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Bacterial vaginosis: Clinical manifestations and diagnosis

Bacterial vaginosis: Clinical manifestations and diagnosis
Literature review current through: May 2024.
This topic last updated: Dec 07, 2023.

INTRODUCTION — 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.

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: Initial treatment".)

(See "Vaginitis in adults: Initial evaluation".)

(See "Acute cervicitis".)

In this topic, when discussing study results, we will use the terms "woman/en" or "patient(s)" as they are used in the studies presented. However, we encourage the reader to consider the specific counseling and treatment needs of transgender and gender diverse individuals.

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

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 [2].

Resultant rise in vaginal pH to >4.5 (normal vaginal pH of estrogenized females typically ranges from 4.0 to 4.5). (See "Vaginitis in adults: Initial evaluation", section on 'Normal vaginal discharge'.)

EPIDEMIOLOGY — BV is the most common cause of abnormal vaginal discharge in females of childbearing age, accounting for 40 to 50 percent of vaginitis cases [3-5]. 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 [6]. 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 [7,8]. The health consequences of BV infection are presented below. (See 'Clinical consequences of BV' below.)

PATHOGENESIS AND MICROBIOLOGY — Processes that contribute to clinical BV include a shift in vaginal microbiota from hydrogen peroxide-producing lactobacillus 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]. Ethnicity and age are additional factors that appear 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 [15,16]. (See 'Clinical consequences of BV' below.)

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 [9,17,18]. 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 include fastidious bacteria termed "BV-associated bacteria 1, 2, and 3" in the Clostridiales order, which appear to be specific indicators of BV [20]. Subsequent studies have documented several other bacterial species in the human vagina, including the novel strains Peptoniphilaceae DNF01163 and Prevotellaceae DNF00733 [21-24].

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 (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 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 [25-31]. In this model, a cohesive form of G. vaginalis adheres to the vaginal epithelium and then becomes the scaffolding to which other species adhere [32].

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 [25]. 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 [33]. 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.

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 [34]. 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 [35]. Of the patients with neovaginas, four had penile inversion/scrotal graft with sigmoid colon graft and one had penile inversion/scrotal graft only.

-(See "Gender-affirming surgery: Male to female".)

-(See "Transgender women: Evaluation and management".)

Testosterone-dominant vagina – For transmasculine individuals with a vagina who are taking testosterone therapy, one study of 28 individuals reported diverse anaerobic taxa for most patients and three with Lactobacillus-dominant microbiota [36]. In this study, the microbiota were more similar to those of postmenopausal females than those with BV. (See "Transgender men: Evaluation and management".)

RISK FACTORS

Sexual activity – While the majority of epidemiologic data support the hypothesis that BV is a sexually transmitted infection (STI), it is not yet classified as such because of lack of a single causative agent and absence of a clear disease counterpart in males [17,37-41]. In addition, early studies reported mixed results on the impact of treatment of the male sexual partner [42-47]. 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 [48]. 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.

Studies including male and female sexual partners – Sexual activity is a risk factor for BV, and most experts believe that BV does not occur in individuals who have never had sexual contact of any type, including receptive oral sex [49-51].

-Impact of first sexual encounter – An observational study including 400 Kenyan females age 16 to 21 years reported BV prevalence (Nugent score ≥7) increased from 2.8 percent to 13.7 percent in the time period from before first sex to after first sex [51]. First sex was associated with more than two-fold increased risk of BV in both adjusted analysis (adjusted hazard ratio [aHR] 2.44, 95% CI 1.25-4.76) and a generalized estimating equations model (aHR 1.92, 95% 1.12-3.31).

-Epidemiologic data – Epidemiologic studies are strongly supportive of sexual transmission of BV pathogens [52].

-Impact of male partner treatment – A trial evaluating male partner treatment with seven days of oral metronidazole was stopped early after interim analysis reported similar BV recurrence rates in both treatment (81 percent) and placebo (80 percent). However, in a subset analysis, women who stated that their partners had higher adherence to the course of metronidazole had a lower risk for BV recurrence [53].

-Impact of sexual contact – 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 [37].

-Male penile microbiome – Many BV-associated species have been isolated from the male penile skin, semen, urethra, and urine specimens, and the penile microbiome has been reported to correlate with incident BV infections [54-57].

Studies of same-sex female partnerships – BV is highly prevalent (25 to 50 percent) in females who have sex with females 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 [58-63]. However, in one study, sexually active monogamous female same-sex partnerships over six months tended to have concordant, stable, vaginal microbiota, which was most concordant for normal microbiota [60]. This suggests that longer duration, sexually active partnerships led to stability and alignment of a favorable vaginal microbiota in the couples. Accordingly, the majority of investigators believe that BV, as an original or first infection or occurrence, is sexually transmitted.

Infection with sexually transmitted infections – The presence of other STIs 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) type 2 infection, women infected with HSV-2 had a 55 percent higher risk of BV infection compared with women who were HSV-2 uninfected [64]. 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 [65]. Conversely, BV may also be a risk factor for HIV and other STI acquisition [66-71]. (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 some populations, it is not clear if this finding reflects genetic, socioeconomic, behavioral, or other differences [6,14,72,73]. In the United States National Health and Nutrition Examination Survey (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 White women [6]. By contrast, in a small study comparing the vaginal microbiota of White women and Black women by both cultivation-dependent and cultivation-independent methods, there were no differences in colonization and density of bacterial species by race once women with BV by Nugent criteria were removed [74].

Other – In addition to sexual and infectious risk factors, most studies indicate that douching and cigarette smoking are risk factors for acquisition of BV among sexually active females [3,4,60,75-80]. Other risk factors may include:

Diet – 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 [81]. A diet high in fiber has been associated with higher likelihood of a Lactobacillus-dominant vaginal microbial community [82]. While these dietary factors were associated with differences in the vaginal microbiota, further studies are needed to determine causality.

Body mass index – One study that evaluated Nugent scores for nearly 6000 women reported that overweight (body mass index [BMI] 25.0 to 29.9 kg/m2) and obese (BMI ≥30 kg/m2) women had higher Nugent scores and rates of BV compared with women of normal BMI (BMI 18.5 to 24.9 kg/m2) [73]. The prevalence rates of BV were 21, 30, and 35 percent for lean, overweight, and obese BMIs, respectively.

No increased risk – BV is not associated with chronic medical conditions (eg, diabetes) or immunosuppressive states. Although some degree of genetic susceptibility to BV is likely, no association between a gene polymorphism and BV has been established [83] .

CLINICAL FEATURES — Individuals can present with classic symptoms, symptoms that suggest multiple etiologies of vaginal discharge, or be asymptomatic.

Classic symptoms – Symptomatic individuals typically present with vaginal discharge and/or vaginal odor [49,84,85]. 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 [86,87].

Although supporting data are limited, in our experience, in the absence of microscopy, a lack of fishy odor (negative whiff test) makes the diagnosis of BV less likely [88-92].

Mixed vaginitis – BV alone typically does not cause dysuria, dyspareunia, pruritus, vulvovaginal burning, or vaginal/vulvar inflammation (erythema, edema) [84,85]. The presence of these symptoms suggests mixed vaginitis (symptoms due to two pathogens) [93]. However, symptoms are poorly predictive of diagnosis; thus, all symptomatic individuals should undergo examination and evaluation [94].

Cervicitis – Although BV does not involve the cervix, the disorder may be associated with acute cervicitis (endocervical mucopurulent discharge or easily induced cervical bleeding) [95]. (See "Acute cervicitis".)

Asymptomatic – Up to 50 to 70 percent of females with BV are asymptomatic [49,84,85]. Small studies with a follow-up durations of 28 to 40 days have reported that 12 to 18 percent of asymptomatic patients will go on to develop symptoms [78,96,97].

CLINICAL CONSEQUENCES OF BV — Presence of BV increases the risk of poor obstetric and gynecologic outcomes as well as risk of acquisition of HIV and other sexually transmitted infections (STIs).

Obstetric outcomes

Preterm delivery [98-101] (See "Bacterial vaginosis: Initial treatment", section on 'Pregnant or lactating persons'.)

Postpartum fever (See "Postpartum endometritis".)

Gynecologic complications [102-104]:

Endometrial bacterial colonization and plasma-cell endometritis (See "Endometritis unrelated to pregnancy".)

Posthysterectomy vaginal cuff cellulitis (See "Posthysterectomy pelvic abscess".)

Postabortal infection (See "Septic abortion: Clinical presentation and management".)

Other infections

HIV – Increased risk of both acquisition and transmission [66,105,106].

Sexually transmitted infections – BV is a risk factor for acquisition of herpes simplex virus (HSV) type 2, gonorrhea, chlamydia, and trichomonas infection [107-109]. It has been hypothesized that the increased risk of acquisition of STIs in those with BV may be due to lack of hydrogen peroxide-producing lactobacilli in the vaginal microbiota of affected persons; other factors associated with BV infection, such as local cytokine production, may also play a role. Additionally, BV has been associated with persistence of chlamydia infection (ie, reduces likelihood of spontaneous clearance of chlamydia) [110].

Pelvic inflammatory disease – BV is more common among patients with pelvic inflammatory disease (PID). While it is not clear whether it is a causal factor or an independent risk factor for this disease [111,112], BV-associated organisms have been found in the endometrium in individuals with PID who do not have any other causes identified [113].

HPV and subsequent cervical pathology – BV appears conducive to the persistence of human papillomavirus infection [114,115], which is a contributor to development of cervical lesions and cancer. (See "Cervical intraepithelial neoplasia: Terminology, incidence, pathogenesis, and prevention", section on 'Role of human papillomavirus'.)

DIAGNOSTIC EVALUATION — As symptoms of BV overlap with those of other vaginal infections, accurate diagnosis is needed to correctly guide treatment.

Physical examination — All patients undergo physical examination to assess the vaginal discharge, evaluate for related findings (eg, vulvar excoriations or edema, erythema, cervicitis), and exclude other causes of the patient's symptoms. Details of physical examination are presented in the algorithm (algorithm 1). (See "Vaginitis in adults: Initial evaluation".)

Approach to test selection

Summary — All patients undergo testing of abnormal vaginal discharge (algorithm 1). Clinician training and test availability drive test selection. Options include laboratory tests, which typically use nucleic acid amplification test (NAAT) technology, clinical evaluation of vaginal discharge with pH testing and microscopy, or gram stain with Nugent criteria (typically in research settings) (table 1). NAAT-based laboratory tests are increasingly used because of their sensitivity and specificity > 90 percent, although they require time for processing that delays diagnosis and treatment. Cervicitis caused by gonorrhea or chlamydia should also be excluded.

The relative advantages, disadvantages, and efficacy of each test approach is briefly presented here and discussed in detail in related content. (See "Vaginitis in adults: Initial evaluation", section on 'Test vaginal discharge'.)

Clinical laboratory tests — Clinical laboratory tests are increasingly used for diagnosing BV because they have improved diagnostic accuracy compared with pH testing and microscopy (ie, greater sensitivity and specificity), are able to identify fastidious bacteria, are easy to use, and can test for multiple infections from the same swab (eg, candidiasis and trichomoniasis) (algorithm 1 and table 1) [52,116-122]. Limitations include the need for clinician education to interpret the tests, time delay for diagnosis, and potential identification of non-pathogenic organisms. (See "Vaginitis in adults: Initial evaluation", section on 'Nucleic acid amplification tests (NAATs)'.)

Nucleic acid amplification tests (NAATs) NAATs are laboratory-based tests that exponentially multiply specific nucleic acid sequences through polymerase chain reactions (PCRs) to identify evidence of various vaginal pathogens, including those specific to the diagnosis of bacterial vaginosis, vaginal candidiasis, and trichomoniasis [116,118,121]. The vaginal swab can be collected by a clinician or patient [121,123]. As noted above, we advise a complete physical examination to guide the differential diagnosis and evaluate for alternative diagnoses. Some of the tests are FDA approved (BD Max vaginal panel, Aptima BV) while other are laboratory-developed tests (NuSwab VG, SureSwab BV, and OneSwab BV panel) that require internal validation prior to use [52]; all have high sensitivity and specificity (ie, >90 percent) [117,119,124]. BV cannot be diagnosed by NAATs that are not specific to BV organisms. (See "Vaginitis in adults: Initial evaluation", section on 'Nucleic acid amplification tests (NAATs)'.)

Details by test type include:

The BD Max vaginal panel (Becton Dickinson) uses quantitative PCR measurement of G. vaginalis, Atopobium vaginae, Megasphaera-1, BV-associated bacteria 2, L. crispatus, L. jensenii, and a proprietary algorithm to provide a positive/negative assessment for the presence of BV [52,125]. In a study of 1763 symptomatic individuals, the sensitivity of the assay compared with a combination of Nugent score and Amsel criteria was 90.5 percent (95% CI 88.3-92.2) and specificity was 85.8 percent (95% CI 83.0-88.3) [121].

The Aptima BV (Hologic) is a NAAT that measures the presence of Lactobacillus, G. vaginalis, and A. vaginae [52,125]. In a study that included 1501 symptomatic women, the sensitivity compared with a combination of Nugent score and Amsel criteria was 95 percent (95% CI 93.1-96.4) and specificity was 89.6 percent (95% CI 87.1-91.6) [123].

NuSwab VG (LabCorp) is a laboratory-developed test that evaluates for Atopobium vaginae, Megasphaera-1, and BV-associated bacterium 2 [52]. Results are reported as positive, negative, or indeterminate.

SureSwab BV (Quest Diagnostics) is a laboratory-developed test that evaluates for Lactobacillus species, G. vaginalis, Atopobium vaginae, Megasphaera-1 and -2, and BV-associated bacterium 2 [52]. Results are reported as supportive of BV, not supportive, or equivocal.

OneSwab BV Panel (MDL) is a laboratory-derived test that uses PCR to assess for G. vaginalis, Atopobium vaginae, Megasphaera-1 and -2, and BV-associated bacteria 2 and uses quantitative PCR for Lactobacillus profiling [52].

Point of care tests – These tests can be done in the office at the time of the physical examination and are to be used in conjunction with physical examination, vaginal pH, and whiff-amine test. All have become less commonly used since the development of NAATs.

OSOM BVBlue – The OSOM BVBlue system is a chromogenic diagnostic test based on the presence of elevated sialidase enzyme activity in vaginal fluid samples [88,126,127].

Affirm VP III – The Affirm VP III test is an automated DNA probe assay for detecting G. vaginalis when present at a high concentration [128].

pH and microscopy using Amsel criteria — When pH testing and microscopy are available, the diagnosis of BV in premenopausal females is usually based upon the presence of at least three Amsel criteria (characteristic vaginal discharge, elevated pH, clue cells seen on microscopy, fishy odor) (figure 1) [87,116,129,130]. Compared with Gram stain for diagnosing BV, reported sensitivity of Amsel criteria for diagnosis of BV is over 90 percent and specificity is 77 percent when used by expert clinicians [131]. However, this approach is limited by availability of microscopy equipment and trained providers; lower sensitivities and specificities have been reported when Amsel criteria are used by general clinicians [117]. Advantages, disadvantages, diagnostic accuracy, and how to perform the vaginal pH and microscopy is reviewed in detail in related content (algorithm 1).

(See "Vaginitis in adults: Initial evaluation", section on 'pH and microscopy'.)

Amsel criteria for diagnosis of BV (at least three criteria must be present) (table 2) [116]:

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 and figure 1). Clue cells are vaginal epithelial cells studded with adherent coccobacilli that are best appreciated at the edge of the cell (picture 2). 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 [132].

However, these criteria are not exclusive to BV; the first three findings are sometimes also present in patients with trichomoniasis (table 3). Mobiluncus species may be noted on microscopy as well (movie 1).

Gram stain with Nugent criteria — Gram stain of vaginal discharge is the gold standard for diagnosis of BV (picture 3A-B) [133], but is mostly performed in research studies because it requires more time, resources, and expertise than Amsel criteria [116,134-136]. The Gram-stained smear is evaluated using Nugent criteria (table 4) or Hay/Ison criteria (table 5). When clinical criteria are used to define infection, the reported sensitivity of Gram stain scoring ranges from 62 to 100 percent [137].

Approaches to avoid — The following methods are unreliable for the diagnosis of BV and therefore are not advised.

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. Additionally, a speculum examination facilitates evaluation for alternative or concurrent diagnoses, such as cervicitis, pelvic inflammatory disease (PID), or retained objects.

In one study of 131 individuals who tested a self-collected vaginal swab for pH and sialidase, self-test pH had a sensitivity of 73 percent and specificity of 67 percent and self-sialidase was 40 percent sensitive and 90 percent specific compared with clinical diagnosis of BV [138].

In another study of the diagnostic accuracy for BV, clinician-performed clinical examination with speculum examination was more likely to result in a correct diagnosis of BV compared with examination of a self-obtained vaginal swab (90 in 125 versus 68 in 125) [139]. Over-diagnosis/over-treatment occurred in 15 patients (105 positive diagnoses versus 61 positive diagnoses).

Diagnosis without testing – In settings where neither microscopy nor commercial tests are available, diagnosis is based upon findings on clinical examination (characteristic vaginal discharge, elevated vaginal pH, fishy odor). In a 2020 study evaluating 303 symptomatic individuals in eight clinics affiliated with an academic medical center, all participants were evaluated for presence of vaginal discharge but pH was assessed in 15 percent and whiff test in 21 percent [140]. As a result, 30 percent of participants with BV diagnosed by the study gold standard received inadequate treatment and 23 percent of participants without BV received inappropriate treatment.

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

Cytology – The Papanicolaou smear is not reliable for diagnosis of BV (sensitivity 49 percent, specificity 93 percent) [141]. 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 microbiota 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 individuals is not routinely indicated. (See "Bacterial vaginosis: Initial treatment", section on 'Asymptomatic nonpregnant'.)

DIAGNOSIS — BV is diagnosed when laboratory or clinical tests find evidence of altered vaginal flora in patients with suggestive physical examination findings. Symptoms may or may not be present.  

DIFFERENTIAL DIAGNOSIS — 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 (table 3).

Dyspareunia and/or vaginal inflammation – Individuals with BV generally do not have dyspareunia or signs of vaginal inflammation; by contrast, those with atrophic vaginitis, desquamative inflammatory vaginitis, and trichomoniasis usually have these signs and symptoms.

Additional microscopy findings

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

White blood cells – Large numbers of white blood cells, specifically polymorphonuclear leukocytes (PMNs), on microscopy are characteristic of desquamative inflammatory vaginitis, trichomoniasis, and atrophic vaginitis with infection, but not BV.

Trichomonads – Visualization of trichomonads readily makes the diagnosis of trichomoniasis in the setting of an elevated pH; in the absence of visible trichomonads or if microscopy is not available, we suggest using more sensitive and specific diagnostic tests to diagnose or exclude trichomoniasis. (See "Trichomoniasis: Clinical manifestations and diagnosis", section on 'Diagnosis'.)

Mixed infections – Mixed infections with BV and a second pathogen, either T. vaginalis or Candida species, are not infrequent, with clinical and laboratory findings reflecting features of both entities.

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

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

Pathogenesis – BV represents a complex change in the vaginal microbiota characterized by a reduction in concentration of the normally dominant hydrogen peroxide- and lactic acid-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.)

Risk factors for BV – The most common risk factor for BV is sexual activity (male and/or female sexual partners). While BV is likely a sexually transmitted infection (STI), it is not yet classified as such because of lack of a single causative agent and absence of a clear disease counterpart in males. Infection with another STI also increases risk of BV. The impact of race and ethnicity are unclear. (See 'Risk factors' above.)

Clinical features – Symptomatic individuals often present with an off-white, thin, homogeneous, and "fishy smelling" vaginal discharge that is more noticeable after coitus and during menses. However, up to 50 to 75 percent of individuals with BV are asymptomatic. (See 'Clinical features' above.)

Clinical sequelae – Sequelae of BV can include an increased risk of preterm birth, plasma-cell endometritis, postpartum fever, posthysterectomy vaginal cuff cellulitis, postabortal infection, pelvic inflammatory disease (PID), and acquisition of other STIs. (See 'Clinical consequences of BV' above.)

Diagnostic evaluation As symptoms of BV overlap with those of other vaginal infections (table 3), accurate diagnosis is needed to correctly guide treatment (algorithm 1). All patients undergo physical examination; the selection of further diagnostic tests is determined by clinical suspicion and test availability. (See 'Diagnostic evaluation' above.)

Clinical laboratory tests – Clinical laboratory tests for diagnosing BV are increasingly used because of improved diagnostic accuracy compared with clinical diagnosis by Amsel criteria, ability to identify fastidious bacteria, and ease of use. In addition to diagnosing BV, nucleic acid amplification tests (NAATs) can identify vaginal candidiasis and trichomonas vaginitis as well as cervicitis caused by gonorrhea and chlamydia. (See 'Clinical laboratory tests' above.)

Microscopy with Amsel criteria – When microscopy is available, the diagnosis of BV is based on the presence of at least three of the following four Amsel criteria. Compared with Gram stain for diagnosing BV, the sensitivity of Amsel criteria for diagnosis of BV is over 90 percent and specificity is 77 percent. However, this approach is limited by availability of microscopy equipment and trained providers (see 'pH and microscopy using Amsel criteria' above):

Amsel criteria include:

-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).

Gram stain with Nugent or Hay/Ison criteria – The Gram-stained smear made from the patient's vaginal discharge is evaluated using Nugent criteria (table 4) or Hay/Ison criteria (table 5). If clinical criteria are used to define infection, then reported sensitivity ranges from 62 to 100 percent. Although Gram stain of vaginal discharge has been the gold standard for diagnosis of BV, it is mainly used in research settings as it requires more time, training, and expertise compared with other methods. (See 'Gram stain with Nugent criteria' above.)

Diagnostic approaches to avoid – Diagnosis of BV should not be made based on history alone or without a speculum examination. Vaginal culture and cytology are not useful for diagnosing BV. (See 'Approaches to avoid' above.)

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Topic 5451 Version 92.0

References

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