When we spot the towering piles of hiking boots, plastic tubs, and spray bottles of disinfectant, we know we’re in the right place.
My husband, son, and I have joined a small group of outdoor enthusiasts at Deer Park in Marin County to “Hike & Bike for Science.” Michelle Cooper, a Sonoma State University (SSU) biology graduate student, is investigating the potential for sudden oak death to be spread by recreational trail users. We stop at measured intervals to carefully rinse the soil from our boots into plastic bags, so Cooper can analyze it later for the presence of the pathogen that causes the disease. Curious hikers, bikers, and horseback riders stop to inquire about our unusual trailside behavior, oblivious to the fact that they, like us, might be agents in spreading a disease that threatens the woodlands they enjoy visiting.
The pathogen that causes sudden oak death (SOD, pronounced ess-o-dee) was first identified in 2000. And though we’ve learned a lot about it in a short time, there’s still much we don’t know. We know that it has spread along the California coast and up into Oregon, and forced quarantines on movement of certain plant materials in 14 California counties, threatening the state’s signature oak woodlands. We also know that it infects many plant species other than oaks. In fact, California bay laurel is playing a starring role in spreading the disease. The big question now is what role humans are playing, and how we can help stop the disease from spreading further.
To answer that, we need to understand how the pathogen works and how it gets around. We know that the primary method of transport from tree to tree seems to be wind-driven rain moving through the forest canopy. However, SOD shows up in isolated patches up and down the coast, too far apart to be explained completely by the movement of water. So it’s highly likely that people play a part, whether by buying and transporting infected garden and nursery plants, bringing home pathogen-laced firewood, or simply hiking along muddy forest trails during the rainy season.
Cooper was unable to successfully culture the pathogen in the lab from the dried mud on our boots, but that doesn’t mean trail users are off the hook. Cooper points out there could be many reasons the pathogen failed to appear under lab conditions, and that dormant spores could remain viable even in dry soil out in the field. In a related experiment, she analyzed fresh soil samples and found that 7 percent of hikers going into Deer Park carried the pathogen on their boots, while 23 percent carried it out. Preventing the movement of pathogen out of infected areas may well be a key to containing the disease.
But that will not be easy, given the history of the pathogen’s close relations. SOD is caused by a fungus-like water mold known as Phytophthora ramorum. Phytophthora (Fy-tahf-thora), meaning “plant killer,” is an apt description for the water mold genus that is responsible for so much destruction around the globe. It was a related Phytophthora that caused the Irish potato blight, and another that has more recently decimated the jarrah forest in Australia, reducing thousands of acres of eucalyptus habitat to grassland and scrub. Phytophthoras are also responsible for many common and potentially devastating agricultural diseases.
P. ramorum was identified as the causal agent of SOD in 2000, a mere five years after dead trees were first observed in Marin County, and only a year before the pathogen first turned up in Oregon. “It’s all so new, and so much remains to be learned,” says David Rizzo, a plant pathologist at UC Davis, who with Matteo Garbelotto, a plant pathologist at UC Berkeley, has spearheaded much of California’s research effort.
In the Rizzo lab, postdoctoral student Liz Fichtner shows me the culprit. Under a microscope, the P. ramorum chlamydospores scraped off a bay laurel leaf from Samuel P. Taylor State Park in Marin look like little beads of shining amber. Chlamydospores—just one of several kinds of spores produced by P. ramorum—are dormant, long-lasting spores primarily found in soil and streams. The pathogen also forms sporangia (structures in which spores are produced), which in turn carry zoospores—self-propelled swimming spores, each equipped with its own flagellum. Zoospores, primarily transported in wind-driven rain, appear to be the main culprit in the pathogen’s spread.
But those various spores aren’t produced by every plant infected with P. ramorum. Some plant species become “canker hosts,” most of which die but don’t spread the disease. Other plants are “foliar hosts,” which rarely die but often spread the disease quite effectively.
Canker hosts have symptoms such as bleeding, trunk cankers, and then sudden browning of the canopy when death finally occurs. Several species of oak—including coast live oak, canyon live oak, California black oak, and Shreve’s oak—are canker hosts. Foliar hosts, on the other hand, usually survive and can produce massive quantities of spores. Plants such as rhododendron, poison oak, and California bay laurel are common foliar hosts, manifesting the disease as leaf lesions and sometimes twig blight; many show few symptoms when infected. Dozens of other plant species are foliar hosts as well. The only exception is tanoak, which behaves as a foliar and canker host, both dying from and spreading the disease. (Tanoak is not a “true oak”; it belongs to the genus Lithocarpus rather than Quercus.)
Tanoaks are the tree most susceptible to infection, and the disease kills anything from seedlings to mature trees. Among the true oaks, generally only large, mature, healthy trees succumb to infection. In oaks, once SOD has gained a foothold, opportunistic organisms such as ambrosia beetles and Hypoxylon fungus may invade as the tree becomes weakened. Either SOD or these new maladies can eventually kill the tree.
- Though SOD kills oak trees, it is spread by California baylaurel and other species that serve as foliar hosts, plants that rarelydie from the disease but nurture large numbers of pathogen spores ininfected leaf tissue. Oaks are actually a dead end for Phytophthora ramorum, the pathogen that causes sudden oak death. Illustration by Fiona Morris.
But it is California bay laurel that appears to be the primary driver of the epidemic. The presence of bay is currently the best predictor of new cases in areas where SOD has already been found, and areas with bay are at higher risk of infection. “There’s no doubt about it that bay is playing a huge role in the dynamics of the disease, which is why, if you want to understand this disease, you really have to focus on bays,” says Hall Cushman, an SSU ecologist who studies human-caused spread of the pathogen.
Bay is far from the only suspect. When I meet longtime oak and SOD researcher Ted Swiecki, a plant pathologist and principal of Phytosphere Research, at Spirit Rock Meditation Center in Woodacre, he is clearly not dressed for meditation. From his hard hat, coveralls, and orange vest hung with gear, to the gaiters that wrap around his shins, he is ready for some serious bushwhacking. “Well, we have found out that poison oak may also be a good predictor of SOD,” he tells me as we head up the hill to his study plots. Poison oak, he says, may be an important source of spores, especially when it twines into the canopy.
SOD is currently found along about 300 miles of coastline in 14 California counties from Big Sur north to Humboldt, as well as Curry County in Oregon, in a swath that extends up to 50 miles inland. The disease isn’t found farther inland due to several interrelated factors, including lower moisture levels, higher temperatures, and absence of hosts and contiguous forest.
Within its current range, the distribution of P. ramorum tends to be patchy, but warm, late rains during the past two springs have promoted the spread of the pathogen between patches. “It is simply exploding in Big Sur,” notes Rizzo. “Sporulation levels in 2006 were the highest we have recorded in the five years since we began.”
When a major plant disease appears suddenly, as SOD did a mere dozen years ago, the obvious questions are, Where did it come from, and what can we do to treat it? The answers to these questions are still not clear, and both remain controversial. Several independent scientists argue that SOD is caused by an array of native diseases and general poor forest health, but mainstream researchers concur that P. ramorum is undoubtedly exotic in origin, though no one knows exactly where it came from.
Regardless of P. ramorum‘s origin, scientists are working on several fronts to find ways to treat the disease. “We’re at a research frontier,” says Cushman. In May, SSU microbiologist Michael Cohen found a native amoeba munching Phytophthora sporangia on bay leaves, and he’s launching an investigation into its potential for SOD control. Swiecki is trying to determine how far apart bays and oaks must be to protect oaks from infection and how thinning of understory tanoak might reduce SOD spread. UC Berkeley’s Garbelotto is particularly concerned with a new P. ramorum lineage, recently discovered in a Washington nursery, that could possibly expand the range of SOD if it escapes into the wild. With just one treatment approved by the state and shown to be effective in oaks and tanoaks, the Garbelotto lab is also testing a variety of other potential treatments.
What about human-caused spread? Cushman and Ross Meentemeyer, a geographer at the University of North Carolina, found that wildlands surrounded by high human density were more likely to have P. ramorum infections, strengthening the case for a human role in its spread. Pathogen “hopscotching” between disparate areas is most likely the result of movement of nursery plants and recreational trail users. Plant movement is certainly having a significant impact on disease spread, and nurseries and gardeners can do a lot to contain the disease. Gardeners should be particularly cautious when considering host plants such as bay laurel, rhododendron, camellia, pieris, and viburnum. But no one is sure how culpable either gardeners or trail users might be in any particular place. In any case, trail users can take measures to reduce the chances that they’re spreading disease.
The California Oak Mortality Task Force (COMTF), a clearinghouse for information, provides guidelines for trail users, homeowners, and forestry and landscaping professionals on its web site. COMTF emphasizes the high risk of moving infected plant material (firewood, soil, or detached leaves) and the necessity for precautions during the rainy season. For visitors at open spaces in infested areas, parking on pavement or gravel is advisable, and parking under bay trees not recommended. Muddy boots, tires, paws, and hooves should all be washed before leaving an infested area, or at the nearest car wash. After removal of soil and plant debris, a disinfectant spray such as Lysol provides extra insurance. Such precautions, though not always easy, are a good practice in any case, considering that exotic weeds and other pathogens can be easily spread from one wildland area to another.
But getting the word out to gardeners and thousands of hikers, bikers, and other trail users has been difficult. Researchers I spoke with say they’re frustrated that their efforts aren’t receiving more attention from regional resource managers, though they recognize that lack of funding is a problem. Very few parks have trailhead signage either warning of the risk of SOD spread or recommending precautions, while warnings about ticks and mountain lions are ubiquitous. State Parks Forester Stephen Bakken notes that human use issues, from campground water treatment to staffing at public beaches, often take priority over problems that don’t directly affect human health and safety.
Rallying legislative support for funding education efforts will be critical, since COMTF lacks the personnel and money for significant outreach efforts. “We rely on mass media, training sessions, word of mouth, written material, [and] then it’s about people power,” says Katie Palmieri, public information officer for COMTF. “Ideally, you’d have volunteers dropping off brochures on doorsteps throughout infected counties.”
Word does seem to be getting out, at least judging by the standing-room-only crowd at a July community meeting in Guerneville organized in part by COMTF. Outreach director Janice Alexander says the task force is available to help citizen groups around the state organize similar meetings.
Even if a massive outreach campaign were mounted, the disease will certainly spread to some degree. What will that mean for our forests? SOD is already having widespread impacts in California. The forest and nursery industries are feeling the economic impacts of regulations governing the movement of lumber, firewood, and plants. Coastal Indian tribes whose cultural traditions depend on oaks, bays, and tanoaks face potentially devastating changes in their forest homelands. Finally, if widespread forest dieback occurs, wildfire risk, habitat loss, and erosion issues will become pressing concerns. As dead wood increases fire danger dramatically, citizens are becoming concerned about fire danger and the absence of effective fire prevention programs.
Sitting on Hall Cushman’s Sonoma County deck, we’re listening to the rustle of oak leaves and gazing at the view of distant Annadel State Park as he speculates on the possible cascade of ecological changes in the forest due to SOD. “Even if you just look at acorn production, it should have a huge impact on a whole variety of mammals and birds. And that’s just talking about acorns. Think about all the insects that feed on the leaves, the shade, the habitat that oaks provide, perching sites, all kinds of things. We have to ask ourselves what [will] replace coast live oak and black oak if there is major dieback?”
The severity and extent of that dieback remain unknown. Contrary to some early predictions, researchers are finding that a significant percentage of true oaks have some resistance to the disease. “Not every oak is going to get infected; not every oak that’s infected is going to die,” says Rizzo. But bay may come to dominate certain areas, and tanoak, now common, may become rare in some places.
I am with Nathan Rank, director of SSU’s Fairfield Osborn Preserve, the site of a number of studies on SOD. Rank is preparing a public seminar on SOD, and we are heading out to the seminar site at Jacob’s Ranch, a recently acquired Sonoma County Agriculture Preservation and Open Space District property. At the ranch, Tom Robinson, a conservation analyst for the district, proudly remarks that with this acquisition, open-space advocates have succeeded in protecting land on most of the major mountains around Santa Rosa. These mountains have been protected from urbanization, logging, and agriculture, three major threats to our California woodlands. But can we protect them from SOD?
We have barely started along the trail when Rank stops next to a bay tree. “Well, we won’t have to go far to show people what SOD looks like,” he comments as he points out the brown-tipped leaves. We continue on our way to the ridge, where we stop to marvel at the “Umbrella Tree,” a magnificent and venerable California bay laurel that can be seen from miles around, across the many acres of oak woodland that surround the Santa Rosa plain. How much will that oak-studded vista change in the decades to come? The answer to that may lie, in part, in the care taken by the hundreds of hikers who make the same trek into the woods.