Specific Infections Vulvovaginitis

VV is considered to be a disturbance in vaginal flora rather than a true infection (6). Prepubertal females are particularly susceptible to bacterial VV because of anatomic, physiologic, and hygienic considerations (6) including the relative unprotected location of the vaginal introitus and its proximity to the anus, lack of estrogen-induced mucosal cornification, and the neutral to alkaline pH of the vagina (6). Behavioral factors include the tendency of some females to wipe the perineum from back-to-front, place contaminated hands and foreign bodies in the introitus and vagina, and use harsh soaps and bubble baths (6). The healthy, normal pH of 3.8 to 4.2 is largely dependent upon the presence of Lactobacillus acidophilus, that produces lactic acid and hydrogen peroxide (7).

In both specific and nonspecific VV, changes occur in the normal vulvovaginal flora that may induce inflammation. The specific organisms that cause infection in the prepubertal female are often respiratory, enteric, or sexually transmitted pathogens. The respiratory pathogens include Group A streptococcus, Streptococcus pneumoniae, Neisseria meningitidis, S. aureus, and Haemophilus influenzae. Other rare pathogens are Shigella (8), Yersinia (9), and Candida (6).

The three most common types of VV include nonspecific VV, or VV caused by candida, or trichomonas. Sexually acquired infections include Neisseria gonorrhoeae, G. vaginalis, Trichomonas vaginalis, Chlamydia trachomatis, herpes simplex virus, and Condyloma accuminata.

Bacterial vaginosis is the most prevalent infectious cause of vaginitis (6,10). It is a synergistic infection caused by a complex alteration in the microbial flora, with 100- to 1000fold increase in the number of G. vaginalis organisms as well as anaerobic bacteria, a decrease in lactobacilli, and an increase in organic acids produced by the abnormal flora (11). Mycoplasma hominis is also associated with nonspecific vaginitis (11). Several investigations have shown an association between bacterial vaginosis and the development of acute PID. The microorganisms associated with bacterial vaginosis include anaerobes such as P. bivia, Prevotella spp., and Peptostreptococcus spp. (10), butyrate-producing Peptostreptococcus spp., a comma-shaped bacterium (12), and Mobiluncus curtisii, a curved motile anaerobic rod (12). The exact role of each of these organisms is unclear and requires more study. Other yet unknown triggers for bacterial overgrowth may exist.

Bacterial vaginitis is characterized by the presence of a gray to white homogenous thin discharge adherent to the vaginal wall, vaginal fluid pH greater than 4.5, a positive whiff test, and the presence of clue cell in 20% of all vaginal epithelial cells. An association has been demonstrated between sexual abuse and bacterial vaginitis (13).

Treatment of bacterial vaginosis attempts to restore the vaginal ecosystem. Loss of dominance of lactobacillus results in overgrowth of facultative and obligate symptom causing anaerobes. Therapy of specific VV should be prescribed according to offending pathogens with either oral or intravaginal cream. Two intravaginal preparations are currently available, clindamycin (2%) vaginal cream or metronidazole gel (0.75%) (14,15). Clindamycin cream is administered once a day, whereas metronidazole gel is administered twice daily. Oral metronidazole is an accepted treatment for bacterial vaginosis administered as a single dose (2 g) or 250 mg three times a day or 500 mg given orally twice a day for seven days (16).

Ampicillin, although less effective, is an alternative drug treatment during pregnancy. Concomitant treatment of the female's sexual partner is still under investigation. The response of patients to metronidazole, although this drug is not effective against any of the nonanaerobic bacteria, supports the role of the anaerobic bacteria in this infection. Furthermore, clindamycin therapy eradicated and/or decreased counts of major bacterial vaginosis-associated microflora such as Gardnerella, gram-negative and gram-positive anaerobes, and M. hominis and was correlated with cure in 22 of 24 (92%) women (17). Possibly the elimination of only the anaerobic component of the infection may help to modify the microbial flora and restore normal condition.

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