IM, Witkin SS (2008). "Mannose-binding lectin gene polymorphism and resistance to therapy in women with recurrent vulvovaginal candidiasis". BJOG. 115 (10): 1225–31. doi:10.1111/j.1471-0528.2008.01830.x. PMID 18715406.
  6. ↑ Sobel JD, Subramanian C, Foxman B, Fairfax M, Gygax SE (2013). "Mixed vaginitis-more than coinfection and with therapeutic implications". Curr Infect Dis Rep. 15 (2): 104–8. doi:10.1007/s11908-013-0325-5. PMID 23354954.
  7. ↑ Anderson MR, Klink K, Cohrssen A (2004). "Evaluation of vaginal complaints". JAMA. 291 (11): 1368–79. doi:10.1001/jama.291.11.1368. PMID 15026404.



Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Candida_vulvovaginitis_pathophysiology&oldid=1262699"