Vaginal colonization by Candida in asymptomatic women with and without a history of recurrent vulvovaginal candidiasis

doi:10.1016/S0029-7844(99)00577-3

Obstetrics & Gynecology

Volume 95, Issue 3, March 2000, Pages 413-416

https://doi.org/10.1016/S0029-7844(99)00577-3 Get rights and content

Abstract

Objective: The asymptomatic carriage of Candida in the vagina of women with a history of recurrent vulvovaginal candidiasis was compared with that of women with no such history.

Methods: Vaginal swabs from 50 women with a history of recurrent vulvovaginal candidiasis and 45 women with one or fewer episodes of candidal vaginaitis within the past 12 months were evaluated for Candida by wet mount/Gram stain, culture, and polymerase chain reaction (PCR). All women were asymptomatic for at least 30 days.

Results: Candida was identified in 28 women by PCR, in 14 women by culture, and in 13 women by wet mount/Gram stain. Candida was identified by PCR in a similar proportion of patients with previous recurrent vulvovaginal candidiasis (30%) and in controls (28.8%). However, Candida was identified by culture in more women with previous recurrent vulvovaginal candidiasis (22%) than in controls (6.6%, P = .04); it also was identified by wet mount/Gram stain in more women with recurrent vulvovaginal candidiasis (22%) than in controls (4.4%, P = .01). For the recurrent vulvovaginal candidiasis patients, culture and wet mount/Gram stain had a sensitivity of 66.6% compared with PCR. For the controls, the sensitivity of the two former assays relative to PCR was only 15.3%.

Conclusion: Women with a history of recurrent vulvovaginal candidiasis have more easily detectable Candida in their vagina, even when asymptomatic, than do other women. A relative inefficiency in regulating the proliferation of Candida in the vagina may increase susceptibility to periodic symptomatic recurrences.

Section snippets

Materials and methods

This study was approved by the committee of ethics from the University of Campinas, and informed oral consent was obtained from all subjects. Ninety-five sexually active reproductive age women took part in this study. Fifty women with a history of three or more episodes of recurrent vulvovaginal candidiasis per year and no vulvovaginal complaints for at least 30 days were recruited. The remaining 45 women, attending the clinic for routine gynecologic check-ups, were invited to take part in the

Results

Candida albicans was detected by PCR in 28 (29.4%) women (Table 1). Only 14 (14.7%) of the women tested (all PCR-positive) were positive for Candida by culture, and 13 (13.6%) were positive by wet mount/Gram stain (P < .02 compared with PCR).

The percentage of women positive for Candida by PCR was similar for recurrent vulvovaginal candidiasis patients (30%) and controls (28.8%). In contrast, detection of Candida by wet mount/Gram stain and culture was more frequent in recurrent vulvovaginal

Discussion

With the use of PCR gene amplification technology, Candida was detected in vaginal samples from 29.4% of the asymptomatic women tested. Similar frequencies of Candida colonization were observed, regardless of history of recurrent vulvovaginal candidiasis. These results reinforce previous studies11 that women may harbor Candida in their vagina in the absence of symptoms. Furthermore, the data demonstrate that in many women with no history of recurrent vulvovaginal candidiasis, Candida

References (15)

J.D Sobel et al.
Vulvovaginal candidiasisEpidemiologic, diagnostic and therapeutic considerations
Am J Obstet Gynecol
(1998)
P Giraldo et al.
Vaginal heat shock protein expression in symptom-free women with a history of recurrent vulvovaginitis
Am J Obstet Gynecol
(1999)
S.S Witkin et al.
A macrophage defect in women with recurrent Candida vaginitis and its reversal in vitro by prostaglandin inhibitors
Am J Obstet Gynecol
(1986)
S.S Witkin et al.
A localized vaginal allergic response in women with recurrent vaginitis
J Allergy Clin Immunol
(1988)
H.L Kent
Epidemiology of vulvovaginitis
Am J Obstet Gynecol
(1991)
J.D Sobel
Pathogenesis and epidemiology of vulvovaginal candidiasis
Ann N Y Acad Sci
(1988)
G.E.M Lindnen et al.
Quantitative studies of the vaginal flora of health women and of obstetrics and gynecological women
J Med Microbiol
(1978)

There are more references available in the full text version of this article.

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Localized provoked vulvodynia (LPV) affects ∼14 million people in the US (9% of women), destroying lives and relationships. LPV is characterized by chronic pain (>3 months) upon touch to the vulvar vestibule, which surrounds the vaginal opening. Many patients go months or years without a diagnosis. Once diagnosed, the treatments available only manage the symptoms of disease and do not correct the underlying problem. We have focused on elucidating the underlying mechanisms of chronic vulvar pain to speed diagnosis and improve intervention and management. We determined the inflammatory response to microorganisms, even members of the resident microflora, sets off a chain of events that culminates in chronic pain. This agrees with findings from several other groups, which show inflammation is altered in the painful vestibule. The vestibule of patients is acutely sensitive to inflammatory stimuli to the point of being deleterious. Rather than protect against vaginal infection, it causes heightened inflammation that does not resolve, which coincides with alterations in lipid metabolism that favor production of proinflammatory lipids and not pro-resolving lipids. Lipid dysbiosis in turn triggers pain signaling through the transient receptor potential vanilloid subtype 4 receptor (TRPV4). Treatment with specialized pro-resolving mediators (SPMs) that foster resolution reduces inflammation in fibroblasts and mice and vulvar sensitivity in mice. SPMs, specifically maresin 1, act on more than one part of the vulvodynia mechanism by limiting inflammation and acutely inhibiting TRPV4 signaling. Therefore, SPMs or other agents that target inflammation and/or TRPV4 signaling could prove effective as new vulvodynia therapies.
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Candida albicans causes 85% to 95% of VC infections, and Candida glabrata causes a majority of the remaining infections.17 Candida does not always result in symptomatic vaginitis, and up to 30% of asymptomatic women may be colonized with Candida as part of their normal vaginal flora.18 Although there are studies suggesting possible anogenital and orogenital transmission of yeast, penile-vaginal transmission is rare, and yeast infections can occur in celibate women.17
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We found L. rhamnosus was prevalent in normal women colonizing Candida, but this association was not significant. Presence of C. albicans in asymptomatic women possibly implies inadequate treatment of any previous incidences of VVC [39]. Interestingly, one third study population with asymptomatic BV co-colonized Candida.
Vaginal microbiota contributes in maintaining and protecting the urogenital niche from infections and their sequelae. Despite extensive research, microbiome studies have often ignored asymptomatic bacterial vaginosis (BV) and vulvovaginal candidiasis (VVC). The present study aimed to explore the cultivable vaginal bacterial and mycological communities in women asymptomatic for BV and VVC using multiplex PCR and species-specific PCR. Vaginal swabs collected from 199 participants asymptomatic for urogenital infections, scored by Nugent criteria indicated 73.9% had normal microbiota, 11.6% intermediate and 14.5% BV. The most frequent Lactobacillus species in normal women were L. iners (69.4%), L. crispatus (24.5%), L. reuteri (20.4%). Women with BV colonized L. iners (62.1%); L. rhamnosus (41.4%); L. salivarius (13.7%) and L. reuteri (7.2%). Furthermore, L. crispatus was associated with normal microbiota, whereas L. iners was a frequent member of normal and dysbiotic microbiota. Lactobacillus abundance and species richness reduced in asymptomatic BV. Also L. crispatus, L. fermentum, L. acidophilus and L. delbruckii were absent in these women. L. iners significantly co-existed with other Lactobacillus species, indicating its failure in independently maintaining the healthy vaginal niche. Of 30.4% women detected with Candida, 72.1% constituted non-albicans Candida. Predominance of C. albicans increased from 18.4% in healthy to 60% in women with asymptomatic BV; whereas distribution of BV related bacteria did not vary across the groups. Heterogeneous population of lactobacilli in 80.8% of normal women calls attention towards cumulative effects of these species in safeguarding the vaginal microenvironment. Since the microbiota of asymptomatic BV was different from healthy, screening and management could be encouraged to avoid further complications of infections.
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Recurrent vulvovaginal candidiasis (RVVC), multiple episodes of vulvovaginal candidiasis (VVC; vaginal yeast infection) within a 12-month period, adversely affects quality of life, mental health, and sexual activity. Diagnosis is not straightforward, as VVC is defined by the combination of often nonspecific vaginal symptoms and the presence of yeast—which is a common vaginal commensal. Estimating the incidence and prevalence is challenging: most VVC is diagnosed and treated empirically, the availability for purchase of effective therapies over the counter enables self-diagnosis and treatment, and the duration of the relatively benign VVC symptoms is short, introducing errors into any estimates relying on medical records or patient recall.
We evaluate current estimates of VVC and RVVC and provide new prevalence estimates using data from a 2011 seven-country (n = 7345) internet panel survey on VVC conducted by Ipsos Health (https://www.ipsos.com/en). We also evaluate information on VVC-associated visits using the National Ambulatory Medical Care Survey.
The estimated probability of VVC by age 50 varied widely by country (from 23% to 49%, mean 39%), as did the estimated probability of RVVC after VVC (from 14% to 28%, mean 23%).
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Our goal was to gain a better understanding of the inflammatory pathways affected during localized vulvodynia, a poorly understood, common, and debilitating condition characterized by chronic pain of the vulvar vestibule.
In a control matched study, primary human fibroblast strains were generated from biopsies collected from localized provoked vulvodynia (LPV) cases and from age- and race-matched controls. We then examined intracellular mechanisms by which these fibroblasts recognize pathogenic Candida albicans; >70% of vulvodynia patients report the occurrence of prior chronic Candida infections, which is accompanied by localized inflammation and elevated production of proinflammatory/pain-associated interleukin (IL)-6 and prostaglandin E2 (PGE₂). We focused on examining the signaling pathways involved in recognition of yeast components that are present and abundant during chronic infection.
Dectin-1, a surface receptor that binds C albicans cell wall glucan, was significantly elevated in vestibular vs external vulvar cells (from areas without pain) in both cases and controls, while its abundance was highest in LPV cases. Blocking Dectin-1 signaling significantly reduced pain-associated IL-6 and PGE₂ production during the response to C albicans. Furthermore, LPV patient vestibular cells produced inflammatory mediators in response to low numbers of C albicans cells, while external vulvar fibroblasts were nonresponsive. Inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (proinflammatory transcription factor) nearly abrogated IL-6 and PGE₂ production induced by C albicans, in keeping with observations that Dectin-1 signals through the nuclear factor kappa-light-chain-enhancer of activated B cells pathway.
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^☆: Supported in part by Fundação de Amparo a Pesquisa do Estado de São Paulo and Universidade Estadual de Campinas.

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Obstetrics & Gynecology

Abstract

Section snippets

Materials and methods

Results

Discussion

References (15)

Vulvovaginal candidiasisEpidemiologic, diagnostic and therapeutic considerations

Am J Obstet Gynecol

Vaginal heat shock protein expression in symptom-free women with a history of recurrent vulvovaginitis

Am J Obstet Gynecol

A macrophage defect in women with recurrent Candida vaginitis and its reversal in vitro by prostaglandin inhibitors

Am J Obstet Gynecol

A localized vaginal allergic response in women with recurrent vaginitis

J Allergy Clin Immunol

Epidemiology of vulvovaginitis

Am J Obstet Gynecol

Pathogenesis and epidemiology of vulvovaginal candidiasis

Ann N Y Acad Sci

Quantitative studies of the vaginal flora of health women and of obstetrics and gynecological women

J Med Microbiol

Cited by (97)

Inflammation, lipids, and pain in vulvar disease

Infectious Vaginitis, Cervicitis, and Pelvic Inflammatory Disease

Vaginal microbiota of asymptomatic bacterial vaginosis and vulvovaginal candidiasis: Are they different from normal microbiota?

Recurrent vulvovaginal candidiasis

Vaginitis: Beyond the Basics

Identification of novel mechanisms involved in generating localized vulvodynia pain

Original ArticlesVaginal colonization by Candida in asymptomatic women with and without a history of recurrent vulvovaginal candidiasis☆

Abstract

Section snippets

Materials and methods

Results

Discussion

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

J Allergy Clin Immunol

Epidemiology of vulvovaginitis

Am J Obstet Gynecol

Pathogenesis and epidemiology of vulvovaginal candidiasis

Ann N Y Acad Sci

Quantitative studies of the vaginal flora of health women and of obstetrics and gynecological women

J Med Microbiol

Original Articles
Vaginal colonization by Candida in asymptomatic women with and without a history of recurrent vulvovaginal candidiasis☆