Over the past 10 years, there have been increasingly frequent reports of colonization of niches in the oral cavity by Non-Candida Albicans Candida (NCAC) species. Among these species, Candida parapsilosis sensu stricto plays a major part both locally and systemically. Evidence shows that it may be the second most frequent yeast isolate, after Candida albicans, as commensal in the oral cavity and as pathogen in blood cultures of patients diagnosed with fungemia. Recent reports suggest that both its distribution and its virulence may be affected by environmental conditions and may increase in situations of oral dysbiosis. Based on this background, we hypothesize that oral mucosa in pathological condition may be a source of candidemia by Candida parapsilosis sensu stricto, when promoted by the conditions in the host. We reviewed the scientific databases in search of evidence which may support such hypothesis.

Introduction: 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 the phenotype and molecular level of the production of biofilm in oral isolates of Candida parapsilosis sensu stricto and correlate the results with the clinical origin (dysbiosis versus eubiosis). Materials 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 metabolic activity. The results were corroborated by confocal fluorescence microscopy, and correlated with the transcriptional activity of CPH2, by RT-qPCR. The data were analysed 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.

Microbial & Biochemical Technology J o u rn al of M ic ro b ia l & Bioc h e m ic a l Te chno lo g y

Over the past 10 years, there have been increasingly frequent reports of colonization of niches in the oral cavity by non-Candida albicans Candida (NCAC) species. Among these species, Candida parapsilosis sensu stricto plays a major part both locally and systemically. Evidence shows that it may be the second most frequent yeast isolate, after Candida albicans, as commensal in the oral cavity and as pathogen in blood cultures of patients diagnosed with fungemia. Recent reports suggest that both its distribution and its virulence may be affected by environmental conditions and may increase in situations of oral dysbiosis. Based on this background, we hypothesize that oral mucosa in pathological condition may be a source of candidemia by Candida parapsilosis sensu stricto, when promoted by the conditions in the host. We reviewed the scientific databases in search of evidence which may support such hypothesis.