Expert Review
Gynecology
Recurrent vulvovaginal candidiasis

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Recurrent vulvovaginal candidiasis (RVVC) is a common cause of significant morbidity in women in all strata of society affecting millions of women worldwide. Previously, RVVC occurrence was limited by onset of menopause but the widespread use of hormone replacement therapy has extended the at-risk period. Candida albicans remains the dominant species responsible for RVVC, however optimal management of RVVC requires species determination and effective treatment measures are best if species-specific. Considerable progress has been made in understanding risk factors that determine susceptibility to RVVC, particularly genetic factors, as well as new insights into normal vaginal defense immune mechanisms and their aberrations in RVVC. While effective control of RVVC is achievable with the use of fluconazole maintenance suppressive therapy, cure of RVVC remains elusive especially in this era of fluconazole drug resistance. Vaccine development remains a critical challenge and need.

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Microbiology

Given that C albicans remains responsible for >90% of episodes of acute sporadic VVC in most studies worldwide, it is not surprising that C albicans similarly is responsible for the majority of infections in women with RVVC.4, 10, 11, 12, 13 Approximately 85-95% of women with RVVC have azole-sensitive C albicans as the causative pathogen, implying that the host rather than the pathogen contributes dominantly to the pathophysiology of RVVC.4, 10 Of the non-albicans Candida species, C glabrata is

Pathogenesis of RVVC

Candida blastospores (yeast) migrate from the lower gastrointestinal tract to the adjacent vestibule and vagina. This is a similar route taken by vaginal Lactobacillus species. Colonization of the vagina follows usually in low numbers after adherence of Candida to vaginal epithelial cells. Colonization resistance is poorly studied and understood but colonization is enhanced by an estrogen-influenced environment following menarche and declines in the postmenopause period. In healthy women not

Clinical aspects of VVC

Cardinal symptoms include vulvovaginal pruritus, irritation, soreness, dyspareunia, and vaginal discharge. Clinical signs are best exemplified by vulva erythema, edema, excoriation, and fissure formation together with introital and vaginal erythema. A nonmalodorous clumpy white discharge is suggestive of VVC but is extremely nonspecific. Diagnosis should never be based on clinical findings alone given their lack of specificity.37 RVVC, by virtue of the frequent, numerous acute recurrences or

Diagnosis of VVC

Vaginal pH is almost always normal in VVC and an elevated pH suggests an alternative diagnosis although mixed infections occasionally occur.4 Traditional bedside laboratory tests, include saline and 10% potassium hydroxide microscopy, are still extremely useful providing rapid confirmation when positive, but these tests are now infrequently performed in an era where more expensive and complex tests have become a new but not necessarily superior diagnostic routine. Saline and KOH microscopy

Treatment of RVVC

Practitioners can offer reassurance and even assurances of high likelihood of symptomatic control but unfortunately not guarantee of cure (Table 1). As indicated in the pathophysiology section, susceptibility to recurrent symptomatic vaginitis likely has a genetic basis predisposing to enhanced vaginal colonization with an azole-susceptible strain of C albicans, and in the presence of secondary triggering mechanisms, the carrier state is transformed into a proinflammatory state by a host

Non-albicans Candida species

The approach to RVVC in women with azole-resistant Candida species such as C glabrata and much less commonly C krusei or even Saccharomyces species does not require the aforementioned strategy, since recurrent diseases is not a function of genetic controlled immune hyperactivity but lack of susceptibility to azole drugs. There are no published data or long-term maintenance therapy for C glabrata. In past studies of RVVC, only women with C albicans were enrolled. The management of chronic and

Fluconazole-resistant RVVC due to C albicans

In the last decade, isolated cases have been reported of women with RVVC who either fail to respond to induction therapy with fluconazole or who break through fluconazole maintenance suppressive therapy. After lack of compliance is excluded, fluconazole resistance should be considered.57 Approximately 50 cases have been identified at the Wayne State University School of Medicine Vaginitis Clinic over the last 10 years, although widespread reports have not been forthcoming and there is no

Role of probiotics for RVVC

In layman literature, probiotic use to treat and prevent VVC is a long-standing tradition.59, 60 Scientific justification for exogenous Lactobacillus replacement is based on the premise that Lactobacillus species exert a significant protective effect in vivo in reducing the virulence expression of Candida organisms colonizing the vagina as well as enhancing the vaginal epithelial cell immune defense mechanisms. There also exists the hypothesis that women with VVC and especially RVVC have

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