Abstract

Oral and vaginal candidiasis are the two most common forms of opportunistic fungal infections. However, the prevalence of each can be quite variable depending on the immune status of the host. While vulvovaginal candidiasis (VVC) is equally common in immunocompetent and immunocompromised women, oropharyngeal candidiasis (OPC) is infrequent except under immunocompromised states. Candida albicans, the causative agent in the majority of cases, is a commensal of the gastrointestinal and lower female reproductive tracts. Thus, most healthy individuals have protective Candida-specific immunity that normally prevents infection. Studies from animal models, women with recurrent VVC (RVVC) and HIV-infected individuals, however, suggest that distinct protective host defense mechanisms may function against OPC and VVC. While local and systemic cell-mediated immunity (CMI) appear important for protection against OPC, there is little evidence to indicate that either local or systemic CMI plays a role against VVC. Innate resistance is also considered distinct at both sites with considerably less activity at the vaginal mucosa, including the newfound anti-Candida activity by epithelial cells. Finally, the protective role of humoral immunity has been and remains uncertain. Taken together, the differential prevalence of VVC and OPC is directly proportional to the levels of demonstrable innate and adaptive host defenses at each site.

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