A history of genital infections is a risk factor for VVS (34). Early etiologic hypotheses focused on epidemiologic links to vulvovaginal candidiasis and genital human papilloma virus (HPV) infection. One study reported a history of recurrent candidiasis in 80% of VVS cases (35); others found the prevalence of Candida infection to be within the range found in normal subjects (36). The diagnosis of candidiasis in the aforementioned studies was often presumptive; hence, early misdiagnosis of VVS as candidiasis could have contributed to the observed statistical linkage. More recent investigations, which corroborated referring physicians' statements or prior laboratory results with patient reports, found VVS risk to be associated with a history of bacterial vaginosis, Candida albicans, pelvic inflammatory disease, trichomoniasis, and vulvar dysplasia (34).
The epidemiological association with HPV has been controversial. Studies investigating this hypothesis (most of which examined a limited number of viral subtypes) have produced mixed but mostly negative results (37,38). Laser or cryogenic treatment for prior HPV also has been suggested as a possible precipitating factor for VVS. Recent case-control studies utilizing physician-reported diagnoses found no increased risk associated with prior HPV infection, genital warts, chlamydia, genital herpes, or gonorrhea (34). Emerging data on host factors, such as reduced immune cell function (30-32) and genetic susceptibility to chronic inflammation (27-29), support the hypothesis that either bacterial or viral infections, or other potential inflammatory triggers (exposure to noxious chemicals, laser treatment, semen allergy), may play a role in VVS pathogenesis.
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The term vaginitis is one that is applied to any inflammation or infection of the vagina, and there are many different conditions that are categorized together under this ‘broad’ heading, including bacterial vaginosis, trichomoniasis and non-infectious vaginitis.