Phytosphere Research

2004 Resurvey of permanent plots for monitoring Phytophthora ramorum canker (sudden oak death) in Sonoma County

T. J. Swiecki and E. A. Bernhardt
Phytosphere Research, Vacaville CA

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Additional key words: SOD, oak and tanoak decline, regeneration


Sudden oak death (SOD), a lethal bark canker disease caused by Phytophthora ramorum, has the potential to severely impact many of the ecologically important woodlands and forests of Sonoma County, California. In 2001 we established permanent research/monitoring plots in Sonoma County woodland and forest types at risk due to P. ramorum canker and collected baseline data on these plots. This report presents the results from the 2004 resurvey of these plots. Within plots, we evaluated the occurrence and progression of symptoms caused by P. ramorum, assessed tree decline and mortality due to other agents, and looked at levels of tree failure and potential regeneration of affected species.

We resurveyed a total of 250 fixed-area plots (0.02 ha each) at 11 study locations in various portions of Sonoma County. The number of locations with confirmed P. ramorum infections of both SOD canker hosts (i.e., coast live oak, California black oak, and tanoak) and California bay increased from three in 2001 to four in 2004. At a fifth location, P. ramorum was confirmed from California bay foliage, but not from SOD canker hosts. Hence, P. ramorum became established within the study areas at two additional locations between 2001 and 2004.

Among all plots containing tanoak (73 plots), the percentage of plots with P. ramorum canker increased from 29% in 2001 to 40% in 2004. For plots containing California black oak (119 plots), the percentage of plots with P. ramorum canker symptoms increased from 2% in 2001 to 10% in 2004. The percentage of plots with coast live oak (114 plots) that had P. ramorum canker symptoms decreased slightly, from 9% in 2001 to 7% in 2004. The slight drop in the incidence of P. ramorum canker symptoms in coast live oak was due to apparent symptom remission in two trees at Sugarloaf Ridge State Park.

Between 2001 and 2004, the percentage of trees with P. ramorum canker symptoms increased at three of the four locations that had symptomatic SOD canker hosts. The percentage of SOD canker hosts with P. ramorum canker symptoms increased from 0% to 6% at Annadel SP, 7% to 23% at Austin Creek SRA, and 44% to 51% at Jack London SP between 2001 and 2004. The remaining location (Sugarloaf Ridge SP) showed a slight drop (12% to 11%) in the percentage of symptomatic SOD canker hosts.

Mortality in SOD canker hosts due to both P. ramorum and other agents increased at 9 of the 11 study locations between 2001 and 2004. The percentage of the mortality increase due to P. ramorum was 27% for California black oak, 49% for coast live oak, and 30% for tanoak. For most locations, annualized background mortality unrelated to P. ramorum was less than 1% per year between 2001 and 2004. Over this period, mortality rates associated with P. ramorum exceeded background mortality at three locations and was equal to it at a fourth location. At tanoak-dominated Sonoma Coast State Beach, mortality associated with an unidentified bark canker greatly exceeded background mortality and was comparable to levels of mortality associated with P. ramorum at other locations. Although no pathogens were successfully isolated from tanoak cankers at Sonoma Coast SB, we isolated both P. nemorosa and P. pseudosyringae from symptomatic California bay foliage within plots.

Overall tree failure rates for the period 1999-2004 were significantly higher for California black oak (11.5%) than for tanoak (7.4%) or coast live oak (5.1%). Bole failures were the most common failure type among tanoaks and coast live oaks, whereas large branch failures and bole failures were equally common in California black oak. Failure rates were significantly higher among coast live oaks with P. ramorum canker symptoms than among asymptomatic trees. At two locations, tanoaks with P. ramorum canker also failed at a higher rate than asymptomatic tanoaks. Most of the coast live oaks and tanoaks with P. ramorum symptoms were dead when they failed. Wood decay was the primary contributing factor in almost all observed failures.

Tanoak seedlings were present in nearly all plots with tanoak trees. All plots with tanoak mortality had tanoak seedlings which could potentially grow to replace dead trees. Coast live oak plots were less well-stocked with seedlings. Twenty five percent of plots with coast live oak mortality lacked coast live oak seedlings, and mean counts of coast live oak seedlings per plot were significantly lower in 2004 than in 2001. Less than half of all plots with California black oak trees had California black oak seedlings. Three-quarters of the plots with California black oak mortality lacked seedlings of this species. Regeneration of California black oak appears inadequate to maintain stand density even without the additional mortality due to P. ramorum in the surveyed woodlands.

Funding for this project was provided by the USDA Forest Service through project CF1052021-130. We thank Dr David Rizzo, Department of Plant Pathology, UC Davis for supporting this research through UC Agreement #K007582-01.