Role of arthroconidia in biofilm formation by Trichosporon asahii
Summary Background Trichosporon asahii is the major causative agent of disseminated and deep‐seated trichosporonosis. It is capable of forming biofilms on surfaces, leading to medical device‐related infection.Trichosporon asahii may be present as yeast form, hyphae and/or arthroconidia; however, the...
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Veröffentlicht in: | Mycoses 2021-01, Vol.64 (1), p.42-47 |
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Sprache: | eng |
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Zusammenfassung: | Summary
Background
Trichosporon asahii is the major causative agent of disseminated and deep‐seated trichosporonosis. It is capable of forming biofilms on surfaces, leading to medical device‐related infection.Trichosporon asahii may be present as yeast form, hyphae and/or arthroconidia; however, the relationship between its biofilm‐forming ability and its morphological transition is unclear.
Objectives
We investigated whether the T. asahii morphological transition contributes to its biofilm formation. We also determined the conditions required to induce each of the morphologies.
Methods
Three high‐ and three low‐biofilm‐producing strains (HBS and LBS, respectively) were selected using a biofilm formation assay, and the cell surface hydrophobicity of these six strains was measured. For each strain, the morphology was observed and the number of each morphological form (yeast form, hypha and arthroconidium) was counted to calculate the ratio. Finally, the ability of cells each morphological type to adhere to the polystyrene substrate was evaluated.
Results
The HBS exhibited abundant arthroconidia and hyphae; in contrast, the LBS produced mainly hyphae with few or no arthroconidia. The production of hyphae was increased by nitrogen‐containing medium, and the production of arthroconidia was increased by nitrogen‐deficient medium. Cells incubated under nitrogen‐deficient conditions showed higher adherence to a polystyrene surface than those incubated in the presence of nitrogen.
Conclusion
Arthroconidia of T. asahii play a key role in biofilm formation by promoting cellular adhesion. |
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ISSN: | 0933-7407 1439-0507 |
DOI: | 10.1111/myc.13181 |