There is an association between bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC), according to a recent study.
Takeaways
- The study establishes a connection between bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC), challenging the traditional view of these infections as separate entities.
- While BV and VVC are commonly perceived as distinct infections, the study reveals mixed interactions between these conditions, emphasizing the need to consider their interrelationship.
- Research in Argentina suggests that antibacterial agents may influence the pathologic microbiome of BV, potentially contributing to the development of recurrent VVC in women.
- Treating a BV episode instead of the underlying BV infection has been linked to future occurrences of VVC, highlighting the importance of understanding the appropriate treatment approach for these conditions.
- The study underscores the role of vaginal microbiota, host mucosal immune factors, and vaginal mucosal inflammation in determining outcomes for BV and VVC, prompting the need for further research in this area.
BV and VVC, 2 of the most common bacterial infections, are seen as separate entities with individual clinical manifestations. However, mixed interactions between these conditions have been observed.
In Argentina, a study found 35% of women with recurrent VVC (RVVC) had associated BV, and 33.2% had intermediate vaginal microbiota. This can be explained as antibacterial agents affected already pathologic microbiome of BV. Treating a BV episode rather than BV infection has been associated with future VVC.
There is currently little data on the relationship between BV and VVC outside the context of a drug induced VVC attack. Investigators conducted a study to evaluate VVC as a consequence of BV.
The Candida species, the primary pathogens behind VVC, form in moderated non-adversarial environments. Estrogen creates a healthy lower genital tract microbiome, leading to Candidacommensalism. Outcomes are determined by yeast, vaginal microbiota, and host mucosal immune factors.
Acute symptomatic Candida vulvovaginitis is seen following vaginal yeast colonization and presents as yeast blastospore proliferation and formation of hyphae. Following these symptoms, signs of acute vulvovaginitis appear.
While VVC has a single or mono-pathogen pathogenesis, BV presents as severe polymicrobial vaginal dysbiosis. During BV, healthy, protective Lactobacillus species disappear while an abundance of anaerobic and facultative species grow, leading to diverse bacterial abundance.
Sexual transmission has been linked to this process, with data associating multiple recurring BV episodes in women with previous sexual transmission. Researchers have also hypothesized Gardnerella species decrease oxidation reduction in the vaginal micro-environment, leading to strict anaerobic bacteria growth.
While there are many women with RVVC who have no associated BV, evidence has indicated BV precedes and sometimes causes RVVC episodes. One mechanism behind this association is increased rates of Candida vaginal colonization in women with BV, which has been observed across multiple studies.
Antibiotic treatment of BV has also been associated with acute VVC. While the source behind this association is not fully understood, investigators have hypothesized antibiotics lysing resident bacterial species leads to Candida proliferation. Currently, antibiotic therapy for recurrent BV is identified as the primary source of RVVC.
BV leads to increased vaginal pH, which is vital for C. albicans growth and severity. Additionally, acidic PH represses yeast-filamentous growth, which leads to yeast colonization and tissue invasion. Interactions may also occur between bacterial species seen in BV dysbiosis besides Lactobacillus, such as Enterococcus faecalis.
These mechanisms may be used to explain an association between BV and VCC. Investigators recommended further research about the impact of vaginal microbiota and vaginal mucosal inflammation.
Reference
Sobel JD, Vempati YS. Bacterial vaginosis and vulvovaginal candidiasis pathophysiologic interrelationship. Microorganisms. 2024;12(1):108. doi:10.3390/microorganisms12010108
