Interactions of bacterial and fungal pathogens in humans

By Dr Jodie Abramovitch

Multi-drug resistant bacteria strains are becoming an increasingly serious problem within a clinical setting. One type of bacteria that can rapidly acquire antibiotic resistance and cause problems in humans is Acinetobacter baumannii. Often A. baumannii is found alongside the fungus Candida albicans which can cause yeast infections, especially within intensive care wards.

Professor Anton Peleg

Monash researchers led by Professor Anton Peleg from the Department of Infectious Diseases and Microbiology had previously noted that A. baumannii and C. albicans were able to inhibit each other’s growth under certain conditions. To explore this interaction further, this study sought to understand the molecular mechanisms behind the inhibition of growth of A. baumannii by C. albicans.

Farnesol is a compound secreted by C. albicans continuously during its growth. This compound was shown to be able to inhibit growth of A. baumannii. Farnesol, upon further investigation, was found to interfere with gene expression that was responsible for maintaining the cell membrane and controlling cell division of the bacterium. The ability of the bacteria to create a biofilm (many bacteria adhere to one another in a protective layer) and move were also greatly impaired by farsenol secreted by C. albicans. This means that the infectivity of A. baumannii was greatly reduced.

This study of bacterial-fungal interactions has increased the understanding of how C. albicans can inhibit the growth and viability of A. baumannii. As such, this study concluded that by understanding how pathogens can compete with one another may allow for the identification of novel antimicrobials for the treatment of problematic human pathogens.

Reference: Kostoulias X, Murray GL, Cerqueira GM, Kong JB, Bantun F, Mylonakis E, Khoo CA, Peleg AY. Impact of a Cross-Kingdom Signaling Molecule of Candida albicans on Acinetobacter baumannii Physiology. Antimicrob Agents Chemother. 2015 Oct; 60:161-7. 

doi: 10.1128/AAC.01540-15.