Vulvovaginal candidiasis

Over the counter treatment doesn't seem to lead to resistance

Like other syndromes affecting the lower genital tract of women, vulvovaginal candidiasis has been regarded as more of a “nuisance infection” than a topic of serious scientific inquiry. New advances in molecular epidemiology, host mucosal immunology, and antifungal treatment have, however, enlivened investigation into this common condition.

Furthermore, the economic costs of vulvovaginal candidiasis treatment have been well documented, along with the extent to which women treat themselves with a variety of antifungal preparations that are available without a prescription. In 2002 women in the United States spent over half a billion dollars on medications to treat vulvovaginal candidiasis, with about half this amount spent on over the counter preparations.1 This is despite the fact that many women may wrongly diagnose vulvovaginal candidiasis and may be equally or more likely to have bacterial vaginosis, with or without vulvovaginal candidiasis.2

Truly representative data on the epidemiology of vulvovaginal candidiasis are hard to come by. Vaginal colonisation with Candida, a prerequisite for development of vulvovaginal candidiasis, occurs in at least 40% of adult women at any given point and possibly in most women at some time during their adult life.3 Most experts agree that at least half of women will have one episode of vulvovaginal candidiasis by the time they reach their mid-20s.4 A minority of these women—up to 25%—will also have recurrent vulvovaginal candidiasis, defined as four or more episodes a year.

Unlike women who have sporadic, uncomplicated vulvovaginal candidiasis, those with recurrent disease do not enjoy the prospect of decreasing frequency of attacks as they age. The pathogenesis of recurrent vulvovaginal candidiasis among women who have no apparent predisposing condition (such as poorly controlled diabetes, systemic immunosuppression or immunodeficiency, and use of antibiotics) is under investigation.

The pathogenesis of recurrent disease probably involves some breakdown of the normal mucosal immune processes that allow for mucosal “tolerance” to the organism.5 The emergence of increasingly resistant Candida species does not seem to play a major part in recurrent vulvovaginal candidiasis, although, as a group, women with recurrent disease do have a slightly higher prevalence (10-15%) of C glabrata, which is inherently less sensitive to the imidazole group of drugs.6 The role of specific behaviours as risk factors for recurrent vulvovaginal candidiasis is unclear, but some investigators have implicated receptive oral sex and increasing frequency of intercourse.7

A recent Cochrane review and both European and US guidelines for managing sexually transmitted diseases say that clinicians should view the topical imidazole drugs for short course treatment as essentially equivalent among themselves and to single dose oral fluconazole given at 150 mg.8–10 Importantly, initial fears that the widespread availability of over the counter vaginal imidazoles would favour the development of increasingly resistant C albicans, or increasing dominance of species less sensitive to imidazoles, such as C glabrata, have not been realised. In most women (90-95%) with sporadic, uncomplicated vulvovaginal candidiasis, sensitive C albicans is the culprit organism.4

A major advance in the treatment of vulvovaginal candidiasis has been the validation of suppressive regimens for women with recurrent disease. After an initial regimen of topical imidazole or oral fluconazole, weekly medication works quite well in suppressing clinical attacks.8–10 The challenge in such cases is deciding when to stop treatment. Once stopped, the same Candida strain seen in the episodes before suppression re-establishes itself and often causes symptomatic disease.5 These events may occur because the fungistatic regimens used for suppression fail to eradicate the organism completely or because of host factors that persistently favour an inability to tolerate the resident yeast. Both these reasons may be implicated to some degree.5

Finally, we should remember that vulvovaginal candidiasis is often not the cause of symptoms commonly ascribed to it. Bacterial vaginosis, the most common cause of vaginitis among women presenting with vaginal symptoms, is often diagnosed together with vulvovaginal candidiasis. Furthermore, genital herpes may be misdiagnosed as recurrent vulvovaginal candidiasis, particularly when epithelial fissures are present in the vulvar area. Other causes of genital dermatitis, such as lichen planus, can cause similar symptoms. In studies evaluating the cause of recurrent vaginitis (presumed to be vulvovaginal candidiasis by most patients), Candida species were isolated in a surprisingly small percentage of subjects (16%).11 Conversely, vulvovaginal candidiasis is imperfectly diagnosed by the potassium hydroxide test (the sensitivity of this test is 85% at best, in obviously symptomatic women).12 The selective use of vaginal fungal cultures can enhance the sensitivity of diagnosis in women with a compatible clinical syndrome. Although there is some debate about the role of vaginal cultures, most experts agree that they are useful (a) in identifying the organism in women with symptoms but a negative potassium hydroxide test, particularly if empirical treatment aimed at uncomplicated vulvovaginal candidiasis has already failed, and (b) before embarking on long term suppressive antifungal treatment.10