Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Vulvovaginitis

  • Author: Jill M Krapf, MD, FACOG; Chief Editor: Christine Isaacs, MD  more...
 
Updated: Mar 29, 2015
 

Practice Essentials

Vulvovaginitis is a general term referring to many types of vaginal infection, although this article focuses on the following disorders, which affect the vulvar region:

  • Vulvovaginal candidiasis
  • Atrophic vaginitis
  • Vulvar vestibulitis
  • Contact dermatitis

Signs and symptoms

Acute vulvovaginal candidiasis

  • Vulvar pruritus and burning - Primary symptoms of the disease
  • Erythema and edema of the vestibule and of the labia majora and minora
  • Thrush patches - Usually found loosely adherent to the vulva
  • Thick, white, curdlike vaginal discharge

Chronic vulvovaginal candidiasis

  • Marked edema and lichenification of the vulva with poorly defined margins
  • Grayish sheen made up of epithelial cells and organism covering the area
  • Severe pruritus and burning
  • Irritation and pain

Atrophic vaginitis

  • Vaginal soreness
  • Postcoital burning
  • Dyspareunia
  • Burning leukorrhea
  • Occasional spotting

Vulvar vestibulitis

  • Primary vulvar vestibulitis (20% of cases) - Introital dyspareunia that starts from initiation of sexual activity or intolerable pain consistently present upon insertion of a tampon or vaginal speculum in women who have never been sexually active
  • Secondary vulvar vestibulitis - Introital dyspareunia that develops after a period of comfortable sexual relations, tampon use, or speculum examinations

Usual symptoms of vulvar vestibulitis include pain, soreness, burning, and a feeling of rawness that is aggravated by stress, exercise, tight clothing, coitus, and tampon use. The pain is usually not considered constant but is elicited by any attempt to enter the vagina.

Other symptoms may include the following:

  • Irritating vaginal discharge
  • Vulvar burning sensation
  • Small spots of erythema around the vestibular glands, with rare ulceration

Contact dermatitis

Pruritus is the cardinal symptom. However, an acute reaction may develop as a result of exposure to a potent irritant that involves the mucosa, leading to the following symptoms:

  • Burning, rawness, and pain
  • Red and edematous skin followed by exudation and weeping
  • Erosion, ulceration, or necrosis - If the irritant is potent enough

Contact dermatitis of long duration may include lichenification, scaling, thickening of the skin, and white plaques.

See Clinical Presentation for more detail.

Diagnosis

See the list below:

  • Vulvovaginal candidiasis - Wet-mount test or potassium hydroxide (KOH) preparation to confirm the presence of Candida; fungal culturing may be used if the diagnosis is uncertain [1]
  • Atrophic vaginitis - Vaginal pH measurement and wet-mount test (although history and physical examination generally provide sufficient diagnostic information); a wet mount often shows white blood cells and a paucity of Lactobacillus

See Workup for more detail.

Management

Vulvovaginal candidiasis

Uncomplicated sporadic vulvovaginal candidiasis usually is caused by strains of C albicans (see the image below). Most of these strains exhibit sensitivity to azole-based antifungal agents. A number of antimycotic regimens are available for the treatment of vulvovaginal candidiasis, including with oral and topical agents.

Candida albicans photomicrograph. Courtesy of Cent Candida albicans photomicrograph. Courtesy of Centers for Disease Control and Prevention (CDC).

Although an optimal regimen has not yet been established for the treatment of recurrent vulvovaginal candidiasis, therapies include ketoconazole (400 mg/day), itraconazole (50-100 mg/day), fluconazole (100 mg/wk) for 6 weeks, and clotrimazole (500-mg vaginal suppositories once per wk).[2] An intravaginally administered boric acid suppository also may be used for treatment.

Atrophic vaginitis

Treatment usually entails the use of topical vaginal estrogen for 1-2 weeks to alleviate symptoms.

Vulvar vestibulitis

Pain management strategies have included the following:

  • Sex therapy
  • Behavior modification
  • Biofeedback
  • Acupuncture
  • Topical anesthetic
  • Topical corticosteroid
  • Petroleum jelly or vitamin A and D ointment - To provide a protective coating
  • Wet compresses with aluminum acetate
  • Anti-inflammatory agents

Surgical excision may be considered as a last resort in the treatment of vulvar vestibulitis. Success rates of 60-80% have been reported.

Contact dermatitis

Treatments include the following:

  • Removal of the inciting agent
  • Triamcinolone ointment (0.1%) - Applied twice daily for irritant contact dermatitis
  • Wet compresses of aluminum acetate - For severe lesions
  • Hydrocortisone (0.5-1%) and fluorinated corticosteroids in lotions or creams

See Treatment and Medication for more detail.

Next

Background

Vulvovaginitis, a general term referring to many types of vaginal infection, is the most common gynecologic condition seen by practitioners rendering primary care to women. Discharge, burning, and pruritus are the most common symptoms, accompanied by signs of vulvar irritation, such as erythema and excoriation of the vulvar skin. (See Presentation.)

Traditionally, the 3 classic entities of vaginitis include bacterial vaginosis, Trichomonas infection, and candidiasis. This article, however, focuses on disorders that affect the vulvar region, including the following (see the image below):

  • Vulvovaginal candidiasis
  • Atrophic vaginitis
  • Vulvar vestibulitis
  • Contact dermatitis
    Candida albicans photomicrograph. Courtesy of Cent Candida albicans photomicrograph. Courtesy of Centers for Disease Control and Prevention (CDC).

The differential diagnosis for women with symptoms of vulvovaginitis is complex. Discharge, burning, and pruritus usually are the presenting symptoms, with signs of vulvar irritation that may include erythema and excoriation of the vulvar skin. Primary or secondary infections, skin irritants, or contact dermatitis may produce vulvar irritation. Irritation from bodily fluids such as urine and normal vaginal secretions may cause symptoms when the environment is kept moist, as with tight-fitting or occlusive clothing. (See Pathophysiology and Etiology, Presentation, and Workup.)

Because each disorder produces a similar clinical presentation, a careful history must be taken, an examination must be performed, and the vaginal discharge should be examined. Along with medical treatment, the patient must be encouraged to avoid etiologic agents and to make necessary changes in her habits. (See Treatment and Medication.)

Patient education

For patient education information, see the Pregnancy Center and the Women's Health Center, as well as Vaginal Infections (Vaginitis), Candidiasis (Yeast Infection), Vaginal Yeast Infection Treatment, Female Sexual Problems, and Trichomoniasis.

Previous
Next

Anatomy

The vulva, the external genitalia of the female, includes the labia majora and minora, the clitoris, and the vestibule of the vagina. The skin of the vulva is sensitive to the vaginal environment and hormonal, metabolic, and allergic influences. It is composed of stratified squamous epithelium that contains hair follicles, sebaceous sweat glands, and apocrine glands.

During the reproductive years of a healthy woman's life, the vagina maintains a moist environment that is in constant fluctuation. The secretion of an alkaline transudate from the vaginal epithelium and cervical glands maintains this moist environment with a pH ranging from 3.8-4.5. In addition, the vagina and its microflora form a unique, balanced environment that can change under pressure from external stimuli but returns to normal with removal of the stimuli. It can vary in degree during sexual activity, pregnancy, and the menstrual cycle.

The vaginal epithelium consists of 3 cell layers; ie, superficial, intermediate, and basal. The cells in these layers are capable of storing glycogen under the influence of estrogen. Glycogen is available in the fully mature cells in the superficial layer of the epithelium. With elevated levels of either exogenous or endogenous estrogen, all levels of the epithelium thicken as a result of glycogen storage. With diminishing levels of estrogen, the layers become thin and atrophic.

Previous
Next

Pathophysiology and Etiology

In an adult woman's reproductive years, the bacterial flora of the healthy vagina contains numerous microorganisms, including aerobic and anaerobic gram-positive and gram-negative bacteria. Lactobacillus and Corynebacterium predominate over other bacteria such as Streptococcus, Bacteroides, Staphylococcus, and Peptostreptococcus.

Lactobacillus and Corynebacterium produce lactic and acetic acid from glycogen, thus maintaining the low vaginal pH. Additional bacteria are kept in check by the acid-producing bacteria and are rarely pathogenic, but they may become pathogenic if the environmental balance is affected.

Vaginal pH may increase with age, menstrual cycle phase, sexual activity, contraceptive choice, pregnancy, the presence of necrotic tissue or foreign bodies, or the use of hygienic products or antibiotics.[3]

Vulvovaginal candidiasis

Vulvovaginal candidiasis can be an acute, chronic, recurrent, or persistent condition that can involve the vulva, vagina, and adjacent crural areas. The specific causative agent belongs to the genus Candida. These organisms are found in almost all humans and many animals. An estimated 10-50% of reproductive-aged American women are considered opportunistic carriers.

The species C albicans is identified approximately 85-90% of the time. However, an increased frequency of other Candida species, such as C glabrata, C tropicalis, and C krusei, has been reported. The emergence of these other Candida species may possibly be due to widespread use of over-the-counter drugs, long-term use of suppressive azoles, and the use of frequent short courses of antifungal drugs.

Pregnancy

Any host factor that affects the vaginal environment or vaginal secretions can play a role in the initiation of Candida vulvovaginitis. Pregnancy is one of the most common predisposing factors. Studies have demonstrated that up to one third of pregnant women worldwide on any day can be affected. The high levels of reproductive hormones and an increase in the vaginal environment’s glycogen content create a favorable environment for Candida species, providing an abundant source of carbon for candidal growth, germination, and adherence.

Furthermore, the acidity of the pregnant vaginal flora can suppress the growth of other microorganisms that are naturally inhibitory to Candida. Although the initial attachment of the organism occurs more readily at high pH values (6-7), the germ tube formation and the development of mycelia are favored by a low vaginal pH (< 5).

Contraception

Older studies of women using high-dose estrogens in oral contraceptives found an increase in vaginal colonization by Candida. The mechanism is believed to be similar to that found in pregnancy. However, newer oral contraceptives with a lower estrogen dose do not seem to predispose the patient to vulvovaginal candidiasis.

Other causes

Disorders associated with an altered immune response, such as acquired immunodeficiency syndrome (AIDS) and diabetes mellitus, also predispose women to Candida vulvovaginitis.

Antimicrobials are thought to predispose a patient to Candida by reducing the number of protective resident vaginal bacteria. The most common offenders are broad-spectrum agents such as tetracycline, cephalosporins, and ampicillin-like agents. Tight-fitting undergarments are another potential factor in the development of vulvovaginal candidiasis.

A study by Horowitz et al demonstrated Candida species in ejaculate fluid of partners of patients with recurrent Candida infections, but they suggested that the carrier rate may be low.[4] Traditionally, vulvovaginal candidiasis is not considered a sexually transmitted disease, because it occurs in celibate women, and Candida itself is considered part of the normal vaginal flora.

Recurrent vulvovaginal candidiasis

Although most women with vulvovaginal candidiasis respond quickly to treatment, the recurrent form of the disease, defined as 4 or more episodes of infection per year, may occur (albeit in less than 5% of healthy women). Predisposing factors for recurrent infection are apparent in only a minority of women; they include poorly controlled diabetes and immunosuppressive therapy.

Other factors that may predispose to recurrent infection include abnormalities in local vaginal mucosal immunity and genetic susceptibility. Studies have found that women with recurrent infections have a higher frequency of certain Lewis blood group antigens and specific gene polymorphisms compared with controls.

Recurrent vulvovaginal candidiasis has also been associated with a decreased in vivo concentration of mannose binding lectin (MBL) and an increased concentration of interleukin-4 (IL-4). Studies have shown that the prevalence of a variant MLB gene is higher in women with recurrent vulvovaginal candidiasis than in controls without candidiasis. Furthermore, IL-4 blocks the anti-Candida response mediated by macrophages; thus, elevation of IL-4 levels results in the inhibition of local defense mechanisms.[5, 6, 7, 8]

The role of sexual transmission in recurrent infection remains unresolved. Although controversial, most studies do not support treatment of sexual partners.[9] Horowitz et al reported on 54 women with recurrent Candida vaginitis and found no significant difference in the rate of relapse between women with untreated or treated partners.[4]

Recurrences may be caused by other species of Candida that are not equally susceptible to the usual first-line treatments. In vitro studies have shown that imidazole antifungal agents, such as miconazole and clotrimazole, are not as effective against non– C albicans fungi. C tropicalis and C glabrata are 10 times less sensitive to miconazole than is C albicans. Appropriate fungal cultures may be taken to identify the species. Treatment entails longer courses of antimycotic therapy (10-14 days), regardless of the route of administration.

Atrophic vaginitis

Extremely low estrogen production, as found after menopause or bilateral oophorectomy, can lead to atrophy of the vaginal and vulvar epithelium. Vulvovaginal atrophy is considered a natural process after estrogen withdrawal. Although menopause is the leading cause of decreased levels of circulating estrogen, atrophy of the vagina can occur in nonmenopausal women due to diminished ovarian estrogen production, as can result from cancer treatments, such as radiation therapy and chemotherapy, and immunologic disorders.

Furthermore, in postpartum women, the decline in estrogen levels in conjunction with the loss of placental estrogen and the antagonistic action of prolactin on estrogen production during lactation can lead to atrophy.

Among its many effects, estrogen helps to maintain the collagen content of the epithelium and thus affects its thickness and elasticity. It also helps to maintain acid mucopolysaccharides and hyaluronic acid, which keep epithelial surfaces moist. During the reproductive years, estrogen stimulation is responsible for maintenance of a well-epithelialized vaginal vault. It causes the nonkeratinized stratified squamous epithelium of the vagina to be thick, rugated, and rich in glycogen. Glycogen is necessary for rapid multiplication and maintenance of lactobacilli.

Menopause

During the perimenopausal period, estrogen secretion, primarily estradiol, remains at approximately 120 ng/L. After menopause, it decreases to approximately 18 ng/L. The reduction of endogenous estrogen causes thinning of the epithelium and a diminished glycogen content. The lack of glycogen contributes to a reduction in lactic acid production and an increase in vaginal pH, thus leading to the overgrowth of nonacidophilic species and the disappearance of Lactobacillus. In some patients, this new flora may include bacteria that can incite a superficial infection in denuded regions and alter vaginal secretions.[10]

In addition, during estrogen withdrawal, the papillae of the vagina flatten and the rugae nearly disappear, leaving the vagina relatively smooth. The mucosa becomes progressively thinner and eventually may become only a few cell layers thick. A moderately thick layer of intermediate cells may be present in some areas, with only a row of basal cells in others. Eventually, the vagina becomes denuded of epithelium.

Vulvar vestibulitis

The classic definition of vulvar vestibulitis, according to Freidrich's criteria, includes the following signs and symptoms confined to the vulvar vestibule:

  • Severe pain upon touching the vestibule or attempted vaginal entry
  • Tenderness to pressure localized within the vulvar vestibule
  • Physical findings confined to vestibular erythema of various degrees

The vestibule consists of nonpigmented and nonkeratinized squamous epithelium devoid of skin. It contains mucus-secreting minor vestibular glands, ductal orifices of the Bartholin glands, Skene glands, and the urethral meatus. It is within this region that the inflammatory entity vulvar vestibulitis arises. While many theories have been proposed, the etiology of this condition remains unknown.

Histology

Histopathologic studies have not been helpful in determining etiology, demonstrating a nonspecific inflammation of the vestibular region affecting mostly the superficial stroma and occasionally the epithelium. In 1988, Pyka et al studied surgically excised specimens of the vulvar vestibule from 41 patients with vulvar vestibulitis. Pyka identified it in 66% of the specimens' minor vestibular glands. All of these glands demonstrated some degree of squamous metaplasia forming vestibular clefts.[11]

Infectious etiologies

Vulvar vestibulitis was not widely recognized until Woodruff and Parmley reported on it in the 1980s.[12] They thought that the etiology was an infection of the vestibular glands that was best treated by perineoplasty.

Marinoff and Pyka proposed that Candida may be a causative organism in vulvar vestibulitis; however, the presence of yeast in patients with the condition has not been confirmed by other reports.

More recent studies have investigated the role of human papillomavirus (HPV) infection; however, the evidence has been controversial.[13] Turner and Marinoff[14] reported a 100% rate of HPV positivity in vulvar biopsies in 7 patients with vestibulitis, while Bergeron reported negative viral findings in all 11 of his biopsies. Further studies are needed to elucidate the relationship, if any, between HPV and vulvar vestibulitis.

Noninfectious etiologies

Possible noninfectious causes of vulvar vestibulitis include the following:

  • Vulvovaginal candidiasis therapy - Some authors believe that the disease may result from allergic sensitization within the vulvar vestibule to several types of topical medication for vulvovaginal candidiasis
  • HPV therapy - Treatments for clinical and subclinical HPV, [15] such as cryosurgery, trichloroacetic acid, podophyllin, and laser treatment, have been implicated in the development of vulvar vestibulitis
  • 5-fluorouracil cream - Several cases of vulvar vestibulitis have been reported after the use of this agent, which is administered for the treatment of actinic keratoses and superficial basal cell carcinoma
  • Chemical irritants - An association between such agents, including those found in feminine hygiene products, and vulvar vestibulitis has been investigated
  • Alkaline vaginal pH - This has been demonstrated to cause irritation to the vestibule; agents that alter the vaginal pH can lead to the overgrowth of anaerobic and/or the disappearance of normal flora (ie, Lactobacillus); hypotheses suggest that the constant bathing of the vestibule by an alkaline vaginal discharge may lead to chronic irritation and inflammation
  • Other - Some authors have associated vulvar vestibulitis with a history of sexual abuse, elective abortions, severe marital conflicts, depression, and anxiety

Neurologic pathophysiology

Studies have begun to focus on specific pain receptors found in the vulvar tissue. As a brief overview, the sensory innervation of the inferior portion of the vulva is primarily from the branches of the pudendal nerve. The ilioinguinal and branches of the genitofemoral nerve innervate the superior portion of the vulva. These nerve fibers are of 2 types: (1) those responsible for touch and (2) those responsible for nociception (perception of noxious stimuli).

The mechanism hypothesized is that the nociception fibers are innervated first instead of the touch fibers. This is followed by a prolonged innervational response of the nociception fibers, leading to an abnormal neurologic response from the dorsal horn of the medulla.

Westrom and Willen tested this theory by obtaining vulvar biopsies of 47 women with clinical vestibulitis. In 44 specimens, they noted that not only were regions of marked increase of vestibular nerve formation present, but a significant correlation was found between inflammation and nerve-bundle density. The authors concluded that a chronic inflammatory reaction in the vestibule might lead to proliferation of nerve fibers. Thus, treatment had entailed surgical removal of these nerve fibers.[16]

Contact dermatitis

The vulvar skin is a frequent site of contact dermatitis; the cutaneous response may be either allergic or irritant induced. An allergic reaction implies previous exposure to an allergen and sensitization. It is a cell-mediated (type IV) immunologic response that can occur in sensitized individuals.

Irritant-induced contact dermatitis can be acute or chronic. It may occur from acute exposure to a potent irritant or upon repeated exposure to a weak irritant. Irritants that can cause contact dermatitis include the following:

  • Moisture
  • Urine
  • Vaginal discharge
  • Topical medications
  • Anticandidal agents
  • Latex
  • Spermicidal agents
  • Cosmetics
  • Douching
  • Fragrances
  • Cleansing products
  • Underwear
Previous
Next

Epidemiology

Occurrence in the United States

Vulvovaginal candidiasis

At some point in their lifetime, nearly 75% of all women experience an attack of vulvovaginal candidiasis, with approximately 50% of college-aged women having an episode. About half of the women who develop the condition have more than 1 episode, and a few have frequent relapses.[17, 18] Patients with recurrent or severe vulvovaginal candidiasis warrant a screening test for diabetes mellitus.

Atrophic candidiasis

After menopause, most women experience some vaginal atrophy as estrogen levels fall. The incidence of atrophic vaginitis depends on how it is defined. Vulvovaginitis related to infection is much less common after menopause. Desquamative inflammatory vaginitis, an exception, has an unknown etiology, but a Gram stain of culture often reveals streptococci. This is treated with intravaginal clindamycin cream or a topical or intravaginal steroid.[19]

International occurrence

An international study by Foxman et al on the rate of vulvovaginal candidiasis in Western nations found a high incidence of the disease in these countries. The investigators examined rates in the United States and 5 European nations, using surveys from about 6000 women aged 16 years and older. They determined that among the 6 countries, rates of vulvovaginal candidiasis ranged from 29-49%. It was also found that the recurrent form of the disease developed in more than one fifth of the reported cases.[20]

Age-related demographics

Candida species infections are most common during childbearing years. Atrophic vaginitis may develop several years after menopause. Most women with vaginal atrophy do not develop symptomatic atrophic vaginitis.

Previous
Next

Prognosis

Vulvovaginal candidiasis

Most women with vulvovaginal candidiasis usually respond quickly to treatment. Despite therapy, however, recurrent vulvovaginal candidiasis, defined as 4 or more episodes of infection per year, can occur, although in less than 5% of healthy women. Predisposing factors for recurrent infection are apparent in only a minority of women, and include poorly controlled diabetes and immunosuppressive therapy. Other factors that may predispose to recurrent infection include abnormalities in local vaginal mucosal immunity and genetic susceptibility. Studies have found that women with recurrent infections have a higher frequency of certain Lewis blood group antigens and specific gene polymorphisms than do controls.

Atrophic vaginitis

Accumulating evidence indicates that the vaginal symptoms readily respond to estrogen treatment. With treatment, mucosal thickening with glandular function can be maintained well into the postmenopausal period.

Vulvar vestibulitis

Generally, no specific cure is available, but spontaneous resolution has been reported; thus, treatment should focus on alleviation of symptoms.

Previous
 
 
Contributor Information and Disclosures
Author

Jill M Krapf, MD, FACOG Assistant Professor, Department of Obstetrics and Gynecology, George Washington University School of Medicine and Health Sciences; Assistant Director, Obstetrics and Gynecology Clerkship, Center for Sexual Health, Women’s Services

Jill M Krapf, MD, FACOG is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Association of Professors of Gynecology and Obstetrics, American Congress of Obstetricians and Gynecologists, International Society for the Study of Women’s Sexual Health

Disclosure: Nothing to disclose.

Specialty Editor Board

Nicole W Karjane, MD Associate Professor, Department of Obstetrics and Gynecology, Virginia Commonwealth University Medical Center

Nicole W Karjane, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, Association of Professors of Gynecology and Obstetrics, North American Society for Pediatric and Adolescent Gynecology

Disclosure: Nothing to disclose.

Chief Editor

Christine Isaacs, MD Associate Professor, Department of Obstetrics and Gynecology, Division Head, General Obstetrics and Gynecology, Medical Director of Midwifery Services, Virginia Commonwealth University School of Medicine

Christine Isaacs, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Acknowledgements

Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David S Howes, MD Professor of Medicine and Pediatrics, Emergency Medicine Residency Program Director Emeritus, Head, Phemister Society, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

David S Howes, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Reza Keshavarz, MD, MPH Clinical Assistant Professor, Departments of Pediatrics and Emergency Medicine, Mount Sinai School of Medicine; Director of Pediatric Emergency Medicine, Mount Sinai Hospital

Disclosure: Nothing to disclose.

Mark J Leber, MD, MPH Assistant Professor of Emergency Medicine in Clinical Medicine, Weill Cornell Medical College; Attending Physician, Lincoln Medical and Mental Health 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.

Deslyn M Mancini, MD Instructor, Department of Obstetrics and Gynecology, MCP Hahnemann University

Disclosure: Nothing to disclose.

Bruce A Meyer, MD, MBA Executive Vice President for Health System Affairs, Executive Director, Faculty Practice Plan, Professor, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical School

Bruce A Meyer, MD, MBA is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Physician Executives, American Institute of Ultrasound in Medicine, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Medical Group Management Association, and Society for Maternal-Fetal Medicine

Disclosure: Nothing to disclose.

Omnia M Samra-Latif, MD Clinical Faculty, Department of Obstetrics and Gynecology, Robert Wood Johnson University, Hamilton Hospital

Omnia M Samra-Latif, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists and American Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Anuritha Tirumani, MD Research Coordinator, Department of Emergency Medicine, Brooklyn Hospital Center

Disclosure: Nothing to disclose.

Ellen Wood, DO, FACOOG Voluntary Assistant Professor, University of Miami, Leonard M Miller School of Medicine

Ellen Wood, DO, FACOOG is a member of the following medical societies: American Society for Reproductive Medicine

Disclosure: Nothing to disclose.

Mark Zwanger, MD, MBA Assistant Professor, Department of Emergency Medicine, Jefferson Medical College of 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.

References
  1. Chatwani AJ, Mehta R, Hassan S, Rahimi S, Jeronis S, Dandolu V. Rapid testing for vaginal yeast detection: a prospective study. Am J Obstet Gynecol. 2007 Apr. 196(4):309.e1-4. [Medline].

  2. Donders G, Bellen G, Byttebier G, Verguts L, Hinoul P, Walckiers R, et al. Individualized decreasing-dose maintenance fluconazole regimen for recurrent vulvovaginal candidiasis (ReCiDiF trial). Am J Obstet Gynecol. 2008 Dec. 199(6):613.e1-9. [Medline].

  3. Katz. Vaginitis. Katz. Comprehensive Gynecology. 5th ed. Mosby; Elsevier; 2007. 588-596.

  4. Horowitz BJ, Edelstein SW, Lippman L. Sexual transmission of Candida. Obstet Gynecol. 1987 Jun. 69(6):883-6. [Medline].

  5. Ip WK, Lau YL. Role of mannose-binding lectin in the innate defense against Candida albicans: enhancement of complement activation, but lack of opsonic function, in phagocytosis by human dendritic cells. J Infect Dis. 2004 Aug 1. 190(3):632-40. [Medline].

  6. Lillegard JB, Sim RB, Thorkildson P, Gates MA, Kozel TR. Recognition of Candida albicans by mannan-binding lectin in vitro and in vivo. J Infect Dis. 2006 Jun 1. 193(11):1589-97. [Medline].

  7. Liu F, Liao Q, Liu Z. Mannose-binding lectin and vulvovaginal candidiasis. Int J Gynaecol Obstet. 2006 Jan. 92(1):43-7. [Medline].

  8. Giraldo PC, Babula O, Gonçalves AK, Linhares IM, Amaral RL, Ledger WJ, et al. Mannose-binding lectin gene polymorphism, vulvovaginal candidiasis, and bacterial vaginosis. Obstet Gynecol. 2007 May. 109(5):1123-8. [Medline].

  9. Fong IW. The value of treating the sexual partners of women with recurrent vaginal candidiasis with ketoconazole. Genitourin Med. 1992 Jun. 68(3):174-6. [Medline]. [Full Text].

  10. Pandit L, Ouslander JG. Postmenopausal vaginal atrophy and atrophic vaginitis. Am J Med Sci. 1997 Oct. 314(4):228-31. [Medline].

  11. Pyka RE, Wilkinson EJ, Friedrich EG Jr, Croker BP. The histopathology of vulvar vestibulitis syndrome. Int J Gynecol Pathol. 1988. 7(3):249-57. [Medline].

  12. Woodruff JD, Parmley TH. Infection of the minor vestibular gland. Obstet Gynecol. 1983 Nov. 62(5):609-12. [Medline].

  13. Bergeron C, Moyal-Barracco M, Pelisse M, Lewin P. Vulvar vestibulitis. Lack of evidence for a human papillomavirus etiology. J Reprod Med. 1994 Dec. 39(12):936-8. [Medline].

  14. Turner ML, Marinoff SC. Association of human papillomavirus with vulvodynia and the vulvar vestibulitis syndrome. J Reprod Med. 1988 Jun. 33(6):533-7. [Medline].

  15. Marinoff SC, Turner ML. Vulvar vestibulitis syndrome. Dermatol Clin. 1992 Apr. 10(2):435-44. [Medline].

  16. Westrom LV, Willen R. Vestibular nerve fiber proliferation in vulvar vestibulitis syndrome. Obstet Gynecol. 1998 Apr. 91(4):572-6. [Medline].

  17. Szumigala JA, Alveredo R. Vulvovaginitis. Ferri. Ferri's Clinical Advisor 2009. Mosby; Elsevier; 2009. 155, 1008-1012.

  18. Eckert LO. Clinical practice. Acute vulvovaginitis. N Engl J Med. 2006 Sep 21. 355(12):1244-52. [Medline].

  19. Margesson LJ. Vulvar disease pearls. Dermatol Clin. 2006 Apr. 24(2):145-55, v. [Medline].

  20. Foxman B, Muraglia R, Dietz JP, Sobel JD, Wagner J. Prevalence of recurrent vulvovaginal candidiasis in 5 European countries and the United States: results from an internet panel survey. J Low Genit Tract Dis. 2013 Jul. 17(3):340-5. [Medline].

  21. Nyirjesy P. Vulvovaginal candidiasis and bacterial vaginosis. Infect Dis Clin North Am. 2008 Dec. 22(4):637-52, vi. [Medline].

  22. Braverman PK. Urethritis, vulvovaginitis, and cervicitis. Principles and Practice of Pediatric Infectious Diseases. 3rd ed. Churchill Livingstone; Elsevier; 2008. 55.

  23. Biggs WS, Williams RM. Common gynecologic infections. Prim Care. 2009 Mar. 36(1):33-51, viii. [Medline].

  24. Johnson E, Berwald N. Evidence-based emergency medicine/rational clinical examination abstract. Diagnostic utility of physical examination, history, and laboratory evaluation in emergency department patients with vaginal complaints. Ann Emerg Med. 2008 Sep. 52(3):294-7. [Medline].

  25. Nyirjesy P, Leigh RD, Mathew L, Lev-Sagie A, Culhane JF. Chronic vulvovaginitis in women older than 50 years: analysis of a prospective database. J Low Genit Tract Dis. 2012 Jan. 16(1):24-9. [Medline].

  26. Halperin R, Zehavi S, Vaknin Z, Ben-Ami I, Pansky M, Schneider D. The major histopathologic characteristics in the vulvar vestibulitis syndrome. Gynecol Obstet Invest. 2005. 59(2):75-9. [Medline].

  27. Esim Buyukbayrak E, Kars B, Karsidag AY, Karadeniz BI, Kaymaz O, Gencer S, et al. Diagnosis of vulvovaginitis: comparison of clinical and microbiological diagnosis. Arch Gynecol Obstet. 2010 Nov. 282(5):515-9. [Medline].

  28. Schwiertz A, Taras D, Rusch K, Rusch V. Throwing the dice for the diagnosis of vaginal complaints?. Ann Clin Microbiol Antimicrob. 2006 Feb 17. 5:4. [Medline]. [Full Text].

  29. [Guideline] Workowski KA, Berman S. Sexually Transmitted Diseases Treatment Guidelines, 2010. MMWR. Dec 17 2010;59(RR-12). Centers for Disease Control and Prevention. Available at http://www.cdc.gov/std/treatment/2010/default.htm. Accessed: August 22, 2013.

  30. Ferris DG, Francis SL, Dickman ED, Miler-Miles K, Waller JL, McClendon N. Variability of vaginal pH determination by patients and clinicians. J Am Board Fam Med. 2006 Jul-Aug. 19(4):368-73. [Medline].

  31. Kulp JL, Chaudhry S, Wiita B, Bachmann G. The accuracy of women performing vaginal pH self-testing. J Womens Health (Larchmt). 2008 May. 17(4):523-6. [Medline].

  32. [Guideline] Huntzinger A. Guideline Briefs. Practice American Family Physician. Nov 2006. 74.

  33. Sobel JD, Wiesenfeld HC, Martens M, Danna P, Hooton TM, Rompalo A, et al. Maintenance fluconazole therapy for recurrent vulvovaginal candidiasis. N Engl J Med. 2004 Aug 26. 351(9):876-83. [Medline].

  34. Sobel JD, Chaim W. Treatment of Torulopsis glabrata vaginitis: retrospective review of boric acid therapy. Clin Infect Dis. 1997 Apr. 24(4):649-52. [Medline].

  35. Nachtigall LD. Use of low-dose premarin, estrace, and estring vaginally. Obstetrical and Gynecological Survey. 1998. 53(10S):62S-65S.

  36. Suckling J, Lethaby A, Kennedy R. Local oestrogen for vaginal atrophy in postmenopausal women. Cochrane Database Syst Rev. 2006 Oct 18. CD001500. [Medline].

  37. The North American Menopause Society. The role of local vaginal estrogen for treatment of vaginal atrophy in postmenopausal women: 2007 position statement of The North American Menopause Society. Menopause. 2007 May-Jun. 14(3 pt 1):355-69; quiz 370-1. [Medline].

  38. Henriksson L, Stjernquist M, Boquist L, Cedergren I, Selinus I. A one-year multicenter study of efficacy and safety of a continuous, low-dose, estradiol-releasing vaginal ring (Estring) in postmenopausal women with symptoms and signs of urogenital aging. Am J Obstet Gynecol. 1996 Jan. 174(1 Pt 1):85-92. [Medline].

  39. Ayton RA, Darling GM, Murkies AL, Farrell EA, Weisberg E, Selinus I, et al. A comparative study of safety and efficacy of continuous low dose oestradiol released from a vaginal ring compared with conjugated equine oestrogen vaginal cream in the treatment of postmenopausal urogenital atrophy. Br J Obstet Gynaecol. 1996 Apr. 103(4):351-8. [Medline].

  40. Eriksen PS, Rasmussen H. Low-dose 17 beta-estradiol vaginal tablets in the treatment of atrophic vaginitis: a double-blind placebo controlled study. Eur J Obstet Gynecol Reprod Biol. 1992 Apr 21. 44(2):137-44. [Medline].

  41. Brossfield J. Herbal Therapies for Menopause. The Resident Reporter. 2000. 5(6):26-30.

  42. Hirata JD, Swiersz LM, Zell B, Small R, Ettinger B. Does dong quai have estrogenic effects in postmenopausal women? A double-blind, placebo-controlled trial. Fertil Steril. 1997 Dec. 68(6):981-6. [Medline].

  43. Lieberman S. A review of the effectiveness of Cimicifuga racemosa (black cohosh) for the symptoms of menopause. J Womens Health. 1998 Jun. 7(5):525-9. [Medline].

  44. Nachtigall LB, LaGrega L, Lee WW. The effects of isoflavones derived from red clover on vasomotor symptoms and endometrial thickness. 9th International Menopause Society World Congress on Menopause. 1999.

  45. Punyahotra S, Dennerstein L, Lehert P. Menopausal experiences of Thai women. Part 1: Symptoms and their correlates. Maturitas. 1997 Jan. 26(1):1-7. [Medline].

  46. Chen J, Geng L, Song X, Li H, Giordan N, Liao Q. Evaluation of the efficacy and safety of hyaluronic acid vaginal gel to ease vaginal dryness: a multicenter, randomized, controlled, open-label, parallel-group, clinical trial. J Sex Med. 2013 Jun. 10(6):1575-84. [Medline].

  47. Bergeron S, Binik YM, Khalifé S, Pagidas K. Vulvar vestibulitis syndrome: a critical review. Clin J Pain. 1997 Mar. 13(1):27-42. [Medline].

  48. Solomons CC, Melmed MH, Heitler SM. Calcium citrate for vulvar vestibulitis. A case report. J Reprod Med. 1991 Dec. 36(12):879-82. [Medline].

  49. Horowitz BJ. Interferon therapy for condylomatous vulvitis. Obstet Gynecol. 1989 Mar. 73(3 Pt 1):446-8. [Medline].

  50. Harris G, Horowitz B, Borgida A. Evaluation of gabapentin in the treatment of generalized vulvodynia, unprovoked. J Reprod Med. 2007 Feb. 52(2):103-6. [Medline].

  51. Marrazzo J. Vulvovaginal candidiasis. BMJ. 2002 Sep 14. 325(7364):586. [Medline]. [Full Text].

 
Previous
Next
 
Candida albicans photomicrograph. Courtesy of Centers for Disease Control and Prevention (CDC).
Table 1. Suggested Treatment Options as Cited in the US Centers for Disease Control and Prevention (CDC) Guidelines for Treatment
Option Treatment
Butoconazole 2% cream, 5 g intravaginally for 3 days
Butoconazole 2% cream, 5 g (butoconazole 1-sustained release), single intravaginal application
Clotrimazole 1% cream, 5 g intravaginally for 7–14 days
Clotrimazole 100 mg vaginal tablet for 7 days
Clotrimazole 100 mg vaginal tablet, 2 tablets for 3 days
Miconazole 2% cream 5 g intravaginally for 7 days
Miconazole 100 mg vaginal suppository, 1 suppository for 7 days
Miconazole 200 mg vaginal suppository, 1 suppository for 3 days
Miconazole 1200 mg vaginal suppository, 1 suppository for 1 day
Nystatin 100,000-unit vaginal tablet, 1 tablet for 14 days
Tioconazole 6.5% ointment 5 g intravaginally in a single application
Terconazole 0.4% cream 5 g intravaginally for 7 days
Terconazole 0.8% cream 5 g intravaginally for 3 days
Terconazole 80 mg vaginal suppository, 1 suppository for 3 days
Fluconazole 150 mg oral tablet, 1 tablet in single dose
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.