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Nightmare on Elm Street

Nightmare on Elm Street. The Elms (genus Ulmus ). - >30 species in genus Europe has 5; N. America 8; Asia has 23 or more. - 2 ssp live in tropics - 6 spps native to the northeastern U.S., including Ulmus americana , the American elm. Many cultivars too.

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Nightmare on Elm Street

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  1. Nightmare on Elm Street

  2. The Elms (genus Ulmus) - >30 species in genus • Europe has 5; N. America 8; Asia has 23 or more. - 2 ssp live in tropics - 6 spps native to the northeastern U.S., including Ulmus americana, the American elm. Many cultivars too. - New species are still being found in China, the center of diversity.

  3. The perfect shade tree • Street liners: fast-growing, easily transported, tolerant of soil compaction and different soil types. Dense canopy borne high above ground, few low branches. • Shade, shelter: When planted in rows, they overhang the street forming a Gothic-style arch. Good for windbreaks. • #1 urban tree in U.S east of the Rockies, and in large parts of Europe and Asia (Heybroek, 1993)

  4. Elms in urban/rural settings • In coastal western Europe, as windbreaks • In dry continental places, the Siberian elm is important. Planted as “shelterbelts” to prevent erosion during the Dustbowl in the 30’s. The most important shelterbelt tree species in the U.S.

  5. In Nature • In general, a riparian, river bottom species (goes through periods of anoxia, explaining it’s tolerance to over-watering and soil compaction). • Long lived (up to 300 years). • Largest trees seem to be most susceptible. • Moller (1992), in Netherlands, 79 ssp of insect are specialized or dependent on elm. Elm seeds are important.

  6. Dutch Elm Disease • Why “Dutch”? First isolated in 1920 by a Dr. Schwarz in the Netherlands. - Wilt disease that attacks elm (Ulmus ssp); caused by ascomycete fungi (genus Ophiostoma, formerly Ceratosystis). Vectored bybeetles (fam. Scolytidae) and root graft. Has a saprophytic and a pathogenic stage.

  7. Life Cycle of Ophiostoma ulmi

  8. Life Cycle of the Disease • Saprophytic stage (in the bark, beetles emerge and carry to healthy tree) and a pathogenic stage (once introduced to a healthy host tree, moves from bark to xylem and begins to attack. May then go back to bark to “reinfect” beetles). • Obligate outcrossers with two sexual compatibility types.

  9. Life cycle of beetles and Ophiostoma are closely matched

  10. 1) Native elm bark beetle (Hylurgopinus rufipes) (above) is the primary vector in parts of the northern United States, New England, and all of Canada. However, temperatures below -6F kill the larvae. 2) European elm bark beetle (Scolytus multistriatus Marsh.) (below) is the major vector of the disease.

  11. Vectors of disease • Insects: 1) the native elm beetle 2) the smaller European elm beetle. The beetles can fly for several miles, allowing the disease to spread over a wide area. • Root grafts: when elms are within 50 feet of one another, their roots can grow together and disease passes easily along. Important in urban settings. • Infected logs: Often transferred long distances in logs.

  12. Management: Sanitation • Includes removing bark from elm logs which are being stored for use as fuel and/or covering or burning all downed wood (so that beetles can’t get in it). AND, removing dead or diseased branches of standing trees (again because of the beetles). • Needs to be community-wide, and coupled w/fungicide use. • Thought of as the most effective way of curbing DED.

  13. Management: Innoculations • Systemic fungicides labeled for preventative control, injected into root flares. Effective on trees showing < 5-10% crown symptoms. • Need new injections every 3 years, expensive.

  14. Management: Spraying • Best when coupled w/sanitation methods. • Timing of spraying is important

  15. Other Management Methods • Development of resistant hybrid elms • Additional treatments: breaking up root grafts is commonly used and efffective. • Timing of pruning: wounded trees attract the bark beetle vectors of DED (Byers et al., 1980), so routine pruning should be done in the dormant season or during periods of beetle inactivity.

  16. History of the Disease (Brasier, 2001) -unknown in Europe and N. America pre-1900. Since then, 2 major pandemics. -caused by 2 different species: 1) Ophiostoma ulmi 2) Ophiostoma novo-ulmi (in both cases, geographic origins unknown- probably Asia)

  17. Pandemic #1 (Ophiostoma ulmi) • Appears in Europe in 1910’s (sweeps across Europe and into Asia); arrives in eastern U.S. in late 1920’s on infested elm timber; transported to Ohio in 1928 via diseased logs. • In Europe it killed 10-40 % of the elms in most countries but by the 1940’s it had slowed, because of the of spread of deleterious viruses. These viruses did not show up in the U.S. and O. ulmi continued to kill trees.

  18. Pandemic #2 (Ophiostoma ulmi-novo) • In the 1940’s, two strains of O. ulmi-novo began a second wave of epidemics: the EAN (Eastern European) strain in Moldova-Ukraine, and the NAN (North American) strain in the Great Lakes region of U.S. Traveled to Asia, W. Europe, and all over the U.S. • Repeated introductions occurred b/c people didn’t realize it was a separate species. • Most mature European elms dead (30 million in UK alone). In N. America, hundreds of millions of elms dead. In these places and in Asia, recurring cycle of recovery of seedlings, and then attack by O. novo-ulmi, are predicted well into the future. • In U.S., in all states besides the desert Southwest.

  19. Spread of O. ulmi and O novo-ulmi

  20. Arrival dates in the U.S.

  21. Dynamics between O. ulmi and O. novo-ulmi • O. ulmi arrives first, but O. novo-ulmi then arrives and outcompetes and replaces. Why? --evolved in tropics vs. temperate --levels of aggression (O. ulmi is moderate pathogen on European elms, O. ulmi-novo is aggressive. American elms are more susceptible to both). Different levels of the cerato- ulmil protein (see later slide).

  22. O. ulmi and O. novo-ulmi: hybridization? • They are anciently diverged taxa but seem to be able to cross under certain conditions, so rare hybrids do occur in nature. These are transient (weak and sterile). But they can act as genetic bridges- allowing unilateral gene flow from one species to the other, when backcrossing occurs.

  23. Hybridization (cont.) • Evidence for gene flow: --has the pathogenicity gene been transferred from O. ulmi to O. ulmi-novo?? • “Field inoculations of the moderately resistant elms Ulmusprocera and Ulmus X Commelin were carried out with progeny of a genetic cross between AST27, a Eurasian (EAN) O. novo-ulmi isolate with an unusually low level of pathogenicity, and H327, a highly aggressive EAN isolate. These confirmed the results of a previous study that indicated that the difference in phenotype was controlled by a single nuclear gene. This pathogenicity gene,designated here Pat1, is the first putative pathogenicity gene to be identified in O. novo-ulmi. (Linkage distances, etc.) suggest that the Pat1 allele conferring unusually low aggressiveness in AST27 may have been acquired from O. ulmi via introgression. “ ( Et-Touil, Brasier, Bernier. 1999. Molecular and Plant Interactions)

  24. Hybridization (cont.) • Evidence for rapid changes in O. ulmi-novo population structure: --Gene acquisition of vegetative compatibility (vc) genes from O. ulmi. (occurs only where O. ulmi and O. novo-ulmi coexist or used to coexist, and the virus is present; allow for resistance to viruses.) --Gene acquisition of virus from O. ulmi? (preliminary data suggests that it’s possible)

  25. Cerato-ulmin • A secreted protein, isolated in 1975, that seems to be directly correlated to aggressive forms of Ophiostoma. May be a “wilt toxin”. • The nucleotide sequences of the cerato-ulmin (cu) genes of two naturally occurring pathogenic CU-deficient mutants, PG470 and MAFf8, of the Dutch elm disease fungus, Ophiostoma novo-ulmi, were determined….. It is likely that the cu gene of MAFf8 has been introgressed from O. ulmi, probably as a result of rare hybrid formation between O. ulmi and O. novo-ulmi, followed by backcrossing of the hybrid with O.novo-ulmi. The presence of an O. ulmi-like cu gene in MAFf8 is consistent with its CU deficiency, since the O. ulmi cu gene is known to be poorly expressed and O. ulmi isolates secrete little or no CU in culture. (Pipe; Brasier; Buck. 2000. Molecular Plant Pathology). • Results from these trials demonstrated that cerato-ulmin was not directly involved in the virulence of the pathogen. All of the epidemiological data, however, indicated a correlation between cerato-ulmin and the pathology of Dutch elm disease. We suggest that the critical evaluation and consideration of these recent data offer opportunities in developing biological control strategies for Dutch elm disease. (Temple and Horgen. 2000. Mycologia)

  26. Hybridization (cont.) • The EAN and NAN forms are hybridizing. -- “swarms of EAN/NAN hybrids are likely to emerge in overlapping sites” (Brasier, 2001) --so O. novo-ulmi is currently undergoing rapid evolutionary development in Europe (accelerated pathogen evolution when it is released from its endemic environment) • Evidence of hybridization in other species as well. --Ophiostoma quercus (saprophytic on oaks) and O. novo-ulmi? --Talk about diversity in O. ulmi and O. novo-ulmi

  27. And.. • The combination of low d-infection frequency, low vc type diversity and the presence of a less efficient Dutch elm disease vector (Scolytus multistriatus) in North America suggests that North American novo-ulmi populations might be potential targets for attempted biological control of Dutch elm disease via the release of d-factors. (Brasier, 1996)

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