|SUDDEN OAK DEATH IN TEXAS
Texas is currently considered a low-risk area for SOD because it is believed the pathogen prefers cool moist environments like that of coastal California.
Confirmed in Texas: In 5 nurseries that have received nursery stock from Monrovia
Oak mortality is caused by a new pathogen, Phytophthora ramorum
Sudden Oak Death (SOD) is a newly discovered, highly infectious disease caused by a fungus-like organism within the genus Phytophthora. The disease was first discovered in Northern California in 1995 where it has since been implicated in large-scale oak mortality. It is estimated that tens of thousands of tan oaks, coast live oaks and black oaks have been killed on the west coast so far.
The pathogen was isolated and identified in 2000 by researchers from the University of California as Phytophthora ramorum. This is an organism that has previously only been known to exist in Germany and the Netherlands, where it was found infecting Rhododendrons and Viburnums.
What is Sudden Oak Death?
Sudden Oak Death has been classified as an invasive species. These organisms are of great concern because history (by the U.S. Department of Agriculture Animal and Plant Health Inspection Survey - APHIS) has shown that an introduced species has the potential to spread easily with devastating effects. Introduced species often have no natural enemies and have potential hosts with no ecologically adapted defenses.
There are numerous examples of introduced tree pathogens and insects that cause devastating problems including chestnut blight, dutch elm disease, gypsy moth caterpillars, white pine blister rust, hemlock woolly adelgid, and fusiform rust.
Given the severity of the effects that invasive species can cause it is justified to give the Sudden Oak Death situation very serious attention.
The common name "Sudden Oak Death" may be misleading due to both the words "sudden" and "oak". The common name was given because of the apparent rapid decline in crowns of infected oak trees, changing from green to brown in sometimes a matter of just a few weeks. But researchers do not yet know how long the disease actually progresses before death. Also, many infected hosts do not decline "suddenly", or even die at all. The disease seems to manifest itself and progress differently depending on many factors including individual tree characteristics, site factors and the species.
The term "oak" in Sudden Oak Death may be misleading because it does not reflect the potential that this disease has for causing serious problems in a wide variety of potential non-oak hosts.
SOD not only causes severe cankering and rapid death of oaks, but has been found causing foliar and twig blights on numerous other trees and shrubs. There are at least 14 different species of ligneous hosts known to be affected by P. ramorum (for current list, see hosts). Many of these hosts, such as those in the genera Quercus, Arbutus, Acer, and Rhododendron have valuable counterparts in native and planted Texas landscapes.
There are many aspects of SOD that are poorly understood For example, the origin of the California outbreak disease is still unknown. There is no information on how long the disease has been on the West Coast, but there is some speculation that it may have been there for quite awhile and the damage is just now escalating due to the accordance of predisposing stress. Changes in environmental conditions such as climatic change, fire suppression, and alterations in land use patterns have all been implicated in the epidemic.
The array of symptoms observed on different hosts currently cannot be explained and there is an unaccountable variable mortality rate among infected plants.There is also some speculation that it originated in Europe and perhaps transported on infected rhododendrons, but there is no direct evidence yet to support this claim. So far, there is no 'cure' yet for SOD, although research is being conducted in this area.
Although SOD has not yet been identified in the United States outside of California and Oregon, laboratory studies have shown that many species outside the current distribution are potential hosts, including eastern and northern red oak, and pin oaks. The spread of Sudden Oak Death to other parts of the country must be considered, given that the pathogen can be moved great distances by transport in nursery stock such as SOD infected rhododendrons, or in soil and bark products.
For more information about "Sudden Oak Death" at Texas A & M University, contact Dr. David Appel at 979-845-8273 or by e-mail at firstname.lastname@example.org
or Sara Service at 979-587-2701 or by e-mail email@example.com
· Phytophthora ramorum is a newly discovered pathogen, and very little is known about it. There is a great deal of research currently being conducted on the disease and there are national monitoring plans being initiated.
· It is believed that the pathogen can be transported from location to location easily by way of infected nursery stock, soil, and bark from SOD infected areas.
· Phytophthora ramorum has not been detected outside of coastal California and Oregon.
· SOD affects a wide variety of hosts, not only oaks but several other species of trees and shrubs as well.
· There are a wide variety of symptoms associated with SOD including bleeding cankers, twig blights and foliar leaf spots.
· Texas is currently considered a low-risk area for SOD because it is believed the pathogen prefers cool moist environments like that of coastal California.
· Not all infected hosts die from SOD. Mortality is most likely among the oaks.
It is important to note that none of the following known hosts are common to Texas. These plants are all indigenous or adapted to the ecology of central California and Oregon. However, the list of susceptible hosts is expanding, and many of these known susceptible host species have relatives in native and planted Texas landscapes.
Known Phytophthera ramorum Hosts
In Texas there are ten plant genera that this pathogen are known to infect. They are Acer, Aesculus, Arbutus, Pseudotsuga, Quercus, Rhamnus, Vaccinium, Vibunum, Castanea and Fagus. These are the suspect hosts in Texas that are being looked at for those nurseries that have received stock from Monrovia.
SYMPTOMS on Trees
· Brown to Black Cankers on lower trunk · Occasional cankers on higher branches · Oozing dark red to black sap
· Cankers on some species may not bleed · Healthy appearing crown in the early stages
· Later stages: thinning or complete browning of crown · Browning of leaves may occur over a period of weeks
· Beetles and Hypoxylon fungus often move opportunistically into SOD weakened trees · Twig dieback on some species · Spontaneous drooping of new growth on some species (tanoak)
· When the outer bark is removed, a dark zone line is evident delimiting healthy tissue from necrotic tissue
Symptoms on Foliar (non-oak) Hosts
· Leaf spots · Twig dieback SOD on foliar hosts can only be identified by laboratory analysis
Joseph G. O’Brien, USDA Forest Service, Northeastern Area
Manfred E. Mielke, USDA Forest Service, Northeastern Area
Steve Oak, USDA Forest Service, Southern Region
Bruce Moltzan, Missouri Dept. of Conservation
|Oak Disorders That Resemble Sudden Oak Death
In eastern hardwood forests, sudden oak death can be confused, in particular, with oak wilt, oak decline, and red oak borer damage. Descriptions of these disorders and comparisons with sudden oak death follow.
Oak wilt is an aggressive fungus disease caused by Ceratocystis fagacearum. It is one of the most serious diseases in the Eastern United States, killing thousands of oak trees in forests, woodlots, and home landscapes. Susceptible hosts include most oaks in the red oak group and Texas live oak. Symptoms include wilting and discoloration of the foliage, premature leaf drop, and rapid death of the tree within days or weeks of the first symptoms. Trees become infected with oak wilt in two ways: through connections between root systems of adjacent trees, and through insects that carry the fungus to other trees that have been wounded.
Similarities: Oak wilt can also kill trees very quickly, especially if infection begins through root grafts. Differences: The oak wilt pathogen does not cause cankers on the stems, and no bleeding is associated with this disease. Dark staining may be evident under the bark of trees with oak wilt, but there are no conspicuous zone lines. Oak wilt typically causes red oak leaves to turn brown around the edges while the veins remain green. Leaves are rapidly shed as the tree dies. Conversely, in live oak with the sudden oak death pathogen, the veins first turn yellow and eventually turn brown. Leaves are often retained on the tree after it dies.
Oak decline is a slow-acting disease complex that can kill physiologically mature trees in the upper canopy. Decline results from interactions of multiple stresses, such as prolonged drought and spring defoliation by late frost or insects, opportunistic root disease fungi such as Armillaria mellea, and inner-bark-boring insects such as the twolined chestnut borer and red oak borer. Progressive dieback of the crown is the main symptom of oak decline and is an expression of an impaired root system. This disease can kill susceptible oaks within 3-5 years of the onset of crown symptoms. Oak decline occurs throughout the range of eastern hardwood forests, but is particularly common in the Southern Appalachian Mountains in North Carolina, Tennessee, and Virginia, as well as the Ozark Mountains in Arkansas and Missouri.
Similarities: Oak decline can cause death of many oaks on a landscape scale. Moist, dark stains may be present on the trunk of trees affected by oak decline. Differences: Oak decline shows evidence that dieback has occurred over several years from the top down and outside inward. Newly killed branches with twigs attached are usually found in the same crown as those in a more advanced state of deterioration killed years before. Dieback associated with sudden oak death occurs over a growing season or two. The inner bark beneath the dark stain associated with stem-boring-insect attacks has a discrete margin with no zone lines or evidence of canker development beyond the attack site.
|Red Oak Borer
Red oak borer (Enaphalodes rufulus (Haldeman)) attacks oaks of both red and white groups throughout the eastern United States, but prefers members of the red oak group; however, it does not kill trees. Outbreaks are associated with stressed trees that eventually die from oak decline. The complete life cycle takes 2 years. Adults are 1-1.5 inches long with antennae one to two times as long as the body. Larvae are the damaging life stage. Adult females lay eggs in mid-summer in refuges in the crevices of the bark. Newly hatched larvae bore into the phloem, where they mine an irregular burrow 0.5-1 inch in diameter before fall. In spring and summer of the second year, dark, moist stains and fine, granular frass may be seen on the trunk. Exposure of the inner bark reveals the frass-packed burrow and the larva, if it has not bored more deeply into the wood to complete development. Mature larvae are stout, round-headed grubs about 2 inches long before they pupate deep in the wood.
Similarities: Moist, dark stains and fi ne frass may be present at sites of red oak borer attack. Differences: With red oak borer the inner bark beneath the dark stain contains a frass-packed burrow and has a discrete margin with no zone lines or evidence of canker development beyond it.
|(Slime Flux) in Trees
Dark amber liquid Ooze bleeds out of canker wound
Description and Diagnosis
Bacterial wetwood involves a liquid that oozes and bubbles through the bark cracks and wounds, also known as slime flux, inspired by the slimy, foul smelling, brown appearance of the liquid. The prime wounding agents are insect borers, mechanical injury, and natural cracks and splits which are rarely observed. This condition is common in oaks, mulberry, sycamore, elm, ash and redbud. There are several common types of anaerobic soil bacteria (bacteria to which oxygen is toxic) which cause of this infection. These bacteria feed on substances in the wood, releasing fatty acids, methane and carbon dioxide gases. These fatty acids go rancid leaving the wood of the tree water soaked and foul smelling.
The gaseous by-products create a hydraulic pressure which forces liquids out of the cracks in the bark which turns brown due to oxidization. The bacteria do not cause any wood decay. However, the liquid raises the internal pH (alkaline) causing the infected wood to resist decay for a few years. Bark tissue will degrade in some cases.
Infection is thought to enter the tree primarily through root uptake, but contaminated pruning tools have all so been reported to transmit this infection. Slime Flux wounds do not close properly as tree tissue involved in wound closure are killed by the infection.
There is no satisfactory control for bacterial wetwood. It does cause die back of branches, but as previously mentioned the raised pH prevents and delays decay fungi from rotting out the heartwood of the tree. Inserting drain tubes around the affected area is no longer recommended. It only helps spread bacterial population within and create wounds conductive to the entry of other pathogens. As a radical effort and with some success with early detection of one or two wounds using a hatchet to expose the infection. Then spray the area with Ammonium Chloride, (Consan 20, a triple action microbial disinfectant), allowing the wound to air dry as oxygen is also toxic to the bacteria. Preventative measures such as avoiding moisture stress, proper pruning and adequate fertilization may invigorate trees. Do not disturb soil around the base of the tree to prevent wounds that the bacteria may enter.
Also see ASIAN AMBROSIA BEETLES http://www.800oakwilt.com/asianambbeetles.html
Scientists Find Sudden Oak Death Defense
By MIELIKKI ORG, Associated Press Writer
BERKELEY, Calif. - The secret to preventing the spread of sudden oak death in coastal trees may be a gigantic booster shot.
University of California scientists have discovered that trees dosed with a chemical product normally used as a fertilizer can fight and even resist the deadly microbe that has killed more than 100,000 oaks throughout California and Oregon since 1995.
The new application, which was just approved by the California Department of Pesticide Regulation, stimulates parts of the tree that produce disease-fighting chemicals.
"It's not a cure, not a solution," said Matteo Garbelottoin, a forest pathologist at the University of California at Berkeley who discovered the effects of phosphite on infected trees in 2001. "But we have something we can use to defend against the disease."
The chemical now is dispensed to the tree in two ways_ through a syringe that puts the product directly into the tree's vascular system, or through a spray that is absorbed through the bark.
Once the phosphite moves up the tree and enters the leaves, it stimulates the production of infection-fighting chemicals within a layer known as the cambium. The chemicals, although they do not affect the pathogen, boost the tree's natural defenses.
At least 60 percent of the oak trees susceptible to sudden oak death are on private coastal property, Garbelottoin said, which means that homeowners may benefit most from the new treatment.
Arborists and foresters who use the phosphite product, which is expected to cost about $30 per application, must be trained and certified before they can use the chemical on private trees.
California's 16 state parks, where an estimated 4,000 acres of oak trees show signs of sudden oak death, stand less to gain from the new product.
"We have so much acreage, so many trees," said Richard Rayburn, chief of natural resources at the California Department of Parks and Recreation. "I'm not sure if we have the physical, or fiscal ability."
United States Department of Agriculture officials said they plan to continue placing quarantines on nurseries and other places in California and Oregon where the pathogen has been known to spread.
Disclaimer: This article may contain pesticide recommendations that are subject to change at any time. These recommendations are provided only as a guide. It is always the pesticide applicator’s responsibility, by law, to read and follow all current label directions for the specific pesticide being used. If any information in these recommendations disagrees with the label, the recommendation must be disregarded. No endorsement is intended for products mentioned, nor is criticism meant for products not mentioned. The Writer assumes no liability resulting from the use of these recommendations. The information given herein is for educational purposes only. Reference to commercial products or trade names is made with the understanding that no discrimination is intended and no endorsement is implied.
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