Tuesday, August 3, 2010: 2:30 PM
321, David L Lawrence Convention Center
Margaret R. Metz1, Kerri M. Frangioso1, Ross K. Meentemeyer2 and Dave M. Rizzo1, (1)Plant Pathology, University of California, Davis, Davis, CA, (2)Forestry and Environmental Resources, North Carolina State University, Raleigh, NC
Background/Question/Methods
Sudden oak death (SOD), caused by
Phytophthora ramorum, is an emerging forest disease associated with extensive tree mortality in coastal California forests. Recent California wildfires provided an opportunity to test a major assumption underlying discussions of SOD and land management, namely that SOD mortality will increase fire severity. An extensive network of monitoring plots examining the impacts of SOD on forest dynamics provided the rare opportunity to link detailed pre-fire measurements of dead woody biomass to post-fire measures of damage. We measured all standing dead woody stems and downed woody debris one to two years prior to the 2008 Basin Fire in Big Sur, CA, and examined how fuels differed in areas with and without the pathogen. The network encompasses a wide range of disease impacts, including uninfested areas, infested areas that have only recently been invaded, and areas where the pathogen has been established for a decade or greater. Immediately following the fire, we conducted a rapid response survey of 61 monitoring plots to assess burn severity. We measured damage to individual trees and several forest strata, including the substrate layers. We quantified tree mortality and forest regeneration one year following the fire in 118 plots, which included infested and uninfested areas within and outside the fire perimeter. We hypothesize that the disturbances interact so that forest damage and recovery vary among infested areas within and outside the fire perimeters.
Results/Conclusions
Despite great differences in fuel abundance, we found no significant difference in burn severity between infested and uninfested plots. Instead, the relationship between SOD and fire reflected the changing nature of the disease impacts over time. Increased SOD mortality contributed to burn severity only in areas where the pathogen had recently invaded. Where the disease had long been established, increasing log volumes led to increased damage to the substrate layers. The impacts for long-term forest recovery and regeneration for mortality from SOD and/or the fire are as yet unknown. We hypothesize longer-term tree mortality following the fire will be higher in areas of highest burn severity and greater in burned, infested plots than in unburned infested plots. The patterns of burn severity in relation to SOD mortality help inform forest management decisions regarding fire, both in Big Sur and in other areas of California as the pathogen continues to expand throughout coastal forests.