The effect of brief exposure to sub-therapeutic concentrations of chlorhexidine gluconate on the germ tube formation of oral Candida albicans and its relationship to post-antifungal effect

Abstract

OBJECTIVES: Adherence of Candida albicans has been implicated as the first step in the pathogenesis of oral candidosis, and germ tube formation a contributory attribute. Recently, these organisms have also been implicated in persistent apical periodontitis. Chlorhexidine gluconate is by far the commonest antiseptic mouth wash prescribed in dentistry. As the intraoral concentrations of this antiseptic fluctuate considerably due to the dynamics of the oral cavity, the main objective of this study was to investigate the effect of brief exposure to three different sub-therapeutic concentrations of chlorhexidine gluconate (0.005%, 0.0025% and 0.00125%) on the germ tube formation of C. albicans. These findings were then correlated with the chlorhexidine-induced post-antifungal effect (PAFE) values we obtained in a study using the identical organisms and experimental conditions. DESIGN: Ten oral isolates of C. albicans were exposed to three different concentrations of chlorhexidine gluconate for 30 min, the antiseptic removed, and the germ tube formation of these isolates quantified following subsequent incubation in a germ tube inducing medium. The PAFE was evaluated by turbidometric measurement of growth. RESULTS: When compared with the controls, exposure to 0.005%, 0.0025% and 0.00125% chlorhexidine gluconate suppressed the ability to form germ tubes by 81.23% (P < 0.01), 42.74% (P < 0.01) and 9.13% (P > 0.05), respectively, while eliciting a mean PAFE of 9.91 h, 1.65 h and 0.67 h respectively. On regression analysis a significant positive correlation was observed between these two parameters (P < 0.0001: r = 0.7325). CONCLUSIONS: Taken together, these findings imply that short exposure to sub-therapeutic levels of chlorhexidine gluconate may modulate candidal germ tube formation as well as its growth, thereby suppressing its pathogencity in vivo.