Abstract
ABSTRACT Background: Candida species have long been recognised as aetiological agents of opportunistic infections of the oral mucosa, and more recently, as players of polymicrobial interactions driving caries, periodontitis and oral carcinogenesis. Methods: We studied the clonal structure of Candida spp. at oral niche resolution in patients (n = 20) with a range of oral health profiles over 22 months. Colonies from oral micro-environments were examined with multilocus sequencing typing. Results: Candida spp. identified were C. albicans, C. glabrata and C. dubliniensis. Increased propensity for micro-variations giving rise to multiple diploid strain types (DST), as a result of loss of heterozygosity, was observed among C. albicans clade 1 isolates compared to other clades. Micro-variations among isolates were also observed in C. dubliniensis contra to expectations of stable population structures for this species. Multiple sequence types were retrieved from patients without clinical evidence of oral candidosis, while single sequence types were isolated from oral candidosis patients. Conclusion: This is the first study to describe the clonal population structure, persistence and stability of Candida spp. at oral niche level. Future research investigating links between Candida spp. clonality and oral disease should recognise the propensity to micro-variations amongst oral niches in C. albicans and C. dubliniensis identified here.
Highlights
The oral cavity comprises a diverse set of niches inhabited by diverse microbial colonisers of prokaryotic and eukaryotic microorganisms
Increased propensity for micro-variations giving rise to multiple diploid strain types (DST), as a result of loss of heterozygosity, was observed among C. albicans clade 1 isolates compared to other clades
Micro-variations among isolates were observed in C. dubliniensis contra to expectations of stable population structures for this species
Summary
The oral cavity comprises a diverse set of niches inhabited by diverse microbial colonisers of prokaryotic (bacteria) and eukaryotic (yeasts and filamentous fungi) microorganisms. Distinct microenvironments harbour microbial communities of planktonic cells in salivary fluids, and of adherent and filamentous multi-species biofilms growing on the surface of teeth, the tongue and mucosal membranes [1,2]. Multi-species and cross-kingdom coaggregations among complex biofilms contribute to ecological homeostasis during host health, and are important factors in the transition to dysbiosis and disease progression [3]. As such most oral diseases are caused by dysbiotic shifts within the microbial communities where ‘pathobionts’ such as Candida spp. thrive quantitatively and functionally. Candida species have long been recognised as aetiological agents of opportunistic infections of the oral mucosa, and more recently, as players of polymicrobial interactions driving caries, periodontitis and oral carcinogenesis
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