Transcript Dutch Elm Disease

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.
- New species are still
being found in China,
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)
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.
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.
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 by beetles (fam. Scolytidae) and root
graft. Has a saprophytic and a pathogenic stage.
Life Cycle of Ophiostoma ulmi
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.
Life cycle of beetles and Ophiostoma are
closely matched
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.
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.
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.
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.
Management: Spraying
• Best when coupled w/sanitation methods.
• Timing of spraying is important
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.
History of the Disease (Brasier, 2001)
-unknown in Europe and N. America pre1900. Since then, 2 major pandemics.
-caused by 2 different species:
1) Ophiostoma ulmi
2) Ophiostoma novo-ulmi
(in both cases, geographic origins unknownprobably Asia)
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.
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.
Spread of O. ulmi and O novo-ulmi
Arrival dates in the U.S.
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).
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.
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 Ulmus procera
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)
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)
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)
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
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)