Bacterial Vaginosis 

  • Author: Diana Curran, MD, FACOG; Chief Editor: Michel E Rivlin, MD   more...
 
Updated: Oct 24, 2011
 

Background

Gardnerella vaginalis is a facultatively anaerobic gram-variable rod. It has been demonstrated to cause a wide variety of infections; however, it is most commonly recognized for its role as one of the organisms responsible for bacterial vaginosis (BV).

For related information, see Medscape's Women's Sexual Health Resource Center.

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Pathophysiology

Bacterial vaginosis (BV), formerly known as nonspecific vaginitis, was named because bacteria are the etiologic agent in this infection and an associated inflammatory response is lacking.

BV is the most common cause of vaginitis and the most common infection encountered in the outpatient gynecologic setting.

An increase in vaginal discharge and vaginal malodor caused by a change in the vaginal flora characterizes BV.

The vaginal discharge of BV is characteristically described as a thin, gray, homogeneous fluid that is adherent to the vaginal mucosa.

Many studies have demonstrated the relationship of Gardnerella vaginalis with other bacteria in causing BV. BV is known to be a synergistic polymicrobic infection. Some of the associated bacteria include Lactobacillus species, Prevotella, and anaerobes, including Mobiluncus, Bacteroides, Peptostreptococcus, Fusobacterium, Veillonella, and Eubacterium species. Mycoplasma hominis, Ureaplasma urealyticum, and Streptococcus viridans may also play a role in BV. Atopobium vaginae is now recognized as a pathogen associated with BV.[1]

Evidence in support of a synergistic relationship includes the following: (1) Gardner and Dukes inoculated pure cultures of G vaginalis into the vaginas of healthy women and failed to produce BV symptoms; (2) inoculation of vaginal discharge fluid from BV patients into the vaginas of healthy women produced symptoms of BV; (3) treatment for BV, an antianaerobic antibiotic (metronidazole), is ineffective against G vaginalis; and (4) the volatile products elaborated from the whiff test are products of anaerobes and not of G vaginalis.

In BV, the vaginal flora becomes altered through known and unknown mechanisms, causing an increase in the local pH. This may result from a reduction in the hydrogen peroxide–producing lactobacilli. Lactobacilli are large rod-shaped organisms that help maintain the acidic pH of healthy vaginas and inhibit other anaerobic microorganisms through elaboration of hydrogen peroxide. Normally, lactobacilli are found in high concentrations in the healthy vagina. In BV, the lactobacilli population is reduced greatly, while populations of various anaerobes and G vaginalis are increased.

G vaginalis forms a biofilm in the vagina.[2] Some studies show that this biofilm may be resistant to some forms of medical treatment. This predominant G vaginalis biofilm has been shown to survive in hydrogen peroxide (H2 O2), lactic acid, and high levels of antibiotics. When the biofilm was subjected in the laboratory to enzymatic dissolution, susceptibility to H2 O2 and lactic acid were restored.[2] These findings may lead to future development of novel therapies involving enzymatic degradation of biofilms. No such products are currently on the market.

In a study published by Fredricks et al, G vaginalis was detected by PCR in 96% of subjects with BV and 70% of those without BV. Multiple other bacterial species were found by PCR in this study. Fredricks' study confirms the polymicrobial nature of BV and the presence of G vaginalis as one of the causative agents.[3]

Although BV is not considered a sexually transmitted disease, sexual activity has been linked to development of this infection. Observations in support of this include the following: (1) incidence of BV increases with an increase in the number of recent and lifetime sexual partners, (2) a new sexual partner can be related to BV, and (3) male partners of women with BV may have urethral colonization by the same organism, but the male is asymptomatic. Evidence that does not support an exclusive sexually transmitted role of BV is its occurrence in virginal females and its colonization of the rectum in virginal boys and girls.

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Epidemiology

Frequency

United States

BV occurs in one third of adult women in the United States, which represents approximately 21 million women. Each year, women make 10 million office visits for vaginal discharge.[4] An increased prevalence is associated with cigarette smoking, obesity, being single/never married, prior pregnancy, and a history of induced abortion.[5]

Gardnerella vaginalis has been reported to occur in up to 100% of women with signs and symptoms of BV and in up to 70% of women with no signs or symptoms of BV.

G vaginalis has been isolated in up to 80% of the urethras of male sexual partners of women with BV. However, treatment of male partners is not recommended as it has not been shown to alter rates of BV in their female partners.

The incidence of BV in patients attending obstetric clinics is 10-25% and may be as high as 30-65% in patients attending sexually transmitted disease clinics.

Mortality/Morbidity

Uncomplicated bacterial vaginosis that is assessed promptly typically resolves with standard antibiotic treatment.

  • Long-standing or untreated BV may lead to more serious sequelae, such as endometritis, salpingitis, pelvic inflammatory disease, or complications of pregnancy, including premature rupture of membranes, premature labor, chorioamnionitis, and postpartum endometritis.
  • BV leads to an increased risk for acquiring HIV.[3]
  • Postgynecologic procedure infections, such as vaginal cuff cellulitis (status posthysterectomy) and postabortion infection may also occur.
  • Suspect concomitant infections (such as candida vaginitis) or newer, resistant organisms (Atopobium vaginae) in patients whose symptoms do not resolve after treatment of BV. See Treatment.

Race

Some studies have shown that bacterial vaginosis appears to occur more commonly among African American women than non-Hispanic white women.[5] The reasons for this are not entirely clear.

Sex

Gardnerella vaginalis colonization and/or infection predominantly occurs in women. Men rarely develop infections with G vaginalis; however, the urethras of men whose sexual partners have symptoms of BV are frequently colonized with the same strain of G vaginalis. A recent study by Bradshaw et al found that G vaginalis is not associated with nongonococcal urethritis.

Age

G vaginalis infections typically occur in women of reproductive age. Studies have documented G vaginalis colonization in prepubertal and/or virginal girls and boys and cases of BV occurring in prepubertal and/or virginal girls.

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Contributor Information and Disclosures
Author

Diana Curran, MD, FACOG  Assistant Professor, Residency Program Director, Department of Obstetrics and Gynecology, University of Michigan Health Systems

Diana Curran, MD, FACOG is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, and Central Association of Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Specialty Editor Board

Thomas Michael Price, MD  Associate Professor of Reproductive Endocrinology, Director of Reproductive Fellowship Training Program, Duke University Medical Center

Thomas Michael Price, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Obstetricians and Gynecologists, American Society for Reproductive Medicine, Phi Beta Kappa, and Society for Gynecologic Investigation

Disclosure: Clinical Advisors Group Consulting fee Consulting; MEDA Corp Consulting Consulting fee Consulting; Gerson Lehrman Group Advisor Consulting fee Consulting; Adiana Grant/research funds PI

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

A David Barnes, MD, PhD, MPH, FACOG  Consulting Staff, Department of Obstetrics and Gynecology, Mammoth Hospital (Mammoth Lakes, California), Pioneer Valley Hospital (Salt Lake City, Utah), Warren General Hospital (Warren, Pennsylvania), and Mountain West Hospital (Tooele, Utah)

A David Barnes, MD, PhD, MPH, FACOG is a member of the following medical societies: American College of Forensic Examiners, American College of Obstetricians and Gynecologists, American Medical Association, Association of Military Surgeons of the US, and Utah Medical Association

Disclosure: Nothing to disclose.

Frederick B Gaupp, MD  Consulting Staff, Department of Family Practice, Hancock Medical Center

Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians

Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD  Professor, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine

Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Eric A Hansen, DO and Burke A Cunha, MD to the development and writing of this article.

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Table. Differential Diagnosis of the Vaginitides
Clinical ElementsBacterial VaginosisTrichomoniasisVaginal Candidiasis
SymptomsVaginal odor++/--
Vaginal dischargeThin, gray, homogenousGreen-yellowWhite, curdlike
Vulvar irritation+/-++
Dyspareunia-+-
SignsVulvar erythema-+/-+/-
Bubbles in vaginal fluid++/--
Strawberry cervix-+/--
MicroscopySaline wet mount
Clue cells+--
Motile protozoa-+-
KOH test
Pseudohyphae--+
Whiff test++/--
pH>4.5>4.5< 4.5
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