ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Candida vulvovaginitis: Clinical manifestations and diagnosis

Candida vulvovaginitis: Clinical manifestations and diagnosis
Literature review current through: Sep 2023.
This topic last updated: May 25, 2023.

INTRODUCTION — Vulvovaginal candidiasis is one of the most common causes of vulvovaginal itching and discharge. The disorder is characterized by inflammation in the setting of Candida species and results in the common vaginitis symptoms of itching and erythema. While Candida vulvovaginitis is frequently self-diagnosed, office diagnosis with microscopy is preferred.

This topic will discuss the clinical presentation, diagnostic approach, and diagnosis of vulvovaginal candidiasis. Related topics on the treatment of vulvovaginal candidiasis and vaginitis in general are presented separately:

(See "Candida vulvovaginitis in adults: Treatment of acute infection".)

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

(See "Bacterial vaginosis: Clinical manifestations and diagnosis".)

(See "Trichomoniasis: Clinical manifestations and diagnosis".)

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 — Vulvovaginal candidiasis refers to a disorder characterized by signs and symptoms of vulvovaginal inflammation in the presence of Candida species. Identification of vulvovaginal Candida alone is not indicative of disease, as Candida species are part of the normal flora of approximately 25 percent of women [1]. In contrast to oropharyngeal candidiasis, it is generally not considered an opportunistic infection. Vulvovaginal candidiasis is not considered a sexually transmitted disease.

EPIDEMIOLOGY — Vulvovaginal candidiasis is the second most common cause of vaginitis symptoms (after bacterial vaginosis) and accounts for approximately one-third of vaginitis cases [2]. The prevalence of vulvovaginal candidiasis is difficult to determine because:

Candida species, without inflammation, can be identified in the lower genital tract in 10 to 20 percent of healthy women in the reproductive age group, 6 to 7 percent of menopausal women, and 3 to 6 percent of prepubertal girls [3,4].

The widespread use of over-the-counter antifungal drugs makes epidemiologic studies difficult to perform.

The clinical diagnosis is often based on symptoms and not confirmed by microscopic examination or culture.

As many as one-half of clinically diagnosed women may have another condition [5].

Culture performed without clinical correlation is likely to overestimate the prevalence of disease.

In surveys, the prevalence of vulvovaginal candidiasis is highest among women in their reproductive years: 55 percent of female university students report having had at least one health care provider-diagnosed episode by age 25 years, 29 to 49 percent of premenopausal women report having had at least one lifetime episode, and 9 percent of women report having had four or more infections in a 12-month period (ie, recurrent vulvovaginal candidiasis [RVVC]) [6,7]. In a separate study, in women with an initial infection, the probability of RVVC was 10 percent by age 25 years and 25 percent by age 50 years [7]. (See "Candida vulvovaginitis in adults: Recurrent infection".)

The incidence of a single or sporadic infection increases with age up to menopause and is higher in African-American women than in other ethnic groups. The disorder is uncommon in postmenopausal women unless they are taking estrogen therapy. It is also uncommon in prepubertal girls, in whom it is frequently overdiagnosed.

MICROBIOLOGY AND PATHOGENESIS — Candida albicans is responsible for 80 to 92 percent of episodes of vulvovaginal candidiasis in the United States [8,9], and Candida glabrata accounts for almost all of the remainder [10]. Some, but not all, investigators have reported an increasing frequency of nonalbicans species, particularly C. glabrata [11,12], possibly due to widespread use of over-the-counter drugs, long-term use of suppressive azoles, and the use of short courses of antifungal drugs.

All Candida species produce similar vulvovaginal symptoms, although the severity of symptoms is milder with C. glabrata and C. parapsilosis. Candida organisms probably access the vagina via migration from the rectum across the perianal area [13]; cultures of the gastrointestinal tract and vagina often show identical Candida species. Less commonly, the source of infection is sexual or relapse from a vaginal reservoir. In contrast to bacterial vaginosis, vulvovaginal candidiasis is not associated with a reduction in vaginal lactobacilli [14-17].

Symptomatic disease is associated with an overgrowth of the organism and penetration of superficial epithelial cells [18-21]. The mechanism by which Candida species transform from asymptomatic colonization to an invasive form causing symptomatic vulvovaginal disease is complex, involving host inflammatory responses and yeast virulence factors. One study comparing histologic specimens from women with confirmed vulvovaginal candidiasis, women without infection, and women with active bacterial vaginosis has reported co-invasion with Gardnerella or Lactobacillus species organisms in women with Candida infection but absence of a biofilm (in contrast with bacterial vaginosis) [21]. (See "Bacterial vaginosis: Clinical manifestations and diagnosis", section on 'Pathogenesis and microbiology'.)

RISK FACTORS — While sporadic attacks of vulvovaginal candidiasis often occur without an identifiable precipitating factor, some risk factors have been identified [22,23]:

Demonstrated impact — Some diseases, endocrine changes, and medication use predispose to candida infections.

Diabetes mellitus – Women with diabetes mellitus who have poor glycemic control are more prone to vulvovaginal candidiasis than euglycemic women [24,25]. In particular, women with type 2 diabetes appear prone to nonalbicans Candida species [26]. Treatment with sodium glucose cotransporter 2 inhibitors may increase the risk for vulvovaginal candidiasis [27,28]. (See "Susceptibility to infections in persons with diabetes mellitus".)

Antibiotic use – Use of broad-spectrum antibiotics significantly increases the risk of developing vulvovaginal candidiasis [29]. As many as one-quarter to one-third of women develop the disorder during or after taking these antibiotics because inhibition of normal bacterial flora favors growth of potential fungal pathogens, such as Candida. Administration of Lactobacillus (oral or vaginal) during and for four days after antibiotic therapy does not prevent post-antibiotic vulvovaginitis [30].

Increased estrogen levels – Vulvovaginal candidiasis appears to occur more often in the setting of increased estrogen levels, such as pregnancy and postmenopausal estrogen therapy.

Immunosuppression – Candidal infections are more common in immunosuppressed patients, such as those taking glucocorticoids or other immunosuppressive drugs, or with human immunodeficiency virus (HIV) infection [31]. (See "Glucocorticoid effects on the immune system" and "The natural history and clinical features of HIV infection in adults and adolescents".)

Genetic – An analysis of whole exome sequencing from 160 European women with recurrent vulvovaginal candidiasis (RVVC) and 175 controls from the same regions demonstrated an association with polymorphisms in the SIGLEC15 gene, which produces a cell surface protein found on macrophages and dendritic cells [32]. Previous studies that evaluated known pathways identified associations between RVVC and polymorphisms in the TLR2 [33] and mannose-binding lectin genes [34]. Although these genetic variations are not modifiable risk factors, in the future, they may help guide treatment or prevention strategies.

Unclear impact — The role of various contraceptive devices, sexual behaviors, and diet on the risk of Candida vulvovaginitis is less clear.

Combined oral contraceptives (COC) – A 2013 systematic review of the literature found that, of 12 studies including more than 200 women, 7 demonstrated a significant association between COC use and prevalent or incident candidiasis, 2 found an association that was not statistically significant, and 3 found no association or a lower risk of candidiasis. However, the authors note that among the three highest quality studies, results were evenly split: one showed an increased risk in COC users, one showed no association, and one showed reduced risk in COC users [35]. Since that review, in one study of over 1000 HIV serodiscordant couples in Zambia, COC use was associated with lower risk for candidiasis, though pregnancy was associated with a higher risk [36].

Contraceptive devices – Vaginal sponges, diaphragms, and intrauterine devices (IUDs) have been associated with vulvovaginal candidiasis, but not consistently. At least two studies have suggested that recurrent Candida vulvovaginitis in IUD users may be related to the ability of some species to attach to the IUD and form a biofilm rather than related to an intrinsic property of the IUD itself [37,38]. Spermicides are not associated with Candida infection. (See "Pericoital (on demand) contraception: Diaphragm, cervical cap, spermicides, and sponge" and "Intrauterine contraception: Candidates and device selection".)

Sexual behavior – Vulvovaginal candidiasis is not traditionally considered a sexually transmitted disease since it occurs in celibate women and since Candida species are considered part of the normal vaginal flora. This does not mean that sexual transmission of Candida does not occur or that vulvovaginal candidiasis is not associated with sexual activity. For example, an increased frequency of vulvovaginal candidiasis has been reported at the time most women begin regular sexual activity [6,22,39]. In addition, partners of infected women are four times more likely to be colonized than partners of uninfected women, and colonization is often the same strain in both partners. However, the number of episodes of vulvovaginal candidiasis a woman experiences does not appear to be related to her lifetime number of sexual partners or the frequency of coitus [22,40,41]. Women who exclusively have sex with women do not appear to have an increased risk of vulvovaginal infection [42].

The type of sex may be a factor. Infection may be linked to orogenital and, less commonly, anogenital sex. Evidence of a link between vulvovaginal candidiasis and hygienic habits (eg, douching, use of tampons/menstrual pads) or wearing tight or synthetic clothing is weak and conflicting [22,43-50].

Diet – There are few high-quality data examining the link between vulvovaginal candidiasis and diet. Most studies are cross-sectional and have high to moderate risk of bias. A few small studies show no association between consumption of yogurt or fermented dairy products and risk for Candida vulvovaginitis [50,51]. Two studies demonstrate higher dairy consumption among women with symptomatic vulvovaginal yeast infection, though this may be due to the common practice of eating yogurt to try and reduce recurrent infections [43,52].

CLINICAL FEATURES

Symptoms — Vulvar pruritus is the dominant feature of vulvovaginal candidiasis [10,19,53-55]. Vulvar burning, soreness, and irritation are also common and can be accompanied by dysuria (typically perceived to be external or vulvar rather than urethral) or dyspareunia. Symptoms are often worse during the week prior to menses [55]. The intensity of signs and symptoms varies from mild to severe, except among women with C. glabrata or C. parapsilosis infection, who tend to have mild or minimal clinical findings [56].

Physical examination — Physical examination of the external genitalia, vagina, and cervix often reveals erythema of the vulva and vaginal mucosa and vulvar edema (picture 1). Vulvar excoriation and fissures are present in approximately one-quarter of patients. However, these changes reflect generalized inflammation and are not necessarily specific to Candida infections. There can be little or no discharge; when present, it is classically white, thick, adherent to the vaginal sidewalls, and clumpy (curd-like or cottage cheese-like) with no or minimal odor. However, the discharge may be thin and loose, watery, homogeneous, and indistinguishable from that in other types of vaginitis. The cervix usually appears normal.

DIAGNOSTIC APPROACH

Clinical evaluation — At the time of physical examination, a sample of vaginal discharge is collected for testing. Office-based tests include pH and microscopy or point-of-care molecular tests. Office-based tests provide immediate results. Alternately, the vaginal discharge can be sent for laboratory testing with molecular tests, typically nucleic acid amplification tests (NAATs). Laboratory tests may take longer for test results but have a higher accuracy [57].

Vaginal pH and microscopy — The office evaluation consists of swabbing the vaginal sidewall and discharge, assessing the vaginal pH, and performing microscopy [58]. The vaginal pH in women with Candida infection is typically normal (4 to 4.5), which distinguishes candidiasis from trichomoniasis or bacterial vaginosis (table 1). In mixed infections, Candida can be seen at higher pH levels. Candida species can be seen on a wet mount of the discharge; adding 10 percent potassium hydroxide destroys the cellular elements and facilitates recognition of budding yeast, pseudohyphae, and hyphae (picture 2 and picture 3 and picture 4 and picture 5 and picture 6 and picture 7) [59]. Use of Swartz-Lamkins fungal stain (potassium hydroxide, a surfactant, and blue dye) may facilitate diagnosis by staining the Candida organisms blue so they are easier to identify [60]. However, microscopy is negative in up to 50 percent of patients with culture-confirmed vulvovaginal candidiasis [18].

Microscopy is also important for looking for clue cells or motile trichomonads, which indicate bacterial vaginosis and trichomoniasis, respectively, as alternative diagnoses, coinfection, or mixed vaginitis [61]. The general diagnostic approach to women with vaginal complaints is reviewed separately:

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

(See "Bacterial vaginosis: Clinical manifestations and diagnosis".)

(See "Trichomoniasis: Clinical manifestations and diagnosis".)

Molecular and other tests — Data supporting point-of-care tests for Candida are limited [62-68].

A DNA probe test performed in a centralized laboratory offers results comparable to culture with results available in several hours, but no speciation (Affirm VPIII).

Polymerase chain reaction (PCR) methods have high sensitivity and specificity and a shorter turn-around time than culture [69-72] but are costly and offer no proven clinical benefit over culture in symptomatic women [69].

A molecular test (BD MAX) that assays the vaginal microbiome for evidence of bacterial vaginosis, vaginal candidiasis, and trichomonas has shown promise in initial clinical studies, with a sensitivity for Candida species group of 90 percent (95% CI 88.1-93.1 percent) and specificity of 94.1 percent (95% CI 92.6-95.4 percent) compared with culture. Sensitivity for C. glabrata was lower, at 75.9 percent (95% CI 57.9-87.8 percent), but specificity was higher at 99.7 percent (99.3-99.9 percent). Another assay approved by the US Food and Drug Administration, the Aptima CV/TV, had similar sensitivity and specificity for the Candida species group (sensitivity 91.7 percent, specificity 94.9 percent) and higher sensitivity for C. glabrata (sensitivity 84.7 percent, specificity 99.1 percent) [57,73].

Pap smear is positive in 25 percent of patients with culture-positive, symptomatic vulvovaginal candidiasis [10]. It is insensitive because the cells are derived from the cervix, which is not affected by Candida vaginitis. (See "Candida vulvovaginitis in adults: Treatment of acute infection", section on 'Unique populations'.)

Limited role of culture — Culture is not typically required for the routine diagnosis of vulvovaginal candidiasis because vaginal pH and microscopy are reliable tests and because yeast are normal colonizers of the vagina (ie, a culture that confirms yeast may not reflect actual infection).

We obtain a vaginal culture in:

Patients with clinical features of vulvovaginal candidiasis, normal vaginal pH, and no pathogens (yeast, clue cells, trichomonads) visible on microscopy. A positive culture in these patients confirms the diagnosis and reveals the species of Candida, thus avoiding empiric, unindicated, or incorrect therapy.

Patients with persistent or recurrent symptoms because many of these patients have nonalbicans infections and/or infections that are resistant to azoles. C. glabrata is not easily recognized on microscopy because it does not form hyphae or pseudohyphae [2].

(See "Candida vulvovaginitis in adults: Treatment of acute infection", section on 'Non-albicans Candida species'.)

(See "Candida vulvovaginitis in adults: Recurrent infection", section on 'Azole-resistant infection'.)

To perform a culture, a vaginal sample is obtained from the lateral wall using a cotton-tipped swab and inoculated onto Sabouraud agar, Nickerson medium, or Microstix-Candida medium; these media perform equally well [10]. Culture for Candida does not require quantification of in vitro colony count. Speciation of Candida is not essential for primary diagnostic testing, as most isolates are C. albicans; however, species identification is essential in refractory and recurrent disease.

Self-diagnosis — Self-diagnosis of vulvovaginal candidiasis is frequently inaccurate and should be discouraged [58,74,75]. In a study that administered a questionnaire to 600 women to assess their knowledge of the symptoms and signs of vulvovaginal candidiasis (and other infections) after reading classic case scenarios, only 11 percent of women without a previous diagnosis of vulvovaginal candidiasis correctly diagnosed this infection [74]. Women who had had a prior episode were more often correct (35 percent) but were likely to use over-the-counter drugs inappropriately to treat other, potentially more serious, gynecologic disorders.

In another report, the actual diagnoses in 95 women who self-diagnosed vulvovaginal candidiasis were vulvovaginal candidiasis (34 percent), bacterial vaginosis (19 percent), mixed vaginitis (21 percent), normal flora (14 percent), Trichomonas vaginitis (2 percent), and other (11 percent) [75]. Women with a previous episode of vulvovaginal candidiasis and those who read the package insert for their over-the-counter medication were not more accurate in making a diagnosis than other women.

Some consequences of misdiagnosis and inappropriate therapy include a delay in correct diagnosis and treatment, wasted monetary expenditure, and precipitation of vulvar dermatitis.

DIAGNOSIS — The diagnosis of vulvovaginal candidiasis is based upon the presence of Candida on wet mount (preferred), Gram stain, culture, or molecular testing of vaginal discharge in a woman with characteristic clinical findings (eg, vulvovaginal pruritus, burning, erythema, edema, and/or curd-like discharge attached to the vaginal sidewall) and no other pathogens to account for her symptoms [58]. (See 'Clinical features' above.)

As none of the clinical manifestations of vulvovaginal candidiasis are pathognomonic, suspected clinical diagnosis should always be confirmed by laboratory methods (ie, microscopy, Gram stain, or culture). Once the diagnosis is confirmed, the infection is then categorized as complicated or uncomplicated to facilitate treatment (table 2). Treatment of Candida vulvovaginitis is reviewed separately. (See "Candida vulvovaginitis in adults: Treatment of acute infection".)

DIFFERENTIAL DIAGNOSIS — Importantly, although vulvar pruritus is a cardinal symptom of the disorder, less than 50 percent of women with genital pruritus have vulvovaginitis candidiasis [76].

Normal vaginal pH – Other conditions considered in the differential diagnosis of vulvovaginitis with normal vaginal pH include hypersensitivity reactions, allergic or chemical reactions, contact dermatitis, neuropathic itch, and inflammatory dermatoses (eg, lichen sclerosus and lichen planus) [77]. Recognizing local adverse reactions to topical agents avoids the prescribing of additional agents that can worsen symptoms. These conditions are discussed in detail elsewhere. (See "Vulvar dermatitis".)

In addition, mechanical irritation due to insufficient lubrication during coitus can also result in vaginal discomfort.

Elevated vaginal pH – If vaginal pH exceeds 4.5 or excess white cells are present, mixed infection with bacterial vaginosis or trichomoniasis may be present. Mixed infection (≥2 pathogens and all are symptomatic) is estimated to occur in <5 percent of patients; coinfection (≥2 pathogens but some are not symptomatic) is more common: 20 to 30 percent of women with bacterial vaginosis are coinfected with Candida species [61]. (See "Bacterial vaginosis: Clinical manifestations and diagnosis" and "Trichomoniasis: Clinical manifestations and diagnosis".)

When significant white cells are present, desquamative inflammatory vaginitis should also be considered in the differential [78]. (See "Desquamative inflammatory vaginitis (DIV)".)

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: Gynecologic infectious diseases (non-sexually transmitted)".)

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: Vulvovaginal yeast infection (The Basics)" and "Patient education: Vulvar itching (The Basics)")

Beyond the Basics topics (see "Patient education: Vaginal yeast infection (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

MicrobiologyCandida is considered part of the normal vaginal flora, but overgrowth of the organism can result in vulvovaginitis. Candida albicans accounts for 80 to 92 percent of episodes of vulvovaginal candidiasis; Candida glabrata is the next most common species. (See 'Epidemiology' above and 'Microbiology and pathogenesis' above.)

Risk factors – Risk factors for Candida vulvovaginitis include diabetes mellitus, antibiotic use, elevated estrogen levels, and immunocompromise. However, many women with sporadic or recurrent infection have no identifiable risk factors. (See 'Risk factors' above.)

Clinical presentation – Vulvar pruritus is the dominant symptom. Vulvar burning, soreness, and irritation are common and may result in dysuria and dyspareunia. The vulva and vagina appear erythematous, and vulvar excoriation and fissures may be present. There is often little or no discharge; when present, it is classically white, thick, adherent, and clumpy (curd-like or cottage cheese-like) with no or minimal odor. (See 'Clinical features' above.)

Diagnosis – The diagnosis of vulvovaginal candidiasis is based on the presence of Candida on wet mount (preferred), Gram stain, or culture of vaginal discharge in a woman with characteristic clinical findings. (See 'Clinical evaluation' above.)

Role of vaginal culture – Culture is not necessary for diagnosis if microscopy shows yeast but should be obtained in some individuals (see 'Limited role of culture' above):

Individuals with clinical features of vulvovaginal candidiasis, normal vaginal pH, and negative microscopy.

Individuals with persistent or recurrent symptoms because many of these women have nonalbicans infection resistant to azoles.

Differential diagnosis – The differential diagnosis of vulvar pruritus and erythema varies based on the vaginal pH of the affected women. For women with a normal pH, possible etiologies include hypersensitivity reactions, allergic or chemical reactions, and contact dermatitis. For women with vaginal pH above 4.5, or if excessive white blood cells are present, they can have mixed infection with bacterial vaginosis or trichomoniasis. (See 'Differential diagnosis' above.)

  1. Gardella C, Eckert LO, Lentz GM. Genital tract infections. In: Comprehensive Gynecology, 7th ed, Lobo RA, Gershenson DM, Lentz GM, Valea FA (Eds), Elsevier, Philadelphia 2017. p.542.
  2. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep 2015; 64:1.
  3. Goldacre MJ, Watt B, Loudon N, et al. Vaginal microbial flora in normal young women. Br Med J 1979; 1:1450.
  4. Tibaldi C, Cappello N, Latino MA, et al. Vaginal and endocervical microorganisms in symptomatic and asymptomatic non-pregnant females: Risk factors and rates of occurrence. Clin Microbiol Infect 2009; 15:670.
  5. Berg AO, Heidrich FE, Fihn SD, et al. Establishing the cause of genitourinary symptoms in women in a family practice. Comparison of clinical examination and comprehensive microbiology. JAMA 1984; 251:620.
  6. Geiger AM, Foxman B, Gillespie BW. The epidemiology of vulvovaginal candidiasis among university students. Am J Public Health 1995; 85:1146.
  7. Foxman B, Muraglia R, Dietz JP, et al. 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; 17:340.
  8. Odds FC. Candidosis of the genitalia. In: Candida and Candidosis: A Review and Bibliography, 2nd ed, Odds FC (Ed), Bailliére Tindall, London 1988. p.124.
  9. Gonçalves B, Ferreira C, Alves CT, et al. Vulvovaginal candidiasis: Epidemiology, microbiology and risk factors. Crit Rev Microbiol 2016; 42:905.
  10. Sobel JD. Vulvovaginal candidosis. Lancet 2007; 369:1961.
  11. Horowitz BJ, Giaquinta D, Ito S. Evolving pathogens in vulvovaginal candidiasis: Implications for patient care. J Clin Pharmacol 1992; 32:248.
  12. Vermitsky JP, Self MJ, Chadwick SG, et al. Survey of vaginal-flora Candida species isolates from women of different age groups by use of species-specific PCR detection. J Clin Microbiol 2008; 46:1501.
  13. Bertholf ME, Stafford MJ. Colonization of Candida albicans in vagina, rectum, and mouth. J Fam Pract 1983; 16:919.
  14. Sobel JD, Chaim W. Vaginal microbiology of women with acute recurrent vulvovaginal candidiasis. J Clin Microbiol 1996; 34:2497.
  15. McClelland RS, Richardson BA, Hassan WM, et al. Prospective study of vaginal bacterial flora and other risk factors for vulvovaginal candidiasis. J Infect Dis 2009; 199:1883.
  16. Vitali B, Pugliese C, Biagi E, et al. Dynamics of vaginal bacterial communities in women developing bacterial vaginosis, candidiasis, or no infection, analyzed by PCR-denaturing gradient gel electrophoresis and real-time PCR. Appl Environ Microbiol 2007; 73:5731.
  17. Zhou X, Westman R, Hickey R, et al. Vaginal microbiota of women with frequent vulvovaginal candidiasis. Infect Immun 2009; 77:4130.
  18. Sobel JD. Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis. Am J Obstet Gynecol 1985; 152:924.
  19. Sobel JD, Faro S, Force RW, et al. Vulvovaginal candidiasis: Epidemiologic, diagnostic, and therapeutic considerations. Am J Obstet Gynecol 1998; 178:203.
  20. Merson-Davies LA, Odds FC, Malet R, et al. Quantification of Candida albicans morphology in vaginal smears. Eur J Obstet Gynecol Reprod Biol 1991; 42:49.
  21. Swidsinski A, Guschin A, Tang Q, et al. Vulvovaginal Candidiasis: Histologic lesions are primarily polymicrobial and invasive and do not contain biofilms. Am J Obstet Gynecol 2018.
  22. Foxman B. The epidemiology of vulvovaginal candidiasis: risk factors. Am J Public Health 1990; 80:329.
  23. Sobel JD. Candida vaginitis. Infect Dis Clin Pract 1994; 3:334.
  24. Donders GG. Lower Genital Tract Infections in Diabetic Women. Curr Infect Dis Rep 2002; 4:536.
  25. de Leon EM, Jacober SJ, Sobel JD, Foxman B. Prevalence and risk factors for vaginal Candida colonization in women with type 1 and type 2 diabetes. BMC Infect Dis 2002; 2:1.
  26. Ray D, Goswami R, Banerjee U, et al. Prevalence of Candida glabrata and its response to boric acid vaginal suppositories in comparison with oral fluconazole in patients with diabetes and vulvovaginal candidiasis. Diabetes Care 2007; 30:312.
  27. Nyirjesy P, Zhao Y, Ways K, Usiskin K. Evaluation of vulvovaginal symptoms and Candida colonization in women with type 2 diabetes mellitus treated with canagliflozin, a sodium glucose co-transporter 2 inhibitor. Curr Med Res Opin 2012; 28:1173.
  28. Nyirjesy P, Sobel JD, Fung A, et al. Genital mycotic infections with canagliflozin, a sodium glucose co-transporter 2 inhibitor, in patients with type 2 diabetes mellitus: a pooled analysis of clinical studies. Curr Med Res Opin 2014; 30:1109.
  29. Wilton L, Kollarova M, Heeley E, Shakir S. Relative risk of vaginal candidiasis after use of antibiotics compared with antidepressants in women: postmarketing surveillance data in England. Drug Saf 2003; 26:589.
  30. Pirotta M, Gunn J, Chondros P, et al. Effect of lactobacillus in preventing post-antibiotic vulvovaginal candidiasis: a randomised controlled trial. BMJ 2004; 329:548.
  31. Duerr A, Heilig CM, Meikle SF, et al. Incident and persistent vulvovaginal candidiasis among human immunodeficiency virus-infected women: Risk factors and severity. Obstet Gynecol 2003; 101:548.
  32. Jaeger M, Pinelli M, Borghi M, et al. A systems genomics approach identifies SIGLEC15 as a susceptibility factor in recurrent vulvovaginal candidiasis. Sci Transl Med 2019; 11.
  33. Rosentul DC, Delsing CE, Jaeger M, et al. Gene polymorphisms in pattern recognition receptors and susceptibility to idiopathic recurrent vulvovaginal candidiasis. Front Microbiol 2014; 5:483.
  34. Nedovic B, Posteraro B, Leoncini E, et al. Mannose-binding lectin codon 54 gene polymorphism and vulvovaginal candidiasis: a systematic review and meta-analysis. Biomed Res Int 2014; 2014:738298.
  35. van de Wijgert JH, Verwijs MC, Turner AN, Morrison CS. Hormonal contraception decreases bacterial vaginosis but oral contraception may increase candidiasis: implications for HIV transmission. AIDS 2013; 27:2141.
  36. Haddad LB, Wall KM, Tote K, et al. Hormonal Contraception and Vaginal Infections Among Couples Who Are Human Immunodeficiency Virus Serodiscordant in Lusaka, Zambia. Obstet Gynecol 2019; 134:573.
  37. Auler ME, Morreira D, Rodrigues FF, et al. Biofilm formation on intrauterine devices in patients with recurrent vulvovaginal candidiasis. Med Mycol 2010; 48:211.
  38. Cakiroglu Y, Caliskan S, Doger E, et al. Does removal of CU-IUD in patients with biofilm forming candida really maintain regression of clinical symptoms? J Obstet Gynaecol 2015; 35:600.
  39. Geiger AM, Foxman B. Risk factors for vulvovaginal candidiasis: a case-control study among university students. Epidemiology 1996; 7:182.
  40. Bradshaw CS, Morton AN, Garland SM, et al. Higher-risk behavioral practices associated with bacterial vaginosis compared with vaginal candidiasis. Obstet Gynecol 2005; 106:105.
  41. Reed BD, Zazove P, Pierson CL, et al. Candida transmission and sexual behaviors as risks for a repeat episode of Candida vulvovaginitis. J Womens Health (Larchmt) 2003; 12:979.
  42. Muzny CA, Rivers CA, Parker CJ, et al. Lack of evidence for sexual transmission of genital Candida species among women who have sex with women: a mixed methods study. Sex Transm Infect 2014; 90:165.
  43. Patel DA, Gillespie B, Sobel JD, et al. Risk factors for recurrent vulvovaginal candidiasis in women receiving maintenance antifungal therapy: Results of a prospective cohort study. Am J Obstet Gynecol 2004; 190:644.
  44. Heidrich FE, Berg AO, Bergman JJ. Clothing factors and vaginitis. J Fam Pract 1984; 19:491.
  45. Elegbe IA, Elegbe I. Quantitative relationships of Candida albicans infections and dressing patterns in Nigerian women. Am J Public Health 1983; 73:450.
  46. Heng LS, Yatsuya H, Morita S, Sakamoto J. Vaginal douching in Cambodian women: Its prevalence and association with vaginal candidiasis. J Epidemiol 2010; 20:70.
  47. Corsello S, Spinillo A, Osnengo G, et al. An epidemiological survey of vulvovaginal candidiasis in Italy. Eur J Obstet Gynecol Reprod Biol 2003; 110:66.
  48. Spinillo A, Pizzoli G, Colonna L, et al. Epidemiologic characteristics of women with idiopathic recurrent vulvovaginal candidiasis. Obstet Gynecol 1993; 81:721.
  49. Farage M, Bramante M, Otaka Y, Sobel J. Do panty liners promote vulvovaginal candidiasis or urinary tract infections? A review of the scientific evidence. Eur J Obstet Gynecol Reprod Biol 2007; 132:8.
  50. Janković S, Bojović D, Vukadinović D, et al. Risk factors for recurrent vulvovaginal candidiasis. Vojnosanit Pregl 2010; 67:819.
  51. Merenstein D, Hu H, Wang C, et al. Colonization by Candida species of the oral and vaginal mucosa in HIV-infected and noninfected women. AIDS Res Hum Retroviruses 2013; 29:30.
  52. Pereira LC, Correia AF, da Silva ZDL, et al. Vulvovaginal candidiasis and current perspectives: new risk factors and laboratory diagnosis by using MALDI TOF for identifying species in primary infection and recurrence. Eur J Clin Microbiol Infect Dis 2021; 40:1681.
  53. Anderson MR, Klink K, Cohrssen A. Evaluation of vaginal complaints. JAMA 2004; 291:1368.
  54. Eckert LO. Clinical practice. Acute vulvovaginitis. N Engl J Med 2006; 355:1244.
  55. Eckert LO, Hawes SE, Stevens CE, et al. Vulvovaginal candidiasis: clinical manifestations, risk factors, management algorithm. Obstet Gynecol 1998; 92:757.
  56. Sobel JD, Chaim W. Treatment of Torulopsis glabrata vaginitis: Retrospective review of boric acid therapy. Clin Infect Dis 1997; 24:649.
  57. Gaydos CA, Beqaj S, Schwebke JR, et al. Clinical Validation of a Test for the Diagnosis of Vaginitis. Obstet Gynecol 2017; 130:181.
  58. Vaginitis in Nonpregnant Patients: ACOG Practice Bulletin, Number 215. Obstet Gynecol 2020; 135:e1. Reaffirmed 2022.
  59. National guideline for the management of vulvovaginal candidiasis. Clinical Effectiveness Group (Association of Genitourinary Medicine and the Medical Society for the Study of Venereal Diseases). Sex Transm Infect 1999; 75 Suppl 1:S19.
  60. SWARTZ JH, LAMKINS BE. A RAPID, SIMPLE STAIN FOR FUNGI IN SKIN, NAIL SCRAPINGS, AND HAIRS. Arch Dermatol 1964; 89:89.
  61. Sobel JD, Subramanian C, Foxman B, et al. Mixed vaginitis-more than coinfection and with therapeutic implications. Curr Infect Dis Rep 2013; 15:104.
  62. Dan M, Leshem Y, Yeshaya A. Performance of a rapid yeast test in detecting Candida spp. in the vagina. Diagn Microbiol Infect Dis 2010; 67:52.
  63. Chatwani AJ, Mehta R, Hassan S, et al. Rapid testing for vaginal yeast detection: A prospective study. Am J Obstet Gynecol 2007; 196:309.e1.
  64. Marot-Leblond A, Nail-Billaud S, Pilon F, et al. Efficient diagnosis of vulvovaginal candidiasis by use of a new rapid immunochromatography test. J Clin Microbiol 2009; 47:3821.
  65. Hopwood V, Evans EG, Carney JA. Rapid diagnosis of vaginal candidosis by latex particle agglutination. J Clin Pathol 1985; 38:455.
  66. Matsui H, Hanaki H, Takahashi K, et al. Rapid detection of vaginal Candida species by newly developed immunochromatography. Clin Vaccine Immunol 2009; 16:1366.
  67. Abbott J. Clinical and microscopic diagnosis of vaginal yeast infection: a prospective analysis. Ann Emerg Med 1995; 25:587.
  68. Donders GGG, Ravel J, Vitali B, et al. Role of Molecular Biology in Diagnosis and Characterization of Vulvo-Vaginitis in Clinical Practice. Gynecol Obstet Invest 2017; 82:607.
  69. Tabrizi SN, Pirotta MV, Rudland E, Garland SM. Detection of Candida species by PCR in self-collected vaginal swabs of women after taking antibiotics. Mycoses 2006; 49:523.
  70. Diba K, Namaki A, Ayatolahi H, Hanifian H. Rapid identification of drug resistant Candida species causing recurrent vulvovaginal candidiasis. Med Mycol J 2012; 53:193.
  71. Mahmoudi Rad M, Zafarghandi ASh, Amel Zabihi M, et al. Identification of Candida species associated with vulvovaginal candidiasis by multiplex PCR. Infect Dis Obstet Gynecol 2012; 2012:872169.
  72. Weissenbacher T, Witkin SS, Ledger WJ, et al. Relationship between clinical diagnosis of recurrent vulvovaginal candidiasis and detection of Candida species by culture and polymerase chain reaction. Arch Gynecol Obstet 2009; 279:125.
  73. Schwebke JR, Gaydos CA, Nyirjesy P, et al. Diagnostic Performance of a Molecular Test versus Clinician Assessment of Vaginitis. J Clin Microbiol 2018; 56.
  74. Ferris DG, Dekle C, Litaker MS. Women's use of over-the-counter antifungal medications for gynecologic symptoms. J Fam Pract 1996; 42:595.
  75. Ferris DG, Nyirjesy P, Sobel JD, et al. Over-the-counter antifungal drug misuse associated with patient-diagnosed vulvovaginal candidiasis. Obstet Gynecol 2002; 99:419.
  76. Mendling W, Brasch J, German Society for Gynecology and Obstetrics, et al. Guideline vulvovaginal candidosis (2010) of the German Society for Gynecology and Obstetrics, the Working Group for Infections and Infectimmunology in Gynecology and Obstetrics, the German Society of Dermatology, the Board of German Dermatologists and the German Speaking Mycological Society. Mycoses 2012; 55 Suppl 3:1.
  77. Donders GG, Sobel JD. Candida vulvovaginitis: A store with a buttery and a show window. Mycoses 2017; 60:70.
  78. Paavonen J, Brunham RC. Bacterial Vaginosis and Desquamative Inflammatory Vaginitis. N Engl J Med 2018; 379:2246.
Topic 5452 Version 67.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟