Loading AI tools
Plant disease From Wikipedia, the free encyclopedia
Oak wilt is a fungal disease caused by the organism Bretziella fagacearum that threatens Quercus spp.[3] The disease is limited to the eastern half of the United States; first described in the 1940s in the Upper Mississippi River Valley. The pathogen penetrates xylem tissue, preventing water transport and causing disease symptoms.[5] Symptoms generally consist of leaf discoloration, wilt, defoliation, and death. The disease is dispersed by insect vectors and to adjacent trees through underground root networks. However, human spread is the most consequential dispersal method.[6] Moving firewood long distances can potentially transport diseases and invasive species.
Oak wilt | |
---|---|
![]() Aerial photograph of an oak wilt center (St. Paul, MN) | |
Causal agents | Bretziella fagacearum |
Hosts | Quercus spp. |
Vectors | Nitidulidae |
EPPO code | CERAFA |
Distribution | US |
Symptoms | leaf discoloration, wilt, defoliation and death |
Bretziella fagacearum | |
---|---|
![]() | |
Spores produced by the oak wilt fungus (a) Endoconidia (b) Conidiophore | |
Scientific classification ![]() | |
Domain: | Eukaryota |
Kingdom: | Fungi |
Division: | Ascomycota |
Class: | Sordariomycetes |
Order: | Microascales |
Family: | Ceratocystidaceae |
Genus: | Bretziella |
Species: | B. fagacearum |
Binomial name | |
Bretziella fagacearum (Bretz) Z.W. de Beer, Marincowitz, T.A. Duong & M.J. Wingfield[1] | |
![]() | |
USA counties with oak wilt (2017) | |
Synonyms | |
Oak wilt is a devastating exotic disease, killing some trees rapidly in a single season.[7] Oak wilt is an important disease in urban areas where trees are highly valued. The disease reduces property values because of the loss of trees and is economically costly to the property owner since they or the local government must pay for tree removal. Additionally, preventing the spread of the disease to healthy trees is costly and requires vigilance. Oak wilt is also an important disease in a forest setting, as entire forest stands can die within a few years.[8] There is a narrow window to salvage diseased trees for hardwood lumber and often the disease is not discovered within that logging window.[9] The ecological impacts to forests is also a concern. The disease is currently restricted to North America, but is potentially a serious threat to oaks worldwide.[10]
All Quercus spp. appear susceptible to the disease, with 33 oak species confirmed to be susceptible; including three species of Castanea, one species of Castanopsis, one species of Lithocarpus, and some oaks native to Europe (Q. petraea, Q. pubescens, & Q. robur).[11][12] Generally, red oaks (subsection Lobatae) display more severe symptoms with rapid and frequent mortality (particularly Q. velutina, Q. rubra, Q. ellipsoidalis & Q. coccinea). White oaks (subsection Quercus) develop symptoms more slowly, rarely die, and can recover from the pathogen with damage limited to a few branches (particularly Q. alba, & Q. macrocarpa). Live oaks (Q. fusiformis & Q. virginiana) display intermediate symptoms compared to red or white oaks. However, live oaks are semi-evergreen, can propagate vegetatively by root suckering, and cohabitate with other live oaks in dense stands enabling interconnected root systems. These traits are favorable for local spread of the disease in an oak-grassland savanna.[13]
Oak wilt is one of three devastating North American vascular wilt diseases that appeared in the early 20th century. The other two vascular wilts are chestnut blight (1900–1950) and Dutch elm disease (1928–1980). Each of these diseases have depopulated their respective host tree populations. Chestnut trees were the dominant overstory tree species before chestnut blight and elms were an iconic landscape tree that bordered streets before Dutch elm disease. Oak wilt and the newly emerging emerald ash borer have the potential to devastate other important North American tree species with large geographical and cultural significance. Range expansion of oak wilt to the Western United States (or to other continents) is a major concern.
The asexual stage of oak wilt was first described in 1942 in Wisconsin.[14][15] Soon thereafter the disease was reported throughout the Upper Midwest and Central forests. The early 20th Century coincided with oak regeneration after significant logging in the Mid-Atlantic and Great Lakes region. Deforestation and fire suppression in this region altered the ecology to favor oak–hickory forests, instead of coniferous forests and grasslands.[16][17][18] Subsequently, the host for the disease became more prevalent and promoted oak wilt infections. Moving timber during the late 19th Century and early 20th Century, in the period of railroad expansion, coincides with the discovery of the oak wilt disease in the United States.
The origin of the disease is unknown, but probably emerged from Mexico, Central America, or South America.[19] Mexico is the global center of oak diversity, supporting it as the endemic range of oak wilt.[20][21] Any biocontrol or disease resistance for this pathogen will likely come from Mexico. The disease currently affects much of the eastern and central US, from northern New York to Central Texas.[22] It is particularly common in the Midwest where conditions are usually favorable for spore production and beetle activity during spring and early summer. Oak wilt is a major problem in Illinois, Iowa, Michigan, Minnesota, Texas, and Wisconsin.[23][24][25]
Bottom cycle. Root graft Spread (Expansion of infection center).
The fungus overwinters on dead tissue from diseased trees. Symptoms first appear in spring and summer. Highly susceptible species typically die within one year (often within six weeks) after symptoms appear. Symptoms begin in the tops of trees and can be difficult to notice. The disease progresses inward and downward from the tree top. Leaves become chlorotic beginning at the leaf tip and leaf edges. An abrupt demarcation of chlorotic veins and green tissue is often a distinguishing characteristic in live oak infections.[26] The foliage may droop, curl lengthwise, wilt, and begin to fall. Leaves drop from the tree in the middle of summer, however less susceptible trees may retain leaves longer and resemble seasonal autumn foliage. Highly susceptible species will exhibit rapid crown dieback, while less susceptible species may only lose a few scattered branches. Live oaks may survive several years with progressive dieback, but often die within six months. Following defoliation, fungal fruiting bodies develop from mycelium under the bark of the tree. The mats grow to 10 – 20 cm in size, elliptical in shape, and grey in color with white margins that darken with age. These mats are not found on live oaks and rarely on white oaks. Trees capable of producing mats are called potential spore-producing trees (PSPT). Brown streaks in the sapwood is also observed in the oak wilt disease. However, this symptom is not always associated with the disease.
The oak wilt fungus can spread from diseased trees to healthy trees in several ways. The disease can spread long distances (overland) by airborne spores in open wounds caused by wind damage, pruning, or other mechanical damage. Alternatively, under ideal conditions (temperature, moisture content, wood pH) spore mats form under the bark of the dead tree. Spore mats develop in the spring or fall for 2–3 weeks. The center of spore mats produce chains of barrel shaped spores, called endoconidia. Conidia are asexual spores dispersed by air, rain, and insects.[27] If compatible mating types are present, these mats will also produce sexual spores called ascospores in fruiting structures called perithecia. Ascospores are spread by water and insects.[27] These spore mats (or pressure pads) increase in size, eventually breaking through the bark and releasing a fruity odor that attracts wildlife, including sap beetles, bark beetles, other insects, birds and animals, such as squirrels. Insect vectors transmit the disease in spring to early summer in the Mid-West and late Winter in Texas. Insect transmission is the primary way new infection foci originate.
The fungus can spread short distances through naturally occurring root grafts. Root grafts form when two or more underground roots merge from adjacent trees. Typically, roots from the same, or similar species, can form root grafts as their cambia are pressed together and combine.[28][29] Fungal spores in the xylem travel to nearby trees through these root grafts and can rapidly kill many trees simultaneously. This transmission method accounts for the vast majority of infections and is particularly devastating as groups of trees are killed. The disease can extend 10 – 20m per year (40m per year in Texas) from the infection foci to surrounding trees. Diseased trees can continue to harbor and transmit the disease for several years through the root network.
The disease results from fungal spores clogging xylem vessels and preventing water and nutrient flow. Mycelia growth between and through vessels end up blocking xylem pits in the vessel endwalls. Tylose protrusion and the accumulation of 'gums' will further obstruct vessels. Tylose is an outgrowth of parenchyma cells created as a plant defense against pathogens, water deficiency, wounding, and heartwood formation. Tylose formation signals senescence of adjacent parenchyma cells and secretion of secondary metabolites (called gums), which may include phenolics.[30] The interruption of the xylem vessels precedes tylose formation. Tylose and secreted gums act as a barrier to slow the colonization of the pathogen and play an important part in plant defenses. However, the action to compartmentalize the oak wilt fungus ultimately obstructs all water conductance, leading to death. The fungus can survive in the xylem for multiple years, if the tree is not killed.
Early detection and prompt action are essential for successful management of oak wilt. The specific measures taken depend on several circumstances but should include appropriate combinations of the following:
- Prevent New Infections
- Remove and dispose of oak wilt-infected red oaks immediately.
- Avoid wounding oak trees, including pruning from,
- February through June in Texas.
- April through October in the Mid-West.
- Sterilize/sanitize all pruning equipment between trees.
- Paint all wounds and fresh stumps immediately regardless of season.
- Handle oak firewood cautiously, burn all firewood before spring, and never store unseasoned oak wood from infected trees near healthy oaks.
- Cover unseasoned firewood (from infection centers and unknown origins) with clear plastic and bury the edges of the plastic.
- Diversify Your Landscape
- Plant trees that are native and/or adapted to your area.
- Favor a diversity of tree species.
- Avoid wounding oaks during planting.
- Stop Spread through Root Connections
- Install a trench at least 4 ft deep and 100 ft beyond the perimeter of infection centers (last symptomatic tree) to break up root connections.
- Cut or uproot all trees within the 100-ft barrier (except those injected with fungicide).
- Inject High-Value Oaks with Fungicide
- Identify susceptible, high-value oak trees in proximity to expanding oak wilt infection centers.
- Consult a trained and licensed arborist (with certified applicator's license) for treatment of susceptible trees with injections of propiconazole.
Seamless Wikipedia browsing. On steroids.
Every time you click a link to Wikipedia, Wiktionary or Wikiquote in your browser's search results, it will show the modern Wikiwand interface.
Wikiwand extension is a five stars, simple, with minimum permission required to keep your browsing private, safe and transparent.