Abstract

PIP: The occurrence of candida vulvovaginitis (CVV) has been estimated based on statistical data from Great Britain to be an increase to 200/100,000 over 10 years to 1984. CVV in the US is the 2nd commonest cause of vaginal infection, with bacterial vaginosis occurring twice as often. 85-90% of the yeasts isolated from the vagina are candida albicans, based on biotyping rather that the newer methods of DNA hybridization. The pathogenesis of CVV is discussed in terms of the microbiology (virulence factors, adherence, germ tube and mycelium formation, proteinase secretion, and switching colonies), asymptomatic vaginal colonization, transformation to symptomatic vaginitis, host predisposing factors (pregnancy, oral contraceptives, diabetes mellitus, antimicrobes, and other), vaginal defense mechanisms (humoral system, phagocytic system, cell mediated immunity, vaginal flora, other), and pathogenesis of recurrent and chronic CVV (internal reservoir, sexual transmission, vaginal relapse, and experimental models) The discussion of the development of virulent symptoms is capsuled in the following comments. Vaginal cell receptivity varies among individuals, but all strains of C. Albicans adhere to both exfoliated vaginal and buccal epithelial cells, or mucosal surfaces, through the yeast surface mannoprotein. It is suggested from in vitro studies that germ tube and mycelium formation facilitates vaginal mucosal invasion. Exogenous and endogenous factors may enhance germination and precipitate symptomatic vaginitis, or inhibit germination. Increased proteinase secretion may be a result of the transformation from the blastoconidium/colonization phase to the germinated invasive vaginitis stage or an independent virulence factor. It is reported that hereditable spontaneous switching may occur spontaneously in vivo also. Colonizing yeasts with a change in environment can transform to a more virulent phase. Colonization rates vary from 10-25%, and the critical issue is understanding the process of asymptomatic colonization to symptomatic vaginitis, which is unclear. Inflammation may be caused by direct hyphal invasion or inducing symptoms of allergic reaction without identification of a specific event. Precipitating factors are pregnancy, where estrogens enhance yeast mycelium formation, or high levels of reproductive hormones. High oral contraceptive use is related to the presence of candida as well as uncontrolled diabetes, during or following use of antimicrobial agents, and use of poorly ventilated clothing.