Bacterial vaginosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alara Ece Dagsali, M.D.[2]
Synonyms and keywords: Anaerobic vaginosis; Nonspecific vaginitis
Overview
Bacterial vaginosis (BV) is a clinical condition characterized by a shift in vaginal microbiota 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 (eg, abnormal vaginal discharge and odor). Future health implications of BV include, but are not limited to, increased susceptibility to other sexually transmitted infections (STIs), including HIV, and preterm birth.
BV is characterized by three alterations in the vaginal environment:
- A shift in vaginal microbiota from Lactobacillus species to one of high bacterial diversity, including facultative anaerobes.
- Production of volatile amines by the new bacterial microbiota and reduced lactic acid production.
- Resultant rise in vaginal pH to >4.5 (normal vaginal pH of estrogenized females typically ranges from 4.0 to 4.5).
Historical Perspective
BV is the most common cause of abnormal vaginal discharge in females of childbearing age, accounting for 40 to 50 percent of vaginitis cases. 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. This included both symptomatic and asymptomatic infection. Worldwide, a meta-analysis of studies from seven regions of the world found that the prevalence of Nugent-diagnosed BV was 23 to 29 percent among women of reproductive age, with small variations according to the population studied.
Pathophysiology
Processes that contribute to clinical BV include a shift in vaginal microbiota from hydrogen peroxide-producing lactobacilli to anaerobic bacteria, release of amines, and production of a protective biofilm.
Altered vaginal microbiota and dysbiosis – BV represents a complex change in the vaginal microbiota characterized by a reduction in concentration of the normally dominant lactobacilli, which produce hydrogen peroxide and lactic acid, and an increase in concentration of other organisms, especially anaerobic Gram-negative rods [9-13]. Age also appears to impact the vaginal microbial community [14]. The absence of clinical signs 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 microbiota that can ultimately impact vaginal function and lead to negative health consequences Processes that contribute to clinical BV include a shift in vaginal microbiota from hydrogen peroxide-producing lactobacilli to anaerobic bacteria, release of amines, and production of a protective biofilm.
- Commonly associated bacteria – The major bacteria detected in females 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. Fusobacterium species and Atopobium vaginae (now renamed Fannyhessea vaginae) [19] are also common.
- Bacteria identified with ribosomal DNA probes – The difference in vaginal microbiota between those with and without BV was illustrated in a study that used broad range ribosomal DNA probes to determine the vaginal microbiota of 27 women with BV and 46 controls [1]. Overall, 35 bacterial phylotypes were identified in women with BV, including 16 that were newly recognized. Women with BV had a mean of 12.6 phylotypes (range 9 to 17) per sample compared with 3.3 phylotypes (range 1 to 6) per sample in women without BV. The organisms newly identified by polymerase chain reaction included fastidious bacteria termed "BV-associated bacteria (BVAB) 1, 2, and 3" in the Clostridiales order, which appear to be specific indicators of BV [20]. Subsequent studies suggest BVAB1, now known as Candidatus lachnonocura vaginae, has likely been mistaken for Mobiluncus on microscopy and Nugent scoring [21-23]. Additional studies have also further characterized BVAB3, which is now known as Mageebacillus indolicus, and identified other bacterial species in the human vagina, including the novel strains Peptoniphilaceae DNF01163 and Prevotellaceae DNF00733, and [24-27].
- Production of amines Hydrogen peroxide-producing lactobacilli appear to be important in preventing overgrowth of the anaerobes normally present in the vaginal microbiota. 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. 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 a 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 microbiota [28-34]. In this model, a cohesive form of G. vaginalis adheres to the vaginal epithelium and then becomes the scaffolding to which other species adhere [35].
- Biopsy data The biofilm hypothesis is supported by a study of microbiota on the epithelial surfaces of vaginal biopsy specimens from individuals 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 [28]. Subsequent desquamation of these epithelial cells would result in the classic clue cells diagnostic of the disorder (see 'Diagnostic evaluation' below). By contrast, most healthy controls had unstructured accumulations of bacteria within secretions loosely attached to epithelial surfaces.
- Role of extracellular DNA (eDNA) 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 [36]. 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.
- Impact of gender-affirming therapy The impact of hormonal and surgical gender-affirming treatment on the microbiota of the vagina and neovagina are not yet well understood. Whether a non-Lactobacillus dominant microbiome in trans people is BV requiring antibiotic treatment is an area needing further study.
- Estrogen-dominant neovagina Transfeminine individuals may elect gender-affirming surgery with creation of a neovagina. Scrotal and penile skin is typically used and may require an extension with colon or skin graft. Individuals with neovaginas who use estrogen therapy have reported symptoms of vaginal discharge and malodor [37]. In one study comparing the microbiome of 5 individuals with neovaginas with 32 individuals with vaginas, the most common taxa in the neovaginas were Porphyromonas (30.2 percent), Peptostreptococcus (9.2 percent), Prevotella (9.0 percent), Mobiluncus (8.0 percent), and Jonquetella (7.2 percent) compared with Lactobacillus and Gardnerella in the vaginas [38]. Of the patients with neovaginas, four had penile inversion/scrotal graft with sigmoid colon graft and one had penile inversion/scrotal graft only.
Causes
Differentiating Bacterial vaginosis from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Amsel Criteria | History and Symptoms | Physical Examination | Laboratory Findings | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies