Abstract
Interactions between plant pathogens and arthropods have been predominantly studied through the prism of herbivorous arthropods. Currently, little is known about the effect of plant pathogens on the third trophic level. This question is particularly interesting in cases where pathogens manipulate host phenotype to increase vector attraction and presumably increase their own proliferation. Indeed, a predator or a parasitoid of a vector may take advantage of this manipulated phenotype to increase its foraging performance. We explored the case of a bacterial pathogen, Candidatus Liberibacter asiaticus (Las), which modifies the odors released by its host plant (citrus trees) to attract its vector, the psyllid Diaphorina citri. We found that the specialist parasitoid of D. citri, Tamarixia radiata, was attracted more toward Las-infected than uninfected plants. We demonstrated that this attractiveness was due to the release of methyl salicylate. Parasitization of D. citri nymphs on Las-infected plants was higher than on uninfected controls. Also, parasitization was higher on uninfected plants baited with methyl salicylate than on non-baited controls. This is the first report of a parasitoid ‘eavesdropping’ on a plant volatile induced by bacterial pathogen infection, which also increases effectiveness of host seeking behavior of its herbivorous vector.
Highlights
There is mounting evidence that vector borne pathogens manipulate the behavior of their vectors by altering the state of the vector’s host
We explored the case of a bacterial pathogen, Candidatus Liberibacter asiaticus (Las), which modifies the odors released by its host plant to attract its vector, the psyllid Diaphorina citri
We explored whether the parasitoid wasp, T. radiata, “eavesdrops” on plant volatiles induced radiata, a known parasitoid of D. citri, that is attracted to volatiles released by the immature nymphal stages of D. citri (d) may be more attracted to this pathogen modified odor release (e) and increase parasitism on D. citri (f)
Summary
There is mounting evidence that vector borne pathogens manipulate the behavior of their vectors by altering the state of the vector’s host This occurs in both plant-pathogen-vector interactions (Ngumbi et al, 2007; Mauck et al, 2010; Davis et al, 2012; Mann et al, 2012), as well as, in animal-pathogen-vector systems (Rogers and Bates, 2007; van den Abbeele et al, 2010; Cornet et al, 2013). This mechanism may drive pathogen spread throughout a community of plant hosts and has been termed the “deceptive host phenotype hypothesis” (Mauck et al, 2010)
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