Details

Autor(en) / Beteiligte

• Ellepola, A. N. B.
• Samaranayake, L. P.

Titel

Adhesion of oral C. albicans to human buccal epithelial cells following limited exposure to antifungal agents

Ist Teil von

• Journal of oral pathology & medicine, 1998-08, Vol.27 (7), p.325-332

Ort / Verlag

Oxford, UK: Blackwell Publishing Ltd

Erscheinungsjahr

1998

Quelle

Wiley Online Library Journals Frontfile Complete

Beschreibungen/Notizen

• The major aetiologic agent of oral candidosis is C. albicans, and adhesion to oral mucosal surfaces is considered a vital prerequisite for successful colonisation and subsequent infection by this agent. Although many antimycotics are available for the treatment of oral candidosis, the diluent effect of saliva and the cleansing action of the oral musculature often tend to reduce the availability of the agents below that of the effective therapeutic concentration. Therefore, the yeasts undergo only a limited exposure to the antifungals during therapy. Hence, the main aim of the present study was to determine the in vitro adhesion of ten isolates of oral C. albicans to buccal epithelial cells (BEC) following a short exposure to sublethal concentrations of four antifungal agents. The yeasts were exposed to sublethal concentrations of nystatin (X6 MIC), 5‐fluorocytosine (X8 MIC), ketoconazole (X4 MIC) and fluconazole (X4 MIC) for a period of 1 h. Following subsequent removal of the drug, the adhesion of these isolates to BEC was assessed by a previously described adhesion assay. The mean percentage reductions of candidal adhesion to BEC following exposure to sublethal concentrations of nystatin, 5‐fluorocytosine, ketoconazole and fluconazole were 72.88%, 16.52%, 40.16% and 24.36%, respectively. Ultrastructural studies revealed that short exposure to nystatin and the azoles (but not 5‐fluorocytosine) resulted in aberrant cellular features. These findings indicate that subtherapeutic levels of antifungals may modulate candiadal colonisation of the oral mucosa and thereby suppress the invasive potential of the pathogen.