Oak wilt is a vascular wilt disease caused by the fungal pathogen Ceratocystis fagacearum (Bretz) Hunt. It is the most damaging disease of oaks in the United States, especially red oaks in the Section Lobatae (MacDonald et al. 2007; Haugen et al. 2007). Ceratocystis fagacearum is of unknown origin (Harrington, 2007). While most species of Ceratocystis are plant pathogens, only C. fagacearum causes a true vascular wilt (Harrington, 2007). Losses associated with oak wilt have been more limited than relative to other notorious vascular wilt tree diseases such as Dutch elm disease and chestnut blight (Appel, 2007) probably due to complex interactions of insect vectors, transmission through root grafts, and climatic and environmental factors.
The pathogen attacks primarily red oaks in the Section Lobatae but also true live oaks in the series Virentes (Quercus virginiana, Q. fusiformis, Q. minima, Q. geminata, Q. brandegei, and Q. oleoides) and rarely white oaks in the Section Quercus (Nixon, 2007 – see for a discussion of the taxonomic divisions of oaks, and where they are found). Red oaks are also more susceptible to sudden oak death.
Wood anatomy might play a role. White oaks have a greater tendency to create tyloses which can block spread of pathogens within the tree’s vascular system. However, some white oaks – especially live oaks – are very vulnerable to oak wilt (Nixon, 2007).
Oak wilt was first detected in the Upper Mississippi River Valley in 1944; however, it was probably killing oak trees in the Upper Midwest by the late 1800’s. It might have been present in Texas since the 1930’s (Harrington, 2007).
As of 2020, oak wilt is widespread in 22 states, from Minnesota south to Arkansas, east to western Pennsylvania and south through western Virginia to North Carolina, and in 76 counties in central Texas. There are outlying outbreaks in New York, South Carolina, South Dakota, and central Kansas.
[See https://www.fs.fed.us/nrs/tools/afpe/maps/pdf/OW.pdf
or https://usfs.maps.arcgis.com/apps/MapSeries/index.html?appid=9aec8460770d46aa9d073ae7ec2c783e – the latter provides information by which to determine the risk at particular locations, including the proportion of forests comprised of oak and presence of other contributing factors. It lists and provides links to additional sources of information, including by individual states.]
While insects capable of transmitting the pathogen are present virtually throughout the range of eastern oak species, their presence is not sufficient. Disease severity, measured by numbers of oaks killed per acre, area affected, and/or number of disease centers per acre, varies considerably in response to a set of conditions [Juzwik, 2007; NE Region story map]:
- basal area of the best reproductive hosts, red oak. (Appel, 2007; MacDonald et al. 2007; Juzwik, 2007; NE Region story map]
- soil conditions suitable for formation of root grafts (Downing et al. 2007; Juzwik, 2007)
climate and other factors suitable for the vectors. - appropriate environmental conditions to promote disease (MacDonald et al. 2007)
The future of this disease could change rapidly if a more efficient vector were to be introduced. The record of insects found in wood imports shows there were multiple opportunities for new vector to be introduced (MacDonald et al. 2007).
Still, oak wilt has proved highly adaptable, as demonstrated by the severity of disease under the very different conditions in the Midwest compared to Texas. In Texas, oak wilt has reached epidemic proportions in a host population that does not support insect-vectored spread and under temperature conditions that limit formation of mycelial/spore mats essential to insect-vectored transmission (Appel, 2007).
The vulnerability of red oaks paired with the demonstrated adaptability of the pathogen has led some experts to predict that oak wilt would probably be highly damaging in Latin America, where red oaks dominate high elevations and wetter forests from Mexico to Colombia (Nixon, 2007).
Varying disease severity [for specifics, visit the website of your state’s department or division of forestry]
Texas
Oak wilt’s extent and impact in Texas was probably assisted by delayed recognition of the disease; the symptoms exhibited by live oak differ from those on red oak, and the fungus was thought to be impeded by heat (Appel, 2007).
In Texas, the disease has reached extremely high levels in live oaks in the Hill Country of the center of the state. Live oaks (primarily Q. fusiformis) have been colonizing the former grasslands now that fires and overgrazing are under control. Live oaks are also planted as a shade tree. Huge monocultures of live oak exist as a result. As of 2007, oak wilt had not moved into the east Texas pineywoods, despite the presence of large numbers of susceptible oak species (Appel, 2007).
The stand structure of live oaks in Central Texas facilitates transmission of oak wilt disease because the dense stands are closely linked by common or grafted root systems. Transmission of the disease through the roots is sufficiently efficient that it overcomes the limits on insect vectors and formation of mycelian mats created by the climate (Appel, 2007).
In central Texas the disease has had extremely high detrimental impact on property values and the non-economic values from trees. Conservationists also feared that widespread oak mortality would harm the federally listed bird species, golden cheeked warbler (Dendroica chrysoparia) (Appel, 2007; Rooni, 2007). Early results of small studies [Camilli et al. 2007; Greene and Reemts, 2007] indicated the warbler actually prefers habitats where oak wilt is less severe. (The same region also supports Texas ash (Fraxinus texensis), which is vulnerable to the emerald ash borer. The ash provides important habitat for a second endangered bird species, the black-capped vireo (Vireo atricapilla).
Eastern North America
As noted above, oak wilt is widespread in 21 eastern states, but both presence and intensity are highly variable (Appel, 2007; Juzwik, 2007]
In the Appalachians, the vulnerable species include northern red oak (Quercus rubra), scarlet oak (Q. coccinea), and black oak (Q. velutina). Chestnut oak (Q. montana), a white oak, has intermediate vulnerability Macdonald et al. 2007). The following other oaks are also vulnerable: pin oak (Q. palustris), southern red oak (Q. falcata), Shumard (Q. shumardii), and blackjack (Q. marilandica) [NE Region story map].
Because oak wilt fungal mats are most commonly formed on red oak species, the density of red oaks is a significant factor in C. fagacearum spread and disease intensification in forest landscapes. For example, there are much higher frequencies of new oak wilt center establishment in Minnesota and Wisconsin than in Illinois, Pennsylvania, or North Carolina (Juzwik, 2007). In the “Great Lakes” subregion, the basal area of vulnerable red oaks constitutes 7% of total forest basal area, whereas in the “big rivers” subregion to its south, they constitute less than 1%. [FTC calculation from data on NE Region story map].
In the Appalachians, the disease has spread slowly, and severity varies considerably. This has occurred in spite of the presence of the pathogen, insect vectors, and some root graft unions. MacDonald et al. (2007) hypothesize that disease spread is hampered by 1) the diversity of hardwood species in the forest, 2) rocky soil interrupting connections of root systems, and – perhaps – 3) diminished effectiveness of the insect vectors. On the other hand, frequent spring storms in the region create fresh wounds which are necessary for inoculation of new hosts.
Oaks are most vulnerable in spring, when the insect vectors are most active, and the vascular vessels in trees are larger in diameter thus more easily invaded. Also, spring storms cause wounds.
Countering factors in warmer states include the fungus Biscogniauxia (Hypoxylon) atropunctatum, which can quickly colonize oak wilt-killed trees and make the bark unsuitable for production of fungal mats. Furthermore, in dry climates the cambium quickly dries out, preventing mat formation.
Spread Mechanisms
Emergent oak wilt infections result from above-ground transmission of the pathogen by animal vectors, primarily insects (Juzwik, 2007). The types of insect involved varies by geographic region. The primary vectors are sap-feeding nitidulid beetles (Appel, 2007; Judzik, 2007; Hayslett et al. 2007), especially Colopterus truncates, and in some areas also Co. semitectus and Co. niger. In other areas the principal vectors appear to be oak bark beetles, especially Pseudopityophthorus minutissimus and P. pruinosus. Juzwik (2007) describes the sequence of actions by which beetles in these groups acquire and transport the pathogen as well as the role of anthropogenic wounds or beetle-feeding wounds in inoculating a healthy oak. In the case of both beetle groups, most transmission occurs in the spring.
Healthy trees become infected only when an insect introduces the pathogen to a wound. Such wounds can result from storm damage or human activity, e.g., pruning; harvesting and thinning; road or home construction (Haugen et al. 2007). Wounding in the spring is particularly risky because the trees’ vascular vessels are larger diameter so more easily invaded [NE Region story map]. Climate affects transmission in other ways, too. In warmer states, the fungus Biscogniauxia (Hypoxylon) atropunctatum can quickly colonize oak wilt-killed trees and make the bark unsuitable for production of fungal mats. Dry climates further reduce the risk of transmission by quickly drying out the cambium, which can also prevent mat formation.
Humans are also the presumed cause of long-distance spread of the pathogen to previously uninfected areas by moving infected firewood or sawlogs. For example, the presence of oak wilt in Michigan’s Upper Peninsula has been attributed to movement of infected firewood to seasonal-use properties (Haugen et al. 2007).
Outward expansion of disease from the initial site occurs below ground when fungal propagules move through vascular root connections between a diseased and a nearby healthy oak. Red and live oaks commonly form such connections. Haugen et al. (2007) and Juzwik (2007) discuss the role of other factors, including oak basal area (combined measure of tree density and tree diameters), soil depth, soil texture, and occurrence of non-oak species – which can either reduce the incidence of root graft spread when inter-mixed among the oaks or stop the below-ground spread when the type changes within the stand.
The result of these factors is that a high red oak component is critical to sustaining an epidemic and thus of increasing spread frequency (Juzwik, 2007).
Management
Haugen et al. (2007) and Juzwik (2007) discuss management strategies. Additional site-specific and up-to-date information is found on state forestry divisions’ websites. All sources stress the prevention of human transport of infected material (i.e., firewood and logs).
While Texas researchers explored breeding a live oak resistant to oak wilt [Gray and Appel, 2007), this initiative has apparently ended without result.
The USDA Forest Service first funded disease suppression efforts targeting oak wilt from the early 1950’s in to the 1970’s. This took place in Pennsylvania, West Virginia, Kentucky, North Carolina, and Tennessee. The program was ended because it was deemed largely ineffective. Detection of the damaging oak wilt outbreaks in central Texas and southeast Minnesota precipitated renewed interest (Starkey, 2007).
A five-year cooperative federal-state demonstration project during 1982-1987 in central Texas showed both the extent of oak wilt disease and the likelihood of successful suppression. Federal funding of a cooperative federal-state suppression project in Texas began in 1988 with $168,600 which was matched by state and local expenditures; the project is ongoing. A similar project in southeastern Minnesota was begun in 1990. It operated for seven years. After a period without federal funding, cooperative funding resumed in 2002, and continues. Spread in both areas is primarily by root grafts so trenching or plowing to sever these grafts helps stop infection center expansion (Starkey, 2007).
Canada has not yet detected the presence of oak wilt. Concerned about the possibility of its introduction from the United States (several states with infections border Canada), the Canadian Food Inspection Agency (CFIA) led the development of an oak wilt response framework to guide an incursion response. Oak wilt is regulated under the federal Plant Protection Act and various CFIA directives related to imports (Allison et al. 2021).
SOURCES
Allison JD, M. Marcotte, M.Noseworthy and T. Ramsfield. 2021. Forest Biosecurity in Canada – An Integrated Multi-Agency Approach. Front. For. Glob. Change 4:700825. doi: 10.3389/ffgc.2021.700825
Frontiers in Forests and Global Change July 2021 | Volume 4 | Article 700825
Appel, D.N. (2007 June 4-7). Oak wilt biology, impact, and host pathogen relationships: a Texas perspective. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/Appel.pdf
Camilli, K., Appel, D.N., Downing, M.C., Thomas, V.L., and Reich, R.M. (2007 June 4-7). Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/Camilli%20AppelDowningThomasReich.pdf
Downing, M.C., Thomas, V.L., Juzwik, J., Appel, D.N., Reich, R.M., and Camilli, K. (2007 June 4-7). Using classification tree analysis to predict oak wilt distribution in Minnesota and Texas. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/DowningThomasJuzwik.pdf
Gray, M.C. and Appel, D.N. (2007 June 4-7). Attempts to develop an oak wilt resistant live oak. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/GrayAppel.pdf
Greene, T.A. and Reemts, C.M. (2007 June 4-7). Oak wilt research at Fort Hood: Inoculum sources at landscape scale. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/GreeneandReemts.pdf
Harrington, T.C. (2007 June 4-7). The genus Ceratocystis: where does the oak wilt fungus fit? Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/Harrington.pdf
Haugen, L., O’Brien, J., Pokorny, J., Mielke, M., and Juznik, J. (2007 June 4-7). Oak wilt in the north central region. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/HaugenO%27BrienPokornyMielkeandJuzwik.pdf
Hayslett, M., Juzwik, J., Moltzan, B., Appel, D., and Camilli, K. (2007 June 4-7). Insect vectors of the oak wilt fungus in Missouri and Texas. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/HayslettJuzwikMoltzanAppelandCamilli.pdf
Juzwik, J. (2007 June 4-7). Epidemiology and occurrence of oak wilt in midwestern, middle, and south Atlantic states. Proceedings of the 2nd National Oak Wilt Symposium [Symposium] Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/Juzwik.pdf
MacDonald, W.L., Double, M.L. Haynes, S.C. (2007 June 4-7). Oak wilt in the Appalachians. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/MacDonaldandDouble.pdf
Nixon, K.C. (2007 June 4-7). An overview of Quercus: Classification and phylogenetics with comments on differences in wood anatomy. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/Nixon.pdf
Rooni, J.B. (2007 June 4-7). Oak wilt: Its impact on a growing Texas. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/Rooni.pdf
Starkey, D. A. (2007 June 4-7). USDA Forest Service perspective on oak wilt suppression. Proceedings of the 2nd National Oak Wilt Symposium [Symposium]. Austin, Texas. Billings, R.F. and Appel, D.N. (Editors). Copyright 2008. Reprinted with permission (2009).
https://texasoakwilt.org/assets/professionals/NOWS/conference_assets/conferencepapers/Strakey.pdf
Additional sources of information (MAPS):
https://www.fs.fed.us/nrs/tools/afpe/maps/pdf/OW.pdf
or https://usfs.maps.arcgis.com/apps/MapSeries/index.html?appid=9aec8460770d46aa9d073ae7ec2c783e
Photo credit: Joseph OBrien, USDA Forest Service, Bugwood.org