Control of corn flea beetle and Stewart's wilt in sweet corn with imidacloprid and thiamethoxam seed treatments

2002 ◽  
Vol 21 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Thomas P Kuhar ◽  
Lydia J Stivers-Young ◽  
Michael P Hoffmann ◽  
Alan G Taylor
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 ◽  
2000 ◽  
Vol 84 (8) ◽  
pp. 901-906 ◽  
Author(s):  
Jerald K. Pataky ◽  
Lindsey J. du Toit ◽  
Noah D. Freeman

Maize accessions were evaluated in 1997, 1998, and 1999 to identify additional sources of Stewart's wilt resistance and to determine if reactions differed among accessions collected from various regions of the United States and throughout the world. The distributions of Stewart's wilt reactions rated from 1 (no appreciable spread of symptoms) to 9 (dead plants) were relatively similar among groups of accessions from all regions of the world except for those from the Mid-Atlantic/Ohio River Valley region of the United States, the southern United States, and the northeastern United States. The mean and median Stewart's wilt rating for 1,991 accessions evaluated in 1997 was 4. The mean Stewart's wilt rating for 245 accessions collected from the Mid-Atlantic/Ohio River Valley region was 3.1, which was significantly lower than that for accessions from all other regions. The mean rating for accessions from the southern United States was 3.7, which also was lower than mean ratings for accessions from all other regions. Ratings from trials in 1997 and 1998 were highly correlated (r = 0.87) for 292 accessions and 15 sweet corn hybrid checks evaluated in both years. Of 20 accessions rated below 2 in 1997 and 1998, seven were from Virginia, seven were from the Ohio River Valley or central Corn Belt of the United States, four were from the northern or western Corn Belt of the United States, and two were from Spain. Ratings for these accessions ranged from 1.7 to 3.1 in 1999. Ratings ranged from 2.6 to 3.7 for F1 hybrids of these accessions crossed with one of two susceptible sweet corn inbreds, CrseW30 or Crse16, which were rated 5.7 and 5.4, respectively. Based on the reactions of this collection of germ plasm, it appears that high levels of Stewart's wilt resistance are prevalent only among accessions collected from areas where the disease has been endemic for several years, whereas moderate levels of resistance can be found in accessions collected from nearly everywhere in the world.


2005 ◽  
Vol 11 (1) ◽  
pp. 27-46 ◽  
Author(s):  
J. C. Bailey ◽  
C. D. Scottdupree ◽  
J. H. Tolman ◽  
C. R. Harris ◽  
B. J. Harris

2014 ◽  
Vol 81 (1) ◽  
pp. 139-148 ◽  
Author(s):  
Lindsey Burbank ◽  
Mojtaba Mohammadi ◽  
M. Caroline Roper

ABSTRACTIron is a key micronutrient for microbial growth but is often present in low concentrations or in biologically unavailable forms. Many microorganisms overcome this challenge by producing siderophores, which are ferric-iron chelating compounds that enable the solubilization and acquisition of iron in a bioactive form.Pantoeastewartiisubsp.stewartii, the causal agent of Stewart's wilt of sweet corn, produces a siderophore under iron-limiting conditions. The proteins involved in the biosynthesis and export of this siderophore are encoded by theiucABCD-iutAoperon, which is homologous to the aerobactin biosynthetic gene cluster found in a number of enteric pathogens. Mutations iniucAandiutAresulted in a decrease in surface-based motility thatP. stewartiiutilizes during the early stages of biofilm formation, indicating that active iron acquisition impacts surface motility forP. stewartii. Furthermore, bacterial movementin plantais also dependent on a functional siderophore biosynthesis and uptake pathway. Most notably, siderophore-mediated iron acquisition is required for full virulence in the sweet corn host, indicating that active iron acquisition is essential for pathogenic fitness for this important xylem-dwelling bacterial pathogen.


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.


1994 ◽  
Vol 19 (1) ◽  
pp. 180-180
Author(s):  
J. P. McCaffrey ◽  
B. L. Harmon
Keyword(s):  

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.


2015 ◽  
Vol 28 (12) ◽  
pp. 1374-1382 ◽  
Author(s):  
M. Caroline Roper ◽  
Lindsey P. Burbank ◽  
Kayla Williams ◽  
Polrit Viravathana ◽  
Hsin-Yu Tien ◽  
...  

Pantoea stewartii subsp. stewartii is the etiological agent of Stewart’s wilt and is a serious bacterial pathogen affecting sweet corn. During the leaf blight phase, P. stewartii colonizes the leaf apoplast and causes a characteristic water-soaked lesion. The Hrp type III secretion system has been implicated in the water-soaking phenotype, and the goal of this study was to investigate other potential factors that contribute to the plant cellular disruption associated with these lesions. The P. stewartii genome contains a gene encoding a large repetitive RTX toxin, designated rtx2. RTX toxins comprise a large family of pore-forming proteins, which are widely distributed among gram-negative bacteria. These cytotoxins usually lyse their target host cells and cause significant tissue damage as a consequence. We hypothesized that this RTX-like toxin plays a role in the water-soaking phase of infection due to its predicted cytolytic properties. Based on the data reported here, we conclude that RTX2 contributes significantly to the development of water-soaked lesions and leakage of plant cellular contents and is an important pathogenicity factor for P. stewartii.


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