Candida 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 C. 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 C. 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.

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