Vulvovaginal candidiasis (VVC; colloquially referred to as a 'yeast infection') is a
prevalent mucosal infection caused by Candida spp. that affects ~75% of women at least once
in their life. VVC usually responds well to treatment, yet a small but significant fraction
of women experience recurrent yeast infections even with weekly treatment. A further
complication in understanding the causes of recurrent infections is that approximately one in
five females have vaginal yeast present without any symptoms at any given point. The link
between fungi, other microbes in the vagina ("microbiome"), and the human immune system
remain poorly understood in the switch from having yeast present in the vagina without any
symptoms and symptomatic yeast infections. Fungi also compose a normal component of the
microbiome at other sites in the body (e.g., oral, skin, gastrointestinal tract, rectum)
where they may serve as a source of re-infection following treatment.
In addition to the commonly prescribed 'first choice' antifungal drug fluconazole, a
second-line treatment, boric acid, has shown promise in the literature and has been used
locally with success at increasing the time between recurrent infections. A drawback of this
therapy, however, is cost, as it is a compounded medication, and patients have to pay out of
pocket. The purpose of this study is to understand how the yeast and bacterial microbial
communities differ for females with recurrent infections from females with their first yeast
infection and females with vaginal yeast present without any symptoms, and to track yeast
diversity following treatment with either boric acid or fluconazole. We hypothesize that we
will identify multiple subpopulations of yeast at multiple anatomical body sites in females
with VVC and recurrent VVC. We anticipate finding evidence for recurrent infection from
secondary sites by linking genomic diversity of vaginal yeast strains during symptomatic
infection to strains from other body sites. We hypothesize that yeast isolated from females
with recurrent infections will exhibit different drug response phenotypes than yeast from
females with asymptomatic vaginal yeast. We hypothesize that the vaginal microbiome of
post-treatment patients treated with boric acid will differ from that of fluconazole.
Combined, we hypothesize that post-treatment response will differ between the drugs,
indicating that treatment specifics influence the vaginal environment.