Impact of brief and sequential exposure to nystatin, amphotericin B, ketoconazole, and fluconazole in modulating adhesion traits of oral Candida dubliniensis isolates.
OBJECTIVE
Candida adherence is implicated in the pathogenesis of oral candidosis. Adhesion to buccal epithelial cells (BEC), germ tube (GT) formation, and relative cell surface hydrophobicity (CSH) are colonization attributes of candidal pathogenicity. Candida dubliniensis (C. dubliniensis) is allied with recurrent oral candidosis, which can be treated with nystatin, amphotericin B, ketoconazole, and fluconazole. Due to the diluent effect of saliva and the cleansing effect of the oral musculature in the oral cavity C. dubliniensis isolates undergo brief and sequential exposure to antifungal agents during therapy. Thus, in the present study, we evaluated the adhesion to BEC, GT formation, and the CSH of oral isolates of C. dubliniensis following brief and sequential exposure to nystatin, amphotericin B, ketoconazole, and fluconazole.


METHODS
After determining the minimum inhibitory concentration (MIC) of the aforementioned drugs, 20 oral isolates of C. dubliniensis were briefly (1 h), and sequentially (10 days) exposed to subcidal concentrations of these drugs. Following drug removal, adhesion to BEC, GT formation, and CSH of these isolates were determined.


RESULTS
The percentage reduction of adhesion to BEC, GT formation, and CSH of the isolates following exposure to antifungal agents were as follows: nystatin: 53.55%, 33.98%, and 29.83% (P < 0.001); amphotericin B: 53.84%, 36.23%, and 28.97% (P < 0.001); ketoconazole: 37.43%, 20.51%, and 16.49% (P < 0.001); and fluconazole: 8.93% (P < 0.001), 1.6%, and 0.63% (P > 0.05).


CONCLUSIONS
Brief and sequential exposure of C. dubliniensis to antifungal agents would continue to wield an antifungal effect by altering its adhesion attributes, and elucidate possible pharmacodynamics by which antifungal agents might operate in modulating candidal adherence.
Departments of Bioclinical and Diagnostic Sciences, Faculty of Dentistry, Kuwait University, Jabriya, Kuwait.
Arjuna N B
AN
Ellepola
Departments of Bioclinical and Diagnostic Sciences, Faculty of Dentistry, Kuwait University, Jabriya, Kuwait.
Bobby K
BK
Joseph
School of Dentistry, University of Queensland, Brisbane, Qld, Australia.
Lakshman P
LP
Samaranayake
College of Pharmacy, University of Texas at Austin, Austin, TX, USA.
H M H N
HM
Bandara
Department of Microbiology, Faculty of Medicine, Kuwait University, Jabriya, Kuwait.
Zia U
ZU
Khan
D000666:Amphotericin B; D000935:Antifungal Agents / Q000494:pharmacology*; D002175:Candida; D002177:Candidiasis / Q000188:drug therapy*; D004847:Epithelial Cells / Q000382:microbiology; D015725:Fluconazole; D006801:Humans; D007654:Ketoconazole; D008826:Microbial Sensitivity Tests; D009061:Mouth Mucosa / Q000382:microbiology; D009761:Nystatin
D000935:Antifungal Agents; D009761:Nystatin; D000666:Amphotericin B; D015725:Fluconazole; D007654:Ketoconazole
Candida dubliniensis; adhesion; antifungal agent; oral candidosis; polyene