95th ESA Annual Meeting (August 1 -- 6, 2010)

COS 56-1 - Species extinction vs. ecosystem transformation with forest disease: Sudden Oak Death in California

Wednesday, August 4, 2010: 8:00 AM
411, David L Lawrence Convention Center
Richard C. Cobb, Department of Plant Pathology, University of Califorina Davis, Davis, CA, Joao A. N. Filipe, Plant Sciences, University of Cambridge, Cambridge, United Kingdom, Ross K. Meentemeyer, Center for Geospatial Analytics, NC State, Raleigh, NC, Christopher A. Gilligan, Plant Sciences, Unvirsity of Cambridge, Cambridge and David M. Rizzo, Plant Pathology, University of California, Davis, Davis, CA
Background/Question/Methods

Pathogen characteristics including generalism, saptrotrophic survival, and asymmetric host impacts are likely to increase species endangerment but few pathogens are implicated as the sole cause of extinction across taxa. Over the last hundred years, several diseases have dramatically altered species distributions and structure of North American forests but lead to few instances of endangerment of species. Here we describe ecosystem level changes caused by the forest disease Sudden Oak Death (SOD) in California redwood forests. We use survival models to estimate mortality and infection rates in tanoak (Lithocarpus densiflorus), a hardwood species which is heavily impacted by Phytophthora ramorum the pathogen which causes SOD disease. Simple mathematical models were parameterized with empirical data and jointly utilized to identify changes in species composition, distribution of biomass, and species abundance in forests impacted by SOD. We ask if disease impacts are heterogeneous across individual hosts and if disease is sufficient to lead to stand-level extirpation of tanoak.

Results/Conclusions

Tanoak mortality rate is positively associated with stand-level inoculum intensity, high levels of spring rains, and large tree size. Large trees also show slightly lower rates of infection but no evidence suggests individual tanoak will escape infection except where environmental and community conditions are unfavorable for pathogen establishment. Previous work has shown spring rain events are important drivers of pathogen establishment and this study demonstrates that these events are important drivers of mortality rates as the disease progresses within stands. Simple SIR models suggest tanoak is likely to persist even in stands with high sporulation levels via resprouting from disease-killed individuals. Species persistence via basal sprouting from disease killed overstory trees occurs in other diseases impacting North American hardwood trees including beech bark disease and chestnut blight. Our models suggest stand level species persistence is driven by an interaction among infection, mortality, and resprouting rates. Sudden Oak Death disease is similar to other damaging forest diseases: species extinctions solely due to disease are unlikely but many ecosystems characterized by overstory hosts will be radically altered as these trees are relegated to the forest understory. Changes in relative tree size are important long-term drivers of ecosystem composition and function.