Sudden oak death


Disease triangle As of 5 May, 2008, there were 45 regulated hosts (hosts proven by Koch's postulates). In 2002 there were only 29. Moreoever, several of the hosts (Camellia, Kalmia, Pieris, Rhododendron, Viburnum) are listed only as genera, and include all species, hybrids and cultivars. An additional 72 plants are considered associated hosts (hosts strongly indicated by isolation or molecular test; up from 31 in 2002 and 58 in 2006). A complete host list can be downloaded from USDA Animal and Plant Health Inspection Service here. Hosts include the following:


Disease triangle The pathogen is a previously unknown species, Phytophthora ramorum, a member of the Oomycota. It produces at least two kinds of spores:

  1. chlamydospores, which are resistant and probably not independently dispersed except with plant matter or soil; and
  2. sporangia that, unlike those in most Phytophthora species, can be deciduous and can germinate directly to infect plants, potentially functioning as airborne conidia as in Phytopthora infestans, the cause of late blight of potato. The sporangia may alternatively give rise to swimming zoospores.

Oospores have not been found in nature, though they may occur. Oospores have been produced in culture by pairing naturally occurring A1 and A2 mating types, both of which occur in Europe.

Other new fungi

Although airborne Phytophthora species that infect above-ground plant parts are known from agriculture, forest pathologists have generally thought of these fungi as soil-borne, root-infecting pathogens. However, looking for Phytophthora ramorum in leaves, stems and branches has opened a window into additional Phytophthora species that had not been studied before. Everett Hansen at Oregon State University has a new species, P. nemorosa, that he will be formally describing shortly, and there are additional new species being found. Some of these cause diseases similar to those caused by P. ramorum, but so far they appear to be less aggressive and are presumably native to western North America.


Disease triangleLittle is known of environmental factors in this disease. The pathogen has a temperature optimum of 15-20 C. The restriction of the disease to coastal areas may indicate restrictive moisture requirements or may simply mean the fungus has not yet had an opportunity to spread to other areas.

The pathogen presumably survives periods unsuitable for growth as mycelium, chlamydospores or as oospores.

Disease Cycle


Strangely, sporulation has not been detected on stem and branch cankers and must be rare if it occurs at all. Thus, the lethal disease on woody hosts apparently does not contribute to inoculum. Hosts that get lethal cankers probably get infected from inoculum produced on foliar hosts. Abundant sporulation has been found on foliar lesions in the field and can readily be induced on lesions in the lab. Lesions on leaves dried for several months can still sporulate.

The pathogen may enter new areas when soil is carried on vehicles or animals or perhaps when infected host material is carried into new areas. The soilborne phase may be mycelium, chlamydospores and perhaps oospores in infested host material, or spores in soil. Inoculum may also be carried in streams. It is most commonly detected by placing a leaf of a highly susceptible host, such as Rhododendron, in the stream as bait.

Infection courts

The pathogen has been found in soil and may be soilborne but infections are exclusively on above-ground plant parts; the fungus does not infect roots. Experimental inoculations indicate that infection can occur without wounding, both on leaves and stems.


As stems die, succulent shoots may wilt and leaves turn brown. Mortality may precipitate or be accompanied by attack by ambrosia beetles, oak bark beetle, the saprot ascomycete Hypoxylon thoursianum, and Armillaria species coming up from the roots.

There is no root infection and cankers do not extend below the soil line.


North America

California. The disease was first reported in 1995 in Mill Valley of Marin County, just north of San Francisco. It is now confirmed in 14 counties of California, from Monterey County in the south to Humboldt county, well into northern California. Humboldt and Contra Costa Counties are recent expansions of the distribution within California. Between 5 and 12% of California's redwood/tanoak forests are infested.

Oregon. The disease was found in southwestern Oregon in July 2001. Near Brookings, in Curry County, Oregon, a number of infection foci were found over an area of nine square miles. An eradication campaign was quickly organized, involving cutting and burning all vegetation in and near the foci. During this process additional foci were discovered and treated. Discoveries continued, however, and as of December 2005, the disease had been found and eradication treatments conducted on 51 sites totaling 88 acres. Monitoring has shown that the pathogen can survive cutting and burning of infested areas. Now treatments include herbicide to prevent sprouting, which can carry the disease, or repeated cutting and burning until no inoculum can be detected. In 2005 and 2006, the number of trees infected and acres infested increased. In 2006, 35 new infested sites were discovered, the highest number since the effort began, and some previous sites expanded. By March 2007, the quarantine area had expanded to over 24 square miles and in January 2008, 162 square miles. It remains to be seen whether this attempt at eradication actually turns out to be more of a slow-the-spread program.

How the fungus made such a large jump (if indeed the forests between Oregon and the California infestation are not more or less continuously infested) is not clear. This disease seems to be spreading as fast as any disease introduced to North America thus far. If there is any reason for optimism at all, it is that, thus far at least, the disease seems to be restricted to coastal areas.

In May 2003 the pathogen was found on some shrubs (arrowwood and andromeda) in a nursery just east of Portland in northwestern Oregon, along interstate highway 5. Apparently the suspicion is that the fungus was introduced there with plants from Europe rather than from the established population in the U.S. To eradicate the pathogen, many plants were destroyed in the nursery, plants recently shipped are being traced and inspected, and the neighborhood within 1/4 mile is being intensively inspected. The nursery has been quarantined to prevent further spread. Since 2003, the pathogen was repeatedly found in Oregon nurseries. In April, 2005, the pathogen was found in four residential landscapes due to a trace-forward from an infested nursery. Genetic evidence suggests that eradication efforts have been successful in nurseries, but the pathogen is reintroduced frequently (®).

Washington. In June 2003 the pathogen was found on rhododendron in a nursery in King County, Washington. This was the first detection in this state. The second was in December 2003, at a nursery in Pierce County. Despite eradication attempts, the nursery continued to test positive. As late as January 2006, the pathogen was found in a stream draining the nursery. Presumably the infestation arose from the infested nursery stock shipped from southern California. In January 2004, the pathogen was detected on rhododendron in a third Washington nursery, in Pacific County. In December 2006 and April 2007, as part of USDA Forest Service national water monitoring protocols, the pathogen was detected in two additional streams in Washington, draining nurseries previously found to be infested.

British Columbia. Also in June 2003, it was found on the same host at a nursery outside Vancouver, British Columbia.

Elsewhere in North America. In early 2004, the disease was found in Monrovia Nursery near Los Angeles, California. This large production nursery ships extensively throughout the United States. Traces of shipments, and surveys in the target states, soon revealed that the disease was present in many other states.

Confirmed positive P. ramorum sites from trace-forward, national, and other surveys, 2004-2007. Blanks represent zeros.
  2004 2005 2006 2007

Other than the Pacific Coast states, there was no confirmation that the pathogen had become established in the wild in any of these states. In April 2007, stream monitoring detected the pathogen in a stream draining a nursery found to be infested in Mississippi. Additional stream sampling in Mississippi led in December 2007 to the detection of an infected willow along a drainage ditch near a nursery. Follow-up sampling has been negative. Infected landscape camellias were detected and eradicated in Harris County, Texas, in March 2008.

Spread of the disease to other parts of the continent and new introductions from abroad are considered likely. The susceptibility of northern red oak and many other important species suggests great devastation may occur if the environment in the eastern U.S. is conducive.


The pathogen itself was discovered and named in The Netherlands (®) at about the same time that the etiology of sudden oak death was being elucidated in California. In Europe the pathogen has been most common in nurseries and gardens on rhododendron and viburnum. The impact on trees in forests has been more limited than in California and Oregon (®). However, in December 2003, the pathogen was found infecting European beech, southern and northern red oak, Holm oak, and horse chestnut trees in the Netherlands and UK. In all cases, the trees were near infected rhododendron.

Recent surveys have discovered the pathogen in the Netherlands, Germany, France, Poland, Italy, Spain, Belgium, Sweden, and the UK. In the UK, where Pieris and Camellia have also been found infected, surveys in 2001 and 2002 showed an apparent rapid infestation of 140 nurseries during that time. Nursery stock is suspected as being the pathway of movement of the pathogen, although genetic evidence suggests that the population in California and that in Europe probably had separate origins. The native range of the pathogen is still unknown.


Realistically, little or nothing can be done to treat infected plants or protect plants from inoculum. An experimental effort to stop local spread in generally infested areas is being conducted in northern California; this consists of removing bay laurel and tanoak, followed by pile and broadcast burning. However, most effort is directed at limiting the spread of the disease into new areas, particularly because the evidence available suggests that eastern oak species are just as susceptible as California oak species in inoculations.

Other Issues

Lineages and mating types. Using molecular phylogenetics, three clades, or lineages, have been found within the species Phytophthora ramorum (®). Analyses revealed no evidence for sexual recombination; the variation observed appears to be due to somatic recombination or mutation. The population in US forests appeared to be almost completely derived from a single introduction. Populations in nurseries, both in North America and in Europe, have more genetic diversity, suggesting that introductions and movement of P. ramorum in nurseries, occurring via trade of infected plant material, have been more frequent than in forests.

In Oregon, the forest population has been dominated by a single genotype that persisted over the years despite eradication efforts, suggesting that eradication has not completely eliminated inoculum sources (®). Nursery populations have been more diverse, including even one genotype from the European lineage. Nuresery populations appear to be eradicated successfully more often than those in forests, but they are also replaced with new introductions more often. Analyses indicate that "leakage" of nursery populations into forests have been rare to date (®,®).

Members of the Oomycota are heterothallic with two mating types (designated A1 and A2); both are required for sexual reproduction. Regarding P. ramorum, originally only A1 mating type was found in Europe, and only A2 was found in North America. Now a few occurrences of the opposite mating types have been found on both continents (see ®). However, there is still no evidence that the fungus is reproducing sexually in nature.

Exotic? Sudden oak death (SOD) is a new disease that became established around the San Francisco Bay of California and has since been found in southern Oregon and Washington and more recently disseminated to other parts of North America.

The fungus is almost certainly introduced to California, and the same species has been found in Europe, but the origin and nature of the introduction are unknown. Virtually all the facts point to a recent introduction:

  1. The disease was unknown until 1995.
  2. The disease is devastating, with little resistance in many of the native hosts.
  3. The disease rapidly expanded its distribution in North America.
  4. Genetic variation of the pathogen in North America and Europe is very limited (®,®), consistent with introduction of only a few genotypes.
  5. The pathogen has been found in Europe in nurseries and gardens. Infection of trees has been uncommon in Europe.

Extent of damage. Sudden oak death may develop into one of the most devastating diseases to hit North American forests, but this is uncertain. Some say its potential was overblown, it is killing relatively unimportant tree species, and doesn't seem to be establishing itself away from the Pacific coast. Even in the 12 California counties that were invaded by 2004, however, the hosts that are readily killed are dominant on 1.5 million acres, and the impact to wildlife and other species may be great (®).

The discovery of the disease on coast redwood and Douglas-fir is another in a line of alarming findings. These are among the most treasured and valued tree species of the Pacific coast. However, occurrence of the disease on these hosts is very limited in distribution and severity, and no symptoms have been seen on overstory trees. Disease on these hosts may be restricted to areas with extremely high inoculum loads (because of more susceptible species, especially bay laurel) and especially conducive environment.


Last modified 11 Feb, 2012