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Candida albicans is responsible for 80 to 92 percent of episodes of vulvovaginal candidiasis in the United States [8,9], and
Candida glabrata accounts for almost all of the remainder [10].
Some, but not all, investigators have reported an increasing frequency of nonalbicans species, particularly C. glabrata [11,12], possibly due to widespread use of over-the-counter drugs, long-term use of suppressive azoles, and the use of short courses of antifungal drugs.
All Candida species produce similar vulvovaginal symptoms, although the severity of symptoms is milder with C. glabrata and C. parapsilosis. Candida organisms probably access the vagina via migration from the rectum across the perianal area [13]; cultures of the gastrointestinal tract and vagina often show identical Candida species. Less commonly, the source of infection is sexual or relapse from a vaginal reservoir. In contrast to bacterial vaginosis, vulvovaginal candidiasis is not associated with a reduction in vaginal lactobacilli [14-17].
Symptomatic disease is associated with an overgrowth of the organism and penetration of superficial epithelial cells [18-21]. The mechanism by which Candida species transform from asymptomatic colonization to an invasive form causing symptomatic vulvovaginal disease is complex, involving host inflammatory responses and yeast virulence factors. One study comparing histologic specimens from women with confirmed vulvovaginal candidiasis, women without infection, and women with active bacterial vaginosis has reported co-invasion with Gardnerella or Lactobacillus species organisms in women with Candida infection but absence of a biofilm (in contrast with bacterial vaginosis) [21]. (See "Biology of Candida infections".)