Bacterial Vaginosis and Vulvovaginal Candidiasis Pathophysiologic Interrelationship

Abstract

Among the infectious causes of vulvovaginal symptoms, bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC) dominate. Apart from infrequent mixed infections, both are considered independent and caused by unrelated pathogenic mechanisms. Clinical experience, however, is strongly suggestive that in some populations these infections are linked with recurrent BV (RBV) serving as the dominant etiopathogenic trigger for development of recurrent VVC (RVVC) with profound clinical and therapeutic consequences. The biologic basis for this critical interrelationship is discussed and suggests that as a consequence of BV dysbiosis, and not necessarily because of antibiotics prescribed, immune defenses are compromised, neutralizing vaginal yeast tolerance. The consequent BV-induced vaginal proinflammatory environment predisposes to mixed infection or consecutive episodes of post-treatment VVC. Recurrent BV and repeated antimicrobial drug exposure also predispose to acquired fluconazole resistance in C. albicans isolates, contributing to refractory vulvovaginal candidiasis.

Keywords: bacterial vaginosis; fluconazole resistance; microbiome; microbiota; pathogenesis; recurrent vaginitis; vulvovaginal candidiasis.

Figure 2

Bacterial vaginosis–vulvovaginal candidiasis pathophysiologic linkage.

Figure 1

Bacterial Vaginosis–Vulvovaginal Candidiasis interrelationship.