AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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).

Pathophysiology

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

Many studies have demonstrated the relationship of G vaginalis with other bacteria in causing BV. BV is known to be a synergistic polymicrobic infection. Some of the associated bacteria include Lactobacillus species 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 (Tabrizi, 2006).

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.

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.

Frequency

United States

G 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.

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

Mortality/Morbidity

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

• Long-standing or untreated BV may lead to more serious sequelae, such as endometritis, salpingitis, pelvic inflammatory disease, or complications of pregnancy, including premature rupture of membranes, premature labor, chorioamnionitis, and postpartum endometritis.
• Postgynecologic procedure infections, such as vaginal cuff cellulitis (status posthysterectomy [suprapubic]) 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 for BV. See Treatment section.

Race

BV appears to occur equally among people of all racial groups.

Sex

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.

Age

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

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Vaginal odor is the most common, and often initial, symptom of BV. Odor may be recognized only after sexual intercourse. The alkalinity of semen may cause a release of volatile amines from the vaginal discharge and cause a fishy odor.
• Increased vaginal discharge is typically mild to moderate.
• Vulvar irritation is less common.
• Dysuria or dyspareunia occur rarely.
• Inquire about risk factors that may predispose patients to developing BV. Predisposing factors can 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, as evidenced by the patient having a new sexual partner, an increased number of sexual partners in the month preceding the onset of BV symptoms, or having an increased number of lifetime sexual partners

Physical

• Vaginal discharge
• • Most often gray, thin, and homogeneous
  • Adherent to the vaginal mucosa
  • May not visualize pooling of discharge in the posterior fornix because of adherence to the vaginal mucosa
  • May observe small bubbles in the discharge fluid
• An increased light reflex of the vaginal walls may be observed, indicating a very wet appearance; however, typically, no or little evidence of inflammation is apparent.
• The labia, introitus, cervix, and cervical discharge appear normal.
• Evidence of cervicitis should prompt a workup for concomitant infection with Neisseria gonorrhoeae, Chlamydia trachomatis, or herpes simplex virus (HSV).

Causes

BV is a polymicrobic synergistic infection. As described in Pathophysiology, the normally predominant lactobacilli population is reduced in the vagina, while populations of G 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.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Vaginal candidiasis

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Clinical diagnosis of BV relies on history, vaginal examination, and microscopic examination (see the Table for a summary of the differential diagnoses). Emerging data support sending vaginal cultures in recalcitrant cases (Schwiertz, 2006).
• Historical information regarding the patient's symptoms and nature of the discharge
• • Most patients experience a vaginal malodor and/or an increase in vaginal discharge.
  • Vulvar irritation may be present or absent.
  • Dysuria, dyspareunia, and abdominal pain are lacking.
• Vaginal examination
• • Typical BV discharge characteristics
  • Lack of significant vulvovaginal inflammation
• Microscopic examination of the discharge: Demonstrating 3 of the following 4 criteria is considered necessary to diagnose BV most accurately.
• • Demonstration of clue cells on a saline smear is the most specific criterion for diagnosing BV. Clue cells are vaginal epithelial cells that have bacteria adherent to their surfaces. The edges of the squamous epithelial cells, which normally have a sharply defined cell border, become studded with bacteria. The epithelial cells appear to be peppered with coccobacilli.
  • A pH greater than 4.5 indicates infection, and pH may be elevated in up to 90% of patients with BV.
  • Characteristic discharge appearance is thin, gray, and homogeneous.
  • The whiff test may be positive in up to 70% of BV patients. This test is performed by placing a drop of 10% KOH on the speculum after the vaginal examination or mixing vaginal fluid with a drop of KOH on a microscope slide. The KOH, by virtue of its alkaline properties, causes the release of volatile amines from the vaginal fluid. The amines are products of anaerobic bacterial metabolism.
• The bacterial flora may be examined microscopically for evidence of changes in the overall bacterial predominance. The healthy vagina has a predominance of lactobacilli (large gram-positive rods). The flora of a patient with BV changes to become dominated by coccobacilli, reflecting an increase in the growth of G vaginalis and other anaerobes.
• The vaginal discharge of patients with BV is notable for its lack of polymorphonuclear leukocytes (PMNs), typically 1 or less than 1 PMN per vaginal epithelial cell.
• Diagnosing BV accurately is more difficult when a coinfection is present. However, finding an increase in the number of PMNs per epithelial cell may lead the clinician to consider BV as a possibility.
• Obtaining routine vaginal cultures in patients with BV has no utility because this is a polymicrobial infection and some women may have asymptomatic carriage of G vaginalis organisms. Although G vaginalis has been demonstrated to grow in up to 100% of vaginal cultures of women with BV, it has also been cultured in up to 70% of asymptomatic women. However, obtaining cultures to exclude other infectious etiologies (eg, Trichomonas species, C trachomatis, N gonorrhoeae) is appropriate. In recurrent cases that have not resolved with standard regimens, cultures may be appropriate.

  Differential Diagnosis of the Vaginitides

  Clinical Elements		Bacterial Vaginosis	Trichomoniasis	Vaginal Candidiasis
  Symptoms	Vaginal odor	+	+/-	-
  	Vaginal discharge	Thin, gray, homogenous	Green-yellow	White, curdlike
  	Vulvar irritation	+/-	+	+
  	Dyspareunia	-	+	-
  Signs	Vulvar erythema	-	+/-	+/-
  	Bubbles in vaginal fluid	+	+/-	-
  	Strawberry cervix	-	+/-	-
  Microscopy	Saline wet mount
  	Clue cells	+	-	-
  	Motile protozoa	-	+	-
  	KOH test
  	Pseudohyphae	-	-	+
  	Whiff test	+	+/-	-
  	pH	>4.5	>4.5	<4.5

Procedures

• No other procedures are necessary in the evaluation of patients with BV other than those listed in Lab Studies.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Antibiotics are the mainstay of therapy for BV.
• Asymptomatic women with G vaginalis colonization do not need treatment.
• Studies of topically applied and orally administered yogurt/lactobacilli preparations, which are used to help reestablish the lactobacilli population in the vagina, have demonstrated inconsistent results.
• Some women with recurrent cases of BV may benefit from evaluation and/or treatment of G vaginalis colonization in their sexual partner. This approach is controversial.
• Treat BV occurring in pregnant women to reduce the risk of pregnancy-associated complications related to infection.
• Although not tested by clinical trials, treatment prior to cesarean delivery, total abdominal hysterectomy, and insertion of an IUD is also recommended.

Surgical Care

Surgery is not indicated for BV.

Consultations

Consultation with an infectious disease specialist or obstetrician/gynecologist may be warranted for patients with nonresolving and/or recurring BV or more serious infections, such as endometritis, pelvic inflammatory disease, and chorioamnionitis.

Diet

Studies are conflicting regarding the efficacy of a diet supplemented with Lactobacillus (acidophilus).

Activity

Restriction of activities is not necessary for patients with BV. Other, more serious Gardnerella infections may require restriction of activity based on the severity and nature of the illness.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Antibiotics are the mainstay of therapy for BV. Medications include metronidazole (Flagyl), clindamycin (Cleocin) oral or vaginal suppositories, and metronidazole vaginal gel (MetroGel-Vaginal).

Drug Category: Antibiotics

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Inpatient care is not necessary for patients with BV.
• Obtain cultures of blood and infected tissue (if feasible) from inpatients who develop obstetric/gynecologic postoperative fever or signs of infection to try to elucidate the infectious etiologic organism. Blood cultures may not demonstrate growth of G vaginalis unless gelatin is added to the media to prevent inhibition from the anticoagulant, sodium polyethanol sulfonate (SPS).

Further Outpatient Care

• Uncomplicated cases of BV typically resolve after the standard antibiotic treatment.
• BV that does not resolve after one course of treatment may be cured by a second course with the same agent. Another option is to switch to another agent (ie, metronidazole to clindamycin, or clindamycin to metronidazole) as other concomitant organisms may respond better to an alternate medication. Metronidazole is favored because it allows faster return of colonization of H₂O₂-producing lactobacilli (De Backer, 2006).
• Some women with recurrent episodes of BV may benefit from treatment of G vaginalis in their sexual partner if colonization is demonstrated. Repeating wet preps is useful because patients can develop new, non-BV infections such as Candida.
• Testing for other infections, such as N gonorrhoeae, C trachomatis, and herpes simplex virus type 1 (HSV-1) may be appropriate in individuals with BV because the incidence of sexually transmitted diseases (STDs) may be increased in this population depending upon the risk factors and demographics.
• Therapy with metronidazole or clindamycin may alter the vaginal flora and predispose the patient to development of vaginal candidiasis.

In/Out Patient Meds

• Metronidazole and clindamycin are the preferred medications used to treat Gardnerella infections. See Medication for specific information on these medications.

Deterrence/Prevention

• Predisposing factors that may contribute to development of BV are listed below. Correction or modification of these factors may help reduce the incidence or recurrence of BV.
• • Recent antibiotic use
  • Decreased estrogen production of the host
  • Wearing an IUD
  • Douching
  • Sexual activity leading to transmission, as evidenced by the patient having a new sexual partner, an increased number of sexual partners in the month preceding the onset of BV symptoms, and having an increased number of lifetime sexual partners

Complications

• 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 with Trichomonas and yeast can occur among patients with BV.
• Bacteremia
• • G 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 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.

Prognosis

• The prognosis for uncomplicated cases of BV generally is excellent.
• The prognosis for complicated cases of BV leading to other infections varies depending on the particular infectious process.

Patient Education

• Educate patients regarding the basic pathophysiology, natural history, and risk factors of the infection. BV is not considered a sexually transmitted disease, although sexual contact may predispose patients to development of this process in some cases.
• For excellent patient education resources, visit eMedicine's Parasites and Worms Center and Pregnancy and Reproduction Center. Also, see eMedicine's patient education articles Trichomoniasis, Birth Control Overview, and Birth Control FAQs.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• For patients presenting with atypical clinical features of BV, the clinician must be aware of the possibility of a coinfection, such as vaginal candidiasis, trichomoniasis, infection with C trachomatis or N gonorrhoeae, HSV infection, or an alternative diagnosis.
• Provide patients at risk of HIV with HIV counseling and testing.

Special Concerns

• No adequate and well-controlled human trials evaluating teratogenicity of clindamycin or metronidazole in pregnant women have been performed.
• The use of the cream formulation of clindamycin may result in preterm birth.
• Several clinical trials using both preparations in pregnancy have been conducted. The use of metronidazole after the first trimester is considered within the standard of care.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Amsel R, Totten PA, Spiegel CA. Nonspecific vaginitis. Diagnostic criteria and microbial and epidemiologic associations. Am J Med. Jan 1983;74(1):14-22. [Medline].
• Avonts D, Sercu M, Heyerick P. Incidence of uncomplicated genital infections in women using oral contraception or an intrauterine device: a prospective study. Sex Transm Dis. Jan-Mar 1990;17(1):23-9. [Medline].
• Barbone F, Austin H, Louv WC. A follow-up study of methods of contraception, sexual activity, and rates of trichomoniasis, candidiasis, and bacterial vaginosis. Am J Obstet Gynecol. Aug 1990;163(2):510-4. [Medline].
• Berardi-Grassias L, Roy O, Berardi JC. Neonatal meningitis due to Gardnerella vaginalis. Eur J Clin Microbiol Infect Dis. Jun 1988;7(3):406-7. [Medline].
• Bradshaw CS, Tabrizi SN, Read TR, et al. Etiologies of nongonococcal urethritis: bacteria, viruses, and the association with orogenital exposure. J Infect Dis. Feb 1 2006;193(3):336-45.
• Bump RC, Buesching WJ 3d. Bacterial vaginosis in virginal and sexually active adolescent females: evidence against exclusive sexual transmission. Am J Obstet Gynecol. Apr 1988;158(4):935-9. [Medline].
• Carney FE. Hemophilus vaginalis septicemia. Obstet Gynecol. Jan 1973;41(1):78-9. [Medline].
• Catlin BW. Gardnerella vaginalis: characteristics, clinical considerations, and controversies. Clin Microbiol Rev. Jul 1992;5(3):213-37. [Medline].
• Chen KC, Amsel R, Eschenbach DA. Biochemical diagnosis of vaginitis: determination of diamines in vaginal fluid. J Infect Dis. Mar 1982;145(3):337-45. [Medline].
• De Backer E, Verhelst R, Verstraelen H, et al. Antibiotic susceptibility of Atopobium vaginae. BMC Infect Dis. 2006;6:51:[Full Text].
• Embree J, Caliando JJ, McCormack WM. Nonspecific vaginitis among women attending a sexually transmitted diseases clinic. Sex Transm Dis. Apr-Jun 1984;11(2):81-4. [Medline].
• Eschenbach DA. Bacterial vaginosis and anaerobes in obstetric-gynecologic infection. Clin Infect Dis. Jun 1993;16 Suppl 4:S282-7. [Medline].
• Eschenbach DA, Hillier S, Critchlow C. Diagnosis and clinical manifestations of bacterial vaginosis. Am J Obstet Gynecol. Apr 1988;158(4):819-28. [Medline].
• Ezzell JH Jr, Many WJ Jr. Gardnerella vaginalis: an unusual case of pyogenic liver abscess. Am J Gastroenterol. Dec 1988;83(12):1409-11. [Medline].
• Gravett MG, Hummel D, Eschenbach DA. Preterm labor associated with subclinical amniotic fluid infection and with bacterial vaginosis. Obstet Gynecol. Feb 1986;67(2):229-37. [Medline].
• Hallen A, Pahlson C, Forsum U. Bacterial vaginosis in women attending STD clinic: diagnostic criteria and prevalence of Mobiluncus spp. Genitourin Med. Dec 1987;63(6):386-9. [Medline].
• Hay PE, Morgan DJ, Ison CA. A longitudinal study of bacterial vaginosis during pregnancy. Br J Obstet Gynaecol. Dec 1994;101(12):1048-53. [Medline].
• Hedges SR, Barrientes F, Desmond RA, Schwebke JR. Local and systemic cytokine levels in relation to changes in vaginal flora. J Infect Dis. Feb 15 2006;193(4):556-62.
• Hill LV. Anaerobes and Gardnerella vaginalis in non-specific vaginitis. Genitourin Med. Apr 1985;61(2):114-9. [Medline].
• Hillier SL, Krohn MA, Rabe LK. The normal vaginal flora, H2O2-producing lactobacilli, and bacterial vaginosis in pregnant women. Clin Infect Dis. Jun 1993;16 Suppl 4:S273-81. [Medline].
• Hodge TW Jr, Levy CS, Smith MA. Disk space infection due to Gardnerella vaginalis. Clin Infect Dis. Aug 1995;21(2):443-5. [Medline].
• Holst E, Wathne B, Hovelius B. Bacterial vaginosis: microbiological and clinical findings. Eur J Clin Microbiol. Oct 1987;6(5):536-41. [Medline].
• Joesoef MR, Wiknjosastro G, Norojono W. Coinfection with chlamydia and gonorrhea among pregnant women and bacterial vaginosis. Int J STD AIDS. Jan-Feb 1996;7(1):61-4. [Medline].
• Johnson AP, Boustouller YL. Extra-vaginal infection caused by Gardnerella vaginalis. Epidemiol Infect. Apr 1987;98(2):131-7. [Medline].
• Jones BM, Geary I, Alawattegama AB. In-vitro and in-vivo activity of metronidazole against Gardnerella vaginalis, Bacteroides spp. and Mobiluncus spp. in bacterial vaginosis. J Antimicrob Chemother. Aug 1985;16(2):189-97. [Medline].
• Josey WE, Campbell WG Jr. Vaginitis emphysematosa. A report of four cases. J Reprod Med. Oct 1990;35(10):974-7. [Medline].
• Klebanoff MA, Andrews WW, Yu KF, et al. A Pilot Study of Vaginal Flora Changes With Randomization to Cessation of Douching. Sex Transm Dis. Apr 11 2006.
• Legrand JC, Alewaeters A, Leenaerts L. Gardnerella vaginalis bacteremia from pulmonary abscess in a male alcohol abuser. J Clin Microbiol. May 1989;27(5):1132-4. [Medline].
• Leighton PM, Bulleid B, Taylor R. Neonatal cellulitis due to Gardnerella vaginalis. Pediatr Infect Dis. Sep-Oct 1982;1(5):339-40. [Medline].
• Lugo-Miro VI, Green M, Mazur L. Comparison of different metronidazole therapeutic regimens for bacterial vaginosis. A meta-analysis. JAMA. Jul 1 1992;268(1):92-5. [Medline].
• Martius J, Eschenbach DA. The role of bacterial vaginosis as a cause of amniotic fluid infection, chorioamnionitis and prematurity--a review. Arch Gynecol Obstet. 1990;247(1):1-13. [Medline].
• Martius J, Krohn MA, Hillier SL. Relationships of vaginal Lactobacillus species, cervical Chlamydia trachomatis, and bacterial vaginosis to preterm birth. Obstet Gynecol. Jan 1988;71(1):89-95. [Medline].
• McCormack WM, Hayes CH, Rosner B. Vaginal colonization with Corynebacterium vaginale (Haemophilus vaginalis). J Infect Dis. Dec 1977;136(6):740-5. [Medline].
• McDonald HM, O''Loughlin JA, Vigneswaran R. Bacterial vaginosis in pregnancy and efficacy of short-course oral metronidazole treatment: a randomized controlled trial. Obstet Gynecol. Sep 1994;84(3):343-8. [Medline].
• Mengel MB, Berg AO, Weaver CH. The effectiveness of single-dose metronidazole therapy for patients and their partners with bacterial vaginosis. J Fam Pract. Feb 1989;28(2):163-71. [Medline].
• Nilsson U, Hellberg D, Shoubnikova M. Sexual behavior risk factors associated with bacterial vaginosis and Chlamydia trachomatis infection. Sex Transm Dis. May 1997;24(5):241-6. [Medline].
• Nugent RP, Krohn MA, Hillier SL. Reliability of diagnosing bacterial vaginosis is improved by a standardized method of gram stain interpretation. J Clin Microbiol. Feb 1991;29(2):297-301. [Medline].
• Pheifer TA, Forsyth PS, Durfee MA. Nonspecific vaginitis: role of Haemophilus vaginalis and treatment with metronidazole. N Engl J Med. Jun 29 1978;298(26):1429-34. [Medline].
• Rein MF. Vulvovaginitis and Cervicitis. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 5th ed. Philadelphia, Pa:. Churchill Livingstone;2000:1218-1235.
• Sadhu K, Domingue PA, Chow AW. Gardnerella vaginalis has a gram-positive cell-wall ultrastructure and lacks classical cell-wall lipopolysaccharide. J Med Microbiol. Jul 1989;29(3):229-35. [Medline].
• Schnadig VJ, Davie KD, Shafer SK. The cytologist and bacterioses of the vaginal-ectocervical area. Clues, commas and confusion. Acta Cytol. May-Jun 1989;33(3):287-97. [Medline].
• Schwebke JR, Hillier SL, Sobel JD. Validity of the vaginal gram stain for the diagnosis of bacterial vaginosis. Obstet Gynecol. Oct 1996;88(4 Pt 1):573-6. [Medline].
• Schwiertz A, Taras D, Rusch K, Rusch V. Throwing the dice for the diagnosis of vaginal complaints?. Ann Clin Microbiol Antimicrob. 2006;5:4. [Full Text].
• Soper DE, Bump RC, Hurt WG. Bacterial vaginosis and trichomoniasis vaginitis are risk factors for cuff cellulitis after abdominal hysterectomy. Am J Obstet Gynecol. Sep 1990;163(3):1016-21; discussion 1021-3. [Medline].
• Spiegel CA. Bacterial vaginosis. Clin Microbiol Rev. Oct 1991;4(4):485-502. [Medline].
• Spiegel CA, Amsel R, Holmes KK. Diagnosis of bacterial vaginosis by direct gram stain of vaginal fluid. J Clin Microbiol. Jul 1983;18(1):170-7. [Medline].
• Spiegel CA. Gardnerella vaginalis and Mobiluncus Species. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 5th ed. Philadelphia, Pa:. Churchill Livingstone;2000:2383-2386.
• Sturm AW. Gardnerella vaginalis in infections of the urinary tract. J Infect. Jan 1989;18(1):45-9. [Medline].
• Swedberg J, Steiner JF, Deiss F. Comparison of single-dose vs one-week course of metronidazole for symptomatic bacterial vaginosis. JAMA. Aug 23-30 1985;254(8):1046-9. [Medline].
• Tabrizi SN, Fairley CK, Bradshaw CS, Garland SM. Prevalence of Gardnerella vaginalis and Atopobium vaginae in Virginal Women. Sex Transm Dis. Apr 4 2006.
• Thomason JL, Gelbart SM, Anderson RJ. Statistical evaluation of diagnostic criteria for bacterial vaginosis. Am J Obstet Gynecol. Jan 1990;162(1):155-60. [Medline].
• Venkataramani TK, Rathbun HK. Corynebacterium vaginale (Hemophilus vaginalis) bacteremia: clinical study of 29 cases. Johns Hopkins Med J. Sep 1976;139(3):93-97. [Medline].
• Vontver LA, Eschenbach DA. The role of Gardnerella vaginalis in nonspecific vaginitis. Clin Obstet Gynecol. Jun 1981;24(2):439-60. [Medline].
• Watson RA. Gardnerella vaginalis: genitourinary pathogen in men. Urology. Mar 1985;25(3):217-22. [Medline].

Article Last Updated: Aug 1, 2006