Cytolytic Vaginosis (CV)
Cytolytic Vaginosis (CV) is a vaginal condition whereby the vaginal microbiome is dominated by an overgrowth of lactobacillus, typically lactobacillus crispatus bacteria. Often there are very few or no other bacteria present, whether that’s other lactobacillus strains, or aerobic or anaerobic bacteria.
It presents in a similar way to Vulvovaginal Candidiasis (VVC), with thick white discharge, itching and possibly a vinegar odour. Other symptoms may include painful urination and dyspareunia (painful sex).
Symptoms may appear worse in the luteal phase and around ovulation but improve during menstruation. The reason for this is that lactobacillus thrive off oestrogen, and higher levels of oestrogen tend to increase lactobacillus numbers.
Excess lactobacillus can lead to excess lactic acid production in the vaginal environment, and this increased acidity can damage the vaginal epithelium, leading to breakdown and shedding of skin cells, and associated pain and discomfort. This skin breakdown manifests as increased vaginal discharge and can be observed under a microscope.1
We recommend seeing a gynaecologist with suspected CV. A vaginal microbiome test is very helpful too to check for levels and types of bacteria. To get a diagnosis of CV, vaginal discharge needs to be examined under a microscope to look for damaged skin cells and lactobacillus bacteria.
Treatment for CV involves increasing the vaginal pH and restoring lactobacilli numbers back to normal. Specific advice should be sought from a healthcare professional. It is thought that triggers for CV include extended anti-microbial use and possibly surgery. However, CV is a less researched condition with conflicting views regarding its existence as a specific diagnosis.2
References
- DermNet. Cytolytic Vaginosis. Available at: https://dermnetnz.org/topics/cytolytic-vaginosis. Last accessed March 12, 2025.
- Kraut R, Carvallo FD, Golonka R, et al. Scoping review of cytolytic vaginosis literature. PLoS One. 2023;18(1):e0280954. Published 2023 Jan 26.
