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Jack D Sobel - One of the best experts on this subject based on the ideXlab platform.
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Mixed Vaginitis—More Than Coinfection and With Therapeutic Implications
Current Infectious Disease Reports, 2013Co-Authors: Jack D Sobel, Chitra Subramanian, Betsy Foxman, Marilyn R Fairfax, Scott E GygaxAbstract:Mixed Vaginitis is due to the simultaneous presence of at least two vaginal pathogens, both contributing to an abnormal vaginal milieu and, hence, symptoms and signs of Vaginitis. In mixed Vaginitis, both pathogens require specific therapy for complete eradication of concurrent manifestations. In coinfection, although two pathogens are identified, a potential pathogen may be present but may not be a cause of existing vaginal symptoms. Although data remain sparse, mixed Vaginitis occurs rarely (
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mixed Vaginitis more than coinfection and with therapeutic implications
Current Infectious Disease Reports, 2013Co-Authors: Jack D Sobel, Chitra Subramanian, Betsy Foxman, Marilyn R Fairfax, Scott E GygaxAbstract:Mixed Vaginitis is due to the simultaneous presence of at least two vaginal pathogens, both contributing to an abnormal vaginal milieu and, hence, symptoms and signs of Vaginitis. In mixed Vaginitis, both pathogens require specific therapy for complete eradication of concurrent manifestations. In coinfection, although two pathogens are identified, a potential pathogen may be present but may not be a cause of existing vaginal symptoms. Although data remain sparse, mixed Vaginitis occurs rarely (<5 %). By contrast, pathogen coinfection occurs frequently in women with Vaginitis. Approximately 20 %–30 % of women with bacterial vaginosis (BV) are coinfected with Candida species. Coexistence of BV pathogens and T. vaginalis is even more common, with coinfection rates of 60 %–80 %. Both coinfection and mixed Vaginitis have significant clinical and therapeutic implications and are worthy of further investigation.
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Fluconazole-resistant Candida albicans vulvoVaginitis.
Obstetrics & Gynecology, 2012Co-Authors: Dror Marchaim, Leslie Lemanek, Suchitha Bheemreddy, Keith S. Kaye, Jack D SobelAbstract:OBJECTIVE: As a result of high recurrence rates of Candida albicans Vaginitis, successful suppressive fluconazole is widely used, and drug resistance is considered rare. We report increased occurrence of secondary fluconazole resistance, analysis of risk factors thereof, and describe management of fluconazole-refractory Vaginitis. METHODS: Patients referred to the Vaginitis Clinic at Wayne State University with clinically refractory fluconazole-resistant (minimum inhibitory concentration [MIC] 2 micrograms/mL or greater) C albicans Vaginitis from 2000 to 2010 were enrolled. Patients completed a questionnaire pertaining to demographics, comorbidities, behavioral characteristics, exposure to antimicrobials and antifungals, fluconazole consumption in defined daily doses in the previous 6 months, management received, and outcomes. With patients not located, data were extracted from charts. Susceptibilities to antifungals were determined by broth microdilution. RESULTS: Twenty-five women with fluconazole-resistant recurrent C albicans Vaginitis were identified, and 16 returned filled questionnaires. Study cohort consisted mainly of married, insured white women with more than 12 years of formal education and average or above average socioeconomic status. Median fluconazole MIC was 8 micrograms/mL (range 2–128 micrograms/mL). Risk factors for mycologic failure included increased fluconazole consumption (P5.03) with 16 of 25 women exposed to low-dose weekly fluconazole maintenance therapy. All patients were clinically controlled successfully, although treatment was difficult and often prolonged. CONCLUSION: Fluconazole-resistant C albicans Vaginitis was previously considered rare. We report 25 cases over an 11-year period, indicating an emerging problem. All patients had fluconazole consumption in the previous 6 months. Management of fluconazole refractory disease is extremely difficult with limited options, and new therapeutic modalities are needed.
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treatment of complicated candida Vaginitis comparison of single and sequential doses of fluconazole
American Journal of Obstetrics and Gynecology, 2001Co-Authors: Jack D Sobel, David E Soper, Peter Kapernick, Marcus J Zervos, Barbara D Reed, Thomas M Hooton, Paul Nyirjesy, M W Heine, J Willems, H PanzerAbstract:Abstract Objective: An attempt was made to validate recent recommendations that women with complicated Candida Vaginitis (severe or recurrent, non- albicans Candida spp or abnormal host) require longer-duration antifungal therapy to achieve clinical cure and mycologic eradication. Study Design: A prospective, multicenter, randomized, double-blind study was performed comparing a single dose of 150 mg of fluconazole with 2 sequential 150-mg doses of fluconazole given 3 days apart. Results: Five hundred fifty-six women with severe or recurrent Candida Vaginitis were enrolled, and 398 had at least one postbaseline evaluation (intent to treat) and of these 309 were fully evaluable (efficacy-valid). At baseline, 92% of vaginal isolates were Candida albicans . The 2-dose fluconazole regimen achieved significantly higher clinical cure rates in women with severe Vaginitis when evaluated on day 14 ( P =.015) and higher clinical and mycologic responses persisted at day 35. Women with recurrent but not severe Vaginitis did not benefit clinically short term by the additional fluconazole dose. Multivariate logistic regression analysis showed that being infected with non- albicans Candida predicted significantly reduced clinical and mycologic response regardless of duration of therapy. Fluconazole therapy was well tolerated and free of serious adverse effects. Conclusion: Treatment of Candida Vaginitis requires individualization, and women with severe Candida Vaginitis achieve superior clinical and mycologic eradication with a 2-dose fluconazole regimen. (Am J Obstet Gynecol 2001;185:363-69.)
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Nontrichomonal Purulent Vaginitis: Clinical Approach.
Current Infectious Disease Reports, 2000Co-Authors: Jack D SobelAbstract:Although trichomonal Vaginitis and cervicitis are responsible for most presentations of a frankly purulent vaginal discharge, nontrichomonal Vaginitis and purulent exudate are being seen in an increasing number of cases. Purulent Vaginitis remains poorly defined and largely ignored, with little increase in the amount of knowledge we have of this not infrequent entity. Accordingly, a variety of empirical therapies, often including multiple simultaneous measures, are prescribed. Considerable numbers of causes are now identified, and this review describes a step-by-step approach to diagnosis and management.
Gaia Piazzi - One of the best experts on this subject based on the ideXlab platform.
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prevalence of and risk factors for fungal Vaginitis caused by non albicans species
American Journal of Obstetrics and Gynecology, 1997Co-Authors: Arsenio Spinillo, Ezio Capuzzo, Roberto Gulminetti, P Marone, Laura Colonna, Gaia PiazziAbstract:Abstract OBJECTIVE: Our purpose was to evaluate the prevalence of symptomatic yeast Vaginitis caused by non- albicans species among patients attending a Vaginitis clinic over an 8-year period. STUDY DESIGN: A retrospective study of 1263 patients with symptomatic yeast Vaginitis confirmed by culture techniques was performed. RESULTS: The prevalence of symptomatic fungal Vaginitis caused by non- albicans species increased from 9.9% (10/101) in 1988 to 17.2% (36/209) in 1995 (χ 2 for trend=9.33, p = 0.002). Non- albicans species were found more frequently in known human immunodeficiency virus–seropositive patients (23/102 vs 143/1161, odds ratio 2.07, 95% confidence interval 1.2 to 3.46) than in seronegative subjects or subjects of unknown status for the virus. Recurrent vaginal candidiasis was an additional risk factor for Vaginitis caused by non- albicans species (odds ratio 2.47, 95% confidence interval 1.72 to 3.52). The increase in non- albicans isolates during the study period was confirmed in stratified analysis and in the subgroup of self-referred patients with no history of either human immunodeficiency virus infection or recurrent vaginal candidiasis. CONCLUSION: The prevalence of fungal Vaginitis caused by non- albicans species has increased sharply in the setting of a Vaginitis clinic. The characteristics of risk factors suggest that fungal cultures should be done routinely in human immunodeficiency virus–seropositive subjects with suspected vaginal candidiasis and in patients with recurrent vaginal infection. (Am J Obstet Gynecol 1997;176:138-41.)
Mairi C Noverr - One of the best experts on this subject based on the ideXlab platform.
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candida Vaginitis when opportunism knocks the host responds
PLOS Pathogens, 2014Co-Authors: Brian M Peters, Junko Yano, Mairi C Noverr, Paul L FidelAbstract:Candida albicans, an opportunistic polymorphic fungus and resident of the normal vaginal microbiota, is the leading causative agent of vulvovaginal candidiasis (VVC) and presents major quality of life issues for women worldwide [1]. Candida Vaginitis is characterized by itching, burning, pain, and redness of the vulva and vaginal mucosa and often accompanied by vaginal discharge. Predisposing factors for primary VVC include high-estrogen oral contraceptive use, hormone replacement therapy, antibiotic usage, and underlying diabetes mellitus. It is estimated that 75% of all women of childbearing age will be afflicted by VVC at least once in their lifetime [2]. Of these, approximately 5–8% (approximately 150 million worldwide) suffer from recurrent VVC (RVVC), resulting in idiopathic chronic episodes of vaginal irritation that require antifungal maintenance therapy (e.g., azoles) to partially control symptoms [1]. Although these treatments are typically effective at reducing organism burden and symptoms, the static function of azole activity and fungal recalcitrance to clearance are key factors resulting in recurrence [3]. It is proposed that RVVC and VVC both involve similar immunopathologies but that the triggers occur with greater sensitivity in individuals with RVVC. Continuously rising Vaginitis-related healthcare costs are estimated at $1.8 billion annually in the United States alone [4]. These unsustainable costs further necessitate a comprehensive understanding of Vaginitis and the host and fungal factors that contribute to its immunopathology. The Role of Host Immunity in Candida Vaginitis: Historical and Contemporary Perspectives Susceptibility to oral, chronic mucocutaneous, and gastrointestinal candidiasis has been clearly linked to deficiencies in cell-mediated immunity (CMI) [5]. Therefore, susceptibility to Candida Vaginitis was also long believed to result from defects in the adaptive immune response. However, numerous clinical studies examining women with RVVC and the use of an experimental mouse model to evaluate roles for CMI or humoral immunity (HI) revealed no appreciable protection provided by local or systemic adaptive immune mechanisms [6], [7], [8]. In support of these findings, relatively high production of immunoregulatory factors (e.g., TGF-β, T-regs, and Υ/δ T-cells) in the vagina may partly explain the lack of functional local CMI [9], [10]. Despite a lack of supportive evidence for a role of adaptive immunity in Vaginitis, the newly characterized Th17 axis of CMI, which links innate and adaptive immune responses, has been shown to be critical for local protection against oropharyngeal candidiasis (OPC) [11]. Accordingly, animal models were used to determine its potential role in mucosal immunity during Vaginitis. However, discrepant findings amongst mouse models have led to contradictory conclusions: one study using a less stringent pharmacologic approach to Th17 blockade demonstrated a modest role for Th17 involvement [12], while a more rigorous approach using Th17 axis-knockout mice showed no such function [12], [13]. Thus, the role of Th17 responses during Vaginitis remains unresolved and lacks any supportive clinical evidence. As for mucosal HI, some animal models have demonstrated modest antibody-mediated protection against Vaginitis [14]. It is conceivable that protective human antibodies do exist but occur naturally at concentrations in vaginal secretions too low to sufficiently mediate protection. While exhaustive efforts have found no major role for adaptive immunity in susceptibility to Vaginitis, recent studies have identified the importance of innate immunity in regulating Vaginitis symptomatology. A paramount study using women volunteers challenged with live C. albicans determined that Vaginitis symptoms were associated with polymorphonuclear leukocyte (PMN) recruitment into the vagina and that organism burden alone was not predictive of disease [15]. Moreover, depletion of PMNs in mice did not result in increased fungal load but did decrease histological evidence of vaginal inflammation [16], [17]. Most recently, a family of calcium-binding proteins termed S100A8 and S100A9 “alarmins” have been implicated in the innate vaginal epithelial cell response to C. albicans (see Figure 1) [18]. Because these proteins have vigorous PMN chemotactic activity, it was hypothesized that epithelial expression of S100s may play a key role in controlling PMN migration into the vaginal lumen. However, while this was confirmed, studies using mice lacking expression of S100A8/9 proteins determined that these factors were sufficient but not necessary for driving the PMN response [19]. Collectively, these exciting new studies highlight the immunopathological response as a crucial element of Vaginitis pathogenesis. Future clinical studies, however, are required to confirm the presence and function of alarmins during human infection. Figure 1 Working model of the immunopathogenesis of C. albicans Vaginitis. As alluded to above, resultant findings from animal models must be translatable to the human host. One important point to consider is that laboratory rodents, unlike humans, do not naturally harbor C. albicans as commensal organisms. Although the estrogen-dependent mouse model of Vaginitis closely mimics clinical infection, observed antifungal immune responses are considered primary and may be exaggerated as compared to human infection, in which repeated exposure, immunotolerance, or higher signaling thresholds to Candida may be encountered. Despite this shortcoming, the mouse model of Vaginitis has been an indispensible tool for dissecting the immunological mechanisms associated with this highly complex disease.
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fungal morphogenetic pathways are required for the hallmark inflammatory response during candida albicans Vaginitis
Infection and Immunity, 2014Co-Authors: Brian M Peters, Paul L Fidel, Glen E Palmer, Andrea K Nash, E A Lilly, Mairi C NoverrAbstract:Vulvovaginal candidiasis, caused primarily by Candida albicans, presents significant health issues for women of childbearing age. As a polymorphic fungus, the ability of C. albicans to switch between yeast and hyphal morphologies is considered its central virulence attribute. Armed with new criteria for defining Vaginitis immunopathology, the purpose of this study was to determine whether the yeast-to-hypha transition is required for the hallmark inflammatory responses previously characterized during murine Vaginitis. Kinetic analyses of vaginal infection with C. albicans in C57BL/6 mice demonstrated that fungal burdens remained constant throughout the observation period, while polymorphonuclear leukocyte (PMN), S100A8, and interleukin-1β levels obtained from vaginal lavage fluid increased by day 3 onward. Lactate dehydrogenase activity was also positively correlated with increased effectors of innate immunity. Additionally, immunodepletion of neutrophils in infected mice confirmed a nonprotective role for PMNs during Vaginitis. Determination of the importance of fungal morphogenesis during Vaginitis was addressed with a two-pronged approach. Intravaginal inoculation of mice with C. albicans strains deleted for key transcriptional regulators (bcr1Δ/Δ, efg1Δ/Δ, cph1Δ/Δ, and efg1Δ/Δ cph1Δ/Δ) controlling the yeast-to-hypha switch revealed a crucial role for morphogenetic signaling through the Efg1 and, to a lesser extent, the Bcr1 pathways in contributing to Vaginitis immunopathology. Furthermore, overexpression of transcription factors NRG1 and UME6, to maintain yeast and hyphal morphologies, respectively, confirmed the importance of morphogenesis in generating innate immune responses in vivo. These results highlight the yeast-to-hypha switch and the associated morphogenetic response as important virulence components for the immunopathogenesis of Candida Vaginitis, with implications for transition from benign colonization to symptomatic infection.
David E Soper - One of the best experts on this subject based on the ideXlab platform.
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treatment of complicated candida Vaginitis comparison of single and sequential doses of fluconazole
American Journal of Obstetrics and Gynecology, 2001Co-Authors: Jack D Sobel, David E Soper, Peter Kapernick, Marcus J Zervos, Barbara D Reed, Thomas M Hooton, Paul Nyirjesy, M W Heine, J Willems, H PanzerAbstract:Abstract Objective: An attempt was made to validate recent recommendations that women with complicated Candida Vaginitis (severe or recurrent, non- albicans Candida spp or abnormal host) require longer-duration antifungal therapy to achieve clinical cure and mycologic eradication. Study Design: A prospective, multicenter, randomized, double-blind study was performed comparing a single dose of 150 mg of fluconazole with 2 sequential 150-mg doses of fluconazole given 3 days apart. Results: Five hundred fifty-six women with severe or recurrent Candida Vaginitis were enrolled, and 398 had at least one postbaseline evaluation (intent to treat) and of these 309 were fully evaluable (efficacy-valid). At baseline, 92% of vaginal isolates were Candida albicans . The 2-dose fluconazole regimen achieved significantly higher clinical cure rates in women with severe Vaginitis when evaluated on day 14 ( P =.015) and higher clinical and mycologic responses persisted at day 35. Women with recurrent but not severe Vaginitis did not benefit clinically short term by the additional fluconazole dose. Multivariate logistic regression analysis showed that being infected with non- albicans Candida predicted significantly reduced clinical and mycologic response regardless of duration of therapy. Fluconazole therapy was well tolerated and free of serious adverse effects. Conclusion: Treatment of Candida Vaginitis requires individualization, and women with severe Candida Vaginitis achieve superior clinical and mycologic eradication with a 2-dose fluconazole regimen. (Am J Obstet Gynecol 2001;185:363-69.)
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bacterial vaginosis and trichomoniasis Vaginitis are risk factors for cuff cellulitis after abdominal hysterectomy
American Journal of Obstetrics and Gynecology, 1990Co-Authors: David E Soper, Richard C Bump, Glenn W HurtAbstract:Abstract To assess the relationship between either bacterial vaginosis or trichomoniasis Vaginitis and posthysterectomy infection, preoperative evaluation of the vaginal secretions was performed in 161 women undergoing abdominal hysterectomy. Thirty-two patients (19.9%) and 27 patients (16.8%), respectively, met the diagnostic criteria for bacterial vaginosis and trichomoniasis Vaginitis. Patients with either bacterial vaginosis or trichomoniasis Vaginitis were more likely than control subjects to have cuff cellulitis, cuff abscess, or both (relative risk 3.2, 95% confidence interval 1.5 to 6.7 for bacterial vaginosis; relative risk 3.4, 95% confidence interval 1.6 to 7.1 for trichomoniasis Vaginitis). Preoperative Vaginitis had no effect with respect to the incidence of postoperative wound infection, urinary tract infection, or intravenous line phlebitis. Bacteroides sp., Peptostreptococcus sp., and/or Gardnerella vaginalis ("bacterial vaginosis organisms") were isolated from the vaginal cuff in the majority of patients with postoperative cuff cellulitis. Bacterial vaginosis and trichomoniasis Vaginitis are risk factors for the development of posthysterectomy cuff cellulitis.
Glenn W Hurt - One of the best experts on this subject based on the ideXlab platform.
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bacterial vaginosis and trichomoniasis Vaginitis are risk factors for cuff cellulitis after abdominal hysterectomy
American Journal of Obstetrics and Gynecology, 1990Co-Authors: David E Soper, Richard C Bump, Glenn W HurtAbstract:Abstract To assess the relationship between either bacterial vaginosis or trichomoniasis Vaginitis and posthysterectomy infection, preoperative evaluation of the vaginal secretions was performed in 161 women undergoing abdominal hysterectomy. Thirty-two patients (19.9%) and 27 patients (16.8%), respectively, met the diagnostic criteria for bacterial vaginosis and trichomoniasis Vaginitis. Patients with either bacterial vaginosis or trichomoniasis Vaginitis were more likely than control subjects to have cuff cellulitis, cuff abscess, or both (relative risk 3.2, 95% confidence interval 1.5 to 6.7 for bacterial vaginosis; relative risk 3.4, 95% confidence interval 1.6 to 7.1 for trichomoniasis Vaginitis). Preoperative Vaginitis had no effect with respect to the incidence of postoperative wound infection, urinary tract infection, or intravenous line phlebitis. Bacteroides sp., Peptostreptococcus sp., and/or Gardnerella vaginalis ("bacterial vaginosis organisms") were isolated from the vaginal cuff in the majority of patients with postoperative cuff cellulitis. Bacterial vaginosis and trichomoniasis Vaginitis are risk factors for the development of posthysterectomy cuff cellulitis.
