What makes UpToDate so powerful?

  • over 11000 topics
  • 22 specialties
  • 5,700 physician authors
  • evidence-based recommendations
See more sample topics
Find Patient Print
0 Find synonyms

Find synonyms Find exact match

Bacterial vaginosis: Clinical manifestations and diagnosis
UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate®
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
Bacterial vaginosis: Clinical manifestations and diagnosis
View in Chinese
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2017. | This topic last updated: Jun 30, 2017.

INTRODUCTION — Bacterial vaginosis (BV) is a clinical condition characterized by a shift in vaginal flora away from Lactobacillus species toward more diverse bacterial species, including facultative anaerobes. The altered microbiome causes a rise in vaginal pH and symptoms that range from none to very bothersome. Future health implications of BV include, but are not limited to, increased susceptibility to other sexually transmitted infections and preterm birth.

This topic will discuss the pathogenesis, clinical presentation, and treatment of BV. Related topics on the treatment of BV, evaluation of vaginitis, and cervicitis are presented separately.

(See "Bacterial vaginosis: Treatment".)

(See "Approach to women with symptoms of vaginitis".)

(See "Acute cervicitis".)

DEFINITION — BV is characterized by three alterations in the vaginal environment [1]:

A shift in vaginal flora from Lactobacillus species to one of high bacterial diversity, including facultative anaerobes.

Production of volatile amines by the new bacterial flora.

Resultant rise in vaginal pH to >4.5 (normal vaginal pH of estrogenized women ranges from 4.0 to 4.5). (See "Approach to women with symptoms of vaginitis", section on 'Vaginal pH'.)

EPIDEMIOLOGY — BV is the most common cause of vaginal discharge in women of childbearing age, accounting for 40 to 50 percent of cases [2-4]. In the United States, the National Health and Nutrition Examination Survey (NHANES), which included results from self-collected vaginal swabs from over 3700 women, estimated the prevalence of BV was 29 percent in the general population of women aged 14 to 49 years and 50 percent in African-American women [5]. This included both symptomatic and asymptomatic infection. Worldwide, BV is common among women of reproductive age, with variations according to the population studied [6]. The health consequences of BV infection are presented below. (See 'Consequences of infection' below.)

PATHOGENESIS AND MICROBIOLOGY

Altered vaginal flora and dysbiosis – BV represents a complex change in the vaginal flora characterized by a reduction in concentration of the normally dominant hydrogen-peroxide producing lactobacilli and an increase in concentration of other organisms, especially anaerobic gram negative rods [7-11]. Ethnicity and age are additional factors that appear to impact the vaginal microbial community [12]. The absence of inflammation is the basis for the term "vaginosis" rather than "vaginitis." Some authors use the term "dysbiosis" to reflect the microbial imbalance in the vaginal flora that can ultimately impact vaginal function and lead to negative health consequences [13,14]. (See 'Consequences of infection' below.)

The major bacteria detected in women with BV are Gardnerella vaginalis, Prevotella species, Porphyromonas species, Bacteroides species, Peptostreptococcus species, Mycoplasma hominis, and Ureaplasma urealyticum, as well as Mobiluncus, Megasphaera, Sneathia, and Clostridiales species [7,15]. Fusobacterium species and Atopobium vaginae are also common.

The difference in vaginal flora between women with and without BV was illustrated in a study that used broad range DNA probes to determine the vaginal flora of 27 women with BV and 46 controls [1]. Overall, 35 bacterial phylotypes were identified in women with BV, including 16 which were newly recognized. Women with BV had a mean of 12.6 phylotypes (range 9 to 17) per sample compared to 3.3 phylotypes (range 1 to 6) per sample in women without BV. The organisms newly identified by polymerase chain reaction (PCR) include fastidious bacteria termed "BV associated bacterium (BVAB) 1, 2 and 3" in the Clostridiales order, which appear to be specific indicators of BV [16]. Subsequent studies have documented several other bacterial species in the human vagina, including the novel strains Peptoniphilaceae DNF01163 and Prevotellaceae DNF00733 [17-20].

Production of amines – Hydrogen-peroxide producing lactobacilli appear to be important in preventing overgrowth of the anaerobes normally present in the vaginal flora. With the loss of lactobacilli, pH rises and massive overgrowth of vaginal anaerobes occurs. These anaerobes produce large amounts of proteolytic carboxylase enzymes, which break down vaginal peptides into a variety of amines that are volatile, malodorous, and associated with increased vaginal transudation and squamous epithelial cell exfoliation, resulting in the typical clinical features observed in patients with BV (see 'Clinical features' below). The rise in pH also facilitates adherence of G. vaginalis to the exfoliating epithelial cells.

Role of biofilm – Increasing evidence suggests that G. vaginalis is the key player in the pathogenesis of BV and the development of a biofilm may be an essential component of this process, in addition to the gradual overgrowth of resident anaerobic vaginal flora [21-26]. In this model, a cohesive form of G. vaginalis adheres to the vaginal epithelium and then becomes the scaffolding to which other species adhere [27]. This hypothesis is supported by a study of microbiota on the epithelial surfaces of vaginal biopsy specimens from women with BV that showed a biofilm adhered to part or all of the epithelium, and G. vaginalis comprised 90 percent of bacteria in the biofilm, while Atopobium vaginae accounted for most of the remainder [21]. Subsequent desquamation of these epithelial cells would result in the classic clue cells diagnostic of the disorder (see 'Diagnosis' below). In contrast, most healthy controls had unstructured accumulations of bacteria within secretions loosely attached to epithelial surfaces.

Extracellular DNA (eDNA) is a factor in the structural stability of biofilms in a variety of bacterial species and appears to play an important role in the establishment and maintenance of the G. vaginalis biofilm in BV [28]. The presence of a biofilm may make it difficult to eradicate BV and increase the rate of recurrence, but discovery of the role of eDNA has led to the hypothesis that a DNase might be able to destroy the eDNA that helps to maintain the BV biofilm.

RISK FACTORS

Sexual activity – While the majority of data support the hypothesis that BV is a sexually transmitted infection, it is not yet classified as such because of lack of a single causative agent and absence of a clear disease counterpart in males [15,29-33]. In addition, early studies reported mixed results on the impact of treatment of the male sexual partner [34-39]. However, a subsequent review of early negative or inconclusive studies reported that these studies lacked sufficient power to detect reasonable effect sizes, had deficient or inadequately reported randomization methods, and lacked information on adherence to therapy [40].

Sexual activity is a risk factor for BV and most experts believe that BV does not occur in women who have never had sexual contact of any type, including receptive oral sex [41,42]. Epidemiologic studies are strongly supportive of sexual transmission of BV pathogens. In a systematic review and meta-analysis of 43 observational studies, sexual contact with new and multiple male and female partners was associated with an increased risk of BV, while condom use was associated with a decreased risk [29]. In addition, many BV-associated species have been isolated from the male penile skin, semen, urethra, and urine specimens [43,44].

BV is highly prevalent (25 to 50 percent) in women who have sex with women (WSW), and is associated with increasing numbers of female sexual partners, a female partner with symptomatic BV, and various sexual practices, suggesting sexual transmission is an important factor [45-50]. However, in one study, sexually active monogamous WSW partnerships over six months tended to have concordant, stable, vaginal microbiota, which was most concordant for normal flora [47]. This suggests that longer duration, sexually active partnerships led to stability and alignment of a favorable vaginal microbiota in WSW couples. Accordingly, the majority of investigators believe that BV, as an original or first infection or occurrence, is sexually transmitted. However, in contrast to trichomoniasis, chlamydial, or gonococcal infection, there is also a high rate of symptomatic recurrence of BV in the absence of sexual activity or reinfection.

Sexually transmitted infections – The presence of other sexually transmitted infections appears to be associated with an increased prevalence of BV. In a systematic review and meta-analysis of studies evaluating the association between BV infection and herpes simplex virus (HSV)-2 infection, women infected with HSV-2 had a 55 percent higher risk of BV infection compared with women who were HSV-2 uninfected [51]. Similarly, a five-year prospective cohort study reported that BV was both more prevalent and more persistent among HIV-infected women compared with those without HIV [52]. Conversely, BV may also be a risk factor for HIV acquisition [53]. (See "HIV and women", section on 'Bacterial vaginosis, genital ulcers, and pelvic inflammatory disease'.)

Race and ethnicity – While higher rates of BV have been reported in minority populations, it is not clear if this finding reflects genetic, socioeconomic, behavioral, or other differences [5,12,54]. In the United States NHANES 2001 to 2004 study, the rates of BV based on self-collected swabs were 51 percent for African-American women, 32 percent for Mexican-American women, and 23 percent for women of European ancestry [5]. In contrast, in a small study comparing the vaginal microbiota of white and black women by both cultivation-dependent and –independent methods, there were no differences in colonization and density of bacterial species by race once women with BV by Nugent criteria were removed [55].

Other – In addition to sexual and infectious risk factors, most studies indicate douching and cigarette smoking are risk factors for acquisition of BV among sexually active women [2,3,47,56-61]. Although some degree of genetic susceptibility to BV is likely, no association between a gene polymorphism and BV has been established [62]. One questionnaire study reported an association between high fat diets and BV as well as an inverse relationship for BV with the intakes of folate, vitamin E, and calcium [63]. While these dietary factors were associated with BV, further studies are needed to determine causality. Of not, BV is not associated with chronic medical conditions (eg, diabetes) or immunosuppressive states.

CLINICAL FEATURES — Fifty to 75 percent of women with BV are asymptomatic [41,64,65]. Symptomatic women typically present with vaginal discharge and/or vaginal odor [41,64,65]. The discharge is off-white, thin, and homogeneous; the odor is an unpleasant "fishy smell" that may be more noticeable after sexual intercourse and during menses [66].

BV alone typically does not cause dysuria, dyspareunia, pruritus, burning, or vaginal inflammation (erythema, edema) [64,65]. The presence of these symptoms suggests mixed vaginitis (symptoms due to two pathogens) [67].

Although BV does not involve the cervix, the disorder may be associated with acute cervicitis (endocervical mucopurulent discharge or easily induced cervical bleeding) [68]. (See "Acute cervicitis".)

CONSEQUENCES OF INFECTION

Pregnant women with BV are at higher risk of preterm delivery (see "Bacterial vaginosis: Treatment", section on 'Pregnant women') [69-72].

BV is a cause of [73-75]:

Endometrial bacterial colonization

Plasma-cell endometritis

Postpartum fever

Posthysterectomy vaginal cuff cellulitis

Postabortal infection

BV is a risk factor for HIV acquisition and transmission [53,76,77].

BV is a risk factor for acquisition of herpes simplex virus type 2 (HSV-2), gonorrhea, chlamydia, and trichomonas infection [78-80]. Although BV is more common among women with pelvic inflammatory disease (PID), it is not clear whether it is a causal factor or an independent risk factor for this disease [81,82].

It has been hypothesized that the increased risk of acquisition of sexually transmitted infections in women with BV may be due to lack of hydrogen peroxide-producing lactobacilli in the vaginal flora of affected women; other factors associated with BV infection, such as local cytokine production, may also play a role.

BV may be a factor in development of precancerous cervical lesions. In a systematic review and meta-analysis of primarily cross-sectional studies, the risk of cervical intraepithelial neoplasia (CIN) or squamous intraepithelial lesions (SIL) was increased in women with BV (odds ratio 1.51, 95% CI 1.24-1.83); however, there was considerable heterogeneity among these studies and both CIN 1 and low-grade SIL, which do not usually progress to cancer, were included as outcomes [83]. BV appears conducive to the persistence of human papillomavirus infection [84,85], which is necessary but not sufficient for development of high-grade cervical lesions and cancer. (See "Cervical intraepithelial neoplasia: Terminology, incidence, pathogenesis, and prevention", section on 'Role of human papillomavirus'.)

DIAGNOSIS — The general diagnostic approach to women with vaginal discharge is reviewed separately. (See "Approach to women with symptoms of vaginitis".)

In clinical practice, the diagnosis of BV in premenopausal women is usually based on the presence of at least three Amsel criteria (characteristic vaginal discharge, elevated pH, clue cells, fishy odor) if microscopy is available [86,87]. Use of Nugent or Hay/Ison criteria to evaluate a Gram-stained smear of vaginal discharge is the diagnostic standard in research studies, but requires more time, resources, and expertise [87]. If microscopy is not available, the diagnosis should be based on findings on clinical examination (characteristic vaginal discharge, elevated vaginal pH, fishy odor). Commercial tests that have acceptable performance compared with gram stain include a DNA probe-based test for high concentrations of G. vaginalis (Affirm VP III) and vaginal fluid sialidase activity test (OSOM BV Blue test). A triple PCR assay for the detection of chlamydia, gonorrhea, and trichomonas has been developed and initial testing reported sensitivity and specificity of 91.5 and 98.6 percent, respectively [88]. More trial data are needed before the routine use of this assay is advised. Use of the proline-aminopeptidase test card (Pip Activity TestCard) is no longer recommended because of low sensitivity and specificity.

Amsel criteria — The diagnosis of BV is usually based on Amsel criteria, which are simple and useful in an office practice where microscopy is available [64]. The first three findings are sometimes also present in patients with trichomoniasis (table 1).

Amsel criteria for diagnosis of BV (at least three criteria must be present) [87]:

Homogeneous, thin, grayish-white discharge that smoothly coats the vaginal walls.

Vaginal pH >4.5.

Positive whiff-amine test, defined as the presence of a fishy odor when a drop of 10 percent potassium hydroxide (KOH) is added to a sample of vaginal discharge.

Clue cells on saline wet mount (picture 1A-B). Clue cells are vaginal epithelial cells studded with adherent coccobacilli that are best appreciated at the edge of the cell. For a positive result, at least 20 percent of the epithelial cells on wet mount should be clue cells. The presence of clue cells diagnosed by an experienced microscopist is the single most reliable predictor of BV [89].

Mobiluncus species may be noted on microscopy as well (movie 1).

Using Gram's stain as the standard for diagnosing BV, the sensitivity of Amsel criteria for diagnosis of BV is over 90 percent and specificity is 77 percent [90].

Gram's stain — Gram's stain of vaginal discharge is the gold standard for diagnosis of BV (picture 2A-B) [91], but is mostly performed in research studies because it requires more time, resources, and expertise than Amsel criteria [92-94]. The Gram-stained smear is evaluated using Nugent criteria (table 2) or Hay/Ison criteria (table 3). If clinical criteria are used to define infection, then reported sensitivity ranges from 62 to 100 percent [95].

Cytology — The Papanicolaou smear is not reliable for diagnosis of BV (sensitivity 49 percent, specificity 93 percent) [96]. No information is available on the sensitivity and specificity of liquid-based cervical cytology screening methods. If a cytology smear suggests BV (ie, shift in flora from predominantly lactobacilli to predominantly coccobacilli with or without clue cells), the patient should be asked about symptoms, and if symptomatic, she should undergo standard diagnostic testing for BV and treatment, if appropriate. Treatment of asymptomatic women is not routinely indicated. (See "Bacterial vaginosis: Treatment", section on 'Asymptomatic infection'.)

Culture — Because BV represents complex changes in the vaginal flora, vaginal culture has no role in diagnosis. Although cultures for G. vaginalis are positive in almost all women with symptomatic infection, the organism is detected in up to 50 to 60 percent of healthy asymptomatic women; thus, its presence alone, no matter how identified, is not diagnostic of BV.

Commercial tests — Commercial tests for diagnosis of BV are not widely used, given the excellent performance of Amsel criteria, but can be useful when microscopy is not available.

The Affirm VP III test is an automated DNA probe assay for detecting G. vaginalis when present at a high concentration [97]. It takes less than one hour to perform and is the best option when findings on physical examination suggest BV (characteristic vaginal discharge and results of pH and whiff test, if available), but microscopy cannot be performed to look for clue cells. In one study, for example, the combination of a positive DNA probe (concentration of G. vaginalis ≥2 times 107 CFU/mL) and vaginal pH >4.5 had a sensitivity and specificity of 95 and 99 percent, respectively, for diagnosis of BV when clinical criteria were used as the diagnostic standard [98]. Not all studies have reproduced these excellent results, and over-diagnosis is possible.

The OSOM BVBlue system is a chromogenic diagnostic test based on the presence of elevated sialidase enzyme activity in vaginal fluid samples. This enzyme is produced by bacterial pathogens associated with BV including Gardnerella, Bacteroides, Prevotella, and Mobiluncus. The test can be performed at the point of care and results are available in 10 minutes (Clinical Laboratory Improvement Amendments [CLIA]-waived). Sensitivity ranging from 88 to 94 percent and specificity ranging from 91 to 98 percent have been reported when compared with Amsel and Nugent criteria [99-101].

Investigational tests — Quantitative polymerase chain reaction (PCR)-based assays are based upon molecular quantification of G. vaginalis and Atopobium vaginae, and other bacteria [102,103], most frequently Megasphaera and BV-associated bacteria (BVAB) 1 and 2. Although these tests have good sensitivity and specificity compared with standard clinical tests [104], they are expensive and of questionable advantage [105]. A molecular test that assays the vaginal microbiome for evidence of bacterial vaginosis, vaginal candidiasis, and trichomonas has shown promise in initial clinical studies [106]. The vaginal specimen swab can be collected by a clinician or the patient. Lastly, A urine test that uses fluorescence in situ hybridization (FISH) to identify the BV biofilm on desquamated vaginal epithelial cells in urine sediment appears promising and is also under investigation [22].

Diagnosis without speculum examination — BV has been diagnosed using a swab of vaginal discharge obtained by the patient or clinician without physical examination. However, omission of the speculum examination results in under-diagnosis and should be avoided.

In one study, young women with or without vaginitis symptoms self-tested for BV using a pH or sialidase test and results were compared with clinician-performed examination with clinical diagnosis of BV by modified Amsel criteria [107]. Compared with diagnosis by clinician examination, self-pH was 73 percent sensitive and 67 percent specific and self-sialidase was 40 percent sensitive and 90 percent specific.

In another study of the diagnostic accuracy for BV among women presenting with vaginal discharge to a sexually transmitted diseases (STD) clinic, all women provided self-obtained vaginal swabs for examination, completed a questionnaire, and then were examined by a clinician [108]. A non-examining clinician reviewed the findings of the questionnaire and self-obtained vaginal swab and diagnosed BV if at least two of three Amsel criteria were positive (pH>4.5, >20 percent clue cells, positive Whiff test). Examining clinicians diagnosed BV if at least three of the four standard Amsel criteria were positive (characteristic discharge, pH >4.5, >20 percent clue cells, positive Whiff test). In all cases, Gram-stained slides for diagnosis of BV by Nugent criteria were made, but the results were not disclosed, and 125 were positive. The investigators found that clinical examination with a speculum exam was more likely to result in a correct diagnosis of BV than just examination of a self-obtained vaginal swab (90/125 versus 68/125), but also resulted in over-diagnosis/over-treatment in 15 patients (105 positive diagnoses versus 61 positive diagnoses).

DIFFERENTIAL DIAGNOSIS — Although supporting data are lacking, in our experience, in the absence of microscopy, a lack of fishy odor (negative whiff test) makes the diagnosis of BV unlikely. BV is usually suspected because of high vaginal pH (>4.5). Other causes of increased pH include trichomoniasis, atrophic vaginitis, and desquamative inflammatory vaginitis. These four entities are easily distinguishable by clinical and microscopic features.

Women with BV do not have dyspareunia or signs of vaginal inflammation; in contrast, women with atrophic vaginitis, desquamative inflammatory vaginitis, and trichomoniasis usually have these signs and symptoms.

Both atrophic vaginitis and desquamative inflammatory vaginitis are associated with an increased number of parabasal cells on microscopy, which is not observed in women with BV.

A large number of polymorphonuclear leukocytes on microscopy are characteristic of desquamative inflammatory vaginitis, trichomoniasis, and atrophic vaginitis with infection, but not BV.

Visualization of trichomonads readily makes the diagnosis of trichomoniasis in the setting of an elevated pH; however, in other cases, we suggest using more sensitive and specific diagnostic tests to diagnose or exclude trichomoniasis. (See "Trichomoniasis", section on 'Diagnosis'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Bacterial vaginosis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Bacterial vaginosis (The Basics)")

Beyond the Basics topics (see "Patient education: Bacterial vaginosis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Bacterial vaginosis (BV) is characterized by a shift in vaginal flora, production of volatile amines, and resultant rise in vaginal pH. BV is the most common cause of vaginitis in women of childbearing age. (See 'Definition' above and 'Epidemiology' above.)

BV represents a complex change in the vaginal flora characterized by a reduction in concentration of the normally dominant hydrogen-peroxide producing lactobacilli and an increase in concentration of other organisms, particularly anaerobic and highly specific fastidious BV-associated bacteria. Vaginal wall biofilms, comprised predominantly of Gardnerella vaginalis, appear to play a role in pathogenesis. (See 'Pathogenesis and microbiology' above.)

Approximately 50 to 75 percent of women with BV are asymptomatic. Those with symptoms often present with an off-white, thin, and homogeneous "fishy smelling" discharge that is more noticeable after coitus and during menses. (See 'Clinical features' above.)

Sequelae of BV can include an increased risk of preterm birth, plasma-cell endometritis, postpartum fever, post-hysterectomy vaginal cuff cellulitis, postabortal infection, pelvic inflammatory disease, and acquisition of other sexually transmitted infections. (See 'Consequences of infection' above.)

When microscopy is available, the diagnosis of BV is based on the presence of at least three of the following four Amsel criteria (see 'Diagnosis' above):

Homogeneous, thin, grayish-white discharge that smoothly coats the vaginal walls.

Vaginal pH greater than 4.5.

Positive whiff-amine test, defined as the presence of a fishy odor when 10 percent potassium hydroxide (KOH) is added to a sample of vaginal discharge.

Clue cells on saline wet mount, comprising at least 20 percent of epithelial cells (picture 1A and picture 1B).

If microscopy is not available, we suggest using physical examination, pH testing, whiff-amine test, and a commercial test using a DNA probe (eg, Affirm VP III) to make the diagnosis of BV. (See 'Commercial tests' above.)

Vaginal culture is not useful for diagnosing BV. (See 'Culture' above.)

Use of UpToDate is subject to the  Subscription and License Agreement.

REFERENCES

  1. Fredricks DN, Fiedler TL, Marrazzo JM. Molecular identification of bacteria associated with bacterial vaginosis. N Engl J Med 2005; 353:1899.
  2. Joesoef, M, Schmid, G. Bacterial vaginosis. In: Clinical evidence, BMJ Publishing Group, London 2001. p.887.
  3. Morris M, Nicoll A, Simms I, et al. Bacterial vaginosis: a public health review. BJOG 2001; 108:439.
  4. Tolosa JE, Chaithongwongwatthana S, Daly S, et al. The International Infections in Pregnancy (IIP) study: variations in the prevalence of bacterial vaginosis and distribution of morphotypes in vaginal smears among pregnant women. Am J Obstet Gynecol 2006; 195:1198.
  5. Allsworth JE, Peipert JF. Prevalence of bacterial vaginosis: 2001-2004 National Health and Nutrition Examination Survey data. Obstet Gynecol 2007; 109:114.
  6. Kenyon C, Colebunders R, Crucitti T. The global epidemiology of bacterial vaginosis: a systematic review. Am J Obstet Gynecol 2013; 209:505.
  7. Hill GB. The microbiology of bacterial vaginosis. Am J Obstet Gynecol 1993; 169:450.
  8. Ling Z, Kong J, Liu F, et al. Molecular analysis of the diversity of vaginal microbiota associated with bacterial vaginosis. BMC Genomics 2010; 11:488.
  9. Eschenbach DA, Davick PR, Williams BL, et al. Prevalence of hydrogen peroxide-producing Lactobacillus species in normal women and women with bacterial vaginosis. J Clin Microbiol 1989; 27:251.
  10. Lamont RF, Sobel JD, Akins RA, et al. The vaginal microbiome: new information about genital tract flora using molecular based techniques. BJOG 2011; 118:533.
  11. Muzny CA, Schwebke JR. Pathogenesis of Bacterial Vaginosis: Discussion of Current Hypotheses. J Infect Dis 2016; 214 Suppl 1:S1.
  12. Fettweis JM, Brooks JP, Serrano MG, et al. Differences in vaginal microbiome in African American women versus women of European ancestry. Microbiology 2014; 160:2272.
  13. Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation. Nat Rev Immunol 2015; 15:30.
  14. Nelson TM, Borgogna JL, Brotman RM, et al. Vaginal biogenic amines: biomarkers of bacterial vaginosis or precursors to vaginal dysbiosis? Front Physiol 2015; 6:253.
  15. Bradshaw CS, Sobel JD. Current Treatment of Bacterial Vaginosis-Limitations and Need for Innovation. J Infect Dis 2016; 214 Suppl 1:S14.
  16. Fredricks DN, Fiedler TL, Thomas KK, et al. Targeted PCR for detection of vaginal bacteria associated with bacterial vaginosis. J Clin Microbiol 2007; 45:3270.
  17. Srinivasan S, Munch MM, Sizova MV, et al. More Easily Cultivated Than Identified: Classical Isolation With Molecular Identification of Vaginal Bacteria. J Infect Dis 2016; 214 Suppl 1:S21.
  18. Diop K, Bretelle F, Fournier PE, Fenollar F. 'Anaerococcus mediterraneensis' sp. nov., a new species isolated from human female genital tract. New Microbes New Infect 2017; 17:75.
  19. Diop K, Diop A, Bretelle F, et al. Olegusella massiliensis gen. nov., sp. nov., strain KHD7(T), a new bacterial genus isolated from the female genital tract of a patient with bacterial vaginosis. Anaerobe 2017; 44:87.
  20. Diop K, Bretelle F, Michelle C, et al. Taxonogenomics and description of Vaginella massiliensis gen. nov., sp. nov., strain Marseille P2517(T), a new bacterial genus isolated from the human vagina. New Microbes New Infect 2017; 15:94.
  21. Swidsinski A, Mendling W, Loening-Baucke V, et al. Adherent biofilms in bacterial vaginosis. Obstet Gynecol 2005; 106:1013.
  22. Swidsinski A, Doerffel Y, Loening-Baucke V, et al. Gardnerella biofilm involves females and males and is transmitted sexually. Gynecol Obstet Invest 2010; 70:256.
  23. Swidsinski A, Mendling W, Loening-Baucke V, et al. An adherent Gardnerella vaginalis biofilm persists on the vaginal epithelium after standard therapy with oral metronidazole. Am J Obstet Gynecol 2008; 198:97.e1.
  24. Alves P, Castro J, Sousa C, et al. Gardnerella vaginalis outcompetes 29 other bacterial species isolated from patients with bacterial vaginosis, using in an in vitro biofilm formation model. J Infect Dis 2014; 210:593.
  25. Patterson JL, Stull-Lane A, Girerd PH, Jefferson KK. Analysis of adherence, biofilm formation and cytotoxicity suggests a greater virulence potential of Gardnerella vaginalis relative to other bacterial-vaginosis-associated anaerobes. Microbiology 2010; 156:392.
  26. Jung HS, Ehlers MM, Lombaard H, et al. Etiology of bacterial vaginosis and polymicrobial biofilm formation. Crit Rev Microbiol 2017; :1.
  27. Verstraelen H, Swidsinski A. The biofilm in bacterial vaginosis: implications for epidemiology, diagnosis and treatment. Curr Opin Infect Dis 2013; 26:86.
  28. Hymes SR, Randis TM, Sun TY, Ratner AJ. DNase inhibits Gardnerella vaginalis biofilms in vitro and in vivo. J Infect Dis 2013; 207:1491.
  29. Fethers KA, Fairley CK, Hocking JS, et al. Sexual risk factors and bacterial vaginosis: a systematic review and meta-analysis. Clin Infect Dis 2008; 47:1426.
  30. Potter J. Should sexual partners of women with bacterial vaginosis receive treatment? Br J Gen Pract 1999; 49:913.
  31. Berger BJ, Kolton S, Zenilman JM, et al. Bacterial vaginosis in lesbians: a sexually transmitted disease. Clin Infect Dis 1995; 21:1402.
  32. Fethers K. Is bacterial vaginosis a sexually transmitted infection. Sex Transm Infect 2001; 77:390.
  33. Bradshaw CS, Morton AN, Garland SM, et al. Higher-risk behavioral practices associated with bacterial vaginosis compared with vaginal candidiasis. Obstet Gynecol 2005; 106:105.
  34. Swedberg J, Steiner JF, Deiss F, et al. Comparison of single-dose vs one-week course of metronidazole for symptomatic bacterial vaginosis. JAMA 1985; 254:1046.
  35. Vutyavanich T, Pongsuthirak P, Vannareumol P, et al. A randomized double-blind trial of tinidazole treatment of the sexual partners of females with bacterial vaginosis. Obstet Gynecol 1993; 82:550.
  36. Mengel MB, Berg AO, Weaver CH, et al. The effectiveness of single-dose metronidazole therapy for patients and their partners with bacterial vaginosis. J Fam Pract 1989; 28:163.
  37. Vejtorp M, Bollerup AC, Vejtorp L, et al. Bacterial vaginosis: a double-blind randomized trial of the effect of treatment of the sexual partner. Br J Obstet Gynaecol 1988; 95:920.
  38. Colli E, Landoni M, Parazzini F. Treatment of male partners and recurrence of bacterial vaginosis: a randomised trial. Genitourin Med 1997; 73:267.
  39. Moi H. Prevalence of bacterial vaginosis and its association with genital infections, inflammation, and contraceptive methods in women attending sexually transmitted disease and primary health clinics. Int J STD AIDS 1990; 1:86.
  40. Mehta SD. Systematic review of randomized trials of treatment of male sexual partners for improved bacteria vaginosis outcomes in women. Sex Transm Dis 2012; 39:822.
  41. Yen S, Shafer MA, Moncada J, et al. Bacterial vaginosis in sexually experienced and non-sexually experienced young women entering the military. Obstet Gynecol 2003; 102:927.
  42. Fethers KA, Fairley CK, Morton A, et al. Early sexual experiences and risk factors for bacterial vaginosis. J Infect Dis 2009; 200:1662.
  43. Nelson DE, Van Der Pol B, Dong Q, et al. Characteristic male urine microbiomes associate with asymptomatic sexually transmitted infection. PLoS One 2010; 5:e14116.
  44. Nelson DE, Dong Q, Van der Pol B, et al. Bacterial communities of the coronal sulcus and distal urethra of adolescent males. PLoS One 2012; 7:e36298.
  45. Fethers K, Marks C, Mindel A, Estcourt CS. Sexually transmitted infections and risk behaviours in women who have sex with women. Sex Transm Infect 2000; 76:345.
  46. Marrazzo JM, Antonio M, Agnew K, Hillier SL. Distribution of genital Lactobacillus strains shared by female sex partners. J Infect Dis 2009; 199:680.
  47. Bradshaw CS, Walker SM, Vodstrcil LA, et al. The influence of behaviors and relationships on the vaginal microbiota of women and their female partners: the WOW Health Study. J Infect Dis 2014; 209:1562.
  48. Marrazzo JM, Koutsky LA, Eschenbach DA, et al. Characterization of vaginal flora and bacterial vaginosis in women who have sex with women. J Infect Dis 2002; 185:1307.
  49. Vodstrcil LA, Walker SM, Hocking JS, et al. Incident bacterial vaginosis (BV) in women who have sex with women is associated with behaviors that suggest sexual transmission of BV. Clin Infect Dis 2015; 60:1042.
  50. Evans AL, Scally AJ, Wellard SJ, Wilson JD. Prevalence of bacterial vaginosis in lesbians and heterosexual women in a community setting. Sex Transm Infect 2007; 83:470.
  51. Esber A, Vicetti Miguel RD, Cherpes TL, et al. Risk of Bacterial Vaginosis Among Women With Herpes Simplex Virus Type 2 Infection: A Systematic Review and Meta-analysis. J Infect Dis 2015; 212:8.
  52. Jamieson DJ, Duerr A, Klein RS, et al. Longitudinal analysis of bacterial vaginosis: findings from the HIV epidemiology research study. Obstet Gynecol 2001; 98:656.
  53. Myer L, Denny L, Telerant R, et al. Bacterial vaginosis and susceptibility to HIV infection in South African women: a nested case-control study. J Infect Dis 2005; 192:1372.
  54. Goldenberg RL, Klebanoff MA, Nugent R, et al. Bacterial colonization of the vagina during pregnancy in four ethnic groups. Am J Obstet Gynecol 1996; 174:1618.
  55. Beamer MA, Austin MN, Avolia HA, et al. Bacterial species colonizing the vagina of healthy women are not associated with race. Anaerobe 2017.
  56. Ness RB, Hillier SL, Richter HE, et al. Douching in relation to bacterial vaginosis, lactobacilli, and facultative bacteria in the vagina. Obstet Gynecol 2002; 100:765.
  57. Schwebke JR, Desmond RA, Oh MK. Predictors of bacterial vaginosis in adolescent women who douche. Sex Transm Dis 2004; 31:433.
  58. Ness RB, Kip KE, Soper DE, et al. Variability of bacterial vaginosis over 6- to 12-month intervals. Sex Transm Dis 2006; 33:381.
  59. Schwebke JR, Desmond RA. A randomized trial of the duration of therapy with metronidazole plus or minus azithromycin for treatment of symptomatic bacterial vaginosis. Clin Infect Dis 2007; 44:213.
  60. Brotman RM, Klebanoff MA, Nansel TR, et al. A longitudinal study of vaginal douching and bacterial vaginosis--a marginal structural modeling analysis. Am J Epidemiol 2008; 168:188.
  61. Klebanoff MA, Nansel TR, Brotman RM, et al. Personal hygienic behaviors and bacterial vaginosis. Sex Transm Dis 2010; 37:94.
  62. Verstraelen H, Verhelst R, Nuytinck L, et al. Gene polymorphisms of Toll-like and related recognition receptors in relation to the vaginal carriage of Gardnerella vaginalis and Atopobium vaginae. J Reprod Immunol 2009; 79:163.
  63. Neggers YH, Nansel TR, Andrews WW, et al. Dietary intake of selected nutrients affects bacterial vaginosis in women. J Nutr 2007; 137:2128.
  64. Amsel R, Totten PA, Spiegel CA, et al. Nonspecific vaginitis. Diagnostic criteria and microbial and epidemiologic associations. Am J Med 1983; 74:14.
  65. Klebanoff MA, Schwebke JR, Zhang J, et al. Vulvovaginal symptoms in women with bacterial vaginosis. Obstet Gynecol 2004; 104:267.
  66. Livengood CH 3rd, Thomason JL, Hill GB. Bacterial vaginosis: diagnostic and pathogenetic findings during topical clindamycin therapy. Am J Obstet Gynecol 1990; 163:515.
  67. Sobel JD, Subramanian C, Foxman B, et al. Mixed vaginitis-more than coinfection and with therapeutic implications. Curr Infect Dis Rep 2013; 15:104.
  68. Marrazzo JM, Wiesenfeld HC, Murray PJ, et al. Risk factors for cervicitis among women with bacterial vaginosis. J Infect Dis 2006; 193:617.
  69. Klebanoff MA, Hillier SL, Nugent RP, et al. Is bacterial vaginosis a stronger risk factor for preterm birth when it is diagnosed earlier in gestation? Am J Obstet Gynecol 2005; 192:470.
  70. Eschenbach DA. Bacterial vaginosis: emphasis on upper genital tract complications. Obstet Gynecol Clin North Am 1989; 16:593.
  71. Flynn CA, Helwig AL, Meurer LN. Bacterial vaginosis in pregnancy and the risk of prematurity: a meta-analysis. J Fam Pract 1999; 48:885.
  72. Hauth JC, Macpherson C, Carey JC, et al. Early pregnancy threshold vaginal pH and Gram stain scores predictive of subsequent preterm birth in asymptomatic women. Am J Obstet Gynecol 2003; 188:831.
  73. Andrews WW, Hauth JC, Cliver SP, et al. Association of asymptomatic bacterial vaginosis with endometrial microbial colonization and plasma cell endometritis in nonpregnant women. Am J Obstet Gynecol 2006; 195:1611.
  74. Oleen-Burkey MA, Hillier SL. Pregnancy complications associated with bacterial vaginosis and their estimated costs. Infect Dis Obstet Gynecol 1995; 3:149.
  75. MacDermott RI. Bacterial vaginosis. Br J Obstet Gynaecol 1995; 102:92.
  76. Martin HL, Richardson BA, Nyange PM, et al. Vaginal lactobacilli, microbial flora, and risk of human immunodeficiency virus type 1 and sexually transmitted disease acquisition. J Infect Dis 1999; 180:1863.
  77. Cohen CR, Lingappa JR, Baeten JM, et al. Bacterial vaginosis associated with increased risk of female-to-male HIV-1 transmission: a prospective cohort analysis among African couples. PLoS Med 2012; 9:e1001251.
  78. Cherpes TL, Meyn LA, Krohn MA, et al. Association between acquisition of herpes simplex virus type 2 in women and bacterial vaginosis. Clin Infect Dis 2003; 37:319.
  79. Wiesenfeld HC, Hillier SL, Krohn MA, et al. Bacterial vaginosis is a strong predictor of Neisseria gonorrhoeae and Chlamydia trachomatis infection. Clin Infect Dis 2003; 36:663.
  80. Balkus JE, Richardson BA, Rabe LK, et al. Bacterial vaginosis and the risk of trichomonas vaginalis acquisition among HIV-1-negative women. Sex Transm Dis 2014; 41:123.
  81. Taylor BD, Darville T, Haggerty CL. Does bacterial vaginosis cause pelvic inflammatory disease? Sex Transm Dis 2013; 40:117.
  82. Ness RB, Hillier SL, Kip KE, et al. Bacterial vaginosis and risk of pelvic inflammatory disease. Obstet Gynecol 2004; 104:761.
  83. Gillet E, Meys JF, Verstraelen H, et al. Association between bacterial vaginosis and cervical intraepithelial neoplasia: systematic review and meta-analysis. PLoS One 2012; 7:e45201.
  84. Guo YL, You K, Qiao J, et al. Bacterial vaginosis is conducive to the persistence of HPV infection. Int J STD AIDS 2012; 23:581.
  85. King CC, Jamieson DJ, Wiener J, et al. Bacterial vaginosis and the natural history of human papillomavirus. Infect Dis Obstet Gynecol 2011; 2011:319460.
  86. Sherrard J, Donders G, White D, et al. European (IUSTI/WHO) guideline on the management of vaginal discharge, 2011. Int J STD AIDS 2011; 22:421.
  87. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep 2015; 64:1.
  88. Van Der Pol B. Profile of the triplex assay for detection of chlamydia, gonorrhea and trichomonas using the BD MAX™ System. Expert Rev Mol Diagn 2017; 17:539.
  89. Eschenbach DA, Hillier S, Critchlow C, et al. Diagnosis and clinical manifestations of bacterial vaginosis. Am J Obstet Gynecol 1988; 158:819.
  90. Landers DV, Wiesenfeld HC, Heine RP, et al. Predictive value of the clinical diagnosis of lower genital tract infection in women. Am J Obstet Gynecol 2004; 190:1004.
  91. Nugent RP, Krohn MA, Hillier SL. Reliability of diagnosing bacterial vaginosis is improved by a standardized method of gram stain interpretation. J Clin Microbiol 1991; 29:297.
  92. Schwebke JR, Hillier SL, Sobel JD, et al. Validity of the vaginal gram stain for the diagnosis of bacterial vaginosis. Obstet Gynecol 1996; 88:573.
  93. Tam MT, Yungbluth M, Myles T. Gram stain method shows better sensitivity than clinical criteria for detection of bacterial vaginosis in surveillance of pregnant, low-income women in a clinical setting. Infect Dis Obstet Gynecol 1998; 6:204.
  94. Gratacós E, Figueras F, Barranco M, et al. Prevalence of bacterial vaginosis and correlation of clinical to Gram stain diagnostic criteria in low risk pregnant women. Eur J Epidemiol 1999; 15:913.
  95. Spiegel CA. Bacterial vaginosis. Clin Microbiol Rev 1991; 4:485.
  96. Greene JF 3rd, Kuehl TJ, Allen SR. The papanicolaou smear: inadequate screening test for bacterial vaginosis during pregnancy. Am J Obstet Gynecol 2000; 182:1048.
  97. Briselden AM, Hillier SL. Evaluation of affirm VP Microbial Identification Test for Gardnerella vaginalis and Trichomonas vaginalis. J Clin Microbiol 1994; 32:148.
  98. Sheiness D, Dix K, Watanabe S, Hillier SL. High levels of Gardnerella vaginalis detected with an oligonucleotide probe combined with elevated pH as a diagnostic indicator of bacterial vaginosis. J Clin Microbiol 1992; 30:642.
  99. Myziuk L, Romanowski B, Johnson SC. BVBlue test for diagnosis of bacterial vaginosis. J Clin Microbiol 2003; 41:1925.
  100. Sumeksri P, Koprasert C, Panichkul S. BVBLUE test for diagnosis of bacterial vaginosis in pregnant women attending antenatal care at Phramongkutklao Hospital. J Med Assoc Thai 2005; 88 Suppl 3:S7.
  101. Bradshaw CS, Morton AN, Garland SM, et al. Evaluation of a point-of-care test, BVBlue, and clinical and laboratory criteria for diagnosis of bacterial vaginosis. J Clin Microbiol 2005; 43:1304.
  102. Menard JP, Fenollar F, Henry M, et al. Molecular quantification of Gardnerella vaginalis and Atopobium vaginae loads to predict bacterial vaginosis. Clin Infect Dis 2008; 47:33.
  103. Cartwright CP, Lembke BD, Ramachandran K, et al. Development and validation of a semiquantitative, multitarget PCR assay for diagnosis of bacterial vaginosis. J Clin Microbiol 2012; 50:2321.
  104. Menard JP, Mazouni C, Fenollar F, et al. Diagnostic accuracy of quantitative real-time PCR assay versus clinical and Gram stain identification of bacterial vaginosis. Eur J Clin Microbiol Infect Dis 2010; 29:1547.
  105. Dumonceaux TJ, Schellenberg J, Goleski V, et al. Multiplex detection of bacteria associated with normal microbiota and with bacterial vaginosis in vaginal swabs by use of oligonucleotide-coupled fluorescent microspheres. J Clin Microbiol 2009; 47:4067.
  106. Gaydos CA, Beqaj S, Schwebke JR, et al. Clinical Validation of a Test for the Diagnosis of Vaginitis. Obstet Gynecol 2017; 130:181.
  107. Huppert JS, Hesse EA, Bernard MC, et al. Accuracy and trust of self-testing for bacterial vaginosis. J Adolesc Health 2012; 51:400.
  108. Singh RH, Zenilman JM, Brown KM, et al. The role of physical examination in diagnosing common causes of vaginitis: a prospective study. Sex Transm Infect 2013; 89:185.
Topic 5451 Version 59.0

All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.