The University of Georgia
College of Agricultural and Environmental Sciences
Georgia Agricultural Experiment Stations

Research Bulletin Number 435
September, 1998

Gale Buchanan, Dean and Director
Jerry A. Cherry, Associate Dean and Senior Associate Director
Gerald F. Arkin, Associate Director, Northern Region

ISSN 0435-4680

Assessment of Crop Protectants for Use in Canola

G. David Buntin, Editor

List of Contributors

Table of Contents

Introduction
List of Registered Pesticides for Canola

Reports

Fungicides/Nematicides
Seedling Diseases and Nematodes in Canola Following Peanut - D.R. Sumner and N.A. Minton
Effect of Fungicides on Foliage and Pod Diseases of Canola - D.N. Sumner and P.L. Raymer
Control of Sclerotinia Stem Rot of Canola with Fungicides - D.V. Phillips and W.D. Spradlin
Fungicides for Control of Blackleg of Canola - D.V. Phillips and W.D. Spradlin

Insecticides
Comparison of Foliar Applied Insecticides for Aphid Control in Rosette and Flowering Canola - G.D. Buntin
Aphid Control in Winter Canola Using Soil-Applied Insecticides - G.D. Buntin
Evaluation of Insecticides for Control of the Cabbage Seedpod Weevil in Canola - G.D. Buntin

Herbicides/Harvest Aids
Canola Tolerance to Residues from Spring-Applied Herbicides - D.C. Bridges and T.R. Murphey
Differential Tolerance of Wild Radish and Canola to Herbicides - D.C. Bridges
Response of Canola Cultivars and Wild Radish to Atrazine - D.C. Bridges and P.L. Raymer
Preharvest and Combine Seed Losses in Canola: Effect of Chemical Harvest Aids and Swathing - D.C. Bridges and P.L. Raymer

Introduction

G. David Buntin, Editor

Canola is the edible oil form of oilseed rape, Brassica napus, and is an important crop in many areas of the world where it is used to produce vegetable oil and protein meal. Canola is defined as having <2% erucic acid and <30 mol/g of glucosinolates in the oil-free meal. Although farmers have grown industrial-oil forms of rape-seed on limited acreage in the United States during the past 50 years, commercial operations have grown canola as a grain crop in the United States only since 1986. In the southeastern United States, farmers grow spring-type canola as a winter crop and typically double crop it with summer annual field crops. Canola acreage in the four southeastern states has been <25,000 acres per year during the past 10 years. Recently, virtually all commercial production has consisted of genetically modified varieties that produce higher than normal amounts of lauric acid. This type of canola is referred to as laurate canola.

The canola research and extension team at the University of Georgia has conducted numerous studies to develop a production system for canola. As part of this effort, team members have conducted trials to evaluate pesticides for managing weed, disease, and insect pests of canola. This bulletin presents the results of these trials. Most reports contain results from multiple trials over several years and provide a conclusion or interpretative summary of the results. Many of the products used in these trials are not currently registered for use on canola. Furthermore, some of the treatments are designed to examine principles of canola pest control and would almost never be cost effective in normal canola production.

As with most new crops, few pesticides are registered for use on canola. The next page lists pesticides labeled for use on canola as of August, 1997. The lack of registered pesticides has greatly limited the development of a canola production system. Results presented in this bulletin have been used to prioritize pesticide registration efforts and to develop a more effective production system for canola in the southeastern United States.

Registered Pesticides* for Canola

Seedling Diseases and Nematodes in Canola Following Peanut

Donald R. Sumner and Norman A. Minton

Introduction

Soilborne pathogenic fungi and nematodes may invade the roots and hypocotyls of canola from seed germination through maturity. The seedling stage is particularly vulnerable to the fungi Rhizoctonia solani and Pythium spp., and the peanut root-knot nematode, Meloidogyne arenaria, may cause root injury throughout the growing season. This investigation attempted to determine the effects of fungicides and a nematicide on seedling and root health, stand establishment, plant growth, and seed yield.

Materials and Methods

A peanut-canola double-crop was planted for two consecutive years (1988-1990) on Tifton loamy sand at the Gibbs farm at the Coastal Plain Experiment Station. Plant residues were buried by tillage with a moldboard plow following each crop. Soil pesticides used on canola were the nematicide Nemacur (fenamiphos) and the fungicides Ridomil (metalaxyl, active against Pythium spp.) and SN-84364 (flutolanil, active against R. solani). Treatments were kept on the same plots in each canola experiment, and are listed in Table 1. A randomized complete block design with five repli-cations was used. Each plot was two raised beds, 6 ft. wide and 10 ft. long, with a 5 ft. alley between plots. The cultivar 'Westar' (seed treated with Vitavax) was planted in eight rows on each bed.

In 1988, Nemacur was applied as a surface spray in 20 gal. water/A and incorporated 1-2 in. deep with a tractor-mounted roto-tiller before planting November 10. The fungicides were sprayed on the surface November 11, and the plots were irrigated with 0.5 in. water with over-head sprinklers. In 1989, plots were planted November 1, but rows could not be seen because of volunteer canola from the previous crop. Therefore, the canola was killed with applications of paraquat and glyphosate, and the experiment was replanted November 15 without tillage or reapplication of Nemacur. On November 17, Ridomil and SN-84364 were applied again, and the plots irrigated with 0.5 in. of water. Very few volunteer canola plants emerged in the second planting.

In 1988, soil was collected from each plot (10 cores, 1 in. diam., 6 in. deep) December 7 and assayed on selective media for R. solani and Pythium spp. Soil was not assayed for soilborne pathogens in 1989. Each year, plants were counted in 3-6 ft. rows one or more times, and plants were dug and evaluated for root and hypocotyl disease severity 20 days after planting. Fungi were isolated from seedlings and identified. Soil was collected periodically from each plot and assayed for nematodes, and plants were rated for root gall injury. In each plot, plant and soil sampling was done in one bed and seed yield was taken in late May or early June in the other bed.

Results and Discussion

Plant stands were improved by Ridomil in 1988 and Nemacur + Ridomil in 1989, but not by other treatments, compared with the control (Tables 1 and 2). Populations of R. solani anastomosis group (AG)-4 and Pythium spp. in soil were not influenced significantly by treatments in 1988 (Table 1). The fungi isolated most frequently from seedlings both years were Pythium spp. and Fusarium oxysporum; R. solani and other Rhizoctonia spp. were isolated infrequently. In previous research in 1987, R. solani AG-4 was frequently isolated from 10-day-old seedlings, and in greenhouse experiments, R. solani AG-4 was the most virulent pathogen on canola seedlings. Pythium ultimum was slightly to moderately virulent.

Seedlings rated for root and hypocotyl diseases exhibited very little discoloration and decay 20 days after planting in 1988. In 1989, there were more seedling diseases, but there was much variation among plots, and there were no significant difference among treatments (Table 2). When canola seeds or seedlings are invaded by soilborne pathogens, the fungi frequently ramify through the tissues so rapidly that the plants die, shrivel, and disappear before seedlings are rated for diseases.

In previous research with rapeseed in 1987-1988, galling from root knot nematodes was relatively severe, and treatments with Nemacur reduced root galling, improved plant height, and increased seed yield. In contrast, populations of M. arenaria were low in these studies, root galling was very light, and there were no differences among treatments. Also, populations of other nematodes (Pratylenchus brachyurus and Criconemoides ornata) were low and not influenced by Nemacur treatments. Because of the low nematode numbers and root-knot indices, data are not shown.

In 1989, seed yields were increased significantly (30%) by the combination of the two fungicides and the nematicide, but not by the other treatments, compared with the control (Table 1). Seed yield was higher in 1990 than in 1989 and not different among treatments (Table 2). There was a severe record low freeze (22 degrees F) on February 24, 1989, and that may account partially for the lower yields in the first experiment.

Conclusions

Seedling diseases, caused primarily by R. solani Ag-4 and Pythium spp., can reduce stand of canola following peanut. Root-knot nematodes, both M. arenaria and M. incognita, can cause root galling and poor growth in canola. Poor stand establishment and stunting induced by soilborne pathogenic fungi and root-knot nematodes can reduce seed yield in canola double-cropped with peanut.

Acknowledgments

Appreciation is expressed to Marlon Breve and Dan Thomas for harvesting the seed in the plots.

References

Johnson, A. W., A. M. Golden, D. L. Auld, and D. R. Sumner. 1992. Effects of rapeseed and vetch as green manure crops and fallow on nematodes and soilborne pathogens. J. Nematology 24: 117-126.

Sumner, D. R. and N. A. Minton. 1991. Seedling diseases and nematodes on rapeseed following peanut in Georgia. Phytopathology 81: 814 (Abstr.).

Thomas, D. L., M. A. Breve, P. L. Raymer, N. A. Minton, and D. R. Sumner. 1990. Improving rapeseed production practices in the Southeastern United States. ORNL/Sub/86-91324/1. Nat. Tech. Inf. Service, U. S. Dept. Commerce.

Effect of Fungicides on Foliage and Pod Diseases in Canola

Donald R. Sumner and Paul L. Raymer

Introduction

Several fungi may induce foliage diseases of canola including Cercospora brassicicola and Pseudocercosporella capsellae that cause Cercospora leaf spot and white leaf spot, respectively. Three Alternaria spp. (A. brassicae, A. brassicicola, and A. raphani) cause gray and black leaf spots on leaves, stems, and pods. A canola crop is in the field for several months, and weather conditions may be favorable for infection by foliar pathogens during much of the growing season. In Europe and Canada, foliage and pod diseases may reduce seed yields as much as 50%. This research sought to determine the severity of foliage pathogens on canola in south Georgia, to evaluate the efficacy of foliar fungicides on foliage diseases, and to determine the effect of foliage diseases on seed yield.

Materials and Methods

The experiments were conducted for three years on Tifton loamy sand at the Blackshank farm at the Coastal Plain Station. In the early fall, soil was deep-turned with a moldboard plow, and beds 6 ft. wide were prepared with a bed shaper. Then 500 lbs/A of commercial fertilizer (5-10-15 NPK) with trace elements was applied and incorporated with a tractor-powered roto-tiller. The cultivar 'Cascade' was planted October 21, 1988 and October 25, 1989, and 'Bingo' was planted October 25, 1990. The plots were planted with a Stan Hay planter in 6 rows/bed (8 lbs/A), 10-15 seed/ft. of row, and 0.25 in. deep. Ammonium nitrate was broadcast as additional fertilizer at 75 and 350 lbs/A four to six weeks after planting and in mid-February, respectively. In late February, Solubor was sprayed on the foliage at 0.25 lb/A to prevent boron deficiencies. The first and third experiments were on soil with a pH of 6.0, but the second experiment was inadvertently conducted on a field of low pH (5.3).

A randomized complete block design with five replications was used. Each plot was one bed 10 ft. long with a 5-ft. alley between plots. Beds of treatments were alternated with nonsprayed border beds. In the first experiment a tractor-mounted boom sprayer was used to apply fungicide treatments (in 50 gal. water/A) directly over the beds until plants were approximately 2 ft. tall. Later sprays were applied by driving the tractor on border beds with the boom over the plots. In sub-sequent experiments, the last two sprays were applied with a hand sprayer. Sprays of foliage fungicides were applied February 27, March 13 and 27, and April 12 and 25 in 1989; March 5 and 19 and April 2 and 16 in 1990; and February 12 and 26 and March 12 and 26 in 1991. Treatments are given in Tables 1-3. The plants were vegetative to just beginning to flower when the first sprays were applied, and lower pods were filling when the last spray was applied. Foliage and pod discoloration and decay were estimated in each plot two to four times from March through early May each year. Fungi from selected lesions were isolated and identified. Experiments were harvested with a plot combine June 19, 1989; May 23, 1990; and May 14, 1991.

SAS least squares analysis of variance and step-wise multiple regression statistical programs were used for data analysis. Duncan's multiple-range test and Fisher's LSD were used as means separation tests.

Results and Discussion

'Cascade' commonly turned red to purple during the winter, apparently a cultivar reaction to low temperatures, and the foliage of 'Bingo' was yellow to purple in early February. Both varieties, however, turned green and grew rapidly after fertilization in mid-February. In the first experiment, there was a record low temperature of 22 degrees F with wind February 24, 1989, but that was before flowering. In the second experiment, there were no nights below 32 degrees F in February and March. In the last experiment, it was 19 degrees F on February 16, but freezing temperatures did not occur in March. In all years, plants flowered abundantly and produced many pods. Rainfall from February 1 to April 30 totaled 8.9, 7.3, and 13.6 in., and total days with rainfall were 24, 26, and 26 in., respectively, in 1989, 1990 and 1991 at the Coastal Plant Station meteorology center three miles from the experiments. Thus, the periods with 10 to 12 hours of foliage wetness favorable for infection by pathogens were probab-ly similar each year during rapid vegetative growth, flowering, and pod maturity.

Each year white leaf spot was identified on the foliage in early winter, but Cercospora leaf spot was observed rarely. The primary fungi isolated from leaf spots and stem and pod lesions were Alternaria spp. A. brassicae was isolated more frequently in late winter and early spring, and A. brassicicola in the spring; the former is considered to be a cool weather pathogen and the latter a warm weather pathogen. A. raphani was isolated rarely. In contrast, in Canada A. brassicae and A. raphani may cause substantial losses in seed yield and quality of rapeseed oil, but A. brassicicola does not occur naturally on rapeseed.

Lesions induced by A. brassicicola caused severe discoloration and decay on seed stalks and pods in control plots each year. In the first experiment, none of the fungicide treatments reduced disease severity, probably because they had low efficacy against Alternaria spp. (Table 1). In the last two experiments, iprodione (Rovral 4F) was included as a treatment, as it was the only fungicide available with good efficacy on Alternaria spp. In the second experiment, black rot (caused by the bacterium Xanthomonas campestris) was identified in February, and the disease spread throughout the test by April. Black rot killed stem apices and pods, and probably did more damage to the plants than the fungal pathogens. The low yields were probably caused by a combination of black rot, A. brassicicola, and low soil pH (Table 2).

In the last experiment, Rovral 4F + Triton CS-7 and Rovral 4F + Triton CS-7 + Bravo 720 reduced disease severity caused by A. brassicicola on pods, but yields of seed were not different from nonsprayed plots (Table 3). Stepwise multiple regression analysis indicated that pod discoloration and decay April 26 and May 3 did not have a significant effect on seed yield and test weight.

Conclusions

This research indicates the difficulty of preventing foliage, stem, and pod diseases with applications of foliar fungicides. Four or five applications will probably be necessary in the late vegetative through pod maturation stages, and an additional application may be necessary in early May in a wet spring. Fungicides are expensive and should not be applied unless there is a measurable economic benefit. More research is necessary to determine the relationship of foliage and pod disease severity to quantity and quality of canola and oilseed rape seed yields in Georgia.

Acknowledgments

Appreciation to Richard E. Baird and Ronald D. Gitaitis for assistance in identifying the fungal and bacterial pathogens in these experiments.

References

Conn, K. L., J. P. Tewari, and R. P. Awasthi. 1990. A disease assessment key for Alternaria blackspot in rapeseed and mustard. Can. Plant Dis. Survey 70: 19-22.

Degenhardt, K. J., G. A. Petrie, and R. A. A. Morrall. 1982. Effects of temperature on spore germination and infection of rapeseed by Alternaria brassicae, A. brassicicola, and A. raphani. Can J. Plant Pathol. 4: 115-118.

Thomas, D. L., M. A. Breve, P. L. Raymer, N. A. Minton, and D. R. Sumner. 1990. Improving rapeseed production practices in the Southeastern United States. ORNL/Sub/86-91324/1. Nat. Tech. Inf. Service, U. S. Dept Commerce.

Control of Sclerotinia Stem Rot of Canola with Fungicides

D. V. Phillips and W. D. Spradlin

Introduction

One of the major disease problems in all oil-seed rape production areas is stem rot caused by Sclerotinia sclerotiorum (Lib.) de Bary. Canola, Brassica napus, planted in Georgia during October or November is consistently damaged in the rosette and/or flowering stage by Sclerotinia stem rot. Most plants killed by stem rot die from girdling stem lesions during or soon after the flowering period, as is typical of stem rot in most areas of the world (Phillips 1992). Most of these lesions result from ascospores that invade organic material, usually fallen flower petals, in contact with stems or leaves. In Georgia, there are rather high rates of Sclerotinia in the rosette stage in addition to the infections at flowering. Some of these infections kill the young plant, but many bolt and develop a lesion at the base later in the season. This situation appears to be unique to the southeastern United States (McQuilken et al. 1994). Most rosette stage infections appear to originate on leaf tissues in direct contact with the soil.

Growers have observed rosette stage infection from early December until bolting (late February-early March), with disease incidence as high as 32 percent. Infection rates during the flowering and early pod-filling stage (late February-early May) are even higher. Disease incidences approaching 100 percent have been observed, with incidences of 30-50 percent frequently observed the first time canola is planted in many fields in northern Georgia. This may be typical of the situation throughout the Piedmont Plateau region of the southeastern United States (Phillips 1992). Losses in southern Georgia were often less severe, but serious losses have occurred in very wet years. This situation is typical of the Coastal Plains regions of the southeastern United States.

Until the 1991-92 season, rosette stage infections were considered relatively unimportant compared to later infections. The remaining healthy plants appeared to compensate for the dead plants, and no relationship existed between levels of rosette infection and infection levels during flowering. In 1992, however, sclerotia that formed on plants killed during the rosette stage, germinated during the flowering period, and contributed many additional apothecia in localized areas (Phillips and Raymer 1993). If the high levels of rosette stage infections observed in the 1991-92 season occur frequently and the resulting sclerotia contribute significantly to the inoculum levels during flowering, attempts to control rosette stage infections may be justified.

In northern Georgia, apothecia are observed between early March and early May each year with the peak numbers observed during late March or early April. This corresponds very closely with the flowering period for all well-adapted cultivars. Apothecia are very rarely found before the plants bolt during the time when rosette stage infections are observed (Phillips and Raymer 1993).

There are no cultivars highly resistant to Sclerotinia stem rot. Research in Georgia and other regions indicates large differences among cultivars in the extent of damage from stem rot (Phillips et al. 1990a, 1990b). Cultivars have been identified that consistently have a lower percentage of infected plants or that are less damaged when they are infected. Efforts to utilize this apparent resistance in high-yielding cultivars are just beginning.

In Canada and Europe, growers sometimes use fungicide applications to control Sclerotinia infections. There is a need to determine if fungicides can be effective in controlling this important disease in the southeastern United States. This research attempted to determine the effectiveness of several fungicides applied at different rates and timings on the incidence and severity of stem rot on commercial cultivars of canola.

Materials and Methods

All experiments were done at the Northwest Georgia Branch Experiment Station, Baty Farm near Rome, Georgia. Canola was planted October 3, 1990 (experiments #1 and 2) at a seeding rate of 8 lb/acre and September 30, 1991 (experiments #3 and 4) at a seeding rate of 6 lb/acre. The 5x25-foot beds were arranged in randomized complete blocks with five replicates. All treatments were applied with a R&D CO₂ spray unit available from R&D Sprayers, Inc., of Opelousas, Louisiana. Three LF3 80-degree spray tips at 19-inch spacing delivered 36.8 gallons per acre at 25 psi.

Disease evaluations were made by counting the number of Sclerotinia lesions, usually on 50 consecutive plants near the center of each plot. Prematurely dead plants were determined by counting those with brown stems at harvest time. Plots were harvested for seed yield with a Hege small plot combine. Yields are reported in lbs/acre at 10% moisture.

Experiment 1. Four rates of ASC-66825 50W and Benlate 50W were applied to the canola variety 'Ceres' (Table 1). Treatments were first applied April 7, 1991 at early bloom (stage at which approximately 50% of the plants have begun blooming). The second application was applied April 22, 1991, at full bloom (stage at which 80% of plants have begun blooming). Sclerotinia disease counts were taken on May 22, 1991; June 6, 1991; and June 19, 1991, and dead plants were counted at harvest on June 19, 1991.

Experiment 2. Two rates of ASC-66825 50W and Benlate 50W were applied to the canola variety 'CC-349' at three different timings (Table 2). The first group of plots received one application at full bloom on April 16, 1991 (80% of plants were blooming). The second group received one application at early bloom on March 31, 1991, (approximately 50% of plants were blooming) and a second application two weeks later (full bloom). The third group also received one application at early bloom and a second application four weeks later. Sclerotinia disease counts were taken on May 22, 1991, and dead plants were counted June 19, 1991, at harvest.

Experiment 3. Two rates of Fluazinam 500 F, Benlate 50W and Ronilan DF were applied to the canola variety 'Ceres' at three different timings. One group of plots received a first applica-tion on April 2, 1992, at the bolt stage (more than 75% of the plants had begun bolting), a second application on April 14, 1992, at the 25% bloom stage (more than 50% of plants had 25% of the flowers open) and a third application 14 days later. The remaining plots received the first application at 25% bloom and a second 14 days later. Sclerotinia disease counts were taken on April 28, 1992, just before the final application and on May 12, 1992, and June 5, 1992.

Experiment 4. Five formulations of Rovral and/or surfactant, Benlate 50W, and Ronilan DF were applied to the canola variety 'Ceres.' All treatments were applied on April 14, 1992, at the 25% bloom stage (more than 50% of the plants had 25% of the flowers open). A second application was applied 14 days later. Sclerotinia disease counts were taken on April 28, 1992, just before the final application, and on May 12, 1992, and June 5, 1992.

Results and Discussion

The disease ratings and seed yields resulting from the various fungicide treatments are pre-sented in Tables 1-4. The disease intensity in both years of this study was moderate. The mean percentage of plants with Sclerotinia lesions for all treatments combined varied from 10.3 to 26.0, and individual treatment means varied from 4.4% to 42.0%. Benlate 50W, Fluazinam 500F, Ronilan DF and Rovral 50WG reduced the percentage of plants with Sclerotinia lesions in, at least, one evaluation. Only Benlate 50W (three applications) and Ronilan DF (two applications) reduced the percentage for the entire evaluation period in one experiment (Table 3).

None of the treatments applied in 1991 reduced the percentage of prematurely dead plants at harvest, and data for this were not collected in 1992. The high percentage of dead plants at harvest in the cultivar 'CC-349' in 1991 was partially due to premature death from Winter Decline Syndrome. At the time counts were made, it was impossible to determine accurately which plants had died from Sclerotinia stem rot and which had died from Winter Decline.

The data from these experiments do not allow any general conclusions about the numbers or timing of treatments, but the data from Table 3 suggests that three applications of Benlate 50W, including a pre-flowering application, warrants further study. Fungicides are usually applied during the flowering period when most infections are initiated (McQuilken et al. 1994). The apparent benefit of fungicides applied before flowering may be related to the early infections frequently observed at the test site.

None of the fungicide treatments resulted in a seed yield that was significantly different from the control. There was no evidence of phytotoxicity from any of the fungicide treatments at the rates and timings used in these experiments.

References

McQuilken, M. P., S. J. Mitchell, and S. A. Archer. 1994. Origin of early attacks of Sclerotinia stem rot on winter oilseed rape (Brassica napus sub. sp. oleifera var. biensis) in the UK. J. of Phytopathology, Berlin, 140: 179-186.

Phillips, D. V. 1992. An overview of Sclerotinia stem rot of canola in the USA. Proc. U.S. Canola Conf. 1: 156-159.

Phillips, D. V. and P. L. Raymer. 1993. Relation-ship between Development of apothecia and Sclerotinia stem rot of canola in Georgia. Phytopathology 83: 1393.

Phillips, D. V., P. L. Raymer, and D. L. Auld. 1990. Apparent resistance to Sclerotinia stem rot in oilseed Brassica. Phytopathology 80: 1039.

Phillips, D. V., P. L. Raymer, and D. L. Auld. 1990. Evaluation of oilseed Brassicas from the USDA World collection for reaction to Sclerotinia stem rot. Proc. Inter. Canola Conf. 1: 306-307.

Fungicides for Control of Blackleg of Canola

D. V. Phillips and W. D. Spradlin

Introduction

Canola (Brassica napus) has excellent potential to become a major winter crop in the southeastern United States, particularly in the Coastal Plain regions. Canola has excellent yield potential and can be doublecropped with soybean and possibly other summer crops (Angus et al. 1991). In the southern United States, canola is planted in the fall and harvested in the spring. Winter types, which require vernalization before flowering, do well in north Georgia but are not well suited to Coastal Plains regions in south Georgia. With average winters, spring-type canolas, which do not have a vernalization requirement, begin flowering in south Georgia in late February and produce excellent seed yields. In other parts of the world where spring types are grown in the winter, the disease Phoma blackleg, caused by the fungus Leptosphaeria maculans, has become a major threat to production (Hill 1990).

Commercial production began in Georgia in 1989, and the first virulent blackleg was observed late in the season at several locations in the 1992-93 crop. It caused substantial yield losses in a few fields in the 1993-94 crop. Phoma blackleg threatens to severely limit expansion of canola production in the South (Hill 1990; Hill and Williams 1988).

As soon as highly virulent strains of the fungus become established, blackleg quickly becomes the most severe disease in other areas where spring-type canola is grown in the winter. Australia has a widespread, severe problem in production areas with climates very similar to southern Georgia (Salisbury and Ballinger 1993). Georgia already has pathogenicity groups (PG) 2, 3, and 4 of the pathogen. This is similar to Australia and is more severe than western Canada, where only PG-2 is widespread. PG-3 and PG-4 usually cause more severe damage than PG-2.

Crop rotation and destruction of crop residue represent important steps in limiting damage from this disease. As acreage increases and more acres are planted to canola, these procedures may not provide adequate protection. Increased protection from diseases will be required to maintain profitable canola production. In other canola production areas, high-yielding cultivars with very high levels of blackleg resistance are just coming into widespread production. Although few of these cultivars are well adapted for use in the southeastern United States, they can provide sources of resistance genes for southeastern breeding programs. The Georgia breeding program is incorporating the highest levels of resistance found in Australian and in European cultivars and selecting types adapted to the southern United States.

A selection of well-adapted cultivars with high levels of resistance to blackleg is still several years away, even longer for many of the highly desirable specialty canolas. The best available resistant cultivars (from Australia) still lose a considerable percentage of plants under severe disease pressure, and the pathogen has an apparently unique ability to produce new biotypes (Plummer and Howlett 1993). Thus, even with resistant cultivars, disease control may require rotation, residue destruction, and fungicides.

Fungicides may be practical for control of blackleg because the highly destructive phase of the disease, girdling basal stem lesions, only occurs if plants are infected early in the season. In plants infected later, superficial stem lesions and leaf spots develop, but little yield loss results. If plants can be protected for about six weeks, the yield-reducing phase declines greatly (Ballinger 1993). In addition, a type of adult plant resistance exists in some European cultivars, but it may be useful only if the plants can be protected from invasion early in the season. In Australia, growers have achieved some disease control with prochloraz used as a seed treatment. But fertilizer amended with flutriafol provides good control of blackleg. This fungicide is applied in the fertilizer because it inhibits germination if in direct contact with the seed (Ballinger 1993). In Canada, propiconazole was recently labeled for use in the rosette stage for control of Phoma blackleg. In the Canadian border states of the United States, where canola is grown during the summer, the fungicide needs are probably very similar to those of Canada. In Georgia, however, the situation may be more closely related to Australia's.

This research attempted to determine the potential of several fungicides, applied as foliar or seed treatments, to control blackleg in the southeastern United States.

Materials and Methods

Fungicide seed treatments were tested in a blackleg disease nursery near Arlington, Georgia. The inoculum for the disease nursery was provided by spreading canola stems, harvested from infected fields the previous season, over the field after planting. The seeds of 'UGA 188-20B' were planted November 14, 1994.

The canola seeds were treated with one of 12 fungicides at the rates shown in Table 1. The treatments were applied by thoroughly mixing the fungicide with the dry seed just before packaging for planting. The treated seeds were planted at the rate of 6 lb/acre. The treatments with the + symbol (Table 1) differed from the others by the addition of an 8X rate of dead seed treated with the same fungicide at the same rate. The treated dead seed was included as a carrier for additional fungicide that would remain in the root zone after germination of the treated seed.

L. maculans continues to invade plants throughout the season, but the girdling stem cankers usually are not apparent until flowering or later. Because many seed treatments protect the plant for only a relatively short time, the entire test was sprayed with a low rate of Benlate 50WP (0.25 lb ai/A) to preserve any differences caused by the seed treatments. Six weekly applications were planned starting December 14, 1994, but because of delayed disease development, eight applications were made.

The foliar fungicide test site was also planted with 'UGA 188-20B' at a rate of 6 lb/A. This site was adjacent to the seed treatment test, and infected canola stems were not put directly on this site. Thus, all inoculum for the foliar fungicide test developed from air-borne spores.

To prevent significant infection before the first fungicide application, three of the four rows in each plot were planted with treated seed. One row was planted with seed treated with Benlate, one with Folicur, and one with Flutriafol at the same rates as in the seed treatment test. As in the seed treatment test, half of each row was planted with seed mixed with an 8X quantity of treated dead seed to provide additional fungicide that would remain in the root zone. The fourth row was planted with untreated seed.

The plots were 20 ft. long, arranged in randomized block design and were sprayed weekly two, three, four, five or eight times starting on December 14, 1994. All treatments were applied with a CO₂ spray unit available from R&D Sprayers, Inc., of Opelousas, Louisiana. Three LF3 80-degree spray tips at 19-inch spacing delivered 36.8 gallons per acre at 25 psi.

Blackleg ratings on both the seed treatment and foliar fungicide tests were taken on May 4 and 25, 1995. The rating scale used was 0 = no disease, 1 = 1%-10% diseased or dead plants, 2 = 11%-20%, ... 10 = 91%-100% diseased or dead plants. Canola plants in pots were taken to the field each week after planting, and after one week's exposure, they were returned to the greenhouse and observed for symptoms of blackleg.

A stunting and a darker green color appeared soon after emergence in the plants from seed treated with Folicur. This stunting was still apparent several weeks later. On February 2, 1995, before bolting, plants were rated by com-paring the height of plants from Folicur-treated seed with plants in the adjacent row that were from seed treated with Benlate. The rating scale was: 1 = plant height at 25% the height of plants from seed treated with Benlate; 2 = plant height at 50% the height of plants from seed treated with Benlate; 3 = plant height at 75% the height of plants from seed treated with Benlate; 4 = plant height the same as the height of plants from seed treated with Benlate.

Results and Discussion

The indicator plants that were placed in the field each week to determine the time of invasion of the pathogen remained disease-free until 12 weeks after planting. Simultaneously, the first foliar lesions were seen on plants in the field. This late onset of disease indicated the stem girdling phase would occur at very low levels (Ballinger 1993; Salisbury and Ballinger 1993).

Dry weather delayed disease onset after planting. The inoculum was kept dry over the summer to prevent decomposition and was scattered over the test site after planting. There was no irrigation available and no significant rain fell until four weeks after planting. Thus, few ascospores ready for discharge existed until six to eight weeks after planting, and a combination of favorable weather for ascospore release and for invasion apparently did not occur until nearly 12 weeks after planting.

The disease ratings in untreated plots were low, despite planting with a highly susceptible cultivar. No significant differences in disease rating occurred because of either foliar applications or seed treatment (Tables 1 and 2). Slightly higher disease ratings occurred in the seed treatment test, where diseased stems were scattered over the plots, than in the foliar fungicide test. This could stem from a higher concentration of spores or to direct invasion of plants in contact with diseased stems.

The plots were not harvested to determine seed yield because of the extreme variability of growth across the test site and because of the low level of disease development. Folicur applied as a seed treatment affected the growth of plants in the seedling stage. Plants from treated seed were smaller and darker green than plants from untreated seed. This could be seen at all stages before bolting. Plants from treated seed bolted normally, and no apparent height difference occurred after bolting. No apparent effect on seedling size or color resulted from any of the other fungicides in these tests.

The ratings in Table 3 compare plant size before bolting between plants from seed treated with Folicur and plants from seed treated with Benlate. This comparative rating was done rather than a simple height measurement, because considerable variation occurred in plant height due to other factors across the plot area. The planting plan of the foliar fungicide test had Folicur-treated seed planted in a row 7 inches from a row of seed treated with Benlate, in all parts of the test site. Thus, the comparative rating eliminated much of the variability from other factors.

Folicur applied to seed resulted in a mean rating of 2.9. This is equivalent to about a 25% reduction in height. When the 8X quantity of treated dead seed was also planted, the mean rating was 1.9, equivalent to about a 50% reduction. None of the fungicides applied to the foliage influenced plant height. It is interesting that the addition of more fungicide in the root zone (by the treated dead seed) significantly reduced plant size, but the application of two to five foliar sprays had no effect on plant size.

References

Angus, J.F., A. F. van Herwaarde, and C. N. Howe. 1991. Productivity and break crop effects of winter-growing oilseeds. Aust. J. Exp. Agric. 31: 669-677.

Ballinger, D. J. 1993. Effect of seed dressing on establishment and yield of canola. Proc. Aust. Research Assem. Brassicas 9: 100-106.

Hill, C.B. 1990. Blackleg of crucifers, pp. 253-271. In A. N. Mukhopadhyay (ed.) Plant Diseases of Economic Importance. Prentice-Hall, New York.

Hill, C.B. and P. H. Williams. 1988. Leptosphaeria maculans, cause of blackleg of crucifers, pp. 169-174. In G. H. Sidhu,(ed.). Advances in Plant Pathology, Volume 6.

Plummer, K. M. and B. J. Howlett. 1993. Genetic variation in Australian isolates of the blackleg fungus Leptosphaeria maculans. Proc. Aust. Res. Assem. Brassicas 9: 112-117.

Salisbury, P. A. and D. J. Ballinger. 1993. Evaluation of race variability in Leptosphaeria maculans on Brassica species in Australia. Proc. Aust. Res. Assem. Brassicas 9: 107-111.

Comparison of Foliar-Applied Insecticides for Aphid Control in Rosette and Flowering Canola

G. David Buntin

Introduction

Aphids are the most important insect pest of canola in the Coastal Plain of the southeast. Season-long damage can reduce yield by 35% (Buntin and Raymer 1994). Aphids invade canola in the fall and develop throughout the winter. These aphids and new migrants can increase to very large populations in late winter/early spring when canola is flowering. The turnip aphid, Lipaphis erysimi (Kaltenbach), and green peach aphid, Myzus persicae (Sulzer), occur in canola from seedling emergence through flowering. The cabbage aphid, Brevicoryne brassicae (L.), also occurs in canola mostly during flowering.

Aphid populations during flowering in early spring can increase to enormous numbers of sev-eral hundred aphids per plant. Infestations clump on one to a dozen adjacent plants, and infestations become very noticeable to growers when popula-tions reach this level. Infested plants typically are stunted, and aphid injury inhibits flowering and pod formation. Parathion and Thiodan currently are labeled for aphid control in canola. Trials were conducted in three year to evaluate these insecticides and other potential aphicides that are labeled for aphid control in other crops.

Materials and Methods

Studies were conducted in 1990, 1991, and 1993 at the Southwest Branch Experiment Station located near Plains, Georgia. In 1992, the study was conducted at the Bledsoe Research Farm located near Griffin, Georgia. Cultivars were 'Delta' in 1990 and 1991 and 'Bingo' in 1993 at Plains and 'Cobra' at Griffin. Canola seeds were planted on October 27, 1989; October 26, 1990; October 1, 1991; and October 28, 1992, in 7-inch rows using a small plot grain drill. Tillage was conventional, with plowing followed by disk harrowing before planting. Soil pH was near 6.5 in all years. A 7-14-21 fertilizer (N-P-K) was broadcast and incorporated at 700 lb/acre before planting resulting in 49 lb/acre of nitrogen. Nitrogen also was topdress-applied in early March at 100 lb/acre as ammonium nitrate. Treflan was applied before planting to control weeds. Plots measured 5 x 20 ft. in the first two years and 25 by 30 ft. in 1992 and were arranged in a randomized complete block design with four replications.

Spray treatments were applied at about full bloom on March 15, 1990; March 18, 1991; and April 10, 1992. In 1993, treatments were applied at the 6-8 leaf rosette stage on January 15. Treatments were applied using a CO₂-powered back-pack sprayer equipped with 004 flat fan nozzles. Sprayer pressure was 20 psi, which delivered 27 gal/acre. Weather conditions for flowering sprays were sunny, 70-75 degrees F, and light winds, whereas temperature in 1993 was about 60 degrees F. The percentage of infested flower racemes (terminals) was determined by inspecting 100 (200 in 1992) racemes per plot. The number of aphids on infested racemes also was counted on all post-treatment sampling dates. In 1993, aphids were counted on 25 leaves per plot. Aphids were sampled before application and periodically after application in each year. Plots in all years were harvested with a small-plot combine in late May. Seeds were weighed and yield was adjusted to 8% moisture content. Grain test weight also was measured.

Results were analyzed by sample date with an analysis of variance, and means were separated using the least significant difference (LSD) test (P< 0.05). Percentage data were transformed with an square root, angular transformation before analysis.

Results

1990. All insecticide treatments controlled aphid infestations at five days after treatment (Table 1). A very intense rainstorm on March 17 washed aphids from the plants before another sample could be taken. Grain yield and test weight were not significantly affected by the treatments.

1991. Turnip aphids accounted for about 75% of aphids collected, with the remainder being green peach aphids. Treatments of malathion, Cygon 400, Lorsban 4E, and DiSyston 8E effectively controlled aphid infestations (Table 2). Aphids remained in treated plots at three days after treatment but were mostly absent in these plots at 6 and 17 days after treatment. Thiodan 50WP was not effective in this trial. Grain yield and test weight were not significantly affected by the treatments.

1992. The turnip aphid was the predominant species. Cabbage aphids were not found in this study. Treatment effects on turnip aphids, green peach aphids, and total aphids are shown in Tables 3, 4, and 5, respectively. All insecticide treatments significantly reduced the percentage of infested racemes, number of aphids per raceme, and number of aphids per infested raceme for turnip aphids and total aphids on all post-application sampling dates. However, the percentage of infested racemes with turnip aphids did not differ significantly between treatments at 18 days after application. Green peach aphid also were reduced by all insecticides at three and seven days after application, but few green peach aphids were collected on later dates.

Cygon 400 was the most effective insecticide in the study, with essentially no turnip aphids and only a few green peach aphids found after application. The other treatments were equally effective in reducing aphid infestations and numbers, and these treatments were similar in efficacy to Cygon 400 on most sample dates. No significant differences existed between the 0.75-lb and 1.00-lb rates of Thiodan 3E in controlling either aphid species. The insecticides reduced the percentage of infested racemes, but did not eliminate aphids on some infested racemes, particularly on racemes with large initial numbers of aphids and on racemes lower in the canopy.

Treatments also had a large effect on cabbage seedpod weevil damage (see section on cabbage seedpod weevil). Treatments did not significantly (P = 0.58) affect canola grain yield (Table 6). Yield probably was not significantly affected because of poor and variable stands in some plots, and because treatments were applied after some aphid damage had already occurred. All treatments, except Cygon, had significantly greater grain test weight than the untreated check.

1993. Aphids were about an equal mix of turnip and green peach aphids when treatments were applied. All treatments of Thiodan 3E and Cygon exhibited equal effectiveness in controlling turnip and green peach aphids (Table 7). Treatments virtually eliminated turnip aphids for 39 days. All treatments reduced green peach aphid numbers by 85% to 95% for 28 days. Lower rates of both insecticides were as effective as standard rates. Grain yield and test weight did not significantly differ between treatments (Table 8).

Discussion

Most of the insecticides tested controlled turnip and green peach aphids during late rosette and bloom stages. All insecticide treatments tended to be more effective against turnip than against green peach aphids. Dimethoate (Cygon 400) was consistently and noticeably more effective than the other treatments. Furthermore, the low rate of 0.25 lb ai/acre was as effective as higher standard rates. Lorsban 4E, DiSyston 8E, and Malathion also proved effective in trials where they were tested. Efficacy of Thiodan varied; the 50WP formulation was less effective than the 3E formulation. The 0.5-lb and 0.75-lb rates of Thiodan 3E were as effective as the standard 1.0-lb rate. Aphid control during bloom did not affect grain yield in any year, probably because the full bloom stage is less susceptible to aphid injury than earlier plant growth stages.

Reference

Buntin, G. D. and P. L. Raymer. 1994. Pest status of aphids and other insects in winter canola in Georgia. J. Econ. Entomol. 87: 1097-1104.