The forest epidemic known as Sudden Oak Death (SOD), first recognized seven years ago, has been spreading in an enlarging fog belt area of California’s central coast and was recently found as far north as southern Oregon. Tens of thousands of native oaks have already been lost.

Detective work by scientists at the University of California Davis and Berkeley has yielded information in record time about the mysterious killer, a primitive brown alga that loves cool climates and water and can be lethal to susceptible trees.

Now officially known as Phytophthora ramorum (meaning “infector of twigs”) this previously unnamed pathogen seems to be a newcomer to the afflicted forests—as were the Asian and European fungi that, respectively, started the Chestnut Blight in 1900 and Dutch Elm Disease in the 1930s, both of which swept across the country. While these earlier epidemics took decades to decipher, a great deal has been learned in a relatively short time about the SOD pathogen since it was identified in June 2000. The structure of this alga is similar to that of another of its genus, Phytophthora lateralis, cause of Port Orford Root Disease, which is killing Port Orford cedars in the cool, moist forests of the Pacific Northwest. Yet we need to know more, so the search for information that will help us deal with the oak epidemic goes on.

No approved chemical treatment exists that will keep the infected trees alive. Much can be done, however, to prevent humans from spreading the disease and to help healthy trees stay strong. Whether California will lose its oaks, as the country lost its American chestnuts and Dutch elms, will depend on multiple factors, not only on this pathogen. It is noteworthy that in none of the infected areas observed has every tree been affected, nor has every infected tree died. Scientists are hopeful, therefore, that some acorns from these long-lived, wind-pollinated trees will provide genes for natural regeneration, albeit slowly. Eventually, it is expected that SOD will become episodic, flaring up only during climatic conditions it favors. At this point, however, it is believed that the epidemic is in an early stage and its spread is likely to continue.

Discovery

The syndrome now called Sudden Oak Death was observed in the mid-1990s in Marin County. On a slope near Mount Tamalpais, facing the entrance to San Francisco Bay, where cool, moist fogs bathe the hillsides, hikers noted that several clusters of tanoaks had turned brown simultaneously as all their leaves died. (Tanoak, Lithocarpus densiflorus, is not a true oak but a close relative.) Arborists also reported dying tanoaks elsewhere, with unusually large swarms of three common bark beetles on the trunks, attracted to cankers that exuded the scent of death.

These beetles are known to burrow and tunnel in the trunks of dead trees to nest and reproduce. Because the pathogen in the Dutch elm epidemic was transmitted by insects, it was natural to assume that they played the same role in this disease. Before long, however, it became clear that that was not necessarily so.

Pavel Svihra, horticulture advisor at the University of California Cooperative Extension in Marin County, investigated reports and consulted other scientists. They were all puzzled. Soon more afflicted trees were discovered just westward and down the slope from the first site Svihra had seen. This tanoak death was occurring with unusual abruptness and spreading rapidly along creek beds, hillsides, and ridge tops. Scientists soon learned that tanoaks were dying with the same rapidity and symptoms in nearby Muir Woods National Monument.

Marin County Agricultural Commissioner Stacy Carlsen called for help from plant pathologists at the University of California, but the pathogen proved elusive. By 1997, not only tanoaks but also coast live oaks (Quercus agrifolia) were dying in the Marin Municipal Water District lands on the other side of Mt. Tamalpais. Almost simultaneously and yet more easterly, trees in China Camp State Park on San Francisco Bay were dying, as were black oaks (Q. kelloggii) farther north.

Many of these trees had large weeping cankers, swarms of beetles, and the green to black fruiting bodies of Hypoxylon fungus, indicating that tree tissues were dying and the trees were severely weakened. This fungus is believed to be in the tree when it is healthy and to break out and grow rapidly in areas of sapwood that die.

Reports of SOD were confirmed in 1995 in Santa Cruz and Monterey Counties, and later in Sonoma County. By 1998 it had become clear that this disease was spreading very rapidly, that its manifestations differed only slightly by oak species, and that it had to be reckoned with. It had erupted in the urban-wildland interface—an area inhabited and visited by millions of people. It was killing trees on public and private lands, threatening residential and forest landowners, parks, industries, water supply, soil retention, and wildlife. Weakened and dead trees could topple, destroying life and property. They also posed a severe fire hazard.

Clearly, the growing epidemic had to be addressed cooperatively by many landowners and land managers. As news of the oak affliction spread, and homeowners pressed county supervisors for investigation and treatment, several state and federal agencies joined to form the nidus for what would be become, in August 2000, the statewide California Oak Mortality Task Force.

Involved early on were the California Department of Forestry and Fire Protection, the California Forest Pest Council, and the U.S. Forest Service. By now this advisory group has grown to over 800 members and over 65 organizations, including government agencies, research groups, nonprofit organizations, business interests, and individuals. It undertook the challenge of establishing a cooperative, unified approach and offering guidance to funders, lawmakers, management agencies, research institutions, and others concerned with the disease.

A New Pathogen

As word of the epidemic spread, reports of hundreds of thousands of alleged victim trees sprang up all over the state. When investigated, however, not all these trees proved to have SOD. To diagnose the disease, foresters looked for stained bark areas exuding beads of viscous, dark red fluid (bleeding cankers). On seeing one, they peeled away the bark. If they discovered jagged black-pigmented lines surrounding large, expanding areas of dead cambium cells, they presumed they had a case of SOD and took samples for laboratory confirmation.

In all trees, the cambium layer of the inner bark, only a few cell layers thick, is the site of living vascular cells that transport to the roots the nutrients manufactured by photosynthesis in leaves. The pathogen appears to kill the bark all around a tree, girdling it and cutting off the flow of nutrients.

That the cause of SOD was a new pathogen was established in 2000 by David Rizzo, a professor of plant pathology at UC Davis, and Matteo Garbelotto, a forest pathologist at the Department of Environmental Science, Policy, and Management in the School of Ecosystem Sciences at UC Berkeley. Garbelotto showed, through DNA analysis, that this alga was a previously unknown member of the genus Phytophthora. Rizzo isolated the new species, P. ramorum, for the first time, making definitive diagnosis possible on a tree-by-tree basis.

When Rizzo grew the pathogen in his lab he found it had several forms of spores. One type, emerging in large numbers from the fruiting bodies, has flagellae that enable it to swim. Another type, a drought-resistant, resting spore known as a chlamydospore, enables P. ramorum to survive in conditions too warm and dry for the pathogen in its usual growth phase. How long this chlamydospore remains viable is not yet known, but perhaps for years. This is worrisome.

Diagnosis of SOD is laborious and can be difficult. Symptoms are bleeding cankers on trunks, leaf spots, and twig dieback. Fruiting bodies of Hypoxylon fungus and massive attacks by three types of bark beetles may be associated with later stages of tree decline. These symptoms occur on coastal live oak, black oak, and Shreve oak (Q. parvula var. shrevei). In tanoak, in addition to the bleeding, new shoots may droop on trees less than 20 feet tall. But this cluster of external symptoms also occurs with a more common root pathogen, Phytophthora cinnamomi—which can also be fatal if trees are watered or conditions are very favorable for the pathogen—and even with some mechanical injuries. Ultimately, diagnosis requires that the pathogen be cultured.

Trees may be infected as long as two years before they die and the infection becomes obvious to the eye. Often no bleeding is present early on, and in any case, a small spot of ooze is hard to notice, or can be washed off by rain.

It is important to keep in mind that SOD is not the only oak killer. It may not even be the greatest current threat to oaks. Throughout the state, oaks are dying massively of many causes. Many have been uprooted to make way for vineyards and other development; many have died because of land use practices that do not take the needs of oaks into account. (Oaks need dry summer conditions and may not survive in an irrigated landscape. ) Oak forests have been weakened by environmental changes such as habitat fragmentation caused by human actions, as well as by drought and by other pathogens (such as the honey mushroom, Armillaria mellea). When trees are weakened, for whatever reason, they become susceptible to diseases and their life spans are shortened.

Where did it come from?

In 2000 Clive Brasier, a forest pathologist from England, visited Marin County to see SOD, and in Garbelotto’s lab was shown the new pathogen in culture. Shortly thereafter he was consulted by a German plant pathologist about a disease that had appeared on rhododendrons grown in European nurseries, causing dieback in estates and parks in Germany and the Netherlands. Suspecting that the culprit was one and the same, he contacted researchers in California, Germany, and the Netherlands and advised them to investigate further.

In December 2000, in a Santa Cruz rhododendron nursery surrounded by dying oak woodlands, a culture was taken from a plant with spotting on its leaves, and a pathogen identical to the one killing oaks was identified.

Meanwhile in Europe, nursery-grown viburnum and rhododendrons were found to be infected, though not dying. Although rhododendrons from the two affected countries had been imported to the United States, we don’t have enough evidence to assume that they were the source of the disease here. Scientists still do not know for certain when, how, and where the epidemic in California started, but it could have begun a decade ago or longer, going unrecognized until 1995.

From the outset, those studying the epidemic searched for vectors that were able to carry the disease to new sites. Humans became prime suspects because most of the areas where the disease was first reported were popular with bikers, hikers, and horseback riders; dogs and cats were implicated as well. Mud clinging to boots, hooves, paws, and tires could easily have carried the spores. When mud samples from well-visited sites were tested for P. ramorum, they proved culture-positive.

Scientists visiting infected zones began to carry extra pairs of shoes, changing into clean pairs before entering their trucks. They now habitually sterilize shoes and tools with alcohol, 10 percent bleach solution, or Lysol, and wash tires upon leaving an infected area. Advisories were posted urging the public to do the same, and to wash animals’ paws and hooves as well. The public was also asked not to take wood, plants, or parts of plants from infected areas, and, especially, not to take them to distant places not already known to have the disease. Moving infected ornamental plants may be even more likely to spread infestation.

As the search for infected trees went on, so did the scientific research into the nature of the disease. In 2000 Jennifer Davidson, a postdoctoral fellow working with Rizzo, proved that the water-loving Phytophthora could be cultured from rainwater splash. She also found that rainwater splashes onto oak trunks at the height where cankers are usually seen, and that bleeding could be started by applying pathogen spores to the outside of a healthy tree. Researchers concluded that the disease could be transmitted in water vapor and rain.

Meanwhile, Rizzo and colleagues discovered suspicious leaf spots and cane dieback on native huckleberry plants at Muir Woods. Samples were taken and cultured, and the SOD pathogen was found. This discovery opened forests to intense new scrutiny. Subsequently, leaf spots indistinguishable from those caused by a number of other pathogens have been found to grow superabundant cultures of P. ramorum. We now know that at least 15 woody plants carry this infection, including bay laurel, madrone, manzanita, toyon, California coffeeberry, and honeysuckle, in addition to viburnum, rhododendrons, and four or more oak species. The infection can be lethal to madrone, but usually is not to the other non-oaks. More host plants will no doubt be identified as time goes on. Clearly, anything—such as birds, lizards, and small tree-dwelling mammals—or anyone moving any of these plants or parts of them around can spread the disease.

Infection with P. ramorum in oaks and understory associates and their soil has now been found in 10 California counties, along a 250-mile-long swath within 50 miles of the Pacific shore, from Big Sur to Mendocino. The affected area includes parts of Sonoma, Santa Cruz, Monterey, Napa, San Mateo, Santa Clara, Solano, and Alameda Counties. Most recently it was discovered in Mendocino County, near Boonville, by arborist Rob Gross.

The alarming news has continued. In August 2001 the U.S. Forest Service and Oregon Department of Forestry detected SOD in tanoaks in Curry County, Oregon, near the California border. Oregon is cutting and burning known hosts in an attempt to eradicate the pathogen. We know that oaks from Mexico to Canada, including those in California’s Sierra foothills, are genetically susceptible, and pin oaks and red oaks on the East Coast tested positive in greenhouse inoculation trials. We don’t know about oaks in Europe and Asia. Because susceptible oaks seem to be limited to the red and black oak groups—the white (valley) oaks in heavily infected areas in Marin County remain healthy—and most European oaks are white oaks, they will likely remain unaffected.

On a hopeful note, there is reason to believe that some oaks are resistant. Oak genes vary from one acorn to the next because oaks are wind-pollinated. In no affected area are all the trees dying, and some infected oaks are even recovering. From this we take heart that forests may regenerate naturally. It will take many more years of experience with this disease through different weather cycles to learn the outcome. Meanwhile, attempts to restore oak woodlands must be undertaken only with greatest caution, so as not to dilute populations that have genetic resistance.

What to do?

What can be done about the awful fact that we are losing enormous numbers of our beloved oaks, many of them in the urban-forest interface near towns? Garbelotto has tested many chemicals as potential defenses against P. ramorum. Most of those used to eliminate other members of this family of plant pathogens have not been found to be effective. One or two show some promise but only when injected repeatedly into each plant. These are not registered for use as fungicides and thus are not legal to use.

The California Oak Foundation has imported from Germany a product called GreenBox, described as a biologically safe compound that has been used to combat some 60 other Phytophthora strains around the world. Tests are being conducted under the supervision of Walter Mark of California State Polytechnic University, San Luis Obispo, in cooperation with Rizzo and Garbelotto. The foundation hopes it can be used to protect oaks near homes and other structures but sees no prospect of mass application to woodlands.

Svihra and others initially recommended using permethrin (ASTRO) against the beetles that were consistently seen at sites of infection and for a time this pesticide was advised for prevention of tree death and widely used. Once the real cause and mechanism of the problem became known, however, pathologists reasoned that it was not worth the cost or the environmental impacts. As yet, Phytophthora has not been isolated from the bodies of bark beetles, which apparently come to trees only when they are already severely weakened and then set about doing their usual work as biodegraders. Therefore the use of permethrins, toxic to many life forms, is now not recommended for treating SOD. Unfortunately, though, the practice of applying this poison has not been abandoned.

California’s Response

Scientists today agree that widespread treatment for SOD may never be available. The current approach to the epidemic emphasizes research to understand how the pathogen functions in the ecosystem, public education aimed at preventing human spread of the infection, safe removal of infected dead trees, monitoring, and possible reuse of the biomass.

The California Oak Mortality Task Force’s current focus is also on predicting risk, defining impacts, and planning for SOD. It is calling for further research to understand oak forests and woodlands and the ways by which the pathogen spreads. Without adequate knowledge, attempts to manage the problem could be futile or even counterproductive. Monitoring is also needed to understand the impact and distribution of P. ramorum. Regulations need to be adopted and implemented. Agreement has to be reached on how quarantines are to be enforced.

All this requires financial resources. So far, more than $9 million has been made available to address the epidemic—over $4 million from the U.S. Department of Agriculture (USDA), primarily for research; $3.7 million from the State of California; and $1 million from a private foundation. Of the State’s money, $1 million is going to infected counties to pay for the removal of trees that pose a threat to life or to property and public works.

At the initiative of Senator Barbara Boxer, $400,000 for research has been included in the USDA appropriation bill for fiscal year 2002. She is seeking $70 million more in federal funding to combat the disease.

Quarantines and Regulations

In May 2001, the California Department of Food and Agriculture imposed a regulation to limit movement of infected woody materials. To protect their forests, Oregon, Canada, and South Korea have imposed similar quarantines on woody materials from counties (including Curry County, Oregon) in which the disease has been found. In August 2000 and again in September 2001, the USDA Forest Service asked the USDA Animal and Plant Health Inspection Service to issue a regulation preventing interstate and international movement of P. ramorum via commodities.

California’s quarantine is difficult to enforce. County commissioners with enforcement responsibility are underfunded and understaffed for such a huge task. Nevertheless, most hard-hit industries, including nurseries, are being very cooperative to help quell the spread of this disease. All have a great deal at stake.

This is a story whose end will not be known for a long time. Learn how SOD looks, learn how to prevent its spread. Keep up with the latest news on the Task Force’s web site, www.suddenoakdeath.org. We who love our coastal oaks and forests have a duty to keep informed, and to abide by quarantines and regulations. Work with others and let your voice be heard when it is needed to support efforts to limit the spread of Sudden Oak Death.

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