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Bacterial Vaginosis

  • Author: Philippe H Girerd, MD; Chief Editor: Michel E Rivlin, MD  more...
 
Updated: Nov 14, 2015
 

Practice Essentials

Bacterial vaginosis (BV), or nonspecific vaginitis, was named because bacteria are the etiologic agents and an associated inflammatory response is lacking. Many studies have demonstrated the relation of Gardnerella vaginalis with other bacteria in causing BV, such as Lactobacillus, Prevotella, and anaerobes, including Mobiluncus, Bacteroides, Peptostreptococcus, Fusobacterium, Veillonella, and Eubacterium. Mycoplasma hominis, Ureaplasma urealyticum,Streptococcus viridans, and Atopobium vaginae have also been associated with BV.[1]

Signs and symptoms

Typical symptoms of BV include the following:

  • Vaginal odor (the most common, and often initial, symptom of BV); often recognized only after sexual intercourse
  • Mildly to moderately increased vaginal discharge
  • Vulvar irritation (less common)
  • Dysuria or dyspareunia (rare)

Risk factors that may predispose patients to BV include the following:

  • Recent antibiotic use
  • Decreased estrogen production of the host
  • Wearing an intrauterine device (IUD)
  • Douching
  • Sexual activity that could lead to transmission (eg, having a new sexual partner or a recent increase in the number of sexual partners)

Physical findings in BV may include the following:

  • Gray, thin, and homogeneous vaginal discharge, which adheres to the vaginal mucosa
  • Increased light reflex of the vaginal walls, but typically with little or no evidence of inflammation
  • Normal-appearing labia, introitus, cervix, and cervical discharge
  • In some case, evidence of cervicitis

See Clinical Presentation for more detail.

Diagnosis

In addition to the history and vaginal examination, microscopic examination is vital to the clinical diagnosis of BV.

On microscopic examination of the discharge, demonstration of 3 of the following 4 Amsel criteria is considered necessary to diagnose BV most accurately[2] :

  • Demonstration of clue cells on a saline smear (the most specific diagnostic criterion)
  • A pH greater than 4.5 (up to 90% of patients)
  • Characteristic thin, gray, and homogeneous discharge
  • Positive whiff test (up to 70% of patients)

Nugent’s criteria may be used to quantify or grade bacteria via Gram staining of vaginal samples. These criteria evaluate the following 3 types of bacteria and assign scores to each as shown:

  • Lactobacillus (score, 0-4)
  • Bacteroides/Gardnerella (score, 0-4)
  • Mobiluncus (score, 0-2)

Total scores are calculated and interpreted as follows:

  • 0-3: Normal
  • 4-6: Intermediate bacterial count
  • 7-10: BV

See Workup for more detail.

Management

General principles of treatment of BV include the following:

  • Antibiotics are the mainstay of therapy
  • Data on the efficacy of dietary supplementation with Lactobacillus (acidophilus) are conflicting
  • Asymptomatic women with G vaginalis colonization do not need treatment
  • BV occurring in pregnant women should be treated
  • Treatment before cesarean delivery, total abdominal hysterectomy, or insertion of an IUD is also recommended
  • Uncomplicated cases typically resolve after standard antibiotic treatment
  • BV that does not resolve after one course of treatment may be cured by giving a second course of the same agent or by switching to another agent (eg, from metronidazole to clindamycin or from clindamycin to metronidazole)
  • Some women with recurrent BV may benefit from evaluation or treatment of G vaginalis colonization in their sexual partner (controversial)
  • Patients should be advised to stop douching or using bubble bath or any other over-the-counter vaginal hygiene products
  • Patients should wash only with hypoallergenic bar soaps or no soap at all and should avoid liquid soaps and body washes
  • Surgery is not indicated
  • Testing for other infections (eg, N gonorrhoeae, C trachomatis, or herpes simplex virus [HSV]-1) may be appropriate
  • Therapy with metronidazole or clindamycin may alter the vaginal flora and predispose the patient to development of vaginal candidiasis

See Treatment and Medication for more detail.

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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).[3]

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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.[4]

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.[5] 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.[5] 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.[6]

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.

More recent studies indicated that BV is associated with changes in select soluble immune mediators, an increase in HIV target cells, and a reduction in endogenous antimicrobial activity, which may contribute to the increased risk of HIV acquisition.[7]

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Etiology

Bacterial vaginosis is a polymicrobic synergistic infection. As described in Pathophysiology, the normally predominant lactobacilli population is reduced in the vagina, while populations of Gardnerella vaginalis and other anaerobes are increased.

G vaginalis is the only member of its genus. Originally, it was known as Haemophilus vaginalis and then as Corynebacterium vaginale. It is a nonmotile, nonflagellated, nonsporeforming, facultative anaerobic, and nonencapsulated bacteria.

Although G vaginalis appears microscopically as a gram-variable rod, it is officially categorized as a gram-negative rod.

Other factors associated in the development of BV include douching, tub bathing (particularly with bubble bath), use of over-the-counter intravaginal hygiene products, multiple sexual partners, high frequency of intercourse, the use of an IUD and the presence of other sexually transmitted diseases.[8]  The theory for why these factors contribute to the development of BV is that they disrupt the normal vaginal flora. Some evidence shows that hormonal contraception (both combined estrogen/progestin and progestin only) is protective for the development of BV. Recurrent BV may be attributable to previous colonization of the oral cavity or anus with BV-associated bacteria.[9]

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Epidemiology

United States statistics

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.[10] An increased prevalence is associated with cigarette smoking, obesity, being single/never married, prior pregnancy, and a history of induced abortion.[8]

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.

Race-, sex-, and age-related demographics

Some studies have shown that bacterial vaginosis appears to occur more commonly among African American women than non-Hispanic white women.[8] The reasons for this are not entirely clear.

G 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.

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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Prognosis

Uncomplicated cases of bacterial vaginosis (BV) typically resolve after the standard antibiotic treatment.

Mortality/Morbidity

The prognosis for uncomplicated cases of bacterial vaginosis is generally excellent. Uncomplicated bacterial vaginosis that is assessed promptly typically resolves with standard antibiotic treatment.

The prognosis for complicated cases of bacterial vaginosis leading to other infections varies depending on the particular infectious process. Note the following:

  • 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,[6, 11, 12]  and intravaginal practices are an important risk factor for developing BV.[11]
  • 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.

Complications

Bacterial vaginosis (BV) may lead to an increased risk of salpingitis and/or endometritis, postsurgical infections (eg, postcesarean endometritis, posthysterectomy vaginal cuff cellulitis), and adverse outcomes in pregnancy, including premature rupture of membranes, premature labor, chorioamnionitis, and postpartum endometritis.

Mixed infections

Mixed infections with Trichomonas and yeast can occur among patients with BV.

Bacteremia

Gardnerella vaginalis bacteremia occurs much more commonly in women than in men and occurs most commonly in postpartum and postgynecologic procedure infections (eg, postpartum endometritis, chorioamnionitis, septic abortion) but is rare.

SPS, the anticoagulant used in blood culture media, is toxic to G vaginalis and inhibits its growth unless a neutralizing gelatin is added to counteract this effect. Routine blood cultures, therefore, may not grow G vaginalis, leading to underdiagnosis and underrecognition of this organism as the etiologic agent in these types of infections.

Genitourinary infections

Although G vaginalis urinary tract infections (UTI) occur much more frequently in women than in men, the overall occurrence of G vaginalis as a causative etiology in this infection is low (< 0.6%). However, the overall frequency may be underestimated because of a lack of optimal laboratory growth conditions (eg, aerobic incubation, short anaerobic growth period, urine not properly refrigerated prior to being cultured) and absence of associated pyuria occurring in women with concomitantly positive urine cultures.

In men, infections caused by G vaginalis are uncommon. Infection of the prostate and urinary bladder have been documented, although this occurs rarely and probably arises as a result of ascending spread of the organism from the colonized urethra. Balanoposthitis from G vaginalis has also been described.

Other complications

Other infections caused by G vaginalis include chorioamnionitis, endometritis, cervicitis, pelvic inflammatory disease, vaginal cuff cellulitis following hysterectomy, and bacteremia.

Case reports include disc space infection (lumbar spine), vaginitis emphysematosa, liver abscess (postcesarean), neonatal meningitis, and neonatal cellulitis/skin abscess.

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Patient Education

Educate patients regarding the basic pathophysiology, natural history, and risk factors of the bacterial vaginosis. BV is not considered a sexually transmitted disease, although sexual contact may predispose patients to development of this process in some cases.

For patient education resources, see Women's Health Center and Pregnancy Center, as well as Sexually Transmitted Diseases (STDs), Trichomoniasis, Birth Control Overview, and Birth Control Methods.

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Contributor Information and Disclosures
Author

Philippe H Girerd, MD Associate Professor, Department of Obstetrics and Gynecology, Virginia Commonwealth University, Medical College of Virginia

Philippe H Girerd, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, Association of Professors of Gynecology and Obstetrics, Medical Society of Virginia, AAGL

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

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

Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD Former 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, Royal College of Surgeons of Edinburgh, Royal College of Obstetricians and Gynaecologists

Disclosure: Nothing to disclose.

Additional Contributors

Thomas Michael Price, MD Associate Professor, Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Director of Reproductive Endocrinology and Infertility Fellowship 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, Phi Beta Kappa, Society for Reproductive Investigation, Society for Reproductive Endocrinology and Infertility, American Society for Reproductive Medicine

Disclosure: Received research grant from: Insigtec Inc<br/>Received consulting fee from Clinical Advisors Group for consulting; Received consulting fee from MEDA Corp Consulting for consulting; Received consulting fee from Gerson Lehrman Group Advisor for consulting; Received honoraria from ABOG for board membership.

Acknowledgements

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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.

Eric A Hansen, DO, Fellow, Clinical Instructor, Department of Internal Medicine, Division of Infectious Diseases, Winthrop-University Hospital, State University of New York at Stony Brook

Disclosure: Nothing to disclose.

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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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