Stenotrophomonas maltophilia interferes via the DSF-mediated quorum sensing system with Candida albicans filamentation and its planktonic and biofilm modes of growth.

Stenotrophomonas maltophilia is a nosocomial pathogen of increasing importance. S. maltophilia K279a genome encodes a diffusible signal factor (DSF) dependent quorum sensing (QS) system that was first identified in Xanthomonas campestris pv. campestris. DSF from X. campestris is a homologue of farnesoic acid, a Candida albicans QS signal which inhibits the yeast-to-hyphal shift. Here we describe the antagonistic effects of S. maltophilia on C. albicans on filamentation as well as on its planktonic and biofilm modes of growth. To determine the role of the DSF-mediated quorum sensing system in these effects, C. albicans ATCC 10231 and C. albicans tup1 mutant, locked in the filamentous form, were grown with K279a or with its rpfF deletion mutant (DSF-). A significant reduction in viable counts of C. albicans was observed in planktonic cocultures with K279a as well as in mixed biofilms. Furthermore, no viable cells of C. albicans tup1 were recovered from K279a mixed biofilms. Fungal viability was also assessed by labeling biofilms with SYTO 9 and propidium iodide. Confocal images showed that K279a can kill hyphae and also yeast cells. Light microscopic analysis showed that K279a severely affects hyphae integrity. On the other hand, the presence of K279a rpfF did not affect fungal morphology or viability. In conclusion, we report for the first time that S. maltophilia interferes with two key virulence factors of C. albicans, the yeast-to-hyphal transition and biofilm formation. DSF could be directly responsible for these effects or may induce the gene expression involved in antifungal activity.