Pisum Genetics
2007—Volume 39
Brief Communications
The following five papers are summaries of North American Pulse Improvement
Association presentations, November 1 and 2, 2007
Field evaluation of biological control and fungicide seed treatments for pre-emergence damping off of chickpeas
Leisso, R.S. and Burrows, M.E. Dept. of Plant Sci. and Plant Path.
Montana State Univ., Bozeman, MT, U.S.A.
Pre-emergence damping off of chickpeas is a disease caused by a complex of soil-borne pathogens (1). In
Montana, an increasing number of growers are interested in growing chickpeas organically, especially the kabuli
varieties. Montana has the greatest number of acres devoted to organic wheat production in the United States (2),
and organic chickpeas have the potential to be a profitable rotation crop. A number of fungicide seed treatments
for pre-emergence damping off are available (3-5), but growers cultivating chickpeas organically can not use
fungicide seed treatments. Organic growers could use biologically based seed treatments, but little data exists
regarding the efficacy of biocontrol seed treatments for chickpeas in Montana. However, tests of the biological
seed treatment Kodiak (Bacillus subtilis GB03) in Colorado indicated success for this seed treatment (6). Beyond
the use of biological seed treatments in organic systems, they could also be used by conventional growers for
chickpeas as part of an integrated strategy for disease control.
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Pisum Genetics
2007—Volume 39
Brief Communications
The objective of this research was to determine which biological and conventional seed treatments would be
the most useful for both conventional and organic chickpea growers. Biocontrol seed treatments were tested alone
and in combination with conventional seed treatments to determine if commercially available biological control
seed treatments would be effective for managing pre-emergence damping off. Furthermore, this research sought
to determine if biologically based seed treatments, whether used alone, or in combination with standard fungicide
seed treatments, would affect other measures of plant health, ultimately leading to increased yield over untreated
seeds and seeds treated solely with standard fungicides.
Seed treatments were tested on both kabuli and desi varieties. Winter greenhouse results indicated that desi
varieties were less susceptible to pre-emergence damping off than kabuli varieties. Five replicates of twelve seeds
each of a desi variety (CDC-Anna) and a kabuli variety (Dylan) were planted in sterile and non-sterile field soil
obtained from a chickpea field in Big Sandy, Montana. Germination of the desi and kabuli seeds in sterile field soil
were 84% and 70% respectively, whereas germination of desi and kabuli seeds in non-sterile field soil were 80%
and 0% respectively. Results were averaged over two repetitions of the experiment. In collusion with these
results, the desi variety (CDC-Anna) was also less susceptible to pre-emergence damping off than the kabuli
(Sierra) variety in field trials.
The biological seed treatments Actinovate SP (Streptomyces lydicus WYEC108), Kodiak (Bacillus subtilus
GB03), Mycostop (Streptomyces griseoviridis K61), Subtilex (Bacillus subtilus MB1600), T-22 (Trichoderma
harzanium
Rifai strain KLR AG-13), and Yield Shield (Bacillus pumilus GB34), as well as the fungicide seed
treatments Apron XL LS (metalaxyl/mefanoxam) and Maxim (fluidoxonoil) were tested in greenhouse
experiments to determine which were most effective for managing pre-emergence damping off cause by Pythium
ultimum.
Kodiak, T-22, and Yield Shield were the most effective biological seed treatments for reducing pre-
emergence damping off and increasing stand counts over the untreated control. Apron XL LS was the most
effective fungicide treatment and the most effective seed treatment overall for reducing pre-emergence damping
off caused by Pythium ultimum in the greenhouse.
Seed treatments were tested at three field sites near Bozeman, Huntley, and Sidney, Montana in the summer
of 2007. Each biological and conventional seed treatment was tested alone, as well as in combination with one
another to determine if biological and conventional seed treatments would provide additive benefits. Treatments
tested were as follows: Kodiak, T-22, Yield Shield, Apron, Maxim, Apron+Kodiak, Apron+T-22, Apron+Yield
Shield, Maxim+Kodiak, Maxim+T-22, and Maxim+Yield Shield. All seed treatments were applied at the
manufacturer's highest recommended rates two days prior to planting.
Table 1. Seed treatments tested for management of pre-emergence damping off of chickpeas
Treatment
Active ingredient
Type
Rate
Kodiak
Bacillus subtilis GB03
biological control
.125 oz/cwt
T-22
Trichoderma harzanium Rifai
biological control
8 oz/cwt
strain KLR AG-13
Yield Shield
Bacillus pumilus GB34
biological control
.125 oz/cwt
Apron XL LS
metal axyl / mefanoxam
fungicide
.64 oz/cwt
Maxim
fluidoxonil
fungicide
.16 oz/cwt
Stand counts of chickpea seedlings were obtained at each of the field sites approximately three weeks after
planting. Desi variety CDC-Anna had low incidence of pre-emergence damping off and few significant differences
in stand count between the control and seed treatments at all three sites. For the kabuli variety Sierra, seed
treatments containing Apron were most effective for reducing pre-emergence damping-off and increasing stand
count. On average, at Bozeman, seed treatments containing Apron increased Sierra stand counts by 60%, at
Huntley 38%, and at Sidney, where the germination period was cool and wet and disease pressure severe, 900%.
Stand count for seeds treated with biological controls generally did not differ significantly from the untreated
control.
29

Pisum Genetics
2007—Volume 39
Brief Communications
Ascochyta blight was rated in plots to determine if biological controls would have any plant health effects
including induced systemic resistance (7). Plots were monitored and rated for Ascochyta blight using a 1-9 scale
(8) before foliar fungicide applications (Proline 480 and Quadris Opti SC) to control Ascochyta blight. Prior to
applications of fungicides, disease ratings did not differ significantly from the untreated control plot at any of the
locations. Ratings were taken every 7-10 days following the first fungicide application, and the overall AUDPC
(area under the disease progress curve) calculated (9). Seed treatments did not consistently lower the severity of
Ascochyta blight at any of the three locations. Other measures of plant health such as plant height, plant weight,
seed size and yield indicated no differences between seed treatment plots and untreated control plots.
Although significant differences in stand counts for seed treatments were observed, there were few consistent
significant yield differences for the desi or kabuli varieties. At Sidney, no yield data was collected for the kabuli
variety Sierra, due to extremely low initial stands.
Biocontrol seed treatments were ineffective for managing pre-emergence damping-off of kabuli chickpeas in
Montana. Desi chickpeas incurred low incidence of pre-emergence damping off and few significant differences in
stand count were observed at any of the three locations in this study. Seed treatments containing the fungicide
Apron XL LS were most effective for increasing stand count. Despite differences in stand count, there were few
significant differences in seed quality or yield.
1 Trapero-Casas, A., Kaiser, W.J. and Ingram, D.M. 1990. Plant Disease, 74: 563-569.
2. United States Department of Agriculture, Economic Reporting Service. 2005. Montana Organic Production.
3. Chen, W., Paulitz, T.C., Mcphee, K.E. and Muehlbauer, F.J. 2004. Fungicide and Nematicide Tests 59
(ST017).
4. Lauver, M. and S. Guy. 2005. Fungicide and Nematicide Tests, 61 (ST003).
5. Smiley, R.J., Gourlie, J., Whittaker, R, Easley, S., Rhinhart, K., Jacobsen, E., Burnett, A., Jackson, J.,
Kellogg, D. and Zeckman, T. 2001. Oregon Ag. Expt. Sta. Annual Report, Special Report 1054, p. 120-127.
6. Hammon, R. and Berrada, A. 2001. Evaluation of Kodiak (R) Biological Seed Treatment to Control Seedling
Diseases
of Chickpea, C.S.U.C. Extension, Editor.
7. Kloepper, J.W., Ryu, C.-M. and Zhang, S. 2004. Phytopath. 94: 1259-1266.
8. Singh, K.B., Malhotra, R.S. and Witcombe, J.R. 1981. Plant Disease 65: 586-587.
9. Campell, C.L. and Madden, L.V. 1990. Introduction to Plant Disease Epidemiology. John Wiley & Sons, Inc.
New York, p. 532.