Non-traditional partnerships: Salmonella enterica interactions with phytopathogenic bacteria

Jeri Barak (University of Wisconsin-Madison, jeri.barak@wisc.edu)
 

 Human enteric pathogen, such as Salmonella enterica, grow poorly in the phyllosphere; because unlike plant pathogens, they cannot liberate nutrients from plant cells. Nonetheless, many food-borne illness outbreaks have been caused by eating raw leaves. We previously found that if a plant pathogen is present on leaves, S. enterica grows to human infectious doses even under conditions where it cannot do so alone. Recently, we found that effector-triggered susceptibility and suppression of PAMP-triggered immunity by virulent X. perforans created a conducive environment for persistence of S. enterica in the tomato phyllosphere. In contrast, activation of effector-triggered immunity by avirulent Xanthomonas perforans resulted in a dramatic reduction in S. enterica populations suggesting plant defense mechanisms that successfully limit xanthomonad populations can restrict S. enterica as well. The mechanism by which S. enterica benefits from Xanthomonas remains elusive. Co-inoculation with virulent X. perforans increases S. enterica aggregate formation; however, S. enterica does not co-aggregate with X. perforans. Our data supports the conclusion that the benefit gained by S. enterica from the virulent phytopathogen occurs in absence of S. enterica reaching large populations in the apoplast. To characterize the mechanism that confers benefit to Salmonella in infected leaves, we expanded our experiments to include all of the xanthomonads that cause bacterial spot of tomato, X. perforans, X. euvesicatoria, X. vesicatoria, and X. gardneri. We determined that S. enterica grows on leaves infected with either X. euvesicatoria or X. gardneri, but not X. perforans or X. vesicatoria. Moreover, S. enterica populations declined on leaves infected with X. vesicatoria in a similar way to populations on uninfected leaves. We examined the role of cell death caused by the virulent plant pathogen in Salmonella growth. We found that Xanthomonas-infected leaves that had extensive electrolyte leakage corresponded to those where S. enterica growth also occurred. In contrast, leaves infected with X. vesicatoria had little electrolyte leakage and S. enterica populations declined simultaneously. These results suggest that cell death, as reflected in electrolyte leakage, confers a benefit to Salmonella.