eMedicine Specialties > Emergency Medicine > Obstetrics & Gynecology

Vulvovaginitis

Author: Anuritha Tirumani, MD, Research Coordinator, Department of Emergency Medicine, Brooklyn Hospital Center
Coauthor(s): Mark J Leber, MD, MPH, Clinical Assistant Professor of Emergency Medicine, Weill Medical College of Cornell University; Consulting Staff, Department of Emergency Medicine, Brooklyn Hospital Medical Center
Contributor Information and Disclosures

Updated: Oct 17, 2006

Introduction

Background

Vulvovaginitis is common, affecting women of all ages. Vulvovaginitis is an inflammation of the vagina and vulva, most often caused by a bacterial, fungal, or parasitic infection. Vulvovaginitis, one of the most common reasons why women visit their gynecologist, causes vaginal discharge, irritation, and itching. Normally, a woman may have a vaginal discharge, the amount and consistency of which varies during the course of the menstrual cycle; however, vulvovaginitis causes a symptomatic increased vaginal discharge.

Etiologies and the approach of management for a patient with vulvovaginitis are age dependent. Vulvovaginitis can be divided into 3 age categories: premenarchal, childbearing, and postmenopausal.

Pathophysiology

The normal vaginal epithelium cornifies (develops into a thickened layer of epithelial cells) under the influence of estrogen, protecting women against infection. A normal vaginal discharge consists of 1-4 mL of fluid that is white or transparent, thick, and odorless. This physiologic discharge is formed by sloughing epithelial cells, normal bacteria, and vaginal transudate. The discharge may be noticeable during pregnancy, oral contraceptive pill use, or at mid menstrual cycle, close to the time of ovulation.

The normal pH of vaginal secretions is 4.0-4.5. The pH is maintained by lactobacillus, which produce hydrogen peroxide; diphtheroids, and Staphylococcus epidermidis. Vaginal pH may increase with age, phase of menstrual cycle, sexual activity, contraception choice, pregnancy, presence of necrotic tissue or foreign bodies, and use of hygienic products or antibiotics.

Bacterial vaginosis is secondary to bacterial overgrowth and not due to tissue inflammation. One of the organisms associated with bacterial vaginosis is Gardnerella vaginalis. Summarizing, practically any condition changing the vaginal milieu may result in vulvovaginitis.

Frequency

United States

Premenarchal: Vulvovaginitis is the most common gynecologic problem affecting prepubertal girls and is responsible for the largest number of visits to the gynecologist.

Childbearing age: Bacterial vaginosis is the most important cause of vulvovaginitis. Estimating the number of patients presenting with bacterial vaginosis is difficult because G vaginalis can be recovered from the vagina in 30-50% of asymptomatic women.

Trichomonas vaginalis affects 2-3 million women annually in the United States. The organism also is detected in 30-40% of men who are exposed to women with T vaginalis. The prevalence of T vaginalis infection at clinics treating sexually transmitted diseases (STDs) varies from 8-31%. In men, T vaginalis may account for as many as 17% of cases of nongonococcal, nonchlamydial urethritis. T vaginalis infection appears to be more common in the southern United States.

Candidal vulvovaginitis is considered slightly less common than bacterial vaginosis, yet, 3 out of every 4 women in the United States will have at least 1 bout of vulvovaginal candidiasis (VVC) during their lifetime. Patients with recurrent or severe VVC warrant a screening test for diabetes mellitus.

Postmenopausal: After menopause, most women experience some vaginal atrophy as estrogen levels fall. Incidence of atrophic vaginitis depends on how it is defined. Vulvovaginitis related to infection is much less common after menopause. Desquamative inflammatory vaginitis has an unknown etiology, but a Gram stain of culture often reveals streptococci. This is treated with intravaginal clindamycin cream. Postirritation vulvovaginitis may occur in women undergoing pelvic irradiation for cancer.

International

Bacterial vaginosis is the most common cause of vaginitis in women of childbearing age, with prevalence of 50-60% across the globe.

Trichomoniasis affects 180 million women worldwide.

Mortality/Morbidity

No mortality has been documented primarily from vulvovaginitis.

  • Premenarchal: Persistent vulvovaginitis in children is sometimes mistaken for an infection rather than for a foreign body. Labial adhesion, possibly to the point of occlusion of the vaginal orifice, may occur as an isolated finding, be secondary to urinary tract infections (UTIs), or be secondary to vulvovaginitis. These adhesions usually do not cause long-term problems.
  • Childbearing age: A variety of complications has been associated with bacterial vaginosis including the following:
    • Pelvic inflammatory disease
    • Increased incidence of abdominal pain, uterine bleeding, and uterine and adnexal tenderness
    • Increased complications of pregnancy, especially premature delivery, chorioamnionitis, postpartum endometritis, and ectopic pregnancy
    Candidal vulvovaginitis may develop into chronic or recurrent candidal infection related to the following:
    • Diabetes mellitus
    • Oral contraceptive (OCP) use
    • Antibiotic use
    • Immunodeficiency
    • Tight-fitting undergarments
    Some authors have suggested that T vaginalis, being sexually transmitted organisms, may act as vectors for other types of infections. The organism can be identified in 30-40% of male sexual partners of infected women, although carriage in men is self-limited and transient.
  • Postmenarchal: Vaginal bleeding may occur from the thin mucosa. Dyspareunia may also occur as a complication.

Race

  • Premenarchal: Significance of race is not clearly defined.
  • Childbearing age: One study found Trichomonas species to be 3 times more prevalent in black individuals than in white individuals. Bacterial vaginosis does not seem to have any significant racial variation.

Sex

Vulvovaginitis does not occur in males. Males may be carriers of G vaginalis and T vaginalis.

Age

  • Premenarchal: Vulvovaginitis predominately affects school-aged children.
  • Childbearing age
    • Trichomonas species can occur in any age group, yet it is most common in adolescents and women in their 20s, peaking in those aged 20-24 years.
    • Bacterial vaginosis has a fairly equal distribution across all age groups up until menopause. Prevalence does not vary significantly with age.
    • Candida species infections are most common during childbearing years.
  • Postmenarchal: Atrophic vaginitis may develop several years after menopause. Most women with vaginal atrophy do not develop atrophic vaginitis.

Clinical

History

Different historical aspects should be ascertained depending on what vulvovaginitis category the patient may have.

  • Premenarchal
    • Wiping the anus from posterior to anterior, wearing tight-fitting synthetic undergarments, and using vaginal irritants such as bubble baths
    • Recent upper respiratory infection or pharyngitis can lead to group A beta-hemolytic streptococci (GABHS) vaginitis.
    • Vaginal pruritus, especially at night, suggests pinworm infection.
    • Itching, soreness, bleeding, and vaginal discharge; bloody and foul-smelling discharge may suggest a vaginal foreign body.
    • Vulvovaginitis may be secondary to sexual abuse of the child. Parents often equate vulvovaginitis with abuse, although this is not justified in most cases.
    • Asymptomatic vaginal discharge often occurs in the months prior to menarche and represents a physiologic response to increasing estrogen levels.
    • Skin conditions (ie, eczema, psoriasis, seborrhea) occasionally involve the vagina, and a history of these conditions should be sought.
  • In obtaining a history of women in childbearing age, record a complete sexual history, last menstrual period, number of sexual partners, and methods of birth control. A new sexual partner increases the risk of STD and pregnancy. Inquire about antibiotics, high estrogen oral contraceptive pills, and any abdominal pain; ask about the patient's hygienic practices (daily use of panty liners and feminine products).
    • Irritants such as soaps, baths, spermicides, perfumes, douches, and creams can cause vulvovaginitis. Tight-fitting, synthetic undergarments can increase moisture, exacerbating this condition.
    • Vulvovaginitis is usually related to infections secondary to Gardnerella, Trichomonas, or Candida species. Vaginal discharge, pruritus, burning sensation, foul-smelling odor, superficial dyspareunia, and dysuria may be the presenting complaint. With candidiasis, the patient may describe a thick, white, cottage cheese–like discharge associated with pruritus.
  • In postmenopausal women, inquire about vaginal bleeding or spotting, dysuria, pruritus, watery discharge, or dyspareunia and decreased sexual activity.

Physical

  • Premenarchal
    • Genital examination of a prepubertal girl may produce a great deal of anxiety. Explaining the examination to the child and parent, keeping the parent at the patient's side, and explaining the difference between allowing a clinician or anyone else to examine her genitals may make the examination less traumatic. Sedation rarely is necessary.
    • Cultures are not necessary most of the time. History and physical examination should indicate when to obtain a culture from the patient.
  • Childbearing age
    • A complete pelvic examination is needed to evaluate possible upper genital tract infection.
    • Specific clinical descriptions and physical examination findings have been described for each of the 3 etiologies (Gardnerella, Trichomonas, and Candida species), yet these often overlap.
    • More than one infection may be present simultaneously. This usually necessitates additional diagnostic testing to confirm the diagnosis.
    • Pathologic vaginal discharge may be odor producing and may adhere to the vaginal walls, unlike odorless physiologic discharge found in the dependent areas of the vagina.
    • Bacterial vaginosis typically presents with an unpleasant fishy-smelling discharge that is more noticeable after unprotected intercourse. A thin, gray-white vaginal discharge that is homogeneous may adhere to the vaginal walls and be present at the introitus. Pruritus and inflammation are unusual in bacterial vaginosis. The absence of inflammation is the basis for the term vaginosis rather than vaginitis.
    • Trichomonal infection may be asymptomatic or may produce a profuse, frothy, yellow-gray, homogenous discharge. This discharge may adhere to the vaginal walls and may not be present at the vaginal introitus. In contrast to bacterial vaginosis, vulvar and vaginal erythema and edema with Trichomonas species often are present. Punctate hemorrhages may be visible on the vagina and cervix (2% of cases).
    • Candida species infection typically is found as an isolated infection, heralded by pruritus. A thick, odorless, white, cottage cheese–like discharge often is found adhering to the vagina. Erythema, edema, and excoriation may be present. Dysuria and urinary frequency occasionally may be present.
  • Postmenarchal
    • Vaginal mucosa is thin with diffuse erythema, occasional petechiae or ecchymoses, and few or no vaginal folds.
    • Hair loss may occur over the mons and labia majora.
    • Loss of rugae may occur.
    • Thinned mucosa may become friable.

Causes

  • Premenarchal
    • Nonspecific - No defined etiologic agent or poor perineal hygiene
    • Chemical irritants (eg, bubble baths, lotions)
    • Vaginal foreign bodies
    • Pinworm infection
    • GABHS infection
    • Skin conditions - Eczema, psoriasis, seborrhea
    • Etiologies usually associated with women of childbearing age - Bacterial vaginosis, Trichomonas species, Candida species, and gonorrhea (many of these are associated with sexual abuse)
  • Childbearing age
    • Sexual contact especially with multiple sexual contacts
    • No method of birth control
    • History of STD
    • Bacterial or fungal infections such as G vaginalis (bacterial vaginosis), Candida species, and Trichomonas species
    • Chemical irritants
  • Postmenarchal - Atrophic vaginitis (most common cause of vulvovaginitis in postmenarchal women)

More on Vulvovaginitis

Overview: Vulvovaginitis
Differential Diagnoses & Workup: Vulvovaginitis
Treatment & Medication: Vulvovaginitis
Follow-up: Vulvovaginitis
References

References

  1. Braverman PK. Prepubertal vulvovaginitis. In: Long SS, Pickering LK, Prober CG, eds. Principles and Practice of Pediatric Infectious Diseases. 2nd ed. 2002.

  2. Carey JC, Klebanoff MA, Hauth JC, et al. Metronidazole to prevent preterm delivery in pregnant women with asymptomatic bacterial vaginosis. National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units. N Engl J Med. Feb 24 2000;342(8):534-40. [Medline].

  3. Gabbe SG. Vaginal infections. In: Obstetrics - Normal and Problem Pregnancies. 4th ed. 2002.

  4. Johns Hopkins. Diagnostic features and management of vaginal infections. In: The Harriet Lane Handbook: A Manual for Pediatric House Officers. 17th ed. 2005.

  5. Marrazzo J. Vulvovaginal candidiasis. BMJ. Sep 14 2002;325(7363):586. [Medline].

  6. Owen MK, Clenney TL. Management of vaginitis. Am Fam Physician. Dec 1 2004;70(11):2125-32. [Medline].

  7. Sobel JD. Vaginitis, vulvitis, cervicitis and cutaneous vulval lesions. In: Infectious Diseases. 2nd ed. Cohen & Powderly; 2004.

  8. Workowski KA, Levine WC. Centers for Disease Control and Prevention. Sexually Transmitted Diseases Treatment Guidelines. 2002. [Full Text].

Further Reading

Keywords

vulvovaginitis, vaginitis, vaginal yeast infection, vaginosis, lactobacillus, inflammation of vagina, inflammation of vulva, vaginal discharge, vaginal itching, vaginal irritation, vaginal fluid, vaginal pH, bacterial vaginosis, Gardnerella vaginalis, G vaginalis, Staphylococcus epidermis, S epidermis, Trichomonas vaginalis, T vaginalis, vulvovaginal candidiasis, VVC, candidal vulvovaginitis, desquamative inflammatory vaginitis, atrophic vaginitis, trichomoniasis

Contributor Information and Disclosures

Author

Anuritha Tirumani, MD, Research Coordinator, Department of Emergency Medicine, Brooklyn Hospital Center
Disclosure: Nothing to disclose.

Coauthor(s)

Mark J Leber, MD, MPH, Clinical Assistant Professor of Emergency Medicine, Weill Medical College of Cornell University; Consulting Staff, Department of Emergency Medicine, Brooklyn Hospital Medical Center
Mark J Leber, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and American College of Physicians
Disclosure: Nothing to disclose.

Medical Editor

David S Howes, MD, Residency Program Director, Professor of Medicine, Section of Emergency Medicine, University of Chicago/Pritzker School of Medicine
David S Howes, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Mark Zwanger, MD, MBA, Assistant Professor, Department of Emergency Medicine, Thomas Jefferson University
Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Pamela L Dyne, MD, Associate Professor, Program Director, Department of Medicine, Division of Emergency Medicine, University of California at Los Angeles School of Medicine
Pamela L Dyne, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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