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COSEWIC assessment and status report on the Butternut in Canada

Limiting Factors and Threats

The most serious and widespread pressure on butternut is the butternut canker, a disease that was first reported from Wisconsin in 1967 (Renlund 1971). It was originally believed that the causal agent was Melanconis juglandis, and it was not until 1979 that the true pathogen was identified as Sirococcus clavigignenti-juglandacearum (Nair et al. 1979).

Table 2: Summary of Known Occurrences of Butternut in New Brunswick by Estimated Abundance Class
Abundance ClassNumber of AreasNumber of sites

Figure 3: Butternut Distribution in Quebec

Figure 3: Butternut distribution in Quebec (Ministère des Ressources naturelles du Québec, 2002).

Ministère des Ressources naturelles du Québec, 2002).

Figure 4: Quebec Populations where Butternut is ≥ 25% of Basal Area/Canopy Cover

Figure 4: Quebec populations where butternut is ³25% of basal area/canopy cover (Ministère des Ressources naturelles du Québec, 2002).

Ministère des Ressources naturelles du Québec, 2002).

The origin of butternut canker is unknown. However, factors such as its rapid and aggressive spread, the scarcity of resistant trees, apparent lack of genetic diversity in the fungus, and the fact that the oldest cankers appear to be around 50 years old suggests that the disease is a recently introduced exotic (Anderson, 1996). Butternut canker infects all sizes and age classes of trees on all sites and infection can occur through buds, leaf scars and various wounds (Ostry 1995; Davis and Meyer 1997).

Butternut canker can infect and cause mortality in trees of all ages and sizes. Sprouts may be produced, but are generally also infected and do not grow to an appreciable age (Schlarbaum, pers. comm.).

The canker infects trees through leaf scars, buds, lenticels and wounds. Trees are killed by crown dieback or stem girdling. Hyphal pegs (also called stromatal columns) of the fungus rupture the outer bark on branches and stems of infected trees, exposing stromatic tissue and pycnidia of the fungus (Tisserat and Kuntz, 1983). Conidia require free water for release from a gelatinous matrix and are released from pycnidia during periods of rain or high relative humidity (Cree, 1995). Conidia may be carried from branch to branch by rainsplash (Tisserat and Kuntz, 1981). Spores are also carried from the infected crown down the stem by rain wash, causing a number of stem cankers which eventually girdle the tree (Anderson, 1996; Ostry et al., 1994).

During rainstorms, conidia have been trapped in air samples as far as 40 m from the nearest source of inoculum, although spore numbers decreased exponentially with distance from an infected tree (Tisserat and Kuntz, 1983). There is evidence that conidia travel even greater distances (Tissert and Kuntz, 1981). Cankers resulting from natural infection have been found over 100 m from the nearest cankered tree (Tisserat and Kuntz, 1983). Tisserat and Kuntz (1983) concluded that small droplets or aerosols containing conidia could be distributed by wind for distances greater than 1 km. Conidia may survive in an airborne environment for at least 8 hours (Tisserat and Kuntz, 1981).

Following death of a tree, the fungus may continue to sporulate for 20 months (Tisserat and Kuntz, 1984). Several insect species have been found in association with fungus spores on infected trees (Katovich and Ostry, 1998). At least seventeen beetle species have been found to be disease vectors by carrying pathogen conidia (Halik and Bergdahl, 2002). Studies in Quebec have shown that the disease can be transported to new sites on the fruit of black walnut and butternut (Innes, 1998).

Artificial inoculation of black walnut with butternut canker has caused infections, but severe infections in natural stands or plantations have not been found in black walnut.


It is not clear whether resistance to the canker occurs as complete immunity or is present in varying degrees. There are reports of individual trees in infected stands that show no signs of the canker (Ostrey et al. 1994), while other observations suggest trees of varying levels of resistance, but that are nonetheless infected. That is, given the length of time that the butternut canker has been present in the eastern United States, and the reduction in numbers or loss of trees from so many areas, the existence of surviving trees, though infected to some degree, may be evidence of some level of resistance (Schlarbaum, pers. comm.). 

While Ostry et al. (1994) indicate that healthy butternut growing amongst diseased trees may be putatively resistant trees, it has not yet been shown that this putative resistance reflects actual genetic-based resistance.

Butternut Canker in Canada

In Canada, butternut canker was first collected in Quebec in 1990 (Innes and Rainville, 1996), and then in Ontario in 1991 (Davis et al., 1992) and in New Brunswick in 1997 (Harrison et al. 1998). Butternut canker is currently known to exist throughout the range of butternut in Ontario and Quebec, with limited distribution, at present (see Figure 5), in New Brunswick (Hopkin et al. 2001).

Figure 5: Distribution of Butternut and Butternut Canker in Canada

Figure 5. Distribution of butternut and butternut canker in Canada (Hopkin et al., 2001).

Hopkin et al., 2001.

In Ontario, butternut canker was first identified in 1991 by the Forest Insect and Disease Survey (FIDS) unit of the Canadian Forest Service. However, the age of cankers found indicates that the disease had been present in Ontario for at least 20 years. In 1992, the FIDS unit sampled 30 locations in south-western Ontario. The canker was present on 22 of those sites. Whole-tree mortality was most evident in the OMNR Cambridge District where 27% of the trees surveyed had been killed by the disease. Although there was no whole-tree mortality recorded in the eastern half of the province, greater than 90% of the trees examined were infected. Data on growth, health and mortality is collected on growth and yield plots across Ontario. Butternut canker was positively identified in only 3 trees; damage and mortality estimates caused by butternut canker were assumed in the other cases. Records show 40 live butternut trees distributed across 32 plots (Table 3), 17 of which were assessed as potentially infected by canker. Twenty-one dead trees were also recorded with butternut canker listed as the cause for 4 trees.

In Ontario, a voluntary survey of landowners was conducted between 1996 to 1998 to which approximately 500 landowners responded with reports of locations of butternut on their property. Responses from 304 participants provided geographic reference data accurate enough to allow mapping (Figure 6). Of the 500 reports, 263 included data on health of butternut. Trees were in poor condition at 47% of sites for which health was reported. In addition, butternut was identified as a species of concern for the Tree Atlas program conducted from 1996 to 2000. Separate forms were filled out for identified butternut trees with respect to health of the trees located (Figure 6). Tree atlas data indicates that 44% of the 170 individual trees reported on were in poor condition. Tree Atlas data is derived from individual tree forms submitted by volunteer tree atlas surveyors.

Table 3: Summary of OMNR Growth and Yield Data for Butternut in Southern Ontario
OMNR DistrictOntario Township# plots# live treesPotentially cankered# dead treesCanker as possible cause of death
AylmerColchester23 1 
AylmerMosa1  2 
 subtotal 413 
CambridgeLincoln1  1 
 subtotal 1123 
MidhurstGlenelg1  1 
MidhurstOsprey2  52
MidhurstSydenham2  22
 subtotal 7594
TweedS. Fredericksburg11   
 subtotal 1895 
Total  4017214

Butternut canker was positively identified in only 3 trees; damage and mortality estimates caused by butternut canker were assumed in other cases.

Butternut Canker in the United States

In the U.S., the factor having the greatest effect on population size is mortality caused by butternut canker (Sirococcus clavigignenti-juglandacearum V.M.G. Nair, Kostichka and Kuntz ).  Butternut canker was first reported in Wisconsin in 1967 (Renlund, 1971); but the causal agent was not described until 1979 (Nair, 1979). Sinclair (1987) has noted that butternut of all ages and sizes throughout most of its range have signs of the canker. Cankered trees are found growing in mixed and relatively pure stands, on dry, infertile ridgetops with shallow soils, and in moist, fertile bottomlands with deep soils. Infected trees were found in local pockets and over extensive areas (Kuntz et al. 1979, Prey and Kuntz, 1982). Although young butternut has the ability to produce sprouts, asexual sprouts are limited by the fungus and are usually killed in the first year (Ostry et al. 1994).

Figure 6: Tree Atlas Data and Landowner Survey Data for Butternut Health in Ontario

Figure 6: Tree Atlas data and landowner survey data for butternut health in Ontario.

Ostry et al. (1994) indicate that forest inventory data from the USDA Forest Service shows a dramatic decrease in the number of live butternut throughout the United States in the past 10-15 years. The Forest Inventory and Analysis group of the USDA Forest Service reported a 77% reduction in the number of butternut with diameter 5 inches and larger over a 30 year period in North Carolina and Virginia (USDA Forest Service, 2003). Although these results are based on samples, and therefore have some margin of error, they confirm the declines in additional or parallel studies. For example, estimates of the number of butternut infected with the canker in Wisconsin increased from 30 % to 91% between 1976 and 1992, and the number dead butternut trees in the sample areas increased from 8.5% to 27% over the same time period (Cummings Carlson et al. 2004).Tisserat (1984) reported an increase from 5% trees infected to 71% trees infected over a six year period, however this was within one plantation area, which may not be indicative of the natural forest situation. Skilling et al. (1993) have determined that additional surveys are needed to more accurately assess the health of butternut, and several states have now undertaken or are planning to conduct additional surveys.

Disease Symptoms

The following description of butternut canker symptoms has been extracted from "Field Guide to Tree Diseases of Ontario (Davis and Meyer, 1997):

"The most obvious symptoms of the disease are the elongated, sunken cankers, which commonly originate at leaf scars, buds, or wounds. In spring, an inky-black fluid exudes from cracks in the canker; in summer, the cankers appear as sooty black patches, often with a whitish margin. Peeling the bark away reveals brown to black areas of killed cambium. Older cankers can be perennial, are found in bark fissures or loosely covered with shredded bark, and are bordered by successive callous layers. Trees are usually first infected in the lower crown and then die downward as spores from the cankers are washed down. This disease infects trees of all ages and sizes and on all sites. Cankers spread around branches and trunks, eventually girdling and killing the tree".

Disease Control

There is no known control for butternut canker and U.S. researchers suggest that selection of genetically resistant material offers the best potential for recovery programs.

Other Damaging Agents

In addition to butternut canker there are a number of insects and diseases that cause damage to butternut. Only those considered to cause significant damage are included here.

Aside from butternut canker, perhaps the most damaging disease reported on butternut is bunch disease, a witches' broom disease believed to caused by a mycoplasmalike organism (Rink, 1990). Normally-dormant axillary and adventitious buds develop prematurely and form brooms of sucker-like shoots and undersized chlorotic leaves on large limbs and the trunk (Seliskar 1976, Meador et al. 1986). This abnormal growth lacks cold-hardiness and suffers winter-kill. Branches infected with bunch disease do not produce normal nut crops (Berry 1973). In Quebec, one of the most damaging agents in young plantations is Fusarium canker. Phomopsis canker has also been identified in Quebec on tree branches and stems.

There are a number of foliage diseases that are common to butternut as well as to other Juglans species. The most damaging is an anthracnose leaf spot caused by Marssonina juglandis (Lib.) Magnus. This pathogen is reportedly infecting and killing young shoots as well as foliage (Myren 1991; CFS 1994; Black et al. 1977).

Armillaria gallica H. Marxm. & Romagn. has been reported as causing root disease on butternut (McLaughlin, 2001). This species of Armillaria favours hardwood hosts and infects and kills stressed trees. The decline of trees suffering from butternut canker will be accelerated by Armillaria root disease.

The most serious insect pest is the butternut curculio (Conotrachelus juglandis), a beetle that injures young stems and fruit, although damage is usually not major (Rink, 1990). Other insects found on butternut include woodborers, defoliators, nut weevils, lacebugs, and bark beetles (Rink, 1990). Hyphantria cunea (Drury), fall webworm, causes defoliation to a broad range of hardwood trees including Juglans species (Nystron and Britnell 1994). A gregarious feeder (Cannon 1985) that can cause significant defoliation in localized areas when populations are high, it does not cause mortality to healthy trees, although control is sometimes recommended (Anderson 1978). Datana integerrima Grote & Robinson, walnut caterpillar, is common in southern Ontario and the northeastern U.S. (Anon 1985). It feeds on a variety of hardwoods but prefers Juglans species, and is considered an important defoliator of Juglans (Farris and Appleby 1979). 

Acrobasis demotella Grt. is a shoot-borer and one larva can kill a shoot or leader and result in a crooked tree (Martinat and Wallner 1980). It is considered capable of causing serious damage to butternut and walnut in Canada (Nystrom and Britnell 1994).

The common grackle has been reported to destroy immature fruit (Rink, 1990). Butternut is very susceptible to fire and storm damage (Rink, 1990), and is also highly susceptible to frost damage in late spring (OMNR, 2000).