OOS 1-1
Linking epidemiological and ecosystem process models to understand and minimize disease impacts

Monday, August 11, 2014: 1:30 PM
202, Sacramento Convention Center
Richard C. Cobb, Department of Plant Pathology, University of Califorina Davis, Davis, CA
Noam Ross, Department of Environmental Science and Policy, UC Davis, Davis, CA
David M. Rizzo, Plant Pathology, University of California, Davis, Davis, CA
Background/Question/Methods

In this analysis, we examine the form, sources of error, and insights gained from explicit integration of epidemiology and ecosystem ecology. Given the rate of novel pathogen introduction and emergent impacts of widespread native pathogens, linking these fields is needed to understand and respond to the changing conditions caused by forest diseases. What is the magnitude and timing of pathogen impacts in wildland plant systems and how do these impacts alter ecosystem structure and function? We address this question with a series of mathematical and empirical models of the exotic pathogen Phytophthora ramorum (cause of Sudden Oak Death) and native Heterobasidion root pathogens. By linking epidemiological and ecosystem dynamics we also demonstrate the benefits of forest disease management in terms of woody biomass conservation.

Results/Conclusions

Aerial dispersal of P. ramorum leads to patchy pathogen spread and loss of woody biomass over time but over large areas. A series of field and modeling experiments suggesting disease management can result in woody biomass C conservation of up to ~100 Mg Ha-1 C over a 100 year simulation with the overall amounts determined by pre-disease host biomass distribution and the prevalence of pathogen-transmitting hosts. Heterobasidion pathogen spread, impacts, and distribution across the landscape are determined by a combination of establishment opportunities (cut stumps) and local contact structure (root zone of the first infected tree). In contrast to P. ramorum, C losses in Heterobasidion impacted forests are nearly complete across species but are limited to small areas. Host biomass or importance and contact structure, either transmission opportunity or inoculum pressure, are critical drivers of ecosystem change for these and likely most other forest pathogens.