Remaining 1997 Commercial Pesticide Applicator Training and Testing Dates (Categories 1, 2a, 3, 4, 10, 12)
Categories 2a: 8:30 AM - 12:20 PM, Testing at 1:00 PM;
Cat. 3, 10. 12: 8:30 AM - Noon, Testing at 1:00 PM;
Cat. 1, 4, 10, 12: 9:45 AM - 2:00 PM,Testing at 2:00 PM
December 22, 1997
419 Reed Hall
Morehead State University
by Paul Vincelli, Extension Plant Pathologist and Ric Bessin, Extension Entomologist
Background Information
Interest in Fusarium ear rot has grown considerably in recent
years. This ear rot occurs regularly in the region.
Furthermore, the fungi that cause Fusarium ear rot can
produce fumonisins. Fumonisins are mycotoxins discovered
about a decade ago which cause fatal diseases of horses and
swine. Fumonisins also have been shown to cause cancer in
laboratory rats, and have been associated with esophageal
cancer in humans when consumed at high concentration. For
these reasons, a great deal of research effort is currently
being focused on Fusarium ear rot and fumonisin contamination
of corn nationwide. More information on fumonisins and
F. moniliforme is available in the UK Extension
publication, "Mycotoxins in Corn Produced by Fusarium
Fungi. ID-121".
Activity of the European corn borer (ECB) can increase symptoms of Fusarium kernel rot in several ways. Kernel damage caused by second-generation ECB creates infection sites for the development of Fusarium kernel rot. The ECB can carry spores of Fusarium moniliforme and introduced them into maize ears. ECB infestations can also increase the frequency of symptomless infection by F. moniliforme.
Producers are aware that corn hybrids are now commercially available which express the Bt gene for resistance to ECB and other, related insect pests. This Bt gene was originally obtained from a common soil bacterium, Bacillus thuringiensis. It was inserted into corn breeding lines by genetic engineering techniques, and represents one of the first widespread commercial uses of genetically engineered crops in the U. S. The toxin produced by the "Bt hybrids" may or may not be found in the kernels, depending on the specific genetics of the hybrid. If found at adequate doses in the kernels, it protects against feeding damage by the ECB.
The Question
Given that ECB can enhance damage from Fusarium kernel rot,
researchers at Iowa State University asked, do corn hybrids
engineered to produce the Bt toxin suffer less damage from
this ear rot disease? This is a logical, important, and
timely question.
Research Results
A series of detailed field studies to address this question
were conducted by Dr. Gary Munkvold and colleagues at Iowa
State University during 1994-96. They compared hybrids with
and without the Bt-toxin gene. In some experiments,
insecticide treatments were also used for comparison purposes.
The research showed that, when compared to non-engineered
counterparts, genetically engineered corn hybrids which
express the Bt toxin in their kernels consistently had:
1. less damage from ECB, and
2. less damage from Fusarium kernel rot.
This resulted in better grain quality from reduced mold damage.
Note that this conclusion only applies to those hybrids that express the Bt-toxin in the kernel tissue, like YieldGardTM hybrids. When the researchers evaluated hybrids that express the Bt-toxin only in green tissue and pollen and not in kernels (like Maximizer (tm) hybrids), these hybrids did not consistently differ from their non-engineered counterparts. The research suggested that that these hybrids may sometimes experience less Fusarium ear rot than non-engineered hybrids, possibly by preventing a buildup of second-generation ECB populations in the field. However, this effect was not consistent in their studies. The research clearly showed that, for consistent, significant reductions of Fusarium ear rot, the Bt-toxin must be expressed in the kernels.
Based on these conclusions and similar studies in cotton, it seems reasonable to propose that these hybrids would also have less fumonisin contamination under conditions when that mycotoxin is formed. In the Iowa study, fumonisin levels were not measured, so data to address this point are lacking. This will likely be an area of continuing research.
Summary
In recent research in Iowa, corn hybrids that express the
Bt-toxin in kernels consistently suffered less ECB
injury to kernels and less Fusarium ear rot damage. This may
translate into less fumonisin contamination in Bt-hybrids, but
ongoing research on this point is needed. Consistent
reductions in kernel damage from ECB and Fusarium ear rot
were not seen in hybrids that expressed the Bt-toxin in green
tissues and pollen but not in kernels.
by William Nesmith
Japanese agricultural officials have been concerned about importing the tobacco blue mold pathogen, Peronospora tabacina on tomatoes from the U.S., citing reports from the 1930's of blue mold in tomato transplant beds in the southern US as grounds for the embargo. During the past year some import restrictions relative to this issue were lifted by the Japanese officials allowing selected movement of tomatoes from the USA and Canada. This action came about only after convincing data and arguments were presented to support that the current tomato cultivars (foliage, stems and fruit) were not hosts of the tobacco blue mold pathogen. Considerable efforts and extensive testing were done by a number of plant pathologists in the tobacco-producing states cooperating with those in tomato-producing areas. Japanese Ministry of Agriculture scientists also visited many of the laboratories involved to witness the research while it was underway in critical pathogenicity tests and made field visits to observe tobacco, tomatoes, and the combination growing together during epidemics of blue mold on tobacco.
The College of Agriculture, University of Kentucky was significantly involved in this effort. I testified that P. tabacina has not been observed on tomato in Kentucky during the many epidemics of tobacco blue mold even though tomato and tobacco are often cultivated in adjacent fields. After all, this same question is very important to the tobacco industry. We have provided several laboratories in non-tobacco producing areas isolates of the blue mold fungus for pathogenicity testing in tomato. During the summer of 1996, we hosted plant pathologists from the Japanese Ministry of Agriculture and USDA-APHIS, including visits to a number of Kentucky counties to observe tomatoes growing adjacent to tobacco during the worst epidemic of blue mold in the history of Kentucky. This included visiting some farms where no fungicides were being used in the tomato production. We have also conducted laboratory and field tests over the years to determine if tomato is a host of blue mold.
Below are the results of one such test conducted this past season in Clark County during a blue mold epidemic.
Pathogenicity of P. tabacina was tested in a field planting of staked-tomatoes in Clark County, Ky., maintained under commercial production protocols as recommended by the University of Kentucky, and practiced commercially in the state, except that no fungicides were applied and overhead irrigation was used to encourage foliar disease development. Six-week-old plants of four tomato cultivars (Better Boy, Mountain Spring, Mountain Supreme, and Jet Star) were transplanted on June 23 in a randomized complete block design using five plants per treatment (cultivar) and four replications (rows). Burley tobacco (Ky 14) was planted between each row of tomatoes and as a border surrounding the plot area, to help maintain high inoculum pressure at the site. Blue mold was observed in the tobacco on July 8 as scattered, random lesions in the plots; a blue mold epidemic existed in Clark Co. before and during the entire time of this test. In order to increase the uniformity of the fungus in the plot area, nine lesions were collected and sporangiospores induced in the laboratory were removed and applied as an aerial spray to the rows of tobacco at dusk on the evening of July 9. In addition to opportunities for natural infections, P. tabacina was infiltrated into leaves of one of the five tomato plants, three infiltration sites per leaf on each of five leaves, using a 30cc syringe filled with 50,000 spores/ml and delivering about 10 ul/infiltration site. The infiltrations were conducted on July 9 using isolate Ky 97 Laurel Co. and repeated on July 23 using a different tomato plant in each plot. Additionally, 10 infiltrations were made into tobacco plants on the later date. In mid-September when the tobacco flowered and became a less favorable host for blue mold, the tobacco plants were pruned at the soil line, removed from the field and sucker-regrowth allowed to develop to further encourage blue mold development and sustain a natural supply of inoculum. The tomato plants remained in place until damaged by frost in October.
Blue mold developed extensively and uniformly in the tobacco
and sucker-regrowth throughout the plot area, from mid July
until frost, but it was never detected in the tomatoes.
Environmental conditions monitored at this site were
favorable for infections in tobacco on 29 nights. The
percentage of tobacco leaf surface diseased from blue mold was:
0.8% July 16, 3.4% July 23, 17.2% July 30, 39.6% August 8 and
46.9% on August 18.
On July 30, all 10 infiltration sites in
tobacco had excellent lesion development accompanied by
sporulation. At no time during the experiment were symptoms
associated with downy mildew found on any of the tomato
plants, including at the sites of infiltration. Five tomato
leaves that had received infiltration inoculations on July 23
were removed on Aug. 18, placed in plastic bags, misted and
incubated in the dark at 18-20 C overnight and examined
visually on August 19, and microscopically on August 20.
Sporulation signs associated with P. tabacina were
not found. Early blight and Septoria leaf spot developed
extensively in the tomatoes, but green foliage was present
until frost in the tops of most tomato plants and tomato suckers.
These tests and observations suggest that the tomato cultivars tested were not susceptible to blue mold even when artificially inoculated and grown under field conditions conducive to blue mold development in tobacco and in close proximity to infected tobacco.
by Doug Johnson
The cold weather has arrived with a vengeance! The recent cold weather should help our Aphid / BYDV situation a great deal. If you have not had many aphids in the last month then you are unlikely to have much of a problem; but let's look at two situations.
If you planted early, (in most cases before Oct 10-15) then you stand the chance that aphids were able to colonize your fields; most especially if you planted the last week in Sept and / or the first week in Oct. In this case, the recent weather reduced the aphid populations in your fields. Continuing cool weather will stop or slow their spread, BUT it may not kill them all. If the weather warms substantially (high 40's to 50's) then you had best get out and look for them once again.
If you planted later (after OCT 10-15) then the aphid numbers in your fields should be much lower. Likewise the recent cold would have reduced them even more. Your chances of having a problem are much less than for the early plantings. If it does warm a great deal you should scout your fields but you are not likely to find much.
by Doug Johnson
Now would be a real good time to check your stored grain for insect activity, especially anything that has been held over from previous years. I have seen Indian Meal moth activity in this year's wheat. General control recommendations may be found in ENT-19 and crop specific pesticides are found in the appropriate crop recommendations.
Try to ensure that your grain is in good condition and remains that way. This season of big fluctuations in temperature and humidity make it hard to keep the grain mass at an even temperature. Unevenness in temperature within the grain mass and between the grain mass and outside temperatures can lead to condensation and this will lead to compounding insect problems.
Insect infestation within a grain mass is not easy to control and prevention is without doubt the most economic approach.
by John Hartman
Diseases we call yellows or witches broom disease are often caused by phytoplasmas, sometimes referred to in the past as mycoplasmas or mollicutes. In Kentucky landscapes, ash and elm trees have been diagnosed with yellows diseases. Although these diseases only occur occasionally, they are usually lethal when they occur. Both are caused by phytoplasmas, bacteria-like microbes lacking cell walls and which live in the phloem tissues of trees.. Phytoplasmas infect trees systemically and are thought to be vectored by certain leafhoppers and possibly meadow spittlebugs.
Ash yellows. White ash is most frequently infected, and shows a variety of symptoms including: premature spring growth, premature fall color, stunted and folded leaves, very short twig and branch elongation, reduced trunk diameter growth, epicormic shoot growth at the base of the trunk, loss of terminal shoot apical dominance in branches, witches brooms, sometimes chlorotic leaves, branch dieback, decline and death. Trees may survive several years with the disease, but highly susceptible trees often die in just a few years. Infected, declining trees may in the end be attacked also by secondary, weakly parasitic fungi which are not the actual cause of tree mortality.
Ash yellows in Kentucky has been diagnosed primarily by field symptoms. In the laboratory, the disease can be confirmed by microscopic examination of stained phloem tissues, or observation of the phytoplasma in infected tissues using the electron microscope. There have been no controls measures developed to prevent or cure this disease. Although green ash is reported to be more tolerant than white ash, little is known about the susceptibility of others such as blue ash.
Elm Yellows. Formerly called elm phloem necrosis, elm yellows has sometimes been mistaken for Dutch elm disease. The elm yellows phytoplasma is systemic and the disease kills infected trees within a few months or a year. Symptoms include: leaf yellowing, leaf petiole epinasty (bending downward), premature defoliation, branch death, and tree death. These symptoms are probably caused by root deterioration associated with the disease. Roots of infected trees die and discoloration and death of phloem tissues at the base of the tree is evident. Tan to brown discoloration of the inner bark, the phloem tissue, can be observed, and samples of freshly exposed diseased inner bark may yield the odor of wintergreen. Slippery elms may show witches broom symptoms before other yellows symptoms develop.
Elm yellows, like Dutch elm disease may be spread from infected to nearby healthy trees via root grafts, so root graft breakage is a useful tool for preventing disease spread in a cluster of elm trees. Otherwise, there are no treatments for prevention or cure of elm yellows. While American, slippery, and winged elms in Kentucky are susceptible, Asiatic elms are resistant.
by Monte P. Johnson
On Tuesday, Sept. 16, 1997,Vice President Al Gore announced a new website, the Nonprofit Gateway, created for nonprofit groups to access federal information. EPA is one of 15 federal agencies that have created nonprofit pages that link to the central website. Information is available on topics such as loans and grants, federal register notices, community right to know, pollution prevention and partnerships. The website (www.nonprofit.gov) is the result of a year-long partnership between federal agencies and departments and hundreds of nonprofit groups. EPA's website can be located at http://www.epa.gov/epahome/nonprof.htm. (EPA Press Release, Sept. 22, 1997)
NEW SLIDE SHOW FOR THE USDA FEDERAL RECORDKEEPING PROGRAM A new slide program for the USDA Federal Recordkeeping Program may be available for use in pesticide certification training programs. The slide show covers the requirements of the regulations and it written specifically for certified private applicators. Please contact Jeff Haynes at 703-330 -7826 or via E-mail address, jeffery_s_haynes@usda.gov for ordering information.
THIOPHANATE-METHYL (TOPSIN M) USE DELETION OF CELERY Elf Atochem plans to delete CELERY from their label of the fungicide, thiophanate-methyl, due to economic considerations. They plan to continue to support the other registered uses of thiophanate-methyl during reregistration. The following is the current registration status of thiophanate-methyl: REGISTERED USES SUPPORTED by Elf Atochem which are expected to be REREGISTERED: ALMONDS, APPLES, APRICOTS, BEANS, CHERRIES, CONIFER PLANTINGS, CUCUMBERS, MELONS, NECTARINES, ONIONS, ORNAMENTALS (herbaceous and woody), PEACHES, PEANUTS, PECANS, PLUMS, POTATOES, PRUNES, PUMPKINS, SOYBEANS, SQUASH, STRAWBERRIES, SUGAR BEETS, TURF, and WHEAT. For additional information contact: Ms. Rebecca Clemmer, Elf Atochem North, America, Phone 215-419-7667; Fax 215-419-7243. (Reregistration Notification Network, USDA, Oct. 24, 1997)
REDUCED-RISK PESTICIDES REGISTERED Since July, 1993, applicants have sent thirty-nine new chemical or new use submissions to EPA's Office of Pesticide Programs (OPP) for consideration as reduced-risk pesticides. Of the thirty-nine, twenty-two have been accepted by OPP as reduced-risk candidates; and sixteen have been rejected. Of the twenty-two accepted, fourteen have been registered. The following is a list of the registered pesticides by accepted common names (if available) and their trade name (in parenthesis): hexaflumuron (Recruit) - below ground termiticide; flumiclorac-pentyl (Resource) - herbicide; methyl anthranilate (Rejex-It) - bird repellent; tebufenozide (Confirm) - insecticide; hymexazol (Tachigaren) - fungicide; fludioxonil (Maxim) - fungicide; (Cadre) - herbicide; (Mefenoxam) - fungicide; spinosad (Spinosad) - insecticide; azoxystrobin (Heritage) - turf fungicide; alpha-metolachlor (CGA 77102) - herbicide; hexaflumuron (Recruit) - above ground termiticide; imazamox (Raptor) - herbicide; azoxystrobin (Heritage) - fungicide on fruits, etc. (EPA Pesticide Registration Notice 97-3, Sept. 4, 1997)
PESTICIDE COMMON NAME USAGE EXPANDED The EPA has announced a policy to expand the use of common names on pesticide labeling. Chemicals, including pesticide ingredients, have scientific names based upon their chemical structure. In many instances, these names are long, complicated and understandable only by those with a scientific or technical background. Historically, some chemicals have been identified by shorter, acronym-like names, often based upon combinations of the chemical name or chemical family to which the chemical belongs. These are called "common names" and are widely used in lieu of the chemical names. EPA encourages the development of common names and will permit the use of approved ones by the American National Standards Institute (ANSI) in the label ingredients statement without the accompanying scientific chemical names. The EPA also recommends the inclusion on labels of Chemical Abstract Service (CAS) numbers to identify ingredients definitively. (EPA Pesticide Registration Notice 97-5, September, 1997)