# Endowed Polyphenols in Advanced Delivery Systems for Vaginal Infections
## 4 Vaginal Infections
### Vulvovaginal Candidiasis  
VVC is the most common clinical disease caused by _Candida_ spp. and the second most common VI after BV [31]. VVC is thought to affect around 75% women of childbearing age [32], and around half of all college women by age 25, with 50% having a second reoccurrence [31; 32]. Also, it has been reported that around 7% of women will develop recurrent VVC [33], defined as three or more symptomatic episodes within 1 year [34]. VVC includes the spectrum of symptomatic and asymptomatic patients, both fostering the development of positive cultures. The symptoms vary with the host's response and the infectious organism [31].  
Between 85 and 90% of yeasts isolated from women with VCC are _Candida albicans_ strains [35]. This highly versatile pathogen can adapt its growth to several physiological extremes, and it also possesses several genes that encode proteins that increase its virulence through host recognition and binding to the host cells, such as ALS1, HWP1, and INT1, whose proteins provide adherence, and MTN1; strains without this gene in vivo were avirulent [36]. Another protein with significant virulence is candidalysin toxin, which is encoded by the ECE1 gene. Previous research has shown that this gene is regulated in a highly complex way by multiple transcription factors. However, intraspecies heterogeneity is extremely significant to strain-dependent pathogenicity and the virulence mechanisms employed by natural isolates are neglected. Data from previous reports underlined that the capacity to induce damage is linked to neutrophil migration. The _ECE1_ expression alone does not serve as a substitute of a pathogenicity indicator, as ineffective candidalysin secretion would likely impact pathogenicity. Therefore, the variant of ECE1 may also contribute to the reduced pathogenicity associated with _C. albicans_[37]. The remainder is other species, the most common of which are _C. glabrata_ (formerly known as _Torulopsis glabrata_) and _C. tropicalis_[38]. Some of these species possess the ability to cause vagnitis, often more resistant to conventional therapy than _C. albicans_[30].  
VVC is more common and harder to eradicate during pregnancy [31], due to the higher incidence of vaginal colonization, increasing from 9% in the first trimester to 54% in the third trimester [39]. This is most likely due to the higher contents of glycogen and carbon derived from higher levels of reproductive hormones, which are valuable resources for _Candida_ growth and germination [30]. Other factors that increase the prevalence of VCC are high-estrogenic-containing oral contraceptives [31], the use of tight, poorly ventilated clothing, which increases perineal moisture and temperature [30], and the systemic use of antibiotics, mainly tetracycline, ampicillin, and cephalospororin, which end up eliminating the protective vaginal microbiota [30].  
As stated before, the symptoms of VCC vary, but some clinical signs and symptoms include vulvovaginal pruritus, irritation, soreness, burning or micturition, and whitish, cheesy discharge. Most cases of VCC are detected by self-diagnosis, which is the basis for purchasing over-the-counter antimycotics [31]. Laboratory diagnosis methods include a latex agglutination slide technique, microscopic examination of vaginal secretions, or a 10% KOH preparation (whiff test) [30].