Sudden oak death

  Sudden Oak Death (Phytophthora ramorum) is an oomycete infection which afflicts some oak species and some other trees and shrubs, causing them to die rapidly. It also causes a non-fatal leaf disease in many other plants such as rhododendrons and California Bay Laurel. There is no known cure but new studies show that periodic wildfires help protect against the disease.^[1]

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Presence

The disease is known to exist in California's coastal region between Big Sur (in Monterey County) and southern Humboldt County. It is confirmed to exist in all coastal counties in this range, as well as in all immediately inland counties from Santa Clara County north to Lake County. It has not been found east of the California Coast Ranges, however. It was reported in Curry County, Oregon (just north of the California border) in 2002. [1] About the same time, a similar disease in continental Europe and the UK was identified as Phytophthora ramorum.

Hosts and symptoms

It was first discovered in California in 1995 when large numbers of tan oaks (Lithocarpus densiflorus) died mysteriously, and was described as a new species of Phytophthora in 2000. It has subsequently been found in many other areas including Britain, Germany, and some other U.S. states, either accidentally introduced in nursery stock, or already present undetected.

In tan oaks, the disease may be recognized by wilting new shoots, older leaves becoming pale green, and after a period of two to three weeks, foliage turns brown while clinging to the branches. Dark brown sap may stain the lower trunk's bark. Bark may split and exude gum, with visible discoloration. After the tree dies, suckers will sprout next year, but their tips soon bend and die. Ambrosia beetles (Monarthrum scutellare) will most likely infest a dying tree during midsummer, producing piles of fine white dust near tiny holes. Later, bark beetles (Pseudopityophthorus pubipennis) produce fine red boring dust. Small black domes, the fruiting bodies of the Hypoxylon fungus, may also be present on the bark. Leaf death may occur more than a year after the initial infection and months after the tree has been girdled by beetles.

In Coast Live Oaks and Black Oaks, the first symptom is a burgundy-red to tar-black thick sap bleeding from the bark surface. These are often referred to as bleeding cankers.

In addition to oaks, many other forest species may be hosts for the disease, in fact it was observed in the USA that nearly all woody plants in some Californian forests were susceptible to P. ramorum.^[2] including rhododendron, Madrone (Arbutus menziesii), Evergreen Huckleberry (Vaccinium ovatum), California Bay Laurel (Umbellularia californica), Buckeye (Aesculus californica), Bigleaf Maple (Acer macrophyllum), Toyon (Heteromeles arbutifolia), manzanita (Arctostaphylos spp.), Coast Redwood (Sequoia sempervirens), Douglas Fir (Pseudotsuga menziesii), Coffeeberry (Rhamnus californica), Honeysuckle (Lonicera hispidula) and Shreve's Oak (Quercus parvula v. shrevei). P. ramorum more commonly causes a less severe disease known as Ramorum dieback/leaf blight on these hosts. Characteristic symptoms are dark spots on foliage and in some hosts the dieback of the stems and twigs.^[3] The disease is capable of killing some hosts, such as Rhododendron, but most survive. Disease progression on these species is not well documented but hikers have observed dead Douglas Firs with massive quantities of red frass surrounding their base. Redwoods exhibit needle discoloration and cankers on small branches, with purple lesions on sprouts that may lead to sprout mortality.

Transmission

P. ramorum produces both resting spores (chlamydospores) and zoospores, which have flagella enabling swimming. P. ramorum is spread by air;^[4] one of the major mechanisms of dispersal is rainwater splashing spores onto other susceptible plants, and into watercourses to be carried for greater distances.^[4] Chlamydospores can withstand harsh conditions and are able to overwinter.^[4] The pathogen will take advantage of wounding, but it is not necessary for infection to occur.^[5]

As mentioned above, P. ramorum does not kill every plant that can be used as a host, and it is these plants that are most important in the epidemiology of the disease as they act as sources of inoculum.^[6] In the USA bay laurel seems to be the main source of inoculum in forests. Green waste, such as leaf litter and tree stumps are also capable of supporting P. ramorum as a saprophyte and acting as a source of inoculum. Because P. ramorum is able to infect many ornamental plants, it can be transmitted by ornamental plant movement.

Hikers, mountain bikers, equestrians, and other people engaged in various outdoor activities may also unwittingly move the pathogen into areas where it was not previously present. If you are travelling in an area known to be infested with SOD, you can help prevent the spread of the disease by cleaning your (and your animal's) feet, tires, tools, camping equipment, etc. before returning home or entering another uninfected area, especially if you have been in muddy soil.

The two mating types

P. ramorum is heterothallic and has two mating types identified: A1 and A2. Interestingly A1 is found almost exclusively in Europe and A2 in North America. Genetics of the two isolates indicate that they are reproductively isolated.^[7] On average the A1 mating type is more virulent than the A2 mating type but there is more variation in the pathogenicity of A2 isolates.^[8] Because of the genetic and pathological differences it is believed that if the two mating types remain reproductively isolated then two sub-species will be formed.

Possible origins

P. ramorum is a relatively new disease, and there have been several debates about where it may have originated or how it evolved.

Introduction as an exotic species

Evidence exists that suggests P. ramorum may be an introduced exotic species, and that these introductions occurred separately for the European and NA populations, hence why only one mating type exists on each continent – this is called a founder effect.^[9] The differences between the two populations are thus caused by adaptation to separate climates. Evidence includes little genetic variability, as Phytophthora ramorum has not had time to diversify since being recently introduced. What variability there is may be explained by multiple introductions with a few individuals adapting best to their respective environments.^[10] The behavior of the pathogen in California is also indicative of being introduced; it is assumed that such a high mortality rate of trees would have been noticed sooner if P. ramorum was native.

Where Phytophthora ramorum did originate remains unclear but most researchers feel Asia is the most likely, since many of the hosts of P. ramorum originated there.^[11] Since certain climates are best suited to P. ramorum, the most likely sources are the Southern Himalayas, Tibet or Yunnan province.^[12]

Hybridization events

Species of Phytophthora have been shown to have evolved by the interspecific hybridization of two different species from the genus.^[13] When a species is introduced into a new environment it causes episodic selection. The invading species is exposed to other resident taxon, and hybridization may occur to produce a new species. If these hybrids are successful, they may out compete their parent species.^[14] Thus it is possible that Phytophthora ramorum is a hybrid between two species. Its unique morphology does support this. Also, 3 sequences that were studied to establish the phylogeny of Phytophthora: ITS, cox II and nad 5, were identical supporting Phytophthora ramorum having recently evolved.

A native organism

It is possible that Phytophthora ramorum is a native organism. Infection rates could have previously been at a low level, but changes in the environment caused a change to the population structure.^[15] Alternatively, the symptoms of Phytophthora ramorum may have been mistaken for that of other pathogens. When SOD first appeared in the USA, many other pathogens and conditions were blamed before P. ramorum was found to be the causal agent.^[16] With many of the most seriously affected plants being in the forest, the likelihood of seeing diseased trees is also low.

Control

Early detection

Early detection of P. ramorum is essential for its control, as most studies have shown that treatments work best if applied preventively to stop infection.^[17] Techniques were developed to detect P. ramorum even before it becomes symptomatic. One of the most successful techniques uses a real time polymerase chain reaction assay. Researchers developed PCR primers specific to the ITS region of the genome so that DNA is only amplified if it belongs to P. ramorum. The method is more sensitive than direct culturing, the classical method of pathogen identification. Because fluorescence occurs every time the DNA is replicated, it also allows an accurate quantification of the level of infection.^[18] A Pocket Diagnostic on-site test (lateral flow device) is available that can detect any members of the genus Phytophthora and this is useful for field situations. This test is used by plant health inspectors worldwide at the point of inspection. ^[19] Researchers are investigating microsatellite markers in the pathogens genome, that can be used to detect the pathogen and establish the mating type.^[20]

Researchers have built computer models that predict areas at high risk of epidemic P. ramorum based on the preferred climate and hosts of the pathogen. The models predict infections before they emerge, and areas at high risk can be closely monitored and given preventative treatment.^[21]

Chemical control

Several compounds have been identified that are effective against P. ramorum. The most successful compound to be tested was metalaxyl, but at least one resistant strain of P. ramorum has emerged.^[22] Because of this it is recommended metalaxyl is not used. One of the most effective treatments involves injecting phosphonate into the trunk of the plant. This works best preventively, but also is able to reduce canker size and prolong the life of the tree if applied soon after the symptoms develop. Injection or application directly to the bark when coupled with an organosilicate is the only known viable way to deliver the fungicide.^[22] Copper compounds may also be used for a preventative coating of the trunk.^[23]

Disposal of infected plant material

In general, when plants are found to be infected with P. ramorum they are cut and burned, along with any surrounding host plants regardless of infection status.^[24] This technique has its problems, as the pathogen can survive in the tree stumps, soil, and water as well as re-infecting any sprouts. One solution involves spraying stumps with herbicides to prevent such sprouting. Another way to deal with infected plant material, more specifically green waste, utilizes composting. Because P. ramorum is a cool climate pathogen, the high heat involved in the incubation of compost kills the pathogen after two weeks, including the resting spores.^[25]

References

1. ^ Max A. Moritz and Dennis C. Odion. 2005. Examining the strength and possible causes of the relationship between fire history and Sudden Oak Death. Oecologia 144 106 - 114
2. ^ Rizzo, D.M., et al. Phytophthora ramorum and Sudden Oak Death in California 1: Host Reletionships. in Fifth Symposium on Oak Woodlands: Oaks in California's Changing Landscapes. 2001. San Diego, California.
3. ^ Werres, S., et al., Phytophthora ramorum sp. nov., a new pathogen on Rhododendron and Viburnun. Mycological Research, 2001. 105(10): p. 1155-1165.
4. ^ ^{a b c} Davidson, J.M., et al. Phytophthora ramorum and Sudden Oak Death in California: II. Transmission and Survival. in Fifth Symposium on Oak Woodlands: Oaks in California's Changing Landscape. 2001. San Diego, California.
5. ^ Anon, Phytophthora ramorum and Phytophthora kernoviae: Key findings from research, DEFRA, Editor. 2005, DEFRA.
6. ^ Garbelotto, M., et al., Non-oak native plants are the main hosts for sudden oak death pathogen in California. Californian Agriculture, 2003. 57(1): p. 18-23.
7. ^ Ivors, K., et al., AFLP and phylogenetic analyses of North American and European populations of Phytophthora ramorum. Mycological Research, 2004. 108(4): p. 378-392.
8. ^ Brasier, C., et al. Pathogenicity of Phytophthora ramorum isolates from North America and Europe to bark of European Fagaceae, American Quercus rubra and other forest trees. In Sudden Oak Death Science Symposium. 2002. Marriott Hotel, Montery.
9. ^ Brasier, C., Evolutionary Biology of Phytophthora PART I: Genetic System, Sexuality and the Generation of Variation. Annual Review of Phytopathology, 1992. 30: p. 153-171.
10. ^ Garbelotto, M., et al. Phytophthora ramorum and Sudden Oak Death in California: III. Preliminary Studies in Pathogen Genetics. in Fifth Symposium on Oak Woodlands: Oaks in California's Changing Landscape. 2001. San Diego, California.
11. ^ Martin, F.N. and P.W. Tooley, Phylogenetic relationships of Phytophthora ramorum, P. nemorosa and P. pseudosyringae, three species recovered from areas in California with sudden oak death. Mycological Research, 2003. 107(12): p. 1379-1391.
12. ^ Nicholls, H., Stopping the Rot. PLoS Biology, 2004. 2(7): p. 891-895.
13. ^ Brasier, C. and E.M. Hansen, Evolutionary Biology of Phytophthora PART II: Phylogeny, Speciation, and Population Structure. Annual Review of Phytopathology, 1992. 30: p. 173-200.
14. ^ Brasier, C., Episodic Selection as a force in fungal microevolution, with special reference to clonal speciation and hybrid introgression. Canadian Journal of Botany, 1994. 73 (suppl. 1.): p. S1213-S1220.
15. ^ Rizzo, D.M., et al., Phytophthora ramorum as the Cause of Extensie Mortality of Quercus spp. and Luthocarpus densiflorus in California. Plant Disease, 2002. 86(3): p. 205-214.
16. ^ Garbelotto, M., P. Svihra, and D.M. Rizzo, Sudden oak death syndrome fells 3 oak species. Californian Agriculture, 2001. 55(1): p. 9-19.
17. ^ Rizzo, D.M., M. Garbelotto, and E.M. Hansen, Phytophthora ramorum: Integrative Research and Management of an Emerging Pathogen in California and Oregon Forests. Annual Review of Phytopathology 2005. 43: p. 309-335.
18. ^ Hayden, K., et al., Detection and Quantification of Phytophthora ramorum from Californian Forests Using a Real-Time Polymerase Chain Reaction Assay. Phytopathology, 2004. 94(10): p. 1075-1083.
19. ^ Lane, C.R. et al Evaluation of a rapid diagnostic field test kit for identification of Phytophthora species, including P. ramorum and P. kernoviae at the point of inspection. Plant Pathology 2007
20. ^ Prospero, S., J.A. Black, and L.M. Winton, Isolation and charcaterisation of microsatellite markers in Phytophthora ramorum, the causal agent of sudden oak death. Molecular Ecology Notes, 2004. 4: p. 672-674.
21. ^ Meentemeyer, R. Predicting the Risk of Establishment of Phytophthora ramorum Across California. in Spring 2004 Meeting of the California Oak Mortality Task Force. 2004. Sonoma State University, Rohnert Park.
22. ^ ^{a b} Garbelotto, M., A report on a comprehensive series of experiments, both in vitro and in planta, to develop treatments for P. ramorum, the cause of sudden oak death, Department of Environmental Science, Policy and Management. Ecosystem Sciences Division, University of California, Berkeley. p. 1 - 20.
23. ^ Garbelotto, M., D.M. Rizzo, and L. Marais. Phytophthora ramorum and Sudden Oak Death in California: IV. Preliminary Studies on Chemical Control. in Fifth Symposium on Oak Woodlands: Oaks in California's Changing Landscape. 2001. San Diego, California.
24. ^ Kanaskie, A., et al. An Update on Sudden Oak Death in Oregon. in Spring 2004 Meeting of the Californian Oak Mortality Task Force. 2004. Sonoma State University, Rohnert Park.
25. ^ Garbelotto, M., Composting as a Control for Sudden Oak Death Disease. BioCycle -Journal of Composting and Organics Recycling, 2003.