We're moving our quarterly updates about Sudden Oak Death in the north coast to this space. This will be easier to access and will also enable you to interact electronically with us here at UCCE Humboldt-Del Norte by sending us your questions and comments. (We will be able to view your comments in advance so that if it's something sensitive, we can call you rather than posting the answer on this blog.)

Additionally, we will post items and articles of interest here on a more regular basis, so check back here often. Remember that we are here to provide assistance and answer any questions you have about Sudden Oak Death or other forest health-related topics; just post a question to this blog or call Chris or Yana at (707) 445-7351.

Genetics and Pathogen Movement

Although no one knows exactly when the Sudden Oak Death epidemic began in California, scientists are now closer to reconstructing its unseen progress since that unknown point. Using up-to-the-minute DNA fingerprinting technology, Matteo Garbelotto and his laboratory at UC Berkeley have just published a study that traces the movement of P. ramorum throughout California based on tiny similarities and differences among individual P. ramorum isolates (samples) throughout the state. Their conclusions? P. ramorum was probably introduced to North America on ornamental plants and then entered the wild at two specific locations: Santa Cruz and Mount Tamalpais.

The Garbelotto lab’s study uses microsatellites, which are locations on the genome where base pairs of amino acids repeat many times. These base pairs often randomly mutate even in organisms that reproduce asexually (i.e., through cloning), as is the case with P. ramorum in North American forests. Strictly speaking, all the isolates of P. ramorum throughout California forests are genetic clones of each other. However, as these individuals spread out, they are mutating faster than originally thought. Although the differences are tiny, they are enough to enable geneticists to distinguish the individuals one from another.

The Garbelotto lab collected 300 separate isolates of P. ramorum throughout California forests from Humboldt County down to Monterey County and in several nurseries. They then compared selected microsatellites from each isolate to the same microsatellites in all the other isolates. Since these microsatellites mutate step-by-step, this comparison enabled the lab to construct a tree diagram showing which isolates were most closely related to which others.

The sites at the base of the tree—in other words, the isolates that are probably the ancestors of all the others—contained the nursery isolates, the isolates from Santa Cruz, and the isolates from Mount Tamalpais. The probable site of pathogen establishment in Santa CruzCounty was very near a nursery, and from there the pathogen reached Mount Tam, perhaps through human movement of infected plant material. Tracing the relationships of isolates up the tree reveals that from these early establishment nodes, P. ramorum most likely moved from Santa Cruz County to Big Sur and from Marin County to Sonoma County.

With this information, and also looking at the relationships of isolates on a smaller scale by comparing the proportions of genotypes present in each collection locale, the lab determined that natural spread of P. ramorum probably occurs through two main modes: short-distance dispersal of less than 200 m in normal weather conditions, and occasional long-distance dispersal of 1-5 km in extraordinary storm events with extreme winds.

The one question that the lab has unfortunately been unable to answer so far involves how the pathogen got to Humboldt County. The genotypes of the isolates present there apparently do not bear a clear resemblance to any of the other genotypes analyzed for the study, although it is clear that as the pathogen spreads from one place in the county to another, it is mutating. Further clarification about how the pathogen arrived in the county will have to wait for further sample collection and genotyping. Plans for this are in the works.

European Strain in McKinleyville

In 2006, surveyors from UC Cooperative Extension Humboldt-Del Norte (UCCE) and UC Davis were surprised to find P. ramorum in a small watercourse in McKinleyville. The pathogen showed up again in 2007 and has continually confounded every effort to trace its source.

The watercourse in question is Widow White Creek, which begins in the hills east of town and flows through residential neighborhoods before draining to the ocean just north of the mouth of the Mad River. The good news about the pathogen’s presence in the creek is that the stretch of the creek where the pathogen was found features vegetation not known to host P. ramorum, such as willow, red alder, eucalyptus, and Sitka spruce. The pathogen has not been detected in the upper watershed, where tanoaks grow, and almost no bay laurel (pepperwood) occurs in the area at all. This means that the pathogen is not likely to spread throughout the natural environment in the McKinleyville area.

Personnel from UCCE and collaborators have visited the watercourse numerous times searching for plants near the stream that may have been infected by the pathogen. The searchers have submitted numerous samples from planted ornamental hosts as well as from plants not known to be hosts. Most samples did not look highly suspicious, but the surveyors collected and sent everything they could find. All the samples turned up negative for the pathogen, leaving the surveyors scratching their heads and wondering where the inoculum in the stream could have originated.

To complicate the picture further, genetic analysis done at Oregon State University on all the McKinleyville stream samples collected in 2006 and 2007 revealed that two separate strains of P. ramorum—both the North American strain and the European strain—are present. Up until this point, only the North American strain has shown up in the natural environment in North America, the European strain having been limited to nurseries.

Again, there is at least one bright spot in this picture—the absence of host trees along the stream and its short travel time to the ocean. No one knows whether P. ramorum can sustain itself within watercourses perennially or is delivered anew each year from the inoculum source, wherever it is. For the foreseeable future, surveyors will continue to beat the bushes around the stream in an attempt to find that source.

Similar stream finds have recently been recorded in Washington, Mississippi, and Florida. In each case, the pathogen’s presence in the stream has been related to a nearby nursery infested with P. ramorum. While one nursery in McKinleyville has been found with several infected ornamental plants of various species—and at least one of those plants has been infected by the European strain—it is situated in a different watershed from Widow White Creek and cannot be definitively linked to the stream infestation. The nursery, which voluntarily reported the first disease symptoms and has continued to proactively monitor its stock each year since, has implemented control strategies in an attempt to eliminate the infestation. It will continue to be inspected at regular intervals by the Humboldt County Agriculture Department and the California Department of Food and Agriculture.

As searches for the source continue and our understanding of the behavior of P. ramorum in watercourses improves, we will hopefully come closer to knowing whether such infestations are an actual threat to the wildland environment or just minor points of interest useful mostly for detecting the organism in that environment.

Widow White Creek, McKinleyville

2007 Difficult for Oregon Eradication Efforts

The team of scientists and land managers working to eradicate P. ramorum from Oregon forests ran into their most difficult year yet in 2007. Unusually wet conditions (in contrast to the north coast’s generally dry winter and spring) led to some long-distance pathogen “jumps” across the landscape as well as a large increase in the numbers of infected tanoak trees discovered by the group’s aerial, ground, and watercourse surveys. As a result of pathogen movement, the USDA Animal and Plant Health Inspection Service (APHIS) was forced to increase the official regulatory quarantine area in Oregon from 26 square miles to 160.

Altogether, 720 acres were marked for treatment in 2007; only 420 of those acres were treated before money ran out. The Oregon group will treat the remaining 300 acres early this year with the funds they receive for 2008, but they are also mounting an aggressive lobbying effort to secure more funding for a ramped-up program that can keep pace with the pathogen’s expansion in wet years. Altogether, the group estimates that such a program will need $5-10 million per year.

Tanoak Resistance

Here’s one question that comes up time and again when we talk to people about Sudden Oak Death in the north coast: Are any tanoaks naturally resistant to the disease? If scientists find this to be the case, then obviously we have some hope for restoring and reforesting areas where P. ramorum has caused massive tanoak mortality (such as in Point Reyes, where in some individual stands up to 95% of the tanoaks have died).

Unfortunately, the answer to these questions involves more than a trip to a Sudden Oak Death-devastated area to see which tanoaks don’t seem to be affected. Although that certainly is an important first step, assessing resistance to P. ramorum is not so straightforward. The movement of P. ramorum, and thus the incidence of Sudden Oak Death, is extremely patchy and apparently random across the landscape. Which trees escape death may be more a function of “luck” than anything else.

It also may have to do with climate; in wet years, more P. ramorum spores are produced, and more trees are infected. Conversely, during dry years, even extremely susceptible tanoaks may escape infection.

If past experience is a guide, successful programs to identify and/or breed disease-resistant trees take many years and tremendous amounts of money to develop. At the USDA Forest Service’s DorenaTree Improvement Center in Dorena, Oregon, geneticists have spent lots of both in a quest to come up with Port Orford-cedar trees that are resistant to Port Orford-cedar root disease, as well as five-needle pine species resistant to white pine blister rust. In both cases, they have experienced some success in finding resistant individuals and working to enhance that resistance through breeding programs.

Now Bay Area researchers have taken the first steps toward building a similar resistance program for tanoaks to help address the growing problem of mortality caused by Sudden Oak Death. UC Berkeley Professors Richard Dodd and Matteo Garbelotto, graduate student Katy Hayden, and Forest Service conservation geneticist Jessica Wright are exploring some of the preliminary questions that must be answered to get such a program off the ground.

Some of these questions involve the history of tanoak and how tanoaks came to be distributed as they currently are. The answers to this question can help determine whether tanoak acorns taken from one site will be successful in other sites. The scientists have found that tanoaks exist in at least four discrete supergroups in California. This gives clues to tanoak’s evolution and dispersal over the past thousands of years, and it suggests that resistant tanoak acorns taken from, say, the Sierra Nevada may not work for reforestation efforts on the north coast. Dodd has included Humboldt County in his plans for sampling acorns in 2008 as he continues to develop a more complete picture of tanoak’s genetic structure across the state.

Other research efforts involve growing tanoaks from acorns in a common environment and inoculating them directly with P. ramorum to test for greatest resistance to the pathogen. These kinds of projects typically involve a great deal of start-up investment in figuring out how to germinate and grow the seedlings properly; they are now underway at Berkeley.

Such efforts will probably not lead to the discovery or development of genetic individuals that are completely immune to Sudden Oak Death; they are more likely to lead to individuals that are able to live with the disease—a desirable outcome, because it is not likely to stimulate the rapid counter-development of pathogen adaptations that would enable P. ramorum to overcome immune tanoaks. In any case, although resistance may provide a partial answer to the many dilemmas posed by Sudden Oak Death in the north coast, that answer is a long way off.

Bay Removal Information

Recently completed studies suggest that strategic removal of bay laurel (pepperwood) trees near coast live oaks may help prevent the oaks from being infected by P. ramorum. Ted Swiecki and Elizabeth Bernhardt of Phytosphere Research in Vacaville looked at a set of plots containing both infected and uninfected coast live oak trees and noted that plots with more bay trees and a greater percentage of bay foliar cover also contained more infected trees. This observation prompted the researchers to wonder whether removing the bay trees within various distances from oak trees might keep those trees from being infected.

Swiecki and Bernhardt looked closely at the distances of bay trees from oak tree boles in various plots and compared those distances with the severity of symptoms caused by P. ramorum on the oaks (e.g., bleeding cankers on the stems). They concluded that the presence of bay trees within 2.5 m (8.2 ft) of oaks was most strongly correlated with infection. This strongly suggests that removal of bay trees within this distance might help protect susceptible oaks; removal of bay trees within 5 m (16.4 ft) can be expected to have even stronger protective effects.

This result is a straightforward, commonsense one given that bay trees have been shown to be the primary carrier of P. ramorum in California and the primary means of transmitting inoculum to susceptible oak and tanoak species. However, an interesting wrinkle in Swiecki and Bernhardt’s research came from the few cases in which they found coast live oak trees infected although no bay trees were nearby. In each of these cases, the scientists found an abundance of poison-oak growing throughout the oak canopy of the plot. The poison-oak invariably displayed the symptoms of possible P. ramorum infection, including bleeding cankers on the stems and leaf spots. This has led the researchers to speculate that poison-oak could potentially be another carrier of P. ramorum, although how important a carrier it might be no one knows.

The researchers have now begun to test their recommendations about bay removal by cutting bay trees in their study plots. Because coast live oak is more resistant to P. ramorum infection than tanoak, it could be years before they have firm results. Meanwhile, similar studies concerning the latter species will most likely also commence in the near future, and UCCE Humboldt-Del Norte is working on similar studies on a larger scale by coordinating two bay removal projects. The first is at an experimental silvicultural management area southwest of Garberville where other kinds of P. ramorum management studies are ongoing. The other is an attempt to forestall the movement of P. ramorum up the South Fork Eel/Avenue of the Giants corridor between Myers Flat and Weott, which represents the northernmost natural extent of P. ramorum-infected trees in Humboldt County. In this area, only bay trees have been found to be infected, and in 2007 California State Parks, CALFIRE, and UCCE collaborated to remove all bay laurels in an approximately 2 1/2-mile strip between the river and the Avenue. The removal of the bay laurels did not affect habitat value or aesthetics in the treated forest, and so far in 2008, none of the remaining vegetation has been found to be infected.

 

For more information about this research, along with photos that illustrate the study plots where these observations were made, go to http://phytosphere.com/publications/SODmanagementstudy.htm.