[5, 6]. The gold standard for laboratory diagnosis of BV is the Gram stain, which is used to determine the relative concentrations of MCC950 in vitro lactobacilli and the bacteria characteristic of BV [7]. The state of asymptomatic BV has also been recognised, although Gram stains revealed a decrease in lactobacilli and an increase in the abundance of anaerobes specific to BV [8]. The same G. vaginalis that is recovered as the prevailing inhabitant of the vaginal tracts of Selleckchem HDAC inhibitor women diagnosed with BV is also found in BV-negative

women, though at much lower numbers [5, 9, 10]. The issue of G. vaginalis commensalism is still unclear, as the vaginal bacterial community is dynamic and tends to change during the menstrual cycle to produce transient dominance of G. vaginalis in healthy women [11, 12]. Using culture-independent techniques, it was demonstrated that the vaginal microbiota may differ among human populations: Hispanic and non-Hispanic black women have significantly more anaerobes and fewer lactobacilli than Asian and Caucasian women [12]. C188-9 cost Thus, low counts of Lactobacillus do not necessarily indicate the BV state [6, 13]. The association of G. vaginalis with different clinical phenotypes could be explained by different cytotoxicity of the strains,

presumably based on disparities in their gene content. Until recently, surprisingly little has been known about the genetics of G. vaginalis. In 2010, the genomes of several G. vaginalis strains from the vaginas of BV and non-BV patients were sequenced, providing information about Urocanase the bacterium and enabling comparative genomic analyses [14, 15]. Attempts have also been made to expand the knowledge of the genotypic and

phenotypic diversity of G. vaginalis strains in terms of virulence factors: particularly vaginolysin, sialidase, and biofilm-forming proteins [16–18]. The development of methods for the genotypic differentiation of G. vaginalis revealed that the genomes exhibit great variability. Therefore, some conventional methods, including pulse field gel electrophoresis, restriction fragment length polymorphism, classical ribotyping with Southern blot, and restriction enzyme analysis, are not applicable for typing this species [19–21]. The amplified ribosomal DNA restriction analysis method, while applicable to the genotypic differentiation of G. vaginalis, has been found to not be discriminatory enough for pathogenetic and epidemiological studies of G. vaginalis[17, 18]. Recent data from G. vaginalis comparative genomic analyses have indicated that the bacterium possesses a small core genome, consisting of 746 genes, that accounts for only 27% of the pan-genome of the species [22]. The small number of unique genes (21) in the individual strains of G. vaginalis and the genomic plasticity among the strains suggest that horizontal gene transfer (HGT) is active; but there is frequent homologous recombination among G.