Oak Wilt


Oak wilt is a disease of Quercus spp. (oaks). Those in the red oak group (Quercus sect. Lobatae, including black, red, pin, and scarlet oak) are most susceptible. White oaks (Quercus sect. Quercus, bur, overcup, post, white) are more or less resistant. Other members of the Fagaceae may be affected, including chestnut (Castanea), chinkapin (Castanopsis) and tanoak (Notholithocarpus).

Live oaks (evergreen) do not comprise a taxonomic group of species; they occur in both the red oak and white oak sections of the genus. They are characterized by more or less evergreen foliage and oval leaves without distinct lobes. They tend to be fairly susceptible, including those in the white oak group such as Q. fusiformis, Texas live oak.


The pathogen is Ceratocystis fagacearum. It is an ascomycete similar to Ophiostoma and has both sexual perithecia and an asexual conidial stage. Fruiting occurs on dense fungal mats under the bark of recently killed trees.

A new, monotypic genus, Bretziella, has been proposed for this fungus, as molecular phylogeny suggests it does not belong in Ceratocystis or related genera ​[3]​.


Consistent with a wilt disease, symptom expression is exacerbated by hot, dry conditions. On the other hand, the fungus fruits better and vectors are more active under moist, cool conditions. Thus, disease progression is favored by hot, dry conditions, and disease transmission is favored by cool, moist conditions.

Disease Cycle

A few months after the leaves drop, the fungus produces gray mats of mycelium between the bark and wood at various spots on the trunk. Near the middle of the mat, thick ridges of blackish fungal tissue (pressure pads) raise up to crack open the bark.

On the mats, conidia and, if sexually compatible strains are present, perithecia are produced. Perithecia are black with long necks like Ophiostoma. Both kinds of spores are produced in a sticky matrix that facilitates vectoring by insects.

The fungus emits a sweet odor that attracts various beetles especially sap beetles (nitidulids) . The cracking of the bark lets out the odor and lets in the insects, which get coated with spores as they wallow on the mat.

Oak bark beetles breed joyously in diseased trees. When the young emerge, they carry infective spores also. Nitidulids and oak bark beetles operate and transmit the fungus differently.

Oak bark beetles visit healthy oaks and make twig cavities where they feed and transmit the fungus. Nitidulids are attracted to fresh wounds on other trees and transmit the fungus to them. They are active primarily May to June.

The fungus grows primarily in the vessels of the sapwood.

Root-to-root spread through grafts is another form of dispersal and transmission, leading to disease centers. Grafts form most commonly between individuals of the same species and are most common in the red oak group.


Oak wilt in Minnesota.
Oak wilt in Minnesota. Xylem discoloration.

Leaves first fade or turn yellow or bronze and begin to wilt. Then leaf tips and margins become brown and necrotic. In some species, veins become necrotic; this is a diagnostic symptom. Symptoms progress inward and downward in the crown, often accompanied by defoliation, until the tree is dead. In the red oak group the disease may kill the tree in 1-2 months; in the white oak group it may take several years ​[10]​.

The outer annual ring may show brown discoloration where the fungus is actively disrupting xylem. The symptom is more common in white oaks, though it can occur in red oaks. In a cross-section through a diseased branch the discoloration appears as arcs or spotting; in a tangential cut it appears as brown streaks.

Distribution and Damage

Oak wilt is reported only in the U.S. It was first detected in Wisconsin in 1942 and is now known in 22 states. In the early years it was known primarily in the Midwest; it is now common east into the central Appalachians and south into Texas. It appeared in New York in 2008 and has spread since then (see this excellent article for that and more). Except for Texas and a few spots in the Carolinas, it is largely absent from the Gulf and Atlantic coastal states and their coastal live oak populations.

Oak wilt has long taken a heavy annual toll in the Midwest and, more recently, in Texas. In just one mostly urban county in Minnesota, it was estimated that costs only to remove dead trees over a coming decade would be $18-60 million ​[5]​.


Management of oak wilt is not easy but it can be done cost-effectively ​[6, 9]​. Approaches include sanitation, protection, and regulation.

  • Quickly remove and destroy dead oaks to prevent fruiting and transmission.
  • Also destroy neighboring oaks if root spread is suspected.
  • Sever root connections between infected and healthy oaks by trenching.
  • Injection of propiconazole is quite effective at arresting the disease if applied quickly after symptoms first appear ​[4]​.
  • Avoid pruning during periods when mats are produced and vectors are active (spring to mid-summer) ​[10]​. Pruning wounds attract nitidulids. Prune during winter or late summer.
  • If pruning or wounding during the active season is unavoidable, treat with a wound dressing to discourage vectors ​[1]​. This is the only case where a wound dressing is universally recommended.
  • A quarantine is a reasonable exclusionary measure. Among others, California, Canada and Europe have such quarantines, although the details vary. For instance, Canada’s quarantine is against host materials with bark attached from the 22 states known to have the disease. Such quarantines have substantial economic impacts on the forest industry.

Other Issues

Although Ceratocystis fagacearum was long assumed to be native in the US, it has been suggested that it was introduced a century or so ago ​[7]​. This conclusion is based largely on the very low amount of genetic diversity in the species, but also the apparent spread to new areas and the high susceptibility of many native oaks. The disease was not even reported until 1942 and it has become more severe and was found in new areas since then. On the other hand, it has never been found elsewhere. An origin of the fungus in cloud forests of northern South America, Central America, or Mexico has been suggested, and Ceratocystis species from these areas are poorly known ​[7]​. It may cause little or no disease there.

A complicating factor is that, in the US, we are not certain there has been a substantial increase in the range of the pathogen vs. an increase in severity in more of its old range, where it went previously unnoticed. Several factors may explain the disease increase:

  • Transport of firewood from disease-killed trees can move the pathogen into areas where it may not be active. Fruiting mats often form on such firewood, attracting the vectors.
  • Pruning of trees in residential and urban areas creates infection courts. Nitidulid beetles, some of which may have visited mats, are attracted to the pruning wounds.
  • In some areas, the complete loss of chestnut to chestnut blight and the loss of American elm to Dutch elm disease have allowed oaks to colonize areas where they were not abundant before those introduced diseases altered the forest. This may have created new habitat for the pathogen. Reduced forest diversity and increased oak density have also increased opportunities for root-to-root spread in such cases.
  • Forest management has had similar results in some areas, reducing species diversity and increasing density of red oaks, with the same consequences as in the previous point.

Although the disease has not yet been reported from Canada, it was found in Michigan just 500 meters from the border ​[8]​. It is only a matter of time before it is found there. There is increased awareness of and concern for the potential damage from the disease in Ontario ​[2, 8]​.

  1. 1.
    Camilli K, Appel DN, Watson WT. 2007. Studies on pruning cuts and wound dressings for oak wilt control. Arboriculture & Urban Forestry 33(2):132–139 <http://joa.isa-arbor.com/request.asp?JournalID=1&ArticleID=2986&Type=2>.
  2. 2.
    Corrigan J. 2018. Preparing Ontario for an invasive disease: A review of oak wilt management strategies in the Great Lakes region of the United States. Master of Forest Conservation thesis. University of Toronto. 28 pp. <http://www.smithlab.ca/uploads/1/2/0/5/120564888/jessica_corrigan_capstone_2018.pdf>.
  3. 3.
    de Beer ZW, Marincowitz S, Duong TA, Wingfield MJ. 2017. Bretziella, a new genus to accommodate the oak wilt fungus, Ceratocystis fagacearum (Microascales, Ascomycota). MycoKeys 27:1–19 <10.3897/mycokeys.27.20657>.
  4. 4.
    Eggers J, Juzwik J, Bernick S, Mordaunt L. 2005. Evaluation of propiconazole operational treatments of oaks for oak wilt control. Research Note NC-390. USDA Forest Service, North Central Research Station, St. Paul, MN <https://www.fs.usda.gov/treesearch/pubs/13042>.
  5. 5.
    Haight RG, Homans FR, Horie T, Mehta SV, Smith DJ, Venette RC. 2011. Assessing the cost of an invasive forest pathogen: A case study with oak wilt. Environmental Management 47(3):506–517 <10.1007/s00267-011-9624-5>.
  6. 6.
    Juzwik J, Appel DN, MacDonald WL, Burks S. 2011. Challenges and Successes in Managing Oak Wilt in the United States. Plant Disease 95(8):888–900 <10.1094/PDIS-12-10-0944>.
  7. 7.
    Juzwik J, Harrington TC, MacDonald WL, Appel DN. 2008. The origin of Ceratocystis fagacearum, the oak wilt fungus. Annual Review of Phytopathology 46(1):13–26 <10.1146/annurev.phyto.45.062806.094406>.
  8. 8.
    Nienhuis S, Wilson R. 2018. Invasive species in Ontario: The threat, the strategy, and the law. The Forestry Chronicle 94(02):97–102 <10.5558/tfc2018-015>.
  9. 9.
    O’Brien J, Mielke M, Starkey D, Juzwik J. 2017. How to Identify, Prevent and Control Oak Wilt. Report NA-FR-01-11. USDA Forest Service, Northeastern Area, State & Private Forestry, Newtown Square, Pennsylvania, USA <https://www.fs.usda.gov/naspf/index.php?q=publications/how-identify-prevent-and-control-oak-wilt>.
  10. 10.
    Rexrode CO, Brown HD. 1983. Oak Wilt. Forest Insect and Disease Leaflet 29. USDA Forest Service <https://www.fs.usda.gov/Internet/FSE_DOCUMENTS/fsbdev2_043443.pdf>.