Introduction

Contact dermatitis results from the exposure of vulvar epithelium and vaginal mucosa to a primary chemical irritant or an allergen. In either case, characteristic local erythema and edema occur. Severe reactions may progress to ulceration and secondary infection. Common irritants and/or allergens include chemically scented douches; soaps; bubble baths; deodorants; perfumes, dyes, and scents in toilet paper, tampons, and pads; feminine hygiene products; topical vaginal antibiotics; and tight slacks, pantyhose, and synthetic underwear.

Clinically, patients report local swelling and itching or a burning sensation. The gynecologic examination reveals an erythematous and edematous vulvovaginal area. Local vesiculation and ulceration are seen more commonly with allergens or when primary irritants are used in strong concentrations. Vaginal pH changes may promote colonization and infection with C. albicans, thus obscuring the primary cause.

Diagnosis of contact vulvovaginitis is made by ruling out an infectious cause and by identifying the offending agent. Most cases of mild vulvovaginal contact dermatitis resolve spontaneously when the causative agent is withdrawn. For patients with severe, painful reactions, cool sitz baths and wet compresses of dilute boric acid or Burow’s solution may afford relief. Topical corticosteroids, such as hydrocortisone acetate (0.5 to 2.5 percent), fluocinolone acetonide (0.01 to 0.2 percent), or triamcinolone acetonide (.025 percent), relieve symptoms over a few applications and promote healing. Creams can be applied two or three times a day. Oral histamines may be helpful if a true allergic reaction is present. Superinfection with C. albicans, should it occur, should be treated as previously described. In these cases Mycolog (nystatin/triamcinolone) can be used.

Vulvovaginitis in the HIV-1-Positive Woman

Presence of vulvovaginitis may predispose women to infection by the human immunodeficiency virus (HIV) virus. Women who are HIV-1-positive may have an increased incidence of vulvovaginitis and may be more likely to infect others during this period. There is evidence that disturbance of the normal vaginal flora and presence of BV may be a risk factor for acquisition of HIV infection. Among HIV-1-seropositive women, the prevalence of Candida vulvovaginitis is reported to be as high as 62 percent. Rates of colonization are similar in nonimmunocompromised HIV-positive women and HIV-negative women. When CD4₊ T-cell counts are below 200/uL rates of colonization are increased as is symptomatic vaginitis. Recurrence of disease is also more frequent in immunocompromised HIV-positive women, as compared to HIV-positive women with CD4+ T-cell counts >200/uL and HIV-negative women.12 Treatment of VVC infection resulted in decreased viral shedding and thus infectivity in women who have Candida vaginitis. The optimal treatment of HIV-positive patients remains undefined; therefore, these patients should be treated with the same regimen as HIV-negative women. Treatment of patients with trichomoniasis has resulted in decrease of cell-free HIV-1 in vaginal secretions which may lead to decreased infectivity. Herpes genitalis is thought to be associated with an increased risk for HIV infection.