sudden oak death

Sudden Oak Death
Biology 101 – Plant Biology
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Sudden Oak Death
Invasive pathogens are emerging as a potent threat to the forest ecosystems because of their ability to infect and wipe out an individual plant species or broad host range; disrupting the biodiversity of the forest ecosystems. Alarming incidents such as jarrah dieback in Western Australia are reminders that plant infections can have devastating effects on the environment (1). In that incident, almost all the tree species were eliminated over a vast area accumulating to 80 000 hectares and converted to grassland or shrubland as a result of the infection by Phytophthora cinnamomi. Sudden oak death is another plant disease of epidemic proportions joining that list of plant pathogens terrorising forest ecosystem from the Big Sur coastline to Oregon in the USA (2). Similar to sudden oak death is sudden larch death, but it poses threat to the larch species, and is now prevalent in Europe (3). The presence of other infected nurseries was sorely underestimated which led to the establishment of Sudden larch death in parts of Europe through the exchange of contaminated soil or nursery stock (3).
This disease has attracted much attention since its discovery because oak and tanoaks are at greatest risk from this infection and they also are important species in many ecosystems. They can serve as food and habitat for animals, serve as barriers against fire outbreak and host mycorrhizal networks (4).

Therefore, extensive loss of such species which serve as the cornerstone of forests system could irreversibly alter the ecosystem.
Initial reports of oak and tanoak dying were reported by concerned homeowners in Marin County which was then investigated in 1995 (2). The disease was hard to characterise as the symptoms were never encountered before. The disease was so rampant, that by 2000, the disease had affected an area encompassing 300km of the central coast of California. From the initial observations, it took 6 years before Rizzo et al identified Phytophthora ramorum as the causal agent from the infected tissues. P. ramorum was first described in the 1990s from the dying ornamental plant species, rhododendron and viburnum in Germany (5). Since then, there was significant progress in addressing the pathology, potential hosts and potential treatments in an effort to find a permanent cure for the disease.
The term ‘sudden oak death’ was derived as a result of the seemingly short duration of the development of disease to the eventual death of the oak trees. However, inoculation studies have disproved this claim as the development of disease can occur over months or years depending on the host genotype and environment (5). Coast live oak, Californian black oak and Californian tanoak are the most susceptible species to P. ramorum mediated infections, although over 40 species are now thought to be potential hosts (6). P. ramorum can either infect the stem/branch which is lethal or infect the foliage/twigs which are nonlethal (6). This review will discuss more on the fungal pathogen P. ramorum, biological effects of this infection and the management of this infection.
P. ramorum is exotic to California, introduced by infected nursery stocks (7, 8). This is more likely as the distribution of the disease is limited as compared to the distribution of the host range. Extensive surveys were conducted over the period of 2003-2005 to test the presence of the pathogen in the ornamental plant nurseries in California, Oregano and Washington. 31,473 samples were collected from the three states in total over the three years of which 1,243 samples were confirmed to be infected with P. ramorum for an overall infection rate of 3.9% (8). Movement of these ornamental plants for commercial or industrial purposes from their native place to a foreign location is now the primary mode of introducing new pathogens into other places. The host species in California have little or no defence against these pathogens as they have not encountered this pathogen before. As a result, the pathogen can infect other species and introduce a new variability into the ecosystem.
The disease is prevalent in oak sections in Lobatae and Protobalanus while oaks in the section Quercus appear to be naturally resistant (5). Tanoaks so far shows the most susceptibility to the infection as seen from the cankers on the stem and branches and the subsequent rapid death (5). Symptoms displayed by the affected hosts differ according to the environmental conditions and the genotype of the plants. Common symptoms include loss of canopy cover, wilting of apical shoots and stem cankers which produces dark brown or amber sap resembling a bleeding wound (2, 6). In the plots monitored by Swiecki & Bernhardt, over the decade, the mortality rate of the coast live oak has doubled and the mortality rate of tanoaks has quadrupled as a result of the infection (9).
Possible route of transfer of pathogen includes the nonlethal infection of foliar hosts such as bay laurel. It serves as the source of inoculum as the propagation propagules are found on the leaves of these foliar hosts but not as much on the oak hosts (10). The sporulation appears to favour moist conditions and mild temperatures such as 20⁰C (7). Once the infection has been established in a host, the spread of the disease is explosive as the propagation propagules can be dispersed aerially between 10 and 15m from the edges of the stand, leading to increased mortality rates of oak and tanoak (4).
The biological effects of P. ramorum infection have adverse effects on the dynamics of the forest ecosystem beyond the individual tree death (11). The forest ecosystem is altered irreversibly because of the change in the composition of the trees which make up the forest as a result of significant loss of various susceptible oak species. In addition, infection of the coexisting plants can undermine the efforts to treat the afflicted trees, promote the spread of the infection and also affect the regeneration of the infected trees (11). Moreover, P. ramorum infections can alter the physiology of coexisting plant species and as such plants who are able to survive or tolerate P. ramorum infections thrive better outcompeting the other plant species. Signs of these kinds of irreversible changes are already documented in California. In the long run, P. ramorum infections can drastically alter the structure and composition of the forest by introducing new selection pressures that affect the survival of forest species. Other effects which can also impact the dynamics of the ecosystem are the alterations in the interactions between P. ramorum and native fungi pathogens. Increase in rate of mortality in many host species associated the synergic interactions between the P. ramorum and other native opportunistic pathogens such as the canker fungus Botryosphaeria dothidea (12). There might also be other impacts on the ecosystems which are still not obvious yet but will be more pronounced in the near future.
Multiple players need to concert their actions to manage the infection at multiple levels. Scientists need to bridge the knowledge gap in the non-scientific community such as the policymakers, environmental groups and the international community by disseminating latest scientific information on the ecological impact of P. ramorum infection on the forest ecosystems and monitoring the plots for the spread of infection, regeneration of the trees and minimising the impact of the infection while maintaining the ecosystem. All these information would be critical in deciding the best course of treatment or prevention at multiple scales; individual trees, different states within the country and internationally. Modelling studies conducted by Cunniffe et al clearly demonstrated that controlling the spread of the P. ramorum infection is no longer feasible in California as a result of lack of timely action and appropriate policies (13). However, lessons learnt from California have not repeated again in Oregon as eradication program was quickly implemented when the infection was found in concentrated pockets of land (14). Therefore, there are a lot more possibilities for the complete eradication of the disease or at least curb the spread of the infection to other areas.
It is also of fundamental importance to contain the infection within the known zones since not much is known about the geographical origin and the epidemiological data of the P. ramorum species. Therefore, engagement with the international community to implement measures such as, controlling the movement of infected stock and soil from USA and Europe (15) to the other countries, paired with close monitoring of the respective countries’ forest ecosystem for any signs of infection by P. ramorum species is essential. Coordinated proactive efforts from the different players at different levels of control will forestall the progression of P. ramorum infection to other parts of the world.
Plants are also affected by pathogens and can be diseased like humans but unlike humans, plants are rarely cured of their disease. Pathogens exposed to plants may be natural or due to human interactions with nature. P. ramorum is an example of how the human actions inadvertently destroy the environment. P. ramorum is the powerful agent which can spread aerially through inducing sublethal infections in foliar hosts and induce biological effects on the ecosystem by; changing the forest composition, introducing new selection pressure and altering the physiology of the sublethal host. Treating it as an inconvenient problem which might clear out on its own or assume it to be an unfruitful venture is not the ideal approach as seen from the example of California. Henceforth, prevention and management of the spread of disease play a more crucial role in protecting the forest ecosystem from mass destruction. It requires large scale efforts by different groups of people such as the researchers, environmentalists, policy makers among others to make informed decisions which would protect the forest ecosystems from further damage.
References
ADDIN Mendeley Bibliography CSL_BIBLIOGRAPHY 1. ADDIN Mendeley Bibliography CSL_BIBLIOGRAPHY Podger FD. Phytophthora cinnamomi, a cause of lethal disease in indigenous plant communities in Western Australia. Phytopathology. 1972;62(9):972-981.
2. Garbelotto M, Svihra P, Rizzo DM, Moritz R. Sudden oak death syndrome fells 3 oak species Exudate from a canker mats in moss on a coast live oak. Calif Agric. 2001;51(1):9-19.
3. Brasier C, Webber J. Plant pathology: Sudden larch death. Nature. 2010;466(7308):824-825.
4. Davidson JM, Wickland AC, Patterson HA, Kristen RF, Rizzo DM. Transmission of Phytophthora ramorum in Mixed-Evergreen Forest in California. Ecol Epidemiol. 2005;95(5):587-596.
5. Rizzo DM, Garbelotto M, Davidson JM, Slaughter GW, Koike ST. Phytophthora ramorum as the Cause of Extensive Mortality of Quercus spp. and Lithocarpus densiflorus in California. Plant Dis. 2002;86(3):205-214.
6. Davidson JM, Werres S, Garbelotto M, Hansen EM, Rizzo DM. Sudden Oak Death and Associated Diseases Caused by Phytophthora ramorum. Plant Heal Prog. 2003;213(July):143-146.
7. Kozanitas M, Osmundson TW, Linzer R, Garbelotto M. Interspecific interactions between the Sudden Oak Death pathogen Phytophthora ramorum and two sympatric Phytophthora species in varying ecological conditions. 2017.
8. Tubajika KM, Bulluck R, Shiel PJ, Scott SE, Sawyer AJ. The occurrence of Phytophthora ramorum in nursery stock in California, Oregon, and Washington states. Plant Health Progress (Online).
9. Swiecki TJ, Bernhardt E. Evaluation of Stem Water Potential and Other Tree and Stand Variables as Risk Factors for Phytophthora ramorum Canker Development in Coast Live Oak. In: Proceedings of the Fifth Symposium on Oak Woodlands: Oaks in California’s Changing Landscape. ; 2002:787-798.
10. Anacker BL, Rank NE, Hüberli D, et al. Susceptibility to Phytophthora ramorum in a key infectious host: Landscape variation in host genotype, host phenotype, and environmental factors. New Phytol. 2008;177(3):756-766.
11. Garbelotto M, Davidson JM, Ivors K, et al. Non-oak native plants are main hosts for sudden oak death pathogen in California. Calif Agric. 2003;57(1):18-23.
12. Maloney PE, Lynch SC, Kane SF, Rizzo DM. Disease Progression of Phytophthora ramorum and Botryosphaeria dothidea on Pacific Madrone. Plant Dis. 2004;88(8):852-857.
13. Cunniffe NJ, Cobb RC, Meentemeyer RK, Rizzo DM, Gilligan CA. Modeling when, where, and how to manage a forest epidemic, motivated by sudden oak death in California. Proc Natl Acad Sci. 2016;113(20):5640-5645.
14. Kanaskie A, Goheen E, Osterbauer N, Mcwilliams M, Hansen E, Sutton W. Eradication of Phytophthora ramorum From Oregon Forests : Status After 6 Years. In: Proceedings of the Sudden Oak Death Third Science Symposium. Santa Rosa; 2007:15-17.
15. Grünwald NJ, Goss EM, Press CM. Phytophthora ramorum: A pathogen with a remarkably wide host range causing sudden oak death on oaks and ramorum blight on woody ornamentals. Mol Plant Pathol. 2008;9(6):729-740.