Phytosphere Research

Phytophthora ramorum canker: Factors affecting disease progression and failure potential

2002-2003 Contract Year Annual Report

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

Download the report (Adobe Acrobat PDF)

Additional key words: oak decline, tanoak decline, SOD


This report presents data from the third year of observations in a case-control study to examine the role of water stress and various other factors on the development of Phytophthora ramorum stem canker, commonly called sudden oak death, in coast live oak (Quercus agrifolia) and tanoak (Lithocarpus densiflorus). This study compares subject trees that exhibited symptoms of P. ramorum infection (case trees) with symptomless (control) trees. In September 2000, 2001, and 2002 we collected data in 150 circular plots (8 m radius) in areas where disease caused by P. ramorum was prevalent. Each plot was centered around a case or control subject tree. Plots were established at 10 locations in Marin County, and 1 location each in Sonoma and Napa Counties.

Among all surveyed study trees (includes trees dead at the start of the study), the apparent infection rate among tanoaks has increased from 33% in September 2000 to 37% in September 2002. During the same time interval, the apparent infection rate among coast live oaks has increased from 19% to 20%. Disease symptoms and tree decline have progressed more rapidly in infected tanoaks than in infected coast live oaks. Phytophthora-related mortality has increased from 12% of all monitored tanoak in 2000 to 19% in 2002. During the same period, Phytophthora-related mortality among all monitored coast live oak has increased from 5% to 8%.

Between September 2000 and September 2002, failures occurred in 5.6% of the coast live oaks in the plots. Most failures occurred in dead trees, but trees with both P. ramorum cankers and evidence of beetle boring and/or sporulation of H. thouarsianum (i.e., late disease symptoms) also failed at a high rate over the monitoring period. By September 2002, cumulative failure rates had reached 53% among trees which were dead due to P. ramorum infection in September 2000, and 37% among those trees scored as having late symptoms of P. ramorum infection in September 2000. Among trees rated as having early symptoms in September 2000 (i.e., bleeding cankers only), 5% had experienced a failure by September 2002. In comparison, 4% of trees rated as in decline, and none of the trees rated as healthy in September 2000 had failed by September 2002. Of the trees with failures, 57% experienced bole failures and 11% experienced root crown failures. The remaining failures occurred in branches and scaffolds.

For coast live oak, overall levels of canopy dieback increased between 2000 and 2002. Canopy dieback levels were highest in trees with late symptoms of P. ramorum canker and those in decline due to other reasons. Canopy thinning also increased for trees with symptoms of P. ramorum canker. Many coast live oaks with extensive P. ramorum cankers that do not completely girdle the trunk have exhibited a chronic slow decline syndrome characterized by progressive canopy dieback and thinning. These symptoms differ from the more acute syndrome ("sudden oak death") in which canker-girdled trees show synchronous necrosis of the canopy without extensive thinning or fine branch dieback occurring beforehand.

To test the hypothesis that Phytophthora canker in coast live oak is more likely to occur in trees that are vigorous and/or fast-growing than in trees that are suppressed and/or slow-growing, we measured growth rings in a small sample of increment cores collected in September 2002. Growth increments averaged 2.7 mm/year during the high rainfall years 1994 through 1998. The close spacing and relatively wide width of rays in the wood, vague structural demarcation of annual growth increments, and the presence of false annual increments made the cores extremely difficult to read. Average increment growth did not differ significantly between trees with P. ramorum symptoms, trees declining or dead due to other agents, and asymptomatic trees. Given the small sample size and the high amount of variability in the data, this pilot study did not have enough statistical power to detect small to moderate differences in increment growth. On the basis of this limited investigation, we cannot rule out the possibility that differences in increment growth may be related to P. ramorum susceptibility.

Average subject tree stem water potential (SWP) readings for 2002 were intermediate between those measured in 2000 and 2001. Year-to-year changes in SWP can be explained by trends in rainfall totals and potential evapotranspiration. SWP readings for individual trees in all three years were highly correlated. Most trees with symptoms of P. ramorum infection showed year-to-year changes in stem water potential readings that were similar to those of asymptomatic trees. Most coast live oaks with late P. ramorum canker symptoms have maintained high SWP levels and do not show progressive increases in water stress. We hypothesize that SWP levels in these trees remain high because leaf area loss due to diffuse canopy dieback reduces evapotranspiration while roots continue to function normally.

This study was conducted with funding provided by the USDA Forest Service, Pacific Southwest Research Station and Phytosphere Research under cost share agreement 02-JV-11272138-063.