Diagnosis Of Vulvovaginal Candidosis Research Articles

Guideline: Vulvovaginal candidosis (AWMF 015/072, level S2k).

Approximately 70‐75% of women will have vulvovaginal candidosis (VVC) at least once in their lifetime. In premenopausal, pregnant, asymptomatic and healthy women and women with acute VVC, Candida albicans is the predominant species. The diagnosis of VVC should be based on clinical symptoms and microscopic detection of pseudohyphae. Symptoms alone do not allow reliable differentiation of the causes of vaginitis. In recurrent or complicated cases, diagnostics should involve fungal culture with species identification. Serological determination of antibody titres has no role in VVC. Before the induction of therapy, VVC should always be medically confirmed. Acute VVC can be treated with local imidazoles, polyenes or ciclopirox olamine, using vaginal tablets, ovules or creams. Triazoles can also be prescribed orally, together with antifungal creams, for the treatment of the vulva. Commonly available antimycotics are generally well tolerated, and the different regimens show similarly good results. Antiseptics are potentially effective but act against the physiological vaginal flora. Neither a woman with asymptomatic colonisation nor an asymptomatic sexual partner should be treated. Women with chronic recurrent Candida albicans vulvovaginitis should undergo dose‐reducing maintenance therapy with oral triazoles. Unnecessary antimycotic therapies should always be avoided, and non‐albicans vaginitis should be treated with alternative antifungal agents. In the last 6 weeks of pregnancy, women should receive antifungal treatment to reduce the risk of vertical transmission, oral thrush and diaper dermatitis of the newborn. Local treatment is preferred during pregnancy.

Vulvovaginal Candidosis: Current Concepts, Challenges and Perspectives.

Vulvovaginal candidosis (VVC) is a frequently occurring infection of the lower female genital tract, mostly affecting immuno-competent women at childbearing age. Candida albicans is the most prevalent pathogenic yeast—apart from other non-albicans species—related to this fungal infection. Different virulence factors of C. albicans have been identified, which increase the risk of developing VVC. To initiate treatment and positively influence the disease course, fast and reliable diagnosis is crucial. In this narrative review, we cover the existing state of understanding of the epidemiology, pathogenesis and diagnosis of VVC. However, treatment recommendations should follow current guidelines.

Genotyping of Vaginal Candida glabrata Isolates Using Microsatellite Marker Analysis and DNA Sequencing to Identify Mutations Associated with Antifungal Resistance

Vulvovaginal candidosis is the second most common cause of vaginitis (17-39%) after bacterial vaginosis (22-50%). Since the diagnosis of vulvovaginal candidosis mainly depends on clinical findings without mycologic confirmatory tests and treated empirically, the actual incidence rate of vulvovaginal candidosis is unknown. Approximately 70-90% of vulvovaginal candidosis cases are caused by Candida albicans, however the increasing incidence of C.glabrata infections and its reduced susceptibility to azole drug therapy have generated increasing attention. The epidemiology and population structure of vulvovaginal candidosis due to C.glabrata are poorly characterized. This study was aimed to genotype the C.glabrata strains isolated from vaginal samples in Cukurova region, Turkey by microsatellite markers, to investigate the antifungal susceptibility profiles of the strains and to determine the molecular mechanisms leading to phenotypical azole resistance. A total of 34 unrelated vaginal C.glabrata strains isolated from patients with acute (n= 11) and recurrent (n= 14) vulvovaginal candidosis, control group (n= 9) without vaginitis symptoms, and a reference strain of C.glabrata CBS 138 (ATCC 2001) were included in the study. These isolates were genotyped using multiple-locus variable number tandem repeat analysis of three microsatellite markers (RPM2, MTI, and Cg6). Analysis of microsatellite markers was performed by fragment size determination of RPM2, MTI, and Cg6 PCR products through capillary electrophoresis. For each of the evaluated strains, DNA sequence analysis was performed for one gene (CgERG11) and four loci (CgPDR1, NTM1, TRP1, and URA3) to detect mutations possibly associated with antifungal resistance in each strain. In vitro susceptibility profiles of the strains to 13 antifungals and boric acid were determined according to CLSI document M27-A3 to investigate possible relationships between detected mutations and phenotypic resistance. C.glabrata CBS 138 strain was found to be susceptible to all the antifungals tested, while one of (%2.9) 34 vaginal C.glabrata isolates was found to be dose-dependent susceptible to fluconazole, 13 (38.2%) to itraconazole and 3 (8.8%) to voriconazole. No resistant strain were detected in the study population. Only three isolates were found to be resistant to clotrimazole (8.8%), however no relationship was identified between the genotypes and phenotypic resistance (p> 0.05). Thirteen genotypes were detected by microsatellite marker analysis, with high discrimination power (DP= 0.877). As a result, microsatellite marker analysis was validated as a rapid, reliable method for genotyping C.glabrata strains with good, but not optimal discriminatory power. Further studies examining larger numbers of isolates are needed to verify possible relationships between mutations and phenotypic resistance.

Culture and wet smear microscopy in the diagnosis of low-symptomatic vulvovaginal candidosis

To compare the clinical usefulness of culture and wet smear microscopy in low-symptomatic vulvovaginal candidosis (VVC) diagnosis. Study design: Women attending for contraceptive advice were screened for vaginal yeast fungi by culture and wet smear microscopy. A positive culture was found in 130 (13.2%) of the 983 women studied, while a positive wet smear was found in 133 (13.9%). In (30%) of these women both the culture and wet smear was positive. Results: The methods were equally sensitive in predicting symptoms of VVC, such as prutitus, smarting and burning pain, as well as for dyspareunia (35% vs. 36%), but wet smear microscopy was more sensitive in predicting signs of VVC, such as erythema and abnormal discharge (52% vs. 34%). The highest sensitivity was reached when both methods were positive (60% for symptoms, 75% for signs). There was no quantative correlation between number of Candida colonies on culture on the one hand and symptoms, signs or a positive wet smear on the other hand. Using four parameters as a diagnostic battery for VVC, the two methods complemented each other. The correlation between symptoms and/or signs for wet smear was higher than for culture. Conclusion: Wet smear microscopy of vaginal secretion, along with signs found at examination, should be the first-line test in the diagnosis of VVC. Culture must, however, be used when there is a clinical suspicion of VVC and a negative wet smear, or when speciation or antibiotic susceptibility test of isolates are required.