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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 seven 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 2006, 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 2006. The overall percentage of coast live oaks with P. ramorum canker symptoms increased from 23% in 2000 to 30% in 2006. Most of the increase in infection occurred in 2005 and 2006 and was associated with heavy rainfall in the springs of 2005 and 2006. Between 2000 and 2006, tanoaks showed a significantly larger increase in disease incidence, from 31% to 46%. The percentage of newly symptomatic trees was greater for tanoak than coast live oak in all years except 2005. Disease incidence in 2006 varied widely between the 12 locations included in the study, and ranged from 8% to 56%. In 2006, mortality due to P. ramorum ranged from 4% to 24% at locations with coast live oak and from 27% to 39% at the two tanoak locations. Relatively stable differences in disease incidence between nearby locations appeared to be mainly due to factors other than weather and climate variables.
Overall, symptomatic tanoaks tended to survive for a shorter time after the onset of symptoms than did coast live oaks. Among live trees that had P. ramorum canker symptoms in 2000, 63% of tanoaks but only 32% of coast live oaks had died by 2006. For tanoaks that first became symptomatic between 2001 and 2006, 33% died within 2 years from the appearance of symptoms and 45% had died by 2006. In contrast, only 7% of coast live oaks that developed symptoms after 2000 had died by 2006; however, many of these new infections developed in 2005 and 2006. Disease progress and SOD mortality in coast live oak lagged behind that seen in tanoak because fewer new infections developed in coast live oak and infected coast live oaks tended to survive longer than infected tanoaks.
Because many plots had overlapping tree canopies, and contained species which are not killed by P. ramorum, tree mortality did not always result in a decrease in plot canopy cover. Among plots with P. ramorum-related coast live oak mortality, 41% showed reductions in plot canopy cover between 2001 and 2006. In contrast, 14% of plots without P. ramorum-related mortality had reductions in canopy cover over this period. Canopy cover in most tanoak plots had not changed substantially between 2000 and 2006, mainly because redwood overstory was present in many of the tanoak plots.
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 population numbers increased by 17%, and madrone population decreased 7% overall. Two locations had madrone mortality levels greater than 20%. P. cinnamomi has been associated with declining madrone and bay at one of these locations.
Nearly three quarters of the initial substantial failures in SOD-affected coast live oaks occurred in dead trees or dead stems of live trees. However, in live coast live oak trees with P. ramorum canker, more than half of the observed initial failures occurred in live stems or branches. Between 2000 and 2006, the failure rate of trees that had SOD symptoms in 2006 (34%) was about 10 times that of trees that remained free of P. ramorum canker symptoms (3.5%). The failure rate among tanoaks that developed P. ramorum canker symptoms by 2006 was 26%, compared with a 3% failure rate in tanoaks that were asymptomatic in 2006.
Data for the period from September 2000 to September 2006 suggest 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 2006 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 2006. In 2006, all tanoak plots that had P. ramorum-related mortality had tanoak seedlings present. Among plots with P. ramorum-related coast live oak mortality, only 6% lacked coast live oak seedlings.
In 2006, stem water potentials (SWP) of coast live oak trees deviated from the pattern seen in the previous 6 years. Between 2000 and 2005, SWP readings were been closely tied to the total rainfall for the preceding rainfall year (September to August). However, even though total rainfall for 2005-2006 rainfall year was the highest recorded since the start of the study, average SWP levels measured at all locations in September 2006 were lower than seen in September 2005, indicating higher levels of water stress in 2006 than in 2005. We hypothesize that the extreme heat event that affected the area in July 2006 was responsible for the greater levels of water stress seen in late 2006.
This study was conducted with funding provided by the USDA Forest Service, Pacific Southwest Research Station and Phytosphere Research under cost share agreement 05-JV-11272138-051.