Paper presented at the Fourth Sudden Oak Death Science Symposium, Santa Cruz (Scotts Valley), CA, 15-18 June 2009 - Ecological Impacts session
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In 2008, we completed our ninth year of observations in permanent plots that were established in 2000 to examine how tree and site factors affect risk of Phytophthora ramorum stem canker (sudden oak death) and determine how affected stands change over time due to disease. In September of each year from 2000 through 2008, we collected data on P. ramorum symptoms, tree condition, tree failures, regeneration, and various other factors in 150 circular plots (8 m radius) at 12 locations in Marin, Sonoma, and Napa Counties. P. ramorum canker was prevalent in the sampled coast live oak (Quercus agrifolia)or tanoak (Lithocarpus densiflorus) stands in 2000. Data collected through September 2008 will be reported at the symposium; only data through 2007 are reported in this abstract.
Disease development patterns over time differed between tanoak and coast live oak populations in the study. The increase in disease incidence between 2000 and 2007 was greater for tanoaks (31% to 48%) than for coast live oak (23% to 32%). Disease incidence in coast live oaks increased strongly from 2005 through 2007 in response to abundant late season rains that provided favorable conditions for disease spread in the springs of 2005 and 2006. Tanoak showed a less much pronounced increase in disease incidence associated with these favorable years. Based on time lags between favorable conditions for infection and the appearance of visible symptoms, most coast live oaks had latent periods from 0.5 to 1 year, whereas the minimum latent period in tanoaks was commonly about a year.
Compared to coast live oaks, tanoaks show substantially higher rates of mortality within one year after external symptoms appear and have poorer long term survival rates. The increase in SOD mortality has followed a linear trend between 2000 and 2007 (R2=0.98) for both oaks and tanoak. Extrapolation of the linear trends indicates that initial mortality in both plot types would have occurred in 1996. Extrapolation of the linear (R2=0.96) trend in tanoak symptom incidence indicates that the first symptoms in these stands could have developed in the mid 1980's.
In 2007, disease incidence at coast live oak locations ranged from 8 to 55%. The increase in disease incidence since 2000 has varied widely by location. Relatively stable differences in disease incidence between nearby coast live oak locations were mainly associated with differences in California bay cover rather than weather and climate variables. Coast live oak locations also showed varying rates of symptom remission in SOD-affected trees.
The overwhelming majority of all host tree failures through 2007 occurred in trees that had P. ramorum canker symptoms in 2000. Relatively few trees that have become symptomatic since 2000 had failed by 2007. Over three quarters of the initial failures in SOD-affected coast live oaks occurred in dead trees or dead stems of live trees. Early P. ramorum canker symptoms (bleeding only) were not associated with tree failure; only SOD-affected trees colonized by secondary organisms had elevated failure rates. Other factors related to failure risk will be discussed.
Among plots with SOD-related mortality, 27% of the tanoak plots and 45% of the coast live oak plots showed decreases in plot canopy cover. Since 2001, coast live oak plots have shown an increase in Douglas-fir density (+31%), no change in California bay density, and decreased madrone density (−7%). Three locations had relatively high levels of madrone mortality, ranging from 17 to 31 percent. We have determined that P. cinnamomi is associated with declining madrone and bay at one of these locations.