Dutch Elm Disease

dutch elm disease
Ophiostoma ulmi and O. novo-ulmi
(Buis.) Narruf. (ulmi), Brasier (ulmi)
Last updated by:

Faith Campbell

Dutch elm disease (DED) is one of most devastating diseases of tree species in both North America and Europe (Santini and Faccoli, 2015). DED is caused by two fungal pathogens, Ophiostoma ulmi (Buisman) Nannfield and O. novo-ulmi Brasier (Brasier, 1991). The latter species has since been divided into two subspecies: O. novo-ulmi ssp. novo-ulmi, previously known as the Euro-Asian race (EAN), and O. novo-ulmi ssp. americana previously known as the North American race (NAN). Since the 1980’s, these two subspecies have hybridized and the hybrids are now expanding across the continents. These hybrids have the same level of pathogenicity as the original subspecies. A third species, O. himal-ulmi Brasier and Mehrotra, which also causes DED, was identified in the Himalayas in the mid-1990’s. This third species has not yet been reported in Europe or North America (Santini and Faccoli, 2015).

DED is a story of multiple overlapping introductions leading to disaster. In Europe, several native species of elm bark beetles historically had a mutualistic ectosymbiosis with the indigenous saprotrophic fungus Ophiostoma quercus. Late in the 19th Century the Asian congeneric fungus, O. ulmi s.l. arrived in Europe. This fungus has niche requirements similar to O. quercus but is far more aggressive. O. ulmi replaced the endemic fungus, creating a new association with the native beetles. The beetles became an effective DED transmission pathway, with devastating consequences in Europe. Then both the fungus and the beetle were introduced (separately) to North America, resulting in equally tragic consequences. In the middle of the 20th Century, another Asian pathogen, O. novo-ulmi, was somehow introduced to North America, where it set off an even more lethal epidemic. The new pathogen was then introduced to Europe, where it ignited a second wave, more disastrous than the first.


The disease first appeared in Europe in the 1910s, where it rapidly devastated elm populations (Santini and Faccoli, 2015). It caused the death of 10 – 40% of elms in various European countries (UK Forest Research_History of DED). Around 1940, the disease declined in Europe (Santini and Faccoli, 2015) leading some to conclude that disaster had been averted; however, a second epidemic – caused by a different fungus, Ophiostoma novo-ulmi – became apparent in the United Kingdom in the late 1960’s (UK Forest Research_History of DED). This pathogen was introduced on elm logs imported from Canada (UK Forest Research). To date the second pandemic has killed some 30–50 million elms in the UK alone (Brasier, 2008).

In the United Kingdom, the impact has varied by geography and species. By 1980, most mature English elm (Ulmus procera) in lowland central and southern Britain had died. With disappearance of their primary host, populations of the vector beetle crashed and disease intensity waned. However, growth of suckers from surviving roots of English elm and growth of other elm species led to a massive increase in elm resource across much of southern Britain. As expected, the beetles returned and the disease reappeared by 1991. This cycle is expected to repeat approximately every 20 years (UK Forest Research_DED: central and southern Britain).

The disease spread more slowly in other parts of the United Kingdom. While the U. carpinifolia var. cornubiensis populations of East Anglia and Cornwall (on opposite sides of the country) were eventually killed, many mature wych elms (U. glabra) persist in Scotland and northwest England (UK Forest Research_DED: Cornwall and East Anglia). There are thought to be four principal causes: 1) wych elm does not sucker so the disease is less likely to be transmitted via root grafts, 2) wych elm is much less favored by the bark beetles (although it is more susceptible to the fungus), 3) a competitive fungus rapidly enters the bark of newly dying wych elm, interfering with the elm bark beetles, and 4) the colder climate is probably less conducive to to infectivity.

North America

North America is home to six species of elms; all are vulnerable to varying degrees to the DED pathogen (Brunet and Guries, 2016). The species are American elm (Ulmus americana), slippery elm (Ulmus rubra), rock elm (U. thomasii), winged elm (U. alata), cedar elm (U. crassifolia), and September elm (U. serotina).

American elm was an important floodplain species and was commonly planted along city streets and boulevards because of its graceful form and ability to grow relatively well in the harsh urban environment of high summer temperatures, air pollution, and road salt present in northern latitudes (USDA Forest Service_DED).

The first North American DED epidemic began when O. ulmi was introduced in the 1920’s by furniture makers who used imported unpeeled European elm logs to make veneer for cabinets and tables. DED was detected in Ohio in 1930. One of the beetle vectors of the DED pathogens – Scolytus multistriatus – had reached North America earlier. A second vector is the native Hylurgopinus rufipedes. The disease can also be transmitted by root grafts between adjacent trees (APS_DED; USDA Forest Service_DED).

The disease spread up and down the U.S. East Coast and west across the continent, reaching the West Coast in 1973. More than 40 million American elm trees were killed (APS_DED). By 1976, less than half of the estimated 77 million elms present in urban locations before introduction of the DED pathogen remained (USDA Forest Service_DED).

In the 1940’s a new, more aggressive, disease appeared in Illinois (USDA Forest Service_DED). This epidemic was determined to be caused by a different pathogen, O. novo-ulmi. It killed many elms that survived the original epidemic (APS_DED). Elms remain numerous in riparian forests, but the trees are much smaller than before the DED epidemic (Marks, 2017; Schlarbaum pers. comm.).

In 2003, a new elm bark beetle from Asia, Scolytus schevyrewi, was detected in Colorado and Utah (LaBonte, 2003). It is now in 22 states; it primarily attacks the widespread alien species, Siberian elm (U. pumila) (USDA Forest Service_DED).

In Canada, the natural range of elms stretches from Nova Scotia to Saskatchewan. DED reached Eastern Canada in the 1940’s (TreeCanada_Tree Killers: DED); the disease spread to Ontario in 1967, Manitoba in 1975, and Saskatchewan in 1981 (BioForest_DED History). The majority of large elms in Eastern Canada died of the disease in the 1970’s and 1980’s (TreeCanada_Tree Killers: DED). The disease does not occur in Alberta or British Columbia where American elms have been widely planted beyond their natural range. Aggressive measures are being taken to prevent the spread of the disease into Alberta (BioForest_DED History).

One factor contributing to DED’s impact in urban areas is the practice of planting elms in rows along streets and walkways. This practice gives rise to two dangers: 1) monocultures increase vulnerability due to lack of species diversity, 2) DED spreads by root grafts to nearby trees – conditions prevalent along city streets (APS_DED).

Disease Cycle and Spread

The fungi that cause DED are spread by elm bark beetle vectors – especially the introduced smaller European elm bark beetle (Scolytus multistriatus) and the native elm bark beetle (Hylurgopinus rufipes) (APS_DED). DED infectibility and virulence are mainly due to a synchrony between the life cycles of the host tree, pathogen, and elm bark beetle vectors. Beetles attack the tree in the spring, when host plants are more prone to be infected and temperatures are favorable to the fungus growth, enhancing the pathogen’s aggressiveness (Santini and Faccoli, 2015).

The pathogen infects healthy trees when newly emerged bark beetles feed on twigs or small branches. As the beetles feed, they introduce the pathogen spores attached to their body into the sapwood. The fungus quickly spreads throughout the tree in the vessels of the xylem, aided by the production of cell wall-degrading enzymes (Svaldi and Elgersma, 1982). The tree responds by developing tyloses that close off its vascular system and disrupt water movement. This causes the tree to wilt and eventually die. When the fungus reaches the root system, it can infect adjacent trees through root grafts. As trees die, they become more attractive to the next generation of beetles, which form breeding galleries in the recently dead or dying stems and branches of infected trees. The fungus sporulates in the galleries, and spores are picked up by the young beetles maturing in the galleries. This third generation of beetles then carry the spores to a new, healthy host (USDA Forest Service, 2011). For more complete descriptions of the extremely complicated disease cycle, see APS website or Santini and Faccoli (2015).

As noted, breeding elm bark beetles attack trees that are dying or stressed and weakened by various factors (e.g., drought, diseases, pruning, defoliations). They are attracted by a blend of volatiles released by damaged or diseased elms or, later in the process, aggregation pheromones released by conspecific insects. The result is heavy colonization. (Santini and Faccoli, 2015). Scientists have raised concern that the newly detected elm zigzag sawfly (Aproceros leucopoda) might exacerbate the impacts of DED.

Control Strategies

For several decades, cities and foresters tried to minimize the impact of DED to urban and suburban elms by controlling the bark beetles. This involved widespread use of insecticides. (This practice was criticized by Rachel Carson in Silent Spring). The tactic failed (USDA Forest Service_DED).

Sanitation efforts to limit populations of beetles and facilitate spread were more successful (USDA Forest Service_DED). Removal of infected materials can significantly reduce the disease spread of new infections. However, sanitation efforts – removing infected trees and prohibiting the storage of elm wood with attached bark – must be carried out promptly and thoroughly. The fungus can persist in the sapwood for several years after trees die. Sanitation also requires breaking connections between trees’ roots, which is difficult and expensive (USDA Forest Service 2011).

Individual trees can be protected by injection of chemicals, e.g., methoxychlor (CABI). Because the chemicals are injected in the lower stems or upper roots and can only move upward in trees, these treatments are ineffective for root-graft infections. As always, this costly method is appropriate only for high-value trees (USDA Forest Service, 2011).

Efforts to enhance numbers of elm trees with genetic resistance to the Ophiostoma pathogens have been under way for decades. Historically, the objective was to develop DED-resistant elm cultivars to use in urban/suburban plantings. (An alternative strategy is to plant trees not susceptible to the DED pathogen, such as Asian elms or ash trees. [See EAB profile for more info.]) More recent efforts also aim to generate trees suitable for species restoration in rural forests. The focus is on finding remaining healthy, mature American elms and facilitating their reproduction.

Efforts to cross American elm with Asian elms that have some level of resistance to DED have failed, likely due to some incompatibility barrier located on the surface of the flower stigma (Ager and Guries, 1992). While most American elms are tetraploid (i.e., they contain four chromosomes per cell), more than 20% of trees from a range-wide collection are diploid (two chromosomes per cell), like all other elm species (Brunet and Guries, 2016). This finding would seemingly open the possibility of trying, once again, to cross-breed with Asian elms. The focus, however, has shifted to North American elms which have apparently survived the disease to breed trees with greater tolerance to DED and adaptation to conditions in various parts of the species’ huge range.

Since the 1930’s there have been several entities working to breed or select American elms that are tolerant to DED (Marcotrigiano, 2017). Together these programs have tested over 100,000 elm seedlings and clones and have found only a handful with high levels of DED tolerance – some of which are now commercially available (e.g. Valley Forge, Princeton), and commonly planted in cities and towns (Giblin, 2017). While planting DED-tolerant American elm cultivars is acceptable in urban forests, genetically diverse, locally adapted populations of DED tolerant American elm will be required before restoration of rural elm can commence. Toward this goal, The USFS Northern Research Station initiated the American Elm Breeding and Restoration project, which focuses on testing DED tolerance in large survivor American elm trees while also improving methods for testing and assessing DED tolerance. This project aims to ensure the retention of the American elm in forested landscape and provide future trees that are tolerant to new forms of DED that can be added to existing restoration sites to increase genetic diversity (USDA Forest Service_DED).

The American Elm Restoration Project (AERP) has a growing number of partners, including Ohio DNR Division of Forestry, Franklin County Metro Parks, and The Wilds; Northeastern Area State and Private Forestry, Luther College (Iowa), the U.S. Army Corps of Engineers, the Chippewa National Forest, and the Carpenter St. Croix Valley Nature Center (MN); USFWS; Bad River Indian Reservation (WI); TNC in New England (USDA Forest Service_DED; Cornelia Pinchot pers. comm.).

By crossing trees identified in this program, scientists hope to develop three separate genetically-diverse populations of American elm trees that are both DED-tolerant and adapted to growing conditions in New England, the lower Midwest, and the upper Midwest (USDA Forest Service_DED). The eventual goal is to enlist additional partners to establish locally adapted populations of DED tolerant American elm throughout the species’ range (Cornelia Pinchot pers. comm.)

Finally, many of the elm varieties resistant to DED as of a decade ago were susceptible to elm yellows. (USDA Forest Service 2011). Scientists are researching techniques to test trees’ tolerance to the causal phytoplasma (C. Pinchot, pers. comm.).


APS_DED: Dutch Elm Disease by Cleora J. D’Arcy, University of Illinois https://www.apsnet.org/edcenter/disandpath/fungalasco/pdlessons/Pages/DutchElm.aspx [Last updated 2005]

BioForest_DED History: BioForest Technologies Inc.  http://www.dutchelmdisease.ca/history/

Brunet J. and R.P. Guries. 2016. Elm Genetic Diversity and Hybridization in the Presence of Dutch elm Disease. Proceedings of the American elm restoration workshop.

CABI. Insecticides for control of bark beetles that spread Dutch elm disease [Ceratocystis ulmi https://www.cabi.org/isc/abstract/19850699620

Giblin, Chad P. 2017. “Pruning cycles and storm damage: are young American elms failing prematurely?.” In: Pinchot, Cornelia C.; Knight, Kathleen S.; Haugen, Linda M.; Flower, Charles E.; Slavicek, James M., eds. Proceedings of the American elm restoration workshop 2016; 2016 October 25-27; Lewis Center, OH. Gen. Tech. Rep. NRS-P-174. Newtown Square, PA: US Department of Agriculture, Forest Service, Northern Research Station: 122-132., pp. 122-132.

Green, S., D.E.L. Cooke, M. Dunn, L. Barwell, B. Purse, D.S. Chapman, G. Valatin, A. Schlenzig, J. Barbrook, T. Pettitt, C. Price, A. Pérez-Sierra, D. Frederickson-Matika, L. Pritchard, P. Thorpe, P.J.A. Cock, E. Randall, B. Keillor and M. Marzano. 2021. PHYTO-THREATS: Addressing Threats to UK Forests and Woodlands from Phytophthora; Identifying Risks of Spread in Trade and Methods for Mitigation. Forests 2021, 12, 1617 https://doi.org/10.3390/f12121617ý

LaBonte, J.R. 2010. The Banded Elm Bark Beetle, Scolytus schevyrewi Semenov (Coleoptera, Curculionidae, Scolytinae) in North America: a taxonomic review and modifications to the Wood (1982) key to the species of Scolytus Geoffroy in North and Central America. Zookeys. 2010; (56): 207–218. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088333/

Marks, C.O. 2017. The ecological role of American elm (Ulmus americana L.) in floodplain forests of northeastern North America, In: Pinchot, Cornelia C.; Knight, Kathleen S.; Haugen, Linda M.; Flower, Charles E.; Slavicek, James M., eds. Proceedings of the American elm restoration workshop 2016; 2016 October 25-27; Lewis Center, OH. Gen. Tech. Rep. NRS-P-174. Newtown Square, PA: U.S. Department of Agriculture, Forest Service, Northern Research Station: 74-98.
Marcotrigiano, M., 2017. Elms Revisited. Arboriculture & Urban Forestry, 43(6). https://www.fs.usda.gov/treesearch/pubs/54950

Santini, A. and M. Faccoli. 2015. “The elms after 100 years of Dutch Elm disease”. 3rd International Elm Conference, Florence (Italy -2013) [©iForest – Biogeosciences and Forestry has detailed description of beetle/host interactions, seasonality of infectivity]

Svaldi, R. and Elgersma, D.M., 1982. Further studies on the activity of cell wall degrading enzymes of aggressive and non‐aggressive isolates of Ophiostoma ulmi. European Journal of Forest Pathology, 12(1), pp.29-36.

TreeCanada_Tree Killers: DED: https://treecanada.ca/resources/tree-killers/dutch-elm-disease/

UK Forest Research: https://www.forestresearch.gov.uk/

UK Forest Research: History of DED: https://www.forestresearch.gov.uk/tools-and-resources/fthr/pest-and-disease-resources/dutch-elm-disease/dutch-elm-disease-history-of-the-disease/

UK Forest Research_DED: central and southern Britain: https://www.forestresearch.gov.uk/tools-and-resources/fthr/pest-and-disease-resources/dutch-elm-disease/dutch-elm-disease-central-and-southern-britain/

UK Forest Research_DED: Cornwall and East Anglia: https://www.forestresearch.gov.uk/tools-and-resources/fthr/pest-and-disease-resources/dutch-elm-disease/dutch-elm-disease-cornwall-and-east-anglia/

USDA Forest Service_DED: https://www.nrs.fs.fed.us/disturbance/invasive_species/ded/ [Last modified 6/29/2015]

USDA Forest Service Forest Health Protection Rocky Mountain Region. 2011 Dutch Elm Disease A Non-Native Invasive Wilt. https://www.fs.usda.gov/Internet/FSE_DOCUMENTS/stelprdb5342693.pdf