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Additional key words: oak decline, tanoak decline, sudden oak death (SOD), stem water potential, tree failure, disease progress, regeneration, stand structure
This report discusses findings after eight years of observations in a case-control study examining the role of tree and site factors on the development of Phytophthora ramorum stem canker (sudden oak death) in coast live oak (Quercus agrifolia) and tanoak (Lithocarpus densiflorus). In September of each year from 2000 through 2007, we collected data on P. ramorum symptoms, tree condition, midday stem water potential (SWP), and various other factors in 150 circular plots (8 m radius). Each plot was centered around a case (symptomatic) or control (asymptomatic) plot center tree. Plots were located at 12 locations in the California counties of Marin, Sonoma, and Napa in areas where P. ramorum canker was prevalent in 2000. At ten locations the predominant canker host was coast live oak, and at the other two locations the canker host was tanoak.
Across all locations, the percentage of trees with P. ramorum canker increased between September 2000 and September 2007. The overall percentage of coast live oaks with P. ramorum canker symptoms increased from 23% in 2000 to 32% in 2007. Most of the increase in disease incidence occurred between 2005 and 2007. This three-year peak of new disease was associated with abundant late season rains that provided favorable conditions for disease spread in the springs of 2005 and 2006. Between 2000 and 2007, tanoaks showed a significantly larger increase in disease incidence, from 31% to 48%. The percentage of newly symptomatic trees was greater for tanoak than coast live oak in all years except 2005.
Although P. ramorum was established at all study locations in 2000, disease incidence at the various location varied widely by 2007, ranging from 8% to 62%. Mortality due to P. ramorum also varied widely between locations and was higher at the two tanoak locations than at any of the coast live oak locations. 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.
Among other common forest species in plots containing coast live oak, California bay population numbers have remained relatively constant over the study period. Douglas-fir density increased by 31% between 2001 and 2007 due to sapling recruitment. Madrone populations decreased 7% overall. 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.
Over three quarters of the initial substantial failures in SOD-affected coast live oaks occurred in dead trees or dead stems of live trees. If only living coast live oak trees with P. ramorum canker are considered, more than half of the observed initial failures occurred in live stems or branches. However, almost all of these live trees had advanced to the late disease stage, characterized by invasion of cankered areas by secondary decay fungi (primarily Hypoxylon thouarsianum and Phellinus gilvus) and wood-boring beetles. Very few failures have been observed in trees with only bleeding cankers (early disease stage). The overwhelming majority of all recorded failures through 2007 have occurred in trees that had P. ramorum canker symptoms at the start of the study in 2000. Relatively few trees that have become symptomatic since 2000 had failed by 2007.
Data for the period from September 2000 to September 2007 indicate that P. ramorum has not impacted seedling populations of either coast live oak or tanoak. Seedling populations in coast live oak plots have varied widely between and within locations over time. Despite fluctuations during the intervening years, seedling densities in 2007 did not differ significantly from those observed in 2000. Tanoak seedling densities have not fluctuated as widely as coast live oak seedling numbers and also showed no significant change between 2000 and 2007.
We made timed counts of P. ramorum foliar symptoms on California bay at intervals from September 2005 through April 2008 to determine how foliar infection levels changed over time in specific patches or zones of bay foliage. All monitored zones showed peak foliar infection levels in mid 2006 following the abundant and extended rainfall of spring 2006. Foliar infection levels dropped significantly by fall 2006 and remained low into spring 2008. A few monitored bay zones maintained relatively high foliar infection levels into 2008, suggesting that long-term inoculum carryover in bay may be spatially variable. Although repeated bay foliar symptom counts from fall 2005 were not correlated with any subsequent counts, counts from spring and fall 2006 were correlated with each other and with counts made in spring and fall of 2007. Correlations between bay foliar symptom counts may therefore depend to some degree on whether foliar disease levels are increasing or decreasing over the observation period.