OBJECTIVESaccharomyces albicons is the main opportunistic pathogen which is also the common member of oral microflora, and the biofilms they formed have spontaneous drug tolerance compared with planktonic ones. Saccharomyces biofilm population can produce subpopulation of cells which can tolerant high concentration of antifungal drugs. They are called persisters. Many researches indicated that drug efflux gene such as CDR or MDR gene plays the very important roles in yeast drug resistance. The objective of this study is to illuminate the mechanism of Saccharomyces albicons biofilm drug tolerance related with drug efflux gene, especially to the persisters formation.

METHODSTest the minimal inhibitory concentration (MIC) and SMIC80 (sessile minimal inhibitory concentration 80%) of 24 h biofim of totally 7 defective strains of drug efflux pump gene with Amphotercin B. And treat the 24 h biofilm by fluconazole, micronazole, clotrimazole combined with CDR1 inhibitor Enniatin B respectively and antifungal drugs alone as control, then scrapped the biofilm, cultured on the YPD agar. By CFU counting, the numbers of biofilm persisters were determined.

RESULTSAll the defective strains have the similar MIC and SMIC80 for 24 h biofilm with wide type strains. CDR1 inhibitor Enniatin B can help antifungal drugs especially micronazole and clotrimazole to eliminate the biofilm persisters.

CONCLUSIONSaccharomyces albicans drug efflux gene may minor associated with 24 h biofilm drug tolerance. Drug efflux gene CDR1 may play an role in persisiters related biofilm drug tolerance.