Thesis (M.S.)--Oregon State University, 2010. / Printout. Includes bibliographical references (leaves 87-92). Also available on the World Wide Web.

Thesis (M.S.)--Oregon State University, 2009. / Printout. Includes bibliographical references (leaves 58-61). Also available on the World Wide Web.

Thesis (M.S.)--Oregon State University, 2010. / Printout. Includes bibliographical references (leaves 69-72). Also available on the World Wide Web.

Thesis (M.E.S.)--The Evergreen State College, 2008. / Title from title screen viewed (4/7/2009). Includes bibliographical references (leaves 114-126).

The movement of the exotic and destructive plant pathogen Phytophthora ramorum into unquarantined areas via the plant nursery trade provides a potential outlet for transmission into eastern United States forests. A two-year survey of Phytophthora species in a forest adjacent to an ornamental plant nursery in Mississippi isolated P. ramorum 20 times from water and once from vegetation, with an additional detection of 14 Phytophthora species and one provisional species. Isolates were recovered from soil, water, and vegetation using baiting and filtering techniques, and verified by their DNA through Polymerase Chain Reaction (PCR) followed by genomic sequencing. This study confirms the ability of P. ramorum to sustain itself in Mississippi, although disease progression appears to be inhibited by the relatively small window of favorable environmental conditions.

No description available.

Phytophthora ramorum, an oomycete plant pathogen, is the causal agent of sudden oak death, a serious disease of Fagaceous trees in California and Oregon over the last decade. Tanoak (Notholithocarpus densiflorus) is one of the most susceptible host species, but the cause of host mortality is poorly understood. Previous research has implicated disruption in stem water transport, phloem girdling, and activity of a class of secreted proteins known as elicitins as possible mechanisms of pathogenesis. In this study I investigated certain physiological impacts of P. ramorum infection on tanoak saplings and tanoak seedlings. In growth chamber experiments, stems of plants were inoculated with isolates that differed in the amount of elicitin secreted in vitro. Stem-wounded, non-inoculated plants served as controls. Parameters measured included net photosynthetic rate, stomatal conductance, whole plant water usage, stem specific hydraulic conductivity, tylosis production, starch partitioning, and mortality. Inoculated saplings exhibited a reduction in whole plant water usage, followed by a reduction in stem specific hydraulic conductivity implicating an interruption in stem water transport as the primary symptom. A reduction in net photosynthetic rate and stomatal conductance occurred one week later. Experiments conducted on inoculated tanoak seedlings supported the hypothesis that a reduction in stem water transport is the primary disease symptom. Stem specific hydraulic conductivity was the only parameter that appeared to be significantly impacted when treatments were compared during each measurement period. There was, however, a significant difference between treatments over the course of the entire experiment. Due to differences in isolate growth rates and similar levels of elicitin secretion, symptom expression could not be tied to elicitin production. To determine where elicitins are produced in planta, an immunolabeling technique was tested utilizing an elicitin-specific fluorescent antibody. The elicitin protein was most apparent in paratracheal parenchyma cells, although nonspecific staining in control samples confounded interpretation. / Graduation date: 2012

The phytopathogen Phytophthora ramorum (Werres, DeCock & Man in't Veld), causal agent of Sudden Oak Death (SOD) of oaks (Quercus spp.) and tanoaks (Notholithocarpus densiflorus syn. Lithocarpus densiflorus), is established in coastal forests of the western United States. Since the discovery of SOD in the Douglas-fir / tanoak forests of southwest Oregon in 2001, a multiagency effort has ensued with the goal of fully eliminating P. ramorum from this originally small and isolated area. In this study we investigated the epidemiology of SOD in Oregon, particularly as it affects the success of the eradication program. Two approaches were taken to discern the mechanism of long distance dispersal: first, a landscape analysis of the spatial relationship between SOD sites and roads or streams, features associated with movement of infested soils, and, second, a local analysis to discern if understory infection is originating from soil or stream-borne inoculum. Using a restricted randomization test we concluded that SOD sites were no closer to roads than expected by chance, which is inconsistent with soil dispersal by people. While we found evidence that SOD sites were preferentially closer to waterways, inoculum had not moved away from streams into adjacent understory foliage. The local distribution of understory infection around SOD positive trees indicated that primary inoculum is infecting overstory canopies first, suggesting that P. ramorum is dispersing in air currents. Regression modeling indicated that weather conditions two years before detection could explain variation in the maximum distance inoculum moved each year of the epidemic between 2001 and 2010. This two year delay between infection and detection has allowed ample time for infested sites to contribute to further spread. Model results were consistent with observations made the summer of 2011, when trees likely infected by secondary inoculum at non-eradicated sites developed symptoms but were still undetectable by aerial surveys. Due to the prevalence of infection on tanoak, opportunities for sporulation and infection occur more often in Oregon than in California. These data can explain the failure to eliminate P. ramorum. Nevertheless, we did find evidence that the eradication program has significantly reduced the potential size of the SOD epidemic in Oregon. / Graduation date: 2012

No description available.