scholarly journals Control of Stewart's Wilt in Sweet Corn with Seed Treatment Insecticides

Plant Disease ◽  
2000 ◽  
Vol 84 (10) ◽  
pp. 1104-1108 ◽  
Author(s):  
J. K. Pataky ◽  
P. M. Michener ◽  
N. D. Freeman ◽  
R. A. Weinzierl ◽  
R. H. Teyker

Corn flea beetles, Chaetocnema pulicaria, vector Erwinia stewartii (synamorph Pantoea stewartii), which causes Stewart's bacterial wilt of corn (Zea mays). A seed treatment insecticide, imidacloprid, killed flea beetles and reduced the number of feeding wounds and Stewart's wilt symptoms per leaf in greenhouse studies. The objective of our research was to evaluate the ability of imidacloprid and thiamethoxam seed treatments to control Stewart's wilt on sweet corn hybrids under field conditions with naturally occurring populations of the corn flea beetle. Six field trials were planted at four locations in 1998. Eleven field trials were planted at nine locations in 1999. The treatment design was a factorial of sweet corn hybrids and seed treatments. Stewart's wilt incidence ranged from 0 to 54% in the 1998 trials. Incidence of Stewart's wilt in nontreated plots of the susceptible hybrid Jubilee ranged from 2% at the 8-leaf stage to 77% 1 week after mid-silk in the 1999 trials. Seed treatment insecticides reduced the incidence of Stewart's wilt by ≈50 to 85% relative to nontreated controls. The level of control was ≈75 to 85% in seven trials planted before 1 June 1999, when incidence of Stewart's wilt on nontreated Jubilee ranged from 4 to 71%. The level of control was ≈50 to 70% in the three trials planted after 1 July 1999, when incidence of Stewart's wilt on nontreated Jubilee ranged from 44 to 73%. Although comparisons varied, the level of control gained from seed treatment insecticides was similar to the next higher level of host resistance. Seed treatment insecticides appear to control Stewart's wilt during very early growth of corn plants, when foliar applications of insecticides are ineffective and the effectiveness of host resistance varies depending on the proximity of flea beetle feeding sites to the plant's growing point.

Plant Disease ◽  
2005 ◽  
Vol 89 (3) ◽  
pp. 262-268 ◽  
Author(s):  
J. K. Pataky ◽  
P. M. Michener ◽  
N. D. Freeman ◽  
J. M. Whalen ◽  
J. A. Hawk ◽  
...  

Neonicotinoid insecticides applied as seed treatments reduce the incidence of Stewart's wilt. The objectives of this study were to examine the efficacy of different rates of seed treatment insecticides to control Stewart's wilt on susceptible sweet corn hybrids and to compare the economic value of Stewart's wilt control in sweet corn grown for processing and fresh market. Clothianidin (Poncho), imidacloprid (Gaucho), and thiamethoxam (Cruiser) applied to seed at rates ranging from 0.125 to 1.25 mg a.i. per kernel were evaluated in 11 field trials in Illinois and Delaware from 2000 to 2003. Incidence of Stewart's wilt was significantly lower when seed was treated with insecticides than when plants were grown from nontreated seed in all but one trial. The level of control usually was between 50 and 90%. Small but statistically significant differences in incidence of systemically infected plants occurred among rates of insecticides in all trials except those in 2001. Usually, incidence of systemic Stewart's wilt was lower when higher rates of insecticides were applied; however, increasing the rate of insecticides from 0.125 mg a.i. to 1.25 mg a.i. per kernel had a relatively small effect on the level of Stewart's wilt control compared with the difference between treated and nontreated sweet corn seed. Based on a regression analysis, the lowest rates of the insecticides provided 64 to 72% control. The level of control increased about 1.85% with each additional 0.1 mg a.i. of insecticide per kernel from 0.125 mg a.i. to 1.25 mg a.i. Clothianidin provided an 8 or 9% higher level of control than thiamethoxam or imidacloprid at the same rate. Recommendations for application of seed treatment insecticides to processing and fresh market sweet corn differed somewhat due to substantial differences in the value of the crops. Based on estimated costs of $6 to $12 per 0.4 ha for the seed treatments, the economic break even point (i.e., cost of control = value from control) occurred in the range of 3 to 6% Stewart's wilt incidence for processing sweet corn valued at $325 per 0.4 ha and at about 1% Stewart's wilt incidence for fresh market sweet corn valued at $1,625 per 0.4 ha. Relatively small differences in levels of control conferred by commercially available rates of clothianidin (0.25 mg a.i. per kernel) and thiamethoxam (0.125 mg a.i. per kernel) were of little consequence in processing sweet corn but had considerable economic value in fresh market sweet corn.


Plant Disease ◽  
2010 ◽  
Vol 94 (9) ◽  
pp. 1111-1117
Author(s):  
M. D. Meyer ◽  
J. K. Pataky ◽  
D. K. Joos ◽  
R. W. Esgar ◽  
B. R. Henry

Many sweet corn (Zea mays) hybrids commercially available today have higher levels of resistance to Stewart's disease (caused by Pantoea stewartii subsp. stewartii) than the cultivars from which Stevens developed the first forecast of this disease in the 1930s. Incorporating levels of host resistance into forecasts of the seedling wilt phase of Stewart's disease (i.e., Stewart's wilt) could improve control decisions for sweet corn which are made prior to planting. Incidence of systemic infection of seedlings was assessed on 27 sweet corn hybrids with a range of reactions to P. stewartii. In total, 741 observations were collected from 1998 to 2009 in 79 field trials at 15 locations throughout Illinois and one each in Kentucky and Delaware. Relative frequency distributions of the incidence of systemic Stewart's wilt were developed for combinations of hybrids with different levels of resistance and ranges of winter temperature from Stewart's wilt forecasts. The probability of exceeding thresholds of 1 or 5% incidence that warrant the use of seed-treatment insecticides on sweet corn grown for fresh market or processing, respectively, was determined from these frequency distributions. Levels of host resistance affected the incidence of systemic seedling wilt within ranges of winter temperatures used by Stewart's wilt forecasts. For moderate and resistant hybrids, frequency distributions of Stewart's wilt incidence and mean incidence ranging from 0.7 to 1.8% did not differ among three winter temperature ranges above –2.8°C. Conversely, distributions of Stewart's wilt incidence on susceptible hybrids differed among each of the four ranges of winter temperature from the Stevens-Boewe forecast (i.e., >0.6, –1.1 to 0.6, –2.8 to –1.1, and <–2.8°C), with mean incidence ranging from 0.5 to 8.5%. Occurrence of Stewart's wilt also differed among trials varying in number of winter months above –4.4°C, the criterion used by the Iowa State forecast of this disease. Levels of host resistance to P. stewartii also affected the occurrence of Stewart's wilt as predicted by the Iowa State method. The probability of exceeding economic thresholds of 1 or 5% incidence of systemic Stewart's wilt depended on levels of host resistance and winter temperature. Stewart's wilt is unlikely to exceed economic thresholds when the mean winter temperature is below –4.4°C. When mean winter temperature was above –2.8°C, the probability of exceeding 1% incidence of systemic Stewart's wilt was 0.59 for susceptible sweet corn hybrids and 0.28 for moderate and resistant hybrids. When mean winter temperature was below –2.8°C, the probability of exceeding 1% incidence of systemic Stewart's wilt was 0.22 for susceptible hybrids and 0.04 for moderate or resistant sweet corn hybrids. The probability of exceeding 5% incidence was less than 0.1, except when the mean winter temperature was above –2.8°C and susceptible hybrids were grown.


Plant Disease ◽  
2001 ◽  
Vol 85 (12) ◽  
pp. 1278-1284 ◽  
Author(s):  
Noah D. Freeman ◽  
Jerald K. Pataky

Stewart's wilt reactions and yield of a total of 69 sweet corn hybrids were evaluated in trials in 1999 and 2000 in order to determine the level of Stewart's wilt resistance necessary to prevent reduction in yield of sweet corn hybrids. Plants at the 2- to 3-leaf stage were inoculated with Erwinia stewartii using the pinprick method. Stewart's wilt symptoms were rated from 1 to 9, and incidence of systemic infection was determined as a percentage for each experimental unit. Primary ears were harvested about 21 days after midsilk, and yield was measured as ear weight and number of marketable ears. Percent yield was calculated for each hybrid by dividing yield from inoculated treatments by yield from noninoculated treatments and multiplying by 100. Hybrid means for Stewart's wilt ratings in inoculated treatments ranged from 2.0 to 7.3. The relationships between percent yield and Stewart's wilt severity ratings were described best by curvilinear regressions, whereas percent yield decreased linearly with the incidence of systemic infection in 2000. Ear weights of hybrids with ratings below 3 or 3.5 were estimated from the regression equations to be within 95 or 92%, respectively, of those from noninoculated treatments of the same hybrid. The number of marketable ears from hybrids with ratings of 3 or below was estimated from the regression equations to be within 90% of those from noninoculated treatments of the same hybrid. A level of resistance that resulted in Stewart's wilt ratings below 3 or 3.5 corresponded to nonsystemic infection of most plants (i.e., incidence of systemic infection below 5 or 10%, respectively). The adverse effects of Stewart's wilt on ear weight and marketability appeared to be minor for sweet corn hybrids with levels of resistance that prevented or minimized systemic infection.


2002 ◽  
Vol 21 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Thomas P Kuhar ◽  
Lydia J Stivers-Young ◽  
Michael P Hoffmann ◽  
Alan G Taylor

HortScience ◽  
2007 ◽  
Vol 42 (6) ◽  
pp. 1409-1412 ◽  
Author(s):  
Jerald K. Pataky ◽  
Paul M. Richter

Host resistance is the most efficient way to control common smut (Ustilago maydis) in sweet corn, but resistance to U. maydis is not understood well. All meristematic tissues are susceptible, but infection is localized. Ear galls result from infection of ovaries. Infection and resistance can be affected by plant morphology. For example, ovaries are protected from U. maydis infection when an abscission zone forms at the base of the silk 6–24 h after a pollen tube reaches an ovary. The objective of this study was to determine if the rate of silk abscission differed between two related sweet corn hybrids that differed in susceptibility to smut infection of ears. The two hybrids, Green Giant Code 3 (GG3) and Green Giant Code 46 (GG46), were evaluated for the occurrence of infected ears in 58 paired plots at four locations near Le Sueur, MN, from 1993 to 1999. The rate of silk abscission in the two hybrids was evaluated in two field trials in Urbana, IL, in 2002 and 2004. Incidence and severity of ear smut were significantly (P < 0.05) greater and about twice as much on GG3 than on GG46. Silk abscission was more rapid on GG46 than on GG3. Although this association does not prove that decreased susceptibility of GG46 to ear infection is due to silk abscission, it is a logical basis from which to hypothesize that silk dynamics and other aspects of maize floral biology play important roles in resistance to ear infection by minimizing the time period that all ovaries on an ear are exposed to infection by U. maydis. This hypothesis is discussed in relation to the results of this and other research.


Plant Disease ◽  
2002 ◽  
Vol 86 (2) ◽  
pp. 167-172 ◽  
Author(s):  
P. M. Michener ◽  
J. K. Pataky ◽  
D. G. White

Stewart's wilt reactions of 98 food-grade, white corn hybrids, 3 yellow dent corn hybrids, and 23 sweet corn hybrids and infection of kernels by E. stewartii were evaluated in 1998, 1999, and 2000. Stewart's wilt symptoms were rated from 1 (no appreciable spread of symptoms) to 9 (dead plants) following inoculation. The mean Stewart's wilt ratings for the food-grade, white corn and yellow dent corn hybrids were 1.9, 2.4, and 2.9 in 1998, 1999, and 2000, respectively. The mean Stewart's wilt ratings for the sweet corn hybrids were 3.8, 4.2, and 4.6 in 1998, 1999, and 2000, respectively. Hybrids with ratings less than 3 were classified as resistant. Hybrids with ratings between 3 and 4.5 were classified as moderate. Hybrids with ratings greater than 4.5 were classified as susceptible. Ears harvested from each row in 1998 and 1999 were assayed for E. stewartii using an enzyme-linked immunosorbent assay (ELISA)-based seed health test. Kernels from 16 hybrids were positive for E. stewartii in 1998. Kernels from 11 hybrids were positive for E. stewartii in 1999. Kernel infection by E. stewartii was affected considerably by the level of host resistance (i.e., reactions of seed parent plants). For hybrids classified as resistant, estimates of kernel infection were 0.024 and 0.0007% in 1998 and 1999, respectively. For hybrids with moderate reactions to Stewart's wilt, estimates of kernel infection were 0.19 and 0.07% in 1998 and 1999, respectively. For hybrids with susceptible reactions to Stewart's wilt, estimates of kernel infection were 11.6 and 7.8% in 1998 and 1999, respectively. Based on high levels of Stewart's wilt resistance in food-grade, white corn hybrids, and low rates of kernel infection by E. stewartii in resistant and moderate hybrids, there is an exceedingly low probability of introducing E. stewartii to areas where it does not occur by transmitting the bacterium in grain of the food-grade, white corn hybrids evaluated in this study. Although all of the kernels harvested in these experiments were produced as grain on open-pollinated F1 hybrids, the rates of kernel infection observed for hybrids with resistant, moderate and susceptible reactions to Stewart's wilt are applicable to seed produced on inbred lines with equivalent Stewart's wilt reactions.


Plant Disease ◽  
2003 ◽  
Vol 87 (3) ◽  
pp. 223-228 ◽  
Author(s):  
P. M. Michener ◽  
N. D. Freeman ◽  
J. K. Pataky

Relationships between the reactions of sweet corn hybrids to Stewart's wilt and the incidence of natural, systemic infection by Erwinia stewartii differed among trials in which the prevalence of Stewart's wilt differed. Systemic Stewart's wilt infection was assessed for 262, 296, and 245 hybrids planted in seven trials in central Illinois in June and July 1998, 1999, and 2000, respectively. Incidence of systemic infection was calculated in each trial for all hybrids in each of nine categories of Stewart's wilt reactions (i.e., 1 = resistant and 9 = susceptible). When mean incidence was about 5%, incidence ranged from about 1 to 8% on resistant to moderately susceptible hybrids, but incidence was nearly 30% on susceptible hybrids. When mean incidence ranged from 10 to 16%, the relationships between hybrid reactions and incidence were explained by exponential or polynomial regressions. Incidence was less than 10% for hybrids with resistant and moderately resistant reactions, and incidence was greater than 15% for moderately susceptible to susceptible hybrids. When mean incidence was near 50%, the relationship was linear. Incidence was about 18% for resistant hybrids and about 80% for susceptible hybrids. Incidence increased about 8% for each class of hybrid reaction from 1 to 9. The influence of resistance on the development of systemic infection at very early seedling growth stages also was evaluated in six greenhouse trials. A highly resistant hybrid, Bonus, was systemically infected in two of six greenhouse trials when seedlings were inoculated prior to the V3 growth stage; however, systemic infection was not as severe as on a susceptible hybrid, Jubilee. Systemic infection was more severe on Bonus when plants were inoculated at earlier growth stages between VE and V3. The resistant hybrid Bonus was not systemically infected when inoculated after the V4 growth stage except for one greenhouse trial when all Stewart's wilt ratings were higher than usual. Hybrid reactions to Stewart's wilt affected the incidence of systemic infection in field situations and they affected the growth stage at which resistance effectively prevented systemic movement of E. stewartii within plants in greenhouse trials. This information can be used to determine more effectively when to apply other control measures, such as insecticidal seed treatments.


Plant Disease ◽  
2004 ◽  
Vol 88 (6) ◽  
pp. 633-640 ◽  
Author(s):  
J. K. Pataky ◽  
C. C. Block ◽  
P. M. Michener ◽  
L. M. Shepherd ◽  
D. C. McGee ◽  
...  

Two sets of experiments were done to examine whether seed-treatment chemicals affected the ability of an enzyme-linked immunosorbent assay (ELISA)-based seed health test to detect Erwinia stewartii. The chemicals evaluated included Actellic, Apron, Captan, Cruiser, Gaucho, Maxim, Poncho, Thiram, and Vitavax in 11 seed-treatment combinations. In one experiment, seed-treatment chemicals were evaluated quantitatively in a critical region of ELISA absorbance values near 0.5 using maize seed that were spiked with uniform quantities of a liquid suspension of E. stewartii. The number of bacteria in each sample was estimated from ELISA absorbance values using standard curves. Log CFU of E. stewartii per sample were not significantly different among the untreated control and the 11 seed treatments compared with Tukey's Studentized Range Test (P = 0.05). Means of log CFU/ml for all treatments were tightly clustered around 5.70 which corresponded to an absorbance value of 0.440 and a bacterial population of about 500,000 CFU/ml. In a second set of experiments, seed treatment chemicals were evaluated based on qualitative decisions that resulted from the ELISA-based seed health test of seed lots of Jubilee and A632 infected with E. stewartii. The number of negative samples was not substantially greater than expected based on binomial probabilities except for samples of Captan/Vitavax-treated A632, which we considered to be a type I error. The mean absorbance values of positive samples ranged from 1.42 to 1.72 for A632 and from 1.51 to 1.91 for Jubilee and did not differ significantly among the seed treatments. There was no consistent evidence from these experiments that fungicide or insecticide seed treatments interfered with the sensitivity of the ELISA or altered low (e.g., 0.5) or high (e.g. 1.4 to 1.9) absorbance values. The ability of the ELISA-based seed health test to detect E. stewartii in maize seed was not affected by these seed treatments.


HortScience ◽  
1990 ◽  
Vol 25 (9) ◽  
pp. 1067a-1067 ◽  
Author(s):  
A. C. Meyer ◽  
J. K Pataky ◽  
J.A. Juvik

Approximately 200 sweet corn inbred lines were screened for two years for resistance to northern leaf blight, caused by Exserohilum turcicum, and Stewart's wilt, caused by Erwinia stewartii. Inbreds with the best levels of partial resistance to races 1 and 2 of E. turcicum included IL11d, IL676a, IL677a, IL685d, IL766a, IL767a and IL797a. Inbreds with the best partial resistance to E. stewartii included IL126b, IL676a, IL767a, IL772a, IL774g, IL797a, IL798a and M6011. Several of these resistant and moderately resistant inbreds had common ancestors; however, inspection of pedigrees suggested that resistance was derived from Puerto Rican, Bolivian, and other tropical sources and/or dent corn. Thus, many of the sweet corn inbreds may carry different genes for resistance and can be used for the development of populations with improved resistance.


Sign in / Sign up

Export Citation Format

Share Document