T. J. Swiecki1 and E. A. Bernhardt2
This paper reports on the first three years of data from a case-control study that examines the role of water stress and various other factors on the development of Phytophthora ramorum stem canker (sudden oak death) in coast live oak (Quercus agrifolia) and tanoak (Lithocarpus densiflorus). The study compares subject trees that exhibited symptoms of Phytophthora 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 Phytophthora 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.
A number of plot and tree factors were associated with disease in the subject tree in logistic regression models for coast live oak. Vegetation-related plot variables that were positively correlated with disease in coast live oak included the count of California bay (Umbellularia californica) trees in the plot, the number of plot trees with Phytophthora canker symptoms, and the presence of poison oak (Toxicodendron diversilobum) in the plot. Tree-related factors that were associated with disease included multiple stems, large stem cross-sectional area, high levels of canopy exposure, and high stem water potential (SWP). In addition to these factors, logistic models based on plot trees other than the subject trees showed a negative association between Phytophthora canker symptoms and decline symptoms associated with agents other than Phytophthora.
The direction of the effects of a number of variables in several different analyses suggests the possibility that Phytophthora canker in coast live oak is more likely to occur in trees that are vigorous and/or fast-growing (larger, more dominant, less water-stressed, not in decline due to other agents) than in trees that are suppressed and/or slow-growing. To test this hypothesis, we collected increment cores from recently killed trees within the plots in 2002. We will compare recent increment growth in trees that have died due to Phytophthora canker with trees that have died form other causes and live, asymptomatic trees located just beyond the edge of the plot.
We also observed significant positive correlations between canopy dieback and Phytophthora canker among symptomatic trees that have not yet died. From this and other field observations, we conclude that diffuse dieback in the canopy often develops in both coast live oak and tanoak trees that survive for a number of years after initiation of Phytophthora trunk cankers. This symptom is distinct from the rapid and complete necrosis of the canopy that has been commonly associated with the disease.
