Biology Reference
In-Depth Information
the disease did not cause concern, and the fungus
was not described until 1943, since when it has
become a major threat to our forest economy and
to trees in residential areas. All native oak species
are susceptible, also chinquapin, chestnut,
lithocarpus (and apples in experimental inocula-
tion); but red oaks succumb most rapidly. Scout-
ing for the disease has been done largely by
airplane, the discolored foliage being visible up
to a half mile.
First symptoms are a slight crinkling and pal-
ing of leaves, followed by progressive wilting,
bronzing, and browning of leaf blades from mar-
gins toward midribs and defoliation progres-
sively downward and inward throughout the
tree. Red oaks almost never recover and may be
killed within 4 to 8 weeks after symptoms appear.
White and burr oaks may persist for some years,
with affected branches dying in a staghead effect.
The first internal symptoms are the formation
of gums and tyloses in the xylem. After wilting,
mycelial mats are formed between the bark and
wood, and the bark cracks from the pressure
exerted. Perithecia are formed in these mats,
which have a sour odor and attract insects. Nitulid
beetles, fruit flies, brentids, springtails, bark bee-
tles, and possibly other insects get conidia and
ascospores on or in their bodies as they feed, and
can inoculate other trees through wounds. We
know that ascospores remain viable several
months on insects and can be distributed through
fecal pellets, but we do not yet know how great
a role they play in the spread of oak wilt. Birds
have been suspected as carriers but are not yet
indicted. Local spread is largely by root grafts,
one tree infecting others within 50 feet and with
grafts possible between red and white oaks, not
limited to the same species.
Control
In residential areas infected trees should
be removed. In forests, felling may wound other
trees and spread the disease more than letting the
dead tree remain but treated so that it is not
infective. Different states handle the problem in
different ways. In Pennsylvania, each infected
tree is cut, with all other oaks within 50 feet,
and ammate crystals are placed on each stump.
In North Carolina stumps and felled trees are
thoroughly sprayed. In West Virginia the trees
are left standing, but a deep girdle into the heart-
wood dries out the tree so that mycelial mats and
spores do not form.
Ceratocystis (Ceratostomella) ulmi (Graphium
ulmi) (see
O. novo-
ulmi
).
Dutch Elm Disease
, on American,
Sibirian, Slippery and European elms in 31 states,
Maine to North Carolina and west to Oklahoma,
and on cedar.
Ophiostoma ulmi and O. novo-ulmi (formerly
Ceratocystis
(
Ceratostomella
)
ulmi
(
Graphium
ulmi
)).
Dutch Elm Disease
, on American,
Sibirian, Slippery and European elms in 31 states,
Maine to North Carolina and west to Oklahoma,
and on cedar. This fatal disease is not really of
Dutch origin but is so named because it was first
investigated in Holland. It was noticed in Europe
about 1918, first in France, then in Belgium and
Holland. It spread throughout central and south-
ern Europe, then into England and Wales. In
many places it virtually exterminated the elms,
including those on the famous avenues at Ver-
sailles. It is suspected that the fungus came to
Europe from Asia during World War I.
Dutch elm disease was discovered in Ohio in
1930 and in New Jersey in 1933. It has spread
north through New England and has become very
serious in the Midwest. In 1948, the disease was
found in Denver, Colorado, and in 1976 in Cali-
fornia. It is now fairly widespread in reports of its
occurrence in the United States. The spread of the
fungus is linked with the presence of the large and
small European bark beetles,
Scolytus scolytus
and
S. multistriatus
. Only the latter is established
in this country, having arrived in Boston about
1919. Patient detective work established the fact
that the fungus came here in elm burl logs
imported for furniture veneer. After one such
infected elm burl was found in Baltimore in
1934, months of scouting went on in the vicinity
of ports of entry, railroad distributing yards, and
veneer plants. Such backtracking showed the
infected material had come in at four ports of
entry and had been carried by 16 railroads over
13,000 miles in 21 states. From this source the
disease got its start in at least 13 areas in 7 states.
Elm nursery stock is, of course, quarantined,
and elm burls are embargoed; but who would
Ophiostoma ulmi
and
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