COS 24-8
Resprouting and disease dynamics in forests impacted by compounded disturbances: Wildfire and sudden oak death in Big Sur, CA

Tuesday, August 11, 2015: 10:30 AM
322, Baltimore Convention Center
Allison Simler, Graduate Group in Ecology, University of California Davis, Davis, CA
Margaret Metz, Biology, Lewis and Clark College, Portland, OR
Kerri M. Frangioso, Plant Pathology, University of California, Davis, Davis, CA
Ross K. Meentemeyer, Forestry and Environmental Resources, North Carolina State University, Raleigh, NC
David M. Rizzo, Plant Pathology, University of California, Davis, Davis, CA

Novel interactions between multiple disturbances may impact regeneration trajectories, leaving lasting legacies on community structure.  Sudden Oak Death (SOD), caused by Phytophthora ramorum, is an emerging disease causing widespread tree mortality in California’s coastal forests.  In disease-impacted redwood-tanoak forests, wildfire also shapes structure and composition, and the dominant tree species resprout rapidly after being “top-killed.”  In other forest types, some suggest that resprouting trees may be more resilient to changing disturbance regimes, compared to species that only reproduce sexually.  In this redwood-tanoak forest type, tree species differ in resprouting capacity and susceptibility to both fire and disease.

In 2006, 280 forest plots were established to monitor the progression of SOD in California’s Big Sur region.  The 2008 Basin Complex fires burned across infested and disease-free plots in this area, providing an opportunity to investigate impacts of multiple disturbances on forest regeneration.  Burned and unburned forest plots were repeatedly sampled to assess tree mortality, pathogen presence, microclimate, and regeneration, including resprouting vigor and seedling recruitment.  We investigated how the intersection of fire and disease influence resprouting in tanoak, the species most susceptible to SOD, and in turn, whether sprouting in bay laurel, the pathogen’s dominant host, impacts post-fire pathogen prevalence.


Tanoaks in mid-stage SOD-infested areas were more likely to suffer complete (above and belowground) post-fire mortality. This may be due to altered fuels and increased fire severity in SOD-impacted areas, as recorded by preceding studies.  For surviving tanoaks, resprouting vigor was best predicted by pre-fire basal area and degree of aboveground mortality; however, combinations of disease and fire significantly impacted these patterns.  Sprouting in unburned, disease-impacted forests was decreased, compared to disease-free areas.  In plots impacted by fire and disease, tanoak resprouting was significantly greater than expected by our model.  This suggests that the pathogen is not measurably hindering re-growth of tanoak (a susceptible host) in burned, disease-impacted areas.  We hypothesize that this is due to decreased host connectivity and severe microclimates in burned areas.  Additionally, this suggests that tanoaks surviving the bottleneck generated by disease and fire may experience reduced competition and can respond with increased resprouting vigor.

Resprouting vigor also influenced post-fire recovery of P. ramorum.  In burned areas, the pathogen was significantly more likely to be recovered in larger bay laurel sprouting clusters and in areas with more surviving canopy cover, suggesting that resprouting and post-fire microclimates may play a key role in disease reinvasion.