COS 95-4
Disease pressure in plant communities: The joint roles of abundance and phylogenetic structure

Thursday, August 14, 2014: 9:00 AM
Regency Blrm B, Hyatt Regency Hotel
Ingrid M. Parker, Ecology and Evolutionary Biology, University of California, Santa Cruz, Santa Cruz, CA
Gregory S. Gilbert, Environmental Studies, University of California Santa Cruz, Santa Cruz, CA
Megan Saunders, Environmental Studies, University of California Santa Cruz, Santa Cruz, CA
Background/Question/Methods

Rare host species are expected to suffer less damage from pathogens and pests than common hosts. This rare-species advantage is a key feature of hypotheses that explain how pathogens can help maintain diversity (e.g., Janzen-Connell hypothesis) or regulate invasions (e.g., Escape from Natural Enemies hypothesis). However, most pathogens are polyphagous, so the effective host density includes not just conspecifics but also alternative host species. Closely related species are more likely to share pathogens, and therefore effective host density is in turn a function of the phylogenetic structure of the community.  We studied the effects of abundance and phylogenetic structure on plant-pathogen interactions in a coastal grassland community in California.  We quantified the relative abundance of all plant species in the community in 10 randomly located, 20m-diameter circular plots. We then estimated disease pressure on all species by collecting 5-20 random individuals from each species in each plot.  Finally, we introduced experimental arrays of plants novel to California, and we assessed disease symptoms after several weeks in the field.

Results/Conclusions

We found that host relative abundance significantly predicted disease pressure across plant species.  More surprisingly, we found that phylogenetic and numerical structure of the community had an even greater influence on disease pressure than conspecific density.  For novel plants in our experimental introduction, we found that phylogenetic relatedness to the local community predicted disease pressure.  We parameterized models of host sharing using an independent data set of the host range of 95 fungal pathogens; from this we predicted the susceptibility each introduced focal species.  Actual proportion diseased leaf tissue was strongly predicted by this estimator.  This study illustrates the importance of community context in disease ecology.