In most natural environments microorganisms grow predominantly as biofilms rather than as free floating planktonic cells. A biofilm is a complex functional community of one or more species of microbes encased and protected in a self-produced hydrophobic extra cellular matrix (ECM) and, attached to one another or to a solid surface. Biofilms can be composed of a single microbial species or more commonly, mixed species such as bacteria and fungi. A significant proportion of human microbial infections are biofilm-associated and many of these biofilms are formed by multiple microbial species. It has been demonstrated that in mixed-species biofilms containing bacteria and fungi, a range of different interactions can occur, including increased resistance to antimicrobials, enhanced surface colonization as well as interspecies antagonism. Studies with bacteria and fungi have revealed multiple bacterialfungal signal interactions. The effects of these interactions include impact on the production of antimicrobial toxins, fungal morphology, and biofilm formation. The opportunistic pathogens Candida albicans and Pseudomonas aeruginosa frequently colonize the respiratory tract, burn wounds and indwelling medical devices together and know to communicate. Therefore, a number of recent studies were assigned to the interactions of P. aeruginosa with Candida and Aspergillus spp. with potential impact to the oral cavity and the respiratory tract. One study focused on the interactions of Candida spp. and P. aeruginosa during different stages of biofilm development, indicates the latter pathogens have significant mutual growth inhibitory effect at various stages of biofilm development in a dual species environment. It is also evident that there are species specific variations of this modulatory effect. Subsequently others have shown that P. aeruginosa kills C. albicans by forming a dense film on fungal filaments, though, it neither binds nor kills the yeast-form of C. albicans. P. aeruginosa ATCC #27853 at a concentration gradient elicited a significant inhibition of C. albicans biofilms. The Pseudomonas signalling molecule 3-oxo-C12- homoserine lactone (HSL) can impair the yeast-hyphal switch of Candida morphology. Supernatant from cultures of P. aeruginosa can impair C. albicans biofilm formation independently of HSL production, and this occurs in mature biofilm rather than during initial adherence. Transcript profiling revealed HSL-independent changes in gene expression in response to bacterial supernatant. In one study A. fumigatus biofilm formation was inhibited by direct contact with P. aeruginosa, but had no effect on preformed biofilm. A secreted heat-stable soluble factor was also shown to exhibit biofilm formation. P. aeruginosa PAO1 suppressed growth of A. fumigatus, A. niger, A. flavus, A. oryzae, A. terreus and A. nidulans. An increase in phenazine production by P. aeruginosa may contribute to the ability of P. aeruginosa to suppress different Aspergilli. Conclusion: Further studies are warranted to better understand the complex interactions of mixed-species biofilms to identify novel microbial toxins that may not be readily extractable or stable under monoculture conditions and might play an important role in vivo.
Full conference title:
Trends in Medical Mycology, 5th
- TIMM 5th (2013)