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dc.contributor.authorRodriguez Coyago, Maria De lourdes-
dc.contributor.authorRosa, Alcira Cristina-
dc.contributor.authorJewtuchowicz, Virginia Marta-
dc.date.accessioned2021-01-26T14:05:04Z-
dc.date.available2021-01-26T14:05:04Z-
dc.date.issued2020-
dc.identifier.isbn000-000-000-0-
dc.identifier.issn0000-0000-
dc.identifier.urihttps://www.scitcentralconferences.com/accepteddetails/world-summit-on-immunology-microbiology-infectious-diseases/1041-
dc.descriptionCandida parapsilosis sensu stricto is the second to third most frequent cause of candidemia. Studies place this yeast as a frequent colonizer of niches of the oral cavity, predominantly in pathological conditions. We hypothesize that a buccal environment in dysbiosis enhances the virulence of C. parapsilosis sensu stricto. Objective: To evaluate at the phenotype and molecular level the production of biofilm in oral isolates of Candida parapsilosis sensu stricto, and correlate the results with the clinical origin (dysbiosis versus eubiosis). Material and methods: The biofilm-forming ability was compared in 50 oral isolates of Candida parapsilosis sensu stricto obtained from patients with and without oral dysbiosis; by quantification of biofilm biomass and metabolic activity. The results were corroborated by optical and confocal fluorescence microscopy, and correlated with the transcriptional activity of CPH2, by RT-qPCR. The data were analyzed by Excel 2010, and InfoStat 2018, with a 95% confidence interval. Results: The metabolic activity in biofilm was significantly higher in oral dysbiosis relative to control (p = 0.0025). Basal expression of CPH2 increased 2.8 times more in oral dysbiosis related to the control condition, and showed no significant differences with pathogenic isolates of this same yeast, derived from onychomycosis lesions. Conclusion: The oral cavity in dysbiosis increases the virulence of C. parapsilosis sensu stricto due to possible changes in epigenetic marks. This finding suggests that the oral cavity in dysbiosis may be an alternative route to the skin in the epidemiology of nosocomial candidemia.-
dc.description.abstractCandida parapsilosis sensu stricto is the second to third most frequent cause of candidemia. Studies place this yeast as a frequent colonizer of niches of the oral cavity, predominantly in pathological conditions. We hypothesize that a buccal environment in dysbiosis enhances the virulence of C. parapsilosis sensu stricto. Objective: To evaluate at the phenotype and molecular level the production of biofilm in oral isolates of Candida parapsilosis sensu stricto, and correlate the results with the clinical origin (dysbiosis versus eubiosis). Material and methods: The biofilm-forming ability was compared in 50 oral isolates of Candida parapsilosis sensu stricto obtained from patients with and without oral dysbiosis; by quantification of biofilm biomass and metabolic activity. The results were corroborated by optical and confocal fluorescence microscopy, and correlated with the transcriptional activity of CPH2, by RT-qPCR. The data were analyzed by Excel 2010, and InfoStat 2018, with a 95% confidence interval. Results: The metabolic activity in biofilm was significantly higher in oral dysbiosis relative to control (p = 0.0025). Basal expression of CPH2 increased 2.8 times more in oral dysbiosis related to the control condition, and showed no significant differences with pathogenic isolates of this same yeast, derived from onychomycosis lesions. Conclusion: The oral cavity in dysbiosis increases the virulence of C. parapsilosis sensu stricto due to possible changes in epigenetic marks. This finding suggests that the oral cavity in dysbiosis may be an alternative route to the skin in the epidemiology of nosocomial candidemia.-
dc.language.isoes_ES-
dc.publisherSciTech Central Conferences-
dc.sourceSciTech Central Conferences-
dc.subjectCandida parapsilosis sensu stricto-
dc.subjectOraldysbiosis-
dc.subjectOraleubiosis-
dc.subjectVirulence-
dc.titleEcological imbalance of the oral cavity improves the virulence of candida parapsilosis sensu stricto-
dc.title.alternativenull-
dc.typeARTÍCULO DE CONFERENCIA-
dc.description.cityCalifornia-
dc.ucuenca.idautor0704480276-
dc.ucuenca.idautorSGRP-3250-2-
dc.ucuenca.idautorSGRP-3250-3-
dc.ucuenca.versionVersión aceptada-
dc.ucuenca.areaconocimientounescoamplio05 - Ciencias Físicas, Ciencias Naturales, Matemáticas y Estadísticas-
dc.ucuenca.afiliacionRodriguez, M., University of Buenos Aires, Buenos Aires, Argentina; Rodriguez, M., Universidad de Cuenca, Cuenca, Ecuador-
dc.ucuenca.afiliacionRosa, A., University of Buenos Aires, Buenos Aires, Argentina-
dc.ucuenca.afiliacionJewtuchowicz, V., University of Buenos Aires, Buenos Aires, Argentina-
dc.ucuenca.volumenVolumen 0, número 0-
dc.ucuenca.indicebibliograficoSIN INDEXAR-
dc.ucuenca.numerocitaciones0-
dc.ucuenca.areaconocimientofrascatiamplio1. Ciencias Naturales y Exactas-
dc.ucuenca.paisESTADOS UNIDOS-
dc.ucuenca.conferencia10th World Summit on Immunology, Microbiology & Infectious Diseases-
dc.ucuenca.areaconocimientofrascatiespecifico1.6 Ciencias Biológicas-
dc.ucuenca.areaconocimientofrascatidetallado1.6.2 Microbiología-
dc.ucuenca.areaconocimientounescoespecifico051 - Ciencias Biológicas y Afines-
dc.ucuenca.areaconocimientounescodetallado0511 - Biología-
dc.ucuenca.fechainicioconferencia2020-11-23-
dc.ucuenca.fechafinconferencia2020-11-23-
dc.ucuenca.organizadorconferenciaSciTech Central Conferences-
dc.ucuenca.comiteorganizadorconferenciaAP Gupta, Rajeev R Shah, Neeta Mathuria, Jimenez Cardoso Enedina,C S Banushree,Ozan Emre Eyupoglu,Laishram Shantikumar Singh-
dc.ucuenca.urifuentehttps://www.scitcentralconferences.com/details/world-summit-on-immunology-microbiology-infectious-diseases-
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