Candida species are one of the commonest causes of vaginitis in healthy women of reproductive age. Vulvovaginal candidiasis (VVC) is characterized by vulvovaginal itching, redness and discharge. Candida albicans, which is a common genito-urinary tract commensal, has been the prominent species and remains the most common fungal agent isolated from clinical samples of patients diagnosed with VVC. In recent times, however, there has been a notable shift in the etiology of candidiasis with non-albicans Candida (NAC) species gaining prominence. The NAC species now account for approximately 10% to as high as 45% of VVC cases in some studies. This is associated with treatment challenges and a slightly different clinical picture. NAC species vaginitis is milder in presentation, often occur in patients with underlying chronic medical conditions and symptoms tend to be more recurrent or chronic compared with C. albicans vaginitis. C. glabrata is the most common cause of NAC-VVC. C. tropicalis, C. krusei, C. parapsilosis, and C. guilliermondii are the other commonly implicated species. Treatment failure is common in NAC-VVC, since some of these species are intrinsically resistant or show low susceptibilities to commonly used antifungal agents. This article reviews the etiology, pathogenesis, clinical features, diagnosis, and management of NAC vulvovaginitis.

Candida glabrata is a common human fungal commensal and opportunistic pathogen. This fungus shows remarkable resilience as it can form recalcitrant biofilms on indwelling catheters, has intrinsic resistance against azole antifungals, and is causing vulvovaginal candidiasis. As a nosocomial pathogen, it can cause life-threatening bloodstream infections in immune-compromised patients. Here, we investigate the potential role of the high osmolarity glycerol response (HOG) MAP kinase pathway for C. glabrata virulence. The C. glabrata MAP kinase CgHog1 becomes activated by a variety of environmental stress conditions such as osmotic stress, low pH, and carboxylic acids and subsequently accumulates in the nucleus. We found that CgHog1 allows C. glabrata to persist within murine macrophages, but it is not required for systemic infection in a mouse model. C. glabrata and Lactobacilli co-colonise mucosal surfaces. Lactic acid at a concentration produced by vaginal Lactobacillus spp. causes CgHog1 phosphorylation and accumulation in the nucleus. In addition, CgHog1 enables C. glabrata to tolerate different Lactobacillus spp. and their metabolites when grown in co-culture. Using a phenotypic diverse set of clinical C. glabrata isolates, we find that the HOG pathway is likely the main quantitative determinant of lactic acid stress resistance. Taken together, our data indicate that CgHog1 has an important role in the confrontation of C. glabrata with the common vaginal flora.

Vaginal terconazole has not been studied during breastfeeding. Other antifungal agents may be preferred, especially while nursing a newborn or preterm infant

Vaginal tioconazole has not been studied during breastfeeding. Other antifungal agents may be preferred, especially while nursing a newborn or preterm infant.