April 24, 2006
Scientific discovery typically involves a timely convergence of information and, in the April issue of the journal Antimicrobial Agents and Chemotherapy, a team of NIDCR grantees offer such an example in the battle against the bacterium Staphylococcus aureus. S. aureus is a leading cause of hospital-acquired infections from bacteria laden catheters and often plays a role in causing endocarditis, osteomyelitis, toxic shock syndrome, and some skin disorders. This bacterial species is particularly problematic because it embeds itself within biofilms, or microbial communities, where it can avoid antimicrobial agents and/or develop resistance to them. A few years ago, basic scientists discovered that yeast can release a biochemical cell-to-cell signaling molecule called farnesol to communicate within their fungal communities. Subsequent work indicated that this fungal signaling molecule may naturally render certain bacteria less adept at forming mature biofilms. These results led the NIDCR grantees to evaluate in laboratory studies the effect of farnesol on both methicillin resistant and susceptible strains of S. aureus. Their results showed that farnesol inhibited biofilm formation and, when coupled with antimicrobial agents, demonstrated a synergy to reduce substantially the growth of S. aureus in the laboratory, particularly when this bacterial species was in its biofilm mode of growth. The authors concluded, “This observed sensitization of resistant strains to antimicrobials and the observed synergistic effect with gentamicin indicate a potential application for farnesol as an adjuvant therapeutic agent for the prevention of biofilm-related infections and promotion of drug resistance reversal.” Read more about this paper by Jabra-Rizk, Shirtliff, et. al. Interestingly, the researchers also were able to show, in an article soon to be published in the journal FEMS Yeast Research, that farnesol was able to reverse fluconazole resistance in the fungal strains of Candida albicans and Candida dubliensis.