Therapy
Metronidazole and tinidazole, are the treatment
of choice for trichomoniasis. Oral is preferred to local vaginal therapy since systemic administration achieves therapeutic drug levels in the urethra and periurethral glands, which serve as sources for endogenous recurrence. All sexual partners
Most strains of T. vaginalis are highly susceptible to metronidazole.
Refractory cases
In some patients, trichomoniasis is refractory to repeated courses of therapy even when all sexual partners have been treated. These rare patients may have strains of T.vaginalis resistant to metronidazole; this can be confirmed by in vitro culture and sensitivity testing. Women with resistant cases should be given the maximal tolerated dose of metronidazole (2 to 4 g daily for 10 to 14 days). There have been anecdotal reports of success in treating resistant infections with oral tinidazole. Rare patients who do not have a response to both these drugs can be treated with topical paromomycin (250 mg daily for two weeks).
Atrophic vaginitis
Reduced endogenous estrogen causes thinning of the vaginal epithelium, which also lacks glycogen; this contributes to a reduction in lactic acid production and an increase in vaginal pH. These changes in the vaginal environment encourage the overgrowth of nonacidophilic coliforms and the disappearance of lactobacillus species.
Clinically significant atrophic vaginitis is uncommon; the majority of women with mild to moderate atrophy are asymptomatic. Symptoms in women with advanced atrophy include vaginal soreness, postcoital burning, dyspareunia, and occasional spotting. < /p>
On physical examination the vaginal mucosa is thin with diffuse erythema, occasional petechiae or ecchymoses, and few or no vaginal folds. Vulvar atrophy may also be apparent. There may be a serosanguineous or watery discharge with a pH of 5.0 to 7.0. The wet smear shows increased polymorphonuclear leukocytes associated with small, rounded parabasal epithelial cells. The lactobacillus-dominated flora is replaced by a mixed flora of gram-negative rods, although bacteriologic cultures are unnecessary.
Treatment consists of topical vaginal estrogen. Nightly use of one-half of an applicator for one to two weeks is usually sufficient to alleviate symptoms, but symptomatic recurrence is common and may indicate a need for a systemic estrogen regimen.
Noninfectious vaginitis and vulvitis
Noninfectious causes of vaginitis include irritants (eg, minipads, spermicides, povidone-iodine, topical antimycotic drugs, soaps and perfumes, and topical fluorouracil) and allergens that produce immunologic acute and chronic hypersensitivity reactions, including contact dermatitis (eg, latex condoms and antimycotic creams). A syndrome of vaginal hyperacidity due to overgrowth by lactobacilli (cytolytic vaginosis) has been described but not confirmed.
The clinical features of noninfectious vaginitis and vulvitis are indistinguishable from infectious syndromes. Typical symptoms, including pruritus, irritation, burning, soreness, and variable discharge, are most commonly confused with acute candida vaginitis. The diagnosis should be suspected in symptomatic women who do not have an otherwise apparent infectious cause.
Management of noninfectious vaginitis includes identifying and eliminating the offending agent. Sodium bicarbonate sitz baths and topical vegetable oils may provide some local relief. Treatment should not rely upon topical corticosteroids, which frequently cause local burning.
PMN - polymorphonuclear leukocytes; EC = vaginal epithelial cells
