MECHANISMS OF SERRATIA MARCESCENS INTERACTIONS WITH HUMAN PATHOGENIC FUNGI

Tal Maya ¹ Tal Hover ¹ Sapir Ron ¹ Hani Sandovsky ¹ Yana Shadkchan ¹ Nitzan Kijner ¹ Yulia Mitiagin ¹ Boris Fichtman ² Amnon Harel ² Robert M. Q. Shanks ³ Roberto E. Bruna ⁴ Eleonora García-Véscovi ⁴ Nir Osherov ¹

¹Department of Clinical Microbiology and Immunology, Tel Aviv University, Tel Aviv
²Faculty of Medicine in the Galilee, Bar-Ilan University, Safed
³Charles T. Campbell Microbiology Laboratory, Department of Ophthalmology, University of Pittsburgh Medical Center, Pennsylvania, Pittsburgh
⁴Instituto de Biología Molecular y Celular de Rosario (IBR), Consejo Nacional de Investigaciones Científicas y Técnicas, Universidad Nacional de Rosario, Rosario

Objectives: Interactions between bacteria and fungi are commonplace and have major

implications for the environment, agriculture and medicine. However, little is known about

the interactions between medically important bacteria and pathogenic filamentous fungi

despite the fact that they can have dramatic effects on the survival, colonization and

pathogenesis of these organisms. We set out to analyze interactions occurring between

pathogenic species of bacteria and fungi.

Methods: Bacterial and fungal strains were grown on standard SOC medium. Interactions

were parsed on SOC agar plates containing fungal/bacterial pairs grown in an X pattern.

Microscopic analyses were performed using GFP-labeled S. marcescens. Bacterial

spreading and killing of the fungus were measured by plating and enumeration of bacterial

and fungal growth.

Results: We have uncovered a novel interaction between the common mold pathogen

Rhizopus oryzae and the pathogenic gram-negative bacterium Serratia marcescens. S.

marcescens cells initially migrated along the fungal hyphae, forming attached

microcolonies that grew and coalesced to generate a biofilm that covered and killed the

fungus. Flagellum-defective strains of S. marcescens exhibited reduced hyphal spreading

and killing. Mutants defective in type 1 fimbria migrated equally well as or faster than the

wild-type S. marcescens strain. Killing did not depend on the secretion of S. marcescens

chitinases, as mutants in which all three chitinase genes were deleted retained wild-type

killing abilities. Tantalizing initial findings suggest that S. marcescens attacks and destroys

R. oryzae hyphae using a type 6 secretion system.

Conclusions: Our work has revealed novel mechanisms governing microorganismal co-

habitation and antibiosis, and may identify novel antifungal and antibacterial secondary

metabolites produced upon the various interactions with useful antibiotic activity.