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Candida Vulvovaginitis

Historical Perspective

B. Lagenbeck in 1839 in Germany was the first to demonstrate that a yeast-like fungus existed in the human oral infection "thrush." He also found that a fungus was able to cause thrush.[1]

The genera Candida, species albicans was described by botanist Christine Marie Berkhout. She described the fungus in her doctoral thesis, at the University of Utrecht in 1923. Over the years the classification of the genera and species has evolved. Obsolete names for this genus include Mycotorula and Torulopsis. The species has also been known in the past as Monilia albicans and Oidium albicans. The current classification is nomen conservandum, which means the name is authorized for use by the International Botanical Congress (IBC).

The full current taxonomic classification is available at Candida albicans.

The genus Candida includes about 150 different species. However, only a few of those are known to cause human infections. C. albicans is the most significant pathogenic (=disease-causing) species. Other Candida species causing diseases in humans include C. tropicalis, C. glabrata, C. krusei, C. parapsilosis, C. dubliniensis, and C. lusitaniae.


Classification

Candida Vulvovaginitis

Candida vulvovaginitis can be classified based on the duration, as well as the strain of Candida causing the infection.

Duration

Candida vulvovaginitis can be divided based on the duration of the infection into:[2][3][4][5]

  • Acute, uncomplicated: these are usually sporadic cases of Candida vulvovaginitis, which respond to topical anti-fungal therapy and have a high cure rate
  • Acute, complicated: symptoms are more severe than uncomplicated infections and typically require a combination of oral and topical anti-fungal treatment
  • Recurrent: defined as 4 or more cases of Candida vulvovaginitis per year, usually caused by the same strain of Candida. Treatment also requires a combination of oral and topical anti-fungal agents

Microbiology

Candida vulvovaginitis can also be divided based on the strain of Candida causing the infection:[4][6][7]

  • C. albicans: comprises the majority of cases of Candida vulvovaginitis
  • C. glabrata: it is the second most common causative pathogen
  • C. tropicalis
  • C. krusei
  • C. parapsilosis

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.[4][8]
  • 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.[4][8][9]
  • The understanding of the transition from asymptomatic vaginal colonization with Candida to symptomatic vulvovaginitis is not clear.[8][9]

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.[4][10][11]

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 a microscopic image of Candida albicans, grown on cornmeal agar medium.

    This is a a microscopic image of Candida albicans, grown on cornmeal agar medium.

  • 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 is a low-power photomicrograph of one of the Candida colonies from this lymph node. The chains of yeast which are termed "pseudohyphae" are apparent at this magnification.

    This is a low-power photomicrograph of one of the Candida colonies from this lymph node. The chains of yeast which are termed "pseudohyphae" are apparent at this magnification.

  • This higher-power photomicrograph shows the yeasts and pseudohyphae in this focus of Candida organisms.

    This higher-power photomicrograph shows the yeasts and pseudohyphae in this focus of Candida organisms.

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

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

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.[12][13]

Epidemiology and Demographics

Epidemiological studies on Candida vulvovaginitis are hard to perform, because of several factors:[3][4]
1. Candida vulvovaginitis is not a reportable disease
2. The diagnosis of Candida vulvovaginitis is based on clinical presentation, as well as positive laboratory findings. Relying on a positive culture alone would likely overestimate the prevalence of Candida vulvovaginitis
3. The use of over-the-counter (OTC) topical anti-fungals makes epidemiological studies harder to perform

Risk Factors

The following risk factors have been implicated in the development of Candida vulvovaginitis:

History and symptoms

Symptoms of Candida vulvovaginitis include the following:[15][2][3]

Physical Examination

Candida vulvovaginitis requires a careful examination of the external genitalia, the vaginal sidewalls, as well as the cervix. Signs include:[15][2]

  • Vulvar edema or erythema
  • Fissures and excoriations of the external genitalia, and/or
  • Thick, white vaginal discharge.

Laboratory Findings

The following laboratory tests are done in the diagnosis of Candida vulvovaginitis:[2][20][4]

  • Vaginal pH: in Candida vulvovaginitis, vaginal pH is normal (ranges from 4.0-4.5)
  • Microscopy/ wet mount: visualizes Candida hyphae or spores
  • Culture: culture for diagnosing Candida vulvovaginitis is not routinely done. However, it should be done in a symptomatic woman with a negative microscopy and a normal vaginal pH. Sabouraud agar, Nickerson's medium or Microstix-candida culture media may be used
  1. ↑ Barnett JA (2008). "A history of research on yeasts 12: medical yeasts part 1, Candida albicans". Yeast. 25 (6): 385–417. doi:10.1002/yea.1595. PMID 18509848.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Eckert LO (2006). "Clinical practice. Acute vulvovaginitis". N. Engl. J. Med. 355 (12): 1244–52. doi:10.1056/NEJMcp053720. PMID 16990387.
  3. ↑ 3.0 3.1 3.2 Sobel JD, Faro S, Force RW, Foxman B, Ledger WJ, Nyirjesy PR, Reed BD, Summers PR (1998). "Vulvovaginal candidiasis: epidemiologic, diagnostic, and therapeutic considerations". Am. J. Obstet. Gynecol. 178 (2): 203–11. PMID 9500475.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Sobel JD (2007). "Vulvovaginal candidosis". Lancet. 369 (9577): 1961–71. doi:10.1016/S0140-6736(07)60917-9. PMID 17560449.
  5. ↑ Vazquez JA, Sobel JD, Demitriou R, Vaishampayan J, Lynch M, Zervos MJ (1994). "Karyotyping of Candida albicans isolates obtained longitudinally in women with recurrent vulvovaginal candidiasis". J. Infect. Dis. 170 (6): 1566–9. PMID 7995997.
  6. ↑ Buscemi L, Arechavala A, Negroni R (2004). "[Study of acute vulvovaginitis in sexually active adult women, with special reference to candidosis, in patients of the Francisco J. Muñiz Infectious Diseases Hospital]". Rev Iberoam Micol. 21 (4): 177–81. PMID 15709796.
  7. ↑ Corsello S, Spinillo A, Osnengo G, Penna C, Guaschino S, Beltrame A, Blasi N, Festa A (2003). "An epidemiological survey of vulvovaginal candidiasis in Italy". Eur. J. Obstet. Gynecol. Reprod. Biol. 110 (1): 66–72. PMID 12932875.
  8. ↑ 8.0 8.1 8.2 Sobel JD (1985). "Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis". Am. J. Obstet. Gynecol. 152 (7 Pt 2): 924–35. PMID 3895958.
  9. ↑ 9.0 9.1 Sobel JD (1989). "Pathogenesis of Candida vulvovaginitis". Curr Top Med Mycol. 3: 86–108. PMID 2688924.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ Foxman B (1990). "The epidemiology of vulvovaginal candidiasis: risk factors". Am J Public Health. 80 (3): 329–31. PMC 1404680. PMID 2305918.
  15. ↑ 15.0 15.1 15.2 15.3 15.4 Eckert LO, Hawes SE, Stevens CE, Koutsky LA, Eschenbach DA, Holmes KK (1998). "Vulvovaginal candidiasis: clinical manifestations, risk factors, management algorithm". Obstet Gynecol. 92 (5): 757–65. PMID 9794664.
  16. ↑ Wilton L, Kollarova M, Heeley E, Shakir S (2003). "Relative risk of vaginal candidiasis after use of antibiotics compared with antidepressants in women: postmarketing surveillance data in England". Drug Saf. 26 (8): 589–97. PMID 12825971.
  17. ↑ de Leon EM, Jacober SJ, Sobel JD, Foxman B (2002). "Prevalence and risk factors for vaginal Candida colonization in women with type 1 and type 2 diabetes". BMC Infect. Dis. 2: 1. PMC 65518. PMID 11835694.
  18. ↑ Donders GG (2002). "Lower Genital Tract Infections in Diabetic Women". Curr Infect Dis Rep. 4 (6): 536–539. PMID 12433331.
  19. ↑ Duerr A, Heilig CM, Meikle SF, Cu-Uvin S, Klein RS, Rompalo A, Sobel JD (2003). "Incident and persistent vulvovaginal candidiasis among human immunodeficiency virus-infected women: Risk factors and severity". Obstet Gynecol. 101 (3): 548–56. PMID 12636961.
  20. ↑ Mendling W, Brasch J (2012). "Guideline vulvovaginal candidosis (2010) of the German Society for Gynecology and Obstetrics, the Working Group for Infections and Infectimmunology in Gynecology and Obstetrics, the German Society of Dermatology, the Board of German Dermatologists and the German Speaking Mycological Society". Mycoses. 55 Suppl 3: 1–13. doi:10.1111/j.1439-0507.2012.02185.x. PMID 22519657.
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