Vaginitis: Bacterial (Nonspecific) and Bacterial Vaginosis

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Chapter 94 Vaginitis: Bacterial (Nonspecific) and Bacterial Vaginosis

INTRODUCTION

Description: Bacterial vaginitis is a vaginal infection caused by an overgrowth of normal or pathogenic bacteria that results in irritation, inflammation, and clinical symptoms. Bacterial vaginosis is a change in vaginal ecology caused by an overgrowth of anaerobic bacteria, often with an absence of clinical symptoms. It should be noted that bacterial vaginosis does not engender an inflammatory response and is therefore technically not a type of vaginitis.
Prevalence: Roughly 6 million cases per year, 50% of “vaginal infections.”
Predominant Age: 15 to 50 (may occur at any age).
Genetics: No genetic pattern.

ETIOLOGY AND PATHOGENESIS

Causes: Bacterial vaginitis—overgrowth of normal or pathologic bacteria with an inflammatory response (which distinguishes this from bacterial vaginosis). Bacterial vaginosis—a polymicrobial process that involves the loss of normal lactobacilli, an increase in anaerobic bacteria (especially Gardnerella vaginalis, Bacteroides sp., Peptococcus sp., and Mobiluncus sp.), and a change in the chemical composition of the vaginal secretions. There is a 1000-fold increase in the number of bacteria present and a 1000 : 1 anaerobic/aerobic bacteria ratio (normal 5 : 1), high levels of mucinases; phospholipase A2, lipases, proteases, arachidonic acid, and prostaglandins are all present. Amines (cadaverine and putrescine) are made through bacterial decarboxylation of arginine and lysine. These amines are more volatile at an alkaline pH, such as that created by the addition of 10% KOH (potassium hydroxide) or semen (roughly a pH of 7), giving rise to the odor found with the “whiff test” or reported by these patients after intercourse.
Risk Factors: Systemic processes—diabetes, pregnancy, and debilitating disease. Anything that alters the normal vaginal flora—smoking, numbers of sexual partners, vaginal contraceptives used, some forms of sexual expression such as oral sex, antibiotic use, hygiene practices and douching, menstruation, and immunologic status.

CLINICAL CHARACTERISTICS

Signs and Symptoms

Bacterial Vaginitis

• Vulvar burning or irritation
• Increased discharge (often with odor)
• Dysuria
• Dyspareunia
• Edema or erythema of the vulva

Bacterial Vaginosis

• Asymptomatic (20% to 50% of patients)
• Increased discharge
• Vaginal odor (often more pronounced after intercourse)
• Vulvar burning or irritation

Uncommon

• Dysuria
• Dyspareunia
• Edema or erythema of the vulva

DIAGNOSTIC APPROACH

Differential Diagnosis

• Chlamydial cervicitis
• Gonococcal cervicitis
• Trichomonas vaginalis infection
• Vaginal candidiasis

Associated Conditions: Other vaginal or sexually transmitted infections, cervicitis, and vulvitis. Ascending infections including endometritis, pelvic inflammatory disease, postoperative vaginal cuff cellulitis, preterm rupture of the membranes and endomyometritis, increased early pregnancy loss, and decreased success with in vitro fertilization.

Workup and Evaluation

Laboratory: Culture or monoclonal antibody staining may be obtained to evaluate other causes but are seldom necessary. Evaluation for concomitant sexually transmitted infections should be considered.
Imaging: No imaging indicated.
Special Tests: Vaginal pH 5 to 5.5, “whiff” test—the addition of 10% potassium hydroxide to vaginal secretions to liberate volatile amines, causing a “fishy” odor (bacterial vaginosis).
Diagnostic Procedures: Physical examination, microscopic examination of vaginal secretions in normal saline. For bacterial vaginosis, the diagnosis requires three of the following: homogeneous discharge, pH 5 to 5.5, clue cells (>20%), positive “whiff” test. Commercial tests (such as for proline iminopeptidase activity) exist but are generally not necessary to establish the diagnosis.

Pathologic Findings

Increased white blood cells and bacteria when vaginal secretions are viewed under normal saline suggest vaginitis. Clue cells may be present but are often absent in vaginitis. For bacterial vaginosis, clue cells must represent 20% or more of epithelial cells seen.

MANAGEMENT AND THERAPY

Nonpharmacologic

General Measures: Perineal hygiene, education regarding sexually transmitted infections.
Specific Measures: Medical therapy, vaginal acidification.
Diet: No specific dietary changes indicated.
Activity: No restriction.
Patient Education: Reassurance; American College of Obstetricians and Gynecologists Patient Education Pamphlet AP028 (Vaginitis: Causes and Treatments), AP009 (How to Prevent Sexually Transmitted Diseases).

Drug(s) of Choice

Oral—metronidazole (Flagyl, Protostat) 500 mg twice daily for 7 days (90% to 100% cure), oral ampicillin, 500 mg every 6 hours for 7 days.
Topical—clindamycin (5 g of cream, 100 mg of clindamycin) every night at bedtime for 7 days, metronidazole (5 g of cream, 37.5 mg of metronidazole) twice a day for 5 days.
Contraindications: Metronidazole is relatively contraindicated in the first trimester of pregnancy.
Precautions: Oral metronidazole is associated with the potential for systemic side effects including a metallic taste in the mouth and stomach upset. Topical metronidazole is currently available in two forms: one for dermatologic use and one for intravaginal use. The pH of these two preparations is quite different, making it important to specify the form on the prescription to avoid significant chemical irritation. Some concerns have been raised about the risk of inducing antibiotic resistance through the use of topical clindamycin, although the clinical significance is uncertain.
Interactions: Because of a disulfiram-like reaction, patients must be warned to avoid alcohol intake during metronidazole therapy.

Alternative Drugs

Oral—tetracycline, 250 to 500 mg twice a day for 7 days, clindamycin, 300 to 450 mg every 6 hours for 7 days.
Topical—topical triple sulfa (cream or suppositories) twice a day for 7 to 10 days, vaginal acidification (Aci-Jel, Amino-Cerv, boric acid), povidone iodine, as a douche or gel.

FOLLOW-UP

Patient Monitoring: Normal health maintenance.
Prevention/Avoidance: It is thought that bacterial vaginosis develops 5 to 10 days after exposure to the involved bacteria. Gardnerella may be found in 90% of male partners of women with bacterial vaginosis. Hence, sexual transmission is postulated, although bacterial vaginosis can occur in virginal women. The role of condoms in prevention is debated.
Possible Complications: Cystitis, cervicitis, infections of Skene’s or Bartholin’s glands, increased risk of pelvic inflammatory disease, pelvic pain, and infertility. Increased risk of upper genital tract infections and postoperative infections if surgery is performed while bacterial vaginosis is present. Increased risk of premature delivery, premature rupture of the membranes, and chorioamnionitis when bacterial vaginosis is present during pregnancy.

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Expected Outcome: Most treatment failures are actually caused by reinfection or failure to comply with treatment.

MISCELLANEOUS

Pregnancy Considerations: Vaginal infections are associated with an increased risk of prematurity and premature rupture of the membranes.
ICD-9-CM Codes: 616.10.

REFERENCES

Level I

Sanchez S, Garcia PJ, Thomas KK, et al. Intravaginal metronidazole gel versus metronidazole plus nystatin ovules for bacterial vaginosis: a randomized controlled trial. Am J Obstet Gynecol. 2004;191:1898.

Sobel JD, Ferris D, Schwebke J, et al. Suppressive antibacterial therapy with 0.75% metronidazole vaginal gel to prevent recurrent bacterial vaginosis. Am J Obstet Gynecol. 2006;194:1283. Epub 2006 Apr 21

Level II

Beigi RH, Austin MN, Meyn LA, et al. Antimicrobial resistance associated with the treatment of bacterial vaginosis. Am J Obstet Gynecol. 2004;191:1124.

Leitich H, Brunbauer M, Bodner-Adler B, et al. Antibiotic treatment of bacterial vaginosis in pregnancy: a meta-analysis. Am J Obstet Gynecol. 2003;188:752.

Ness RB, Hillier SL, Kip KE, et al. Bacterial vaginosis and risk of pelvic inflammatory disease. Obstet Gynecol. 2004;104:761.

Okun N, Gronau KA, Hannah ME. Antibiotics for bacterial vaginosis or Trichomonas vaginalis in pregnancy: a systematic review. Obstet Gynecol. 2005;105:857.

Ugwumadu A, Reid F, Hay P, Manyonda I. Natural history of bacterial vaginosis and intermediate flora in pregnancy and effect of oral clindamycin. Obstet Gynecol. 2004;104:114.

Level III

American College of Obstetricians and Gynecologists. Assessment of risk factors for preterm birth. ACOG Practice Bulletin 31. Obstet Gynecol. 2001;98:709.

American College of Obstetricians and Gynecologists. Vaginitis. ACOG Practice Bulletin 72. Obstet Gynecol. 2006;107:1195.

Anderson MR, Klink K, Cohrssen A. Evaluation of vaginal complaints. JAMA. 2004;291:1368.

Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2006. MMWR. 2006;55:50.

Eckert LO, Lentz GM. Infections of the lower genital tract. In: Katz VL, Lentz GM, Lobo RA, Gershenson DM, editors. Comprehensive Gynecology. 5th ed. Philadelphia: Mosby/Elsevier; 2007:590.

Faro S. Bacterial vaginitis. Clin Obstet Gynecol. 1991;34:582.

Friese K. The role of infection in preterm labour. BJOG. 2003;110:52.

Ledger WJ. Historical review of the treatment of bacterial vaginosis. Am J Obstet Gynecol. 1993;169:474.

Mitchell H. Vaginal discharge—Causes, diagnosis, and treatment. BMJ. 2004;328:1306.

Owen MK, Clenney TL. Management of vaginitis. Am Fam Physician. 2004;70:2125.

Spiegel CA. Bacterial vaginosis. Clin Microbiol Rev. 1991;4:485.

Sweet RL. New approaches for the treatment of bacterial vaginosis. Am J Obstet Gynecol. 1994;169:479.

Thomason JL, Gelbart SM, Scaglione NJ. Bacterial vaginosis: current review with indications for asymptomatic therapy. Am J Obstet Gynecol. 1991;165:1210.

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