In vitro experimental work has shown this process of adherence, hyphal outgrowth and colonisation is enhanced in the presence of oestrogen, This finding may offer one explanation for the fact that symptomatic vaginal candidosis is more common to women between the menarche and menopause. Symptom severity is not strictly related to yeast cell counts, but most symptomatic patients will have high counts. There is, however, a good correlation between the active clinical disease and the presence of Candida in its mycelial phase. Candida hyphae can invade epithelial cells, and experimental work has shown that mutant strains of Candida which are not able to invade epithelial cells can produce only mild symptoms in animal models. The inflammation of vaginal tissues associated with the symptomatic condition suggests production of a cellular toxin or a protease enzyme.
Proteases can break down proteins and can therefore cause extensive damage to normal cells.
This supports the idea that the growing yeast may produce some factor damaging to vaginal epithelium, thus causing vaginitis. It is likely that a combination of some or all of these factors produce vaginal tissue damage, resulting in the clinical symptoms of vaginal candidosis. A small but significant sub-group of patients suffer with chronic or recurrent episodes of vaginal candidosis. The reasons for this remain uncertain. One hypothesis suggested is that the recurrent episodes might be due to reinfection of the vagina, from other Candida source reservoirs such as the patient's own gut or an infected sexual partner.