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OAK WILT - HOW IS THE DISEASE CAUSED?
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THE
OAK WILT DISEASE: All oak species native to North America are
susceptible to oak wilt. The White oaks are somewhat resistant to the
oak wilt fungus. Red oaks and the live oak are highly susceptible and
this includes the Lacey oak, in spite of it being of the white oak
family.
Many people think
that Oak Wilt Disease is caused by the sap sucking bark-beetle (Nitidulidae
species). But that is not strictly true. The beetles fly to
healthy oaks and feeds in the small twigs crotches and upper branches.
It is actually a fungus called Ceratocystis fagacearum, which
is the cause of trouble. The beetles are just one of the means by
which the fungus can be transferred from tree to tree. The beetle
carries the fungal spores from a spore mat developed only on a red oak
that has succumbed from Oak Wilt and died in late summer and early
fall. During the winter months the spore mat grows and develops. By
mid February, as the mats grow, they push and break out the bark. The
fruiting body has a sour oak sap odor that attracts the beetle and as
he feeds, the spores collect of his body. A sort of honey bee or
humming bird effect of gathering pollen.
Live oaks only, spread the disease via inter-grafted root systems
between trees. The disease can trans-locate through the roots systems
at a rate of about a 75 to 100 feet per year. Live oaks are very bad
parents and do not want to compete from their syblings. So the tree
produces a predisposed a soil borne fungus to kill the germination of
the acorn. They depend on wild life to move the acorns to other
locations for forest diversity. Live oaks propagate from ramets or
buds that form on the root system. A grove or a Mott of live oaks is
actually a clone of one tree and survival is guaranteed because the
new tree has the support of a fully developed, mature root system from
it's clone parent so to speak.
During warm spells in the early spring the young beetles
emerge and are able to fly several furlongs or miles to find an oak
tree and feed on the sap. If successful it gives off a scent to alert
its little friends to the picnic. Incisions are made in the branches
to reach the sap and this is the beginning of the end for the tree
because the beetles infect the sap with the fungal spores. Ingestation
takes about four to six months and there are no noticeable effects of
the disease until you see the start of the foliar effects.
The pathogen has to have a healthy living host to survive, it
can not live in the soil or dead wood tissue. Also during pruning,
fresh cut wounds through molecular evaporation emit an oak sap odor
which is like a loud dinner bell to the beetle. The larger the wounds,
the greater the molecular evaporation. When pruning oak trees these
wounds should be painted immediately with a light application of a
spray paint.
The water conducting vessels (the xylem) are
exposed to the beetle-carried spores as the insect feeds through the
bark. Once established, the fungus can move through the tree’s
vascular and phloem systems, resulting in systemic infection. The
initial fungus spread is relative slow and the developing infections
are not apparent until the fungus moves into the larger branches and
then rapid wilting will occur. The disease is also spread from the
same species by interconnected root grafts. Death of a tree infected
through root graft is much more rapid than caused by the beetle.
The fungus is similar to a yeast and this is carried
systemicly along the vascular system in the tree sap. It excretes
digestive substances which are toxic to the tree. The cells in the
wall of the sap-vessels react to it by producing gum-filled
enlargements (TYLOSIS, a
white rubbery substance, a balloon-like enlargement, protruding into
the cavity of a cell), which
then block the vessels. This most possibly is an effort of
defense by the tree to control the spread of fungi, but in doing so it
suffocates / starves itself.
(A defeatist
attitude, kill yourself , kill the disease,
and the effect is like a serious cholesterol problem in humans )
The flow of nutrients and water is stopped and soon the outwards signs
of the disease can be noted: yellowing leaves, tips of the leaves
turn brown, and veinal necrosis (the main
veinal rib turns brown, the area between the veins remains green or
yellow) within a few weeks a dying branch or the entire
tree. There are different forms of the fungus, which may exist side by
side. One is non-aggressive, whereas the other causes the death of the
tree in a very short time.
Tylosis, balloon-like
enlargement, a white rubbery gum, protruding into the cavity of a
cell and then block the vessels. When a limb is cut off or any trpe
of wound, its' normal function is produced, to seal the wound and to
protect the tree from infection.
The Fungicide
"Propiconazole" 14.3 MEC
How does it work?
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A Sterol biosynthesis Inhibitor
Sterols are essential
compounds in the cells of all living organisms, components of cell
membranes and other important anatomical features.
The triazole
fungicide, Propiconazole is effective in management of the oak wilt
disease, it possesses systemic and some curative properties against
certain fungal diseases. It is a highly systemic sterol inhibitor
that penetrates and trans-locates, preventing fungal cell
development, by interfering with cell wall formation and growth
throughout the plant by inhibiting sterol biosynthesis.
Propoiconazole is
absorbed into the fungus where its two modes of action attack fungal
cells at several sites altering the cell, thereby inhibiting
sulfur-containing enzymes and disrupting fungal energy production.
It has preventive activity, and is primarily active on mycelium with
some anti-sporulant activity, and prevents spore germination.The
commercially available formulation of propiconazole 14.3% MEC (microencapsulated)
is available but not limited to; KESTREL®,
Quali-Pro®, and Alamo®,.
Propiconazole at the highest label rate (therapeutic treatment of 20
mils per diameter inch) may provide protection for multiple seasons.
However there is no residual activity in the tree after 23-24
months. The preventive dosage rate is 10 mils per diameter inch for
trees up to 20 inches in diameter and for trees greater than 20
inches diameter due to their value and size, the 20 mil dosage per
diameter inch is highly recommended. Foliar toxicity of
propiconazole is low, even at rates of up to the highest label rate,
though severe phytotoxicity may occur with high dosage rates on
small diameter trees when treated early in the growing season.
Propiconazole does not require high dilution rates with water so
treatment is considerably faster uptake, and there is less tissue
injury at the injection site due to the fact that it has a near
neutral pH.
The injection treatment is not a universal CURE, however it will
extend the life of the tree, and is effective for inhibiting the
disease in uninfected or newly infected trees. Designed for use on
high-value trees in your landscape, trees should be selected for
preventive treatment based on the risk of the disease pressure. The
chemical residual in the tree is effective for about 24 months and
preventive re-treatment should be considered and applied within the
second and third year. Trees that were infected and are in a
weakened condition should be retreated the following year.
Prevention is better than cure.
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