scholarly journals Relationship Between Sudden Death Syndrome caused by Fusarium virguliforme and Soybean Yield: A Meta-Analysis

Plant Disease ◽  
2020 ◽  
Vol 104 (6) ◽  
pp. 1736-1743
Author(s):  
Yuba R. Kandel ◽  
Carl A. Bradley ◽  
Martin I. Chilvers ◽  
Febina M. Mathew ◽  
Albert U. Tenuta ◽  
...  

In total, 52 uniform field experiments were conducted in Illinois, Indiana, Iowa, Michigan, South Dakota, and Wisconsin in the United States and Ontario, Canada from 2013 to 2017 comparing crop protection products against sudden death syndrome (SDS) of soybean. Data were analyzed using meta-analytic models to summarize the relationship between foliar disease index (FDX) and yield. For each study, correlation and regression analyses were performed separately to determine three effect sizes: Fisher’s transformation of correlation coefficients (Z r ), intercept (β0), and slope (β1). Random- and mixed-effect meta-analyses were used to summarize the effect sizes. Study- and location-specific moderator variables FDX (low < 10% and high ≥ 10%), date of planting (early = prior to 7 May, conventional = 7 to 21 May, and late = after 21 May) cultivar (susceptible and partially resistant to SDS), study location, and growing season were used as fixed effects. The overall mean effect sizes of transformed correlation coefficient [Formula: see text] r was −0.41 and different from zero (P < 0.001), indicating that yield was negatively correlated with FDX. The [Formula: see text] r was affected by disease level (P < 0.01) and cultivar (P = 0.02), with a greater effect at higher disease levels and with susceptible cultivars. The mean [Formula: see text] 0 was 4,121 kg/ha and mean [Formula: see text] 1 was −21 kg/ha/% FDX and were different from zero (P < 0.01). Results from these data indicate that, for every unit of FDX increase, yield was decreased by 0.5%. Study locations and year affected the [Formula: see text] 0 , whereas none of the moderator variables significantly affected [Formula: see text] 1.

Plant Disease ◽  
2001 ◽  
Vol 85 (7) ◽  
pp. 773-779 ◽  
Author(s):  
S. Sanogo ◽  
X. B. Yang ◽  
P. Lundeen

Three-year field experiments were conducted to assess the development of sudden death syndrome (caused by Fusarium solani f. sp. glycines) in three soybean cultivars, tolerant (P9344 and A3071) and nontolerant (BSR101), to glyphosate following foliar application of four herbicides (acifluorfen, glyphosate, imazethapyr, and lactofen) commonly applied to soybeans in the north-central region of the United States. Cultivar A3071 is resistant to sudden death syndrome, whereas cultivars P9344 and BSR101 are susceptible to this disease. There was no statistically significant cultivar-herbicide interaction with respect to the severity of foliar symptoms of the disease and the frequency of isolation of F. solani f. sp. glycines from roots of soybean plants. Across all herbicide treatments, the level of sudden death syndrome was lower in the disease-resistant cultivar than in the susceptible ones. There was an increase in the disease levels under application of acifluorfen, glyphosate, and imazethapyr compared with nontreated or lactofen-treated plants. The results obtained indicate that the response of glyphosate-tolerant soybeans to sudden death syndrome is not different from the response of conventional soybeans to this disease following application of the selected herbicides, and the resistance of soybean to sudden death syndrome was not changed with application of glyphosate.


2011 ◽  
Vol 101 (7) ◽  
pp. 878-886 ◽  
Author(s):  
Andreas Westphal ◽  
Lijuan Xing

The ecology of the complex of soybean cyst nematode (SCN) and sudden death syndrome (SDS) of soybean was investigated under soybean monoculture in two field experiments from 2003 to 2007. Initially, susceptible soybean ‘Spencer’ was planted while inoculating Fusarium virguliforme into nonfumigated or preseason-fumigated plots (methyl bromide, MB, at 450 kg/ha), and SCN and SDS were monitored. In one field, SCN population densities declined in nonfumigated but increased in fumigated plots. After years of limited SDS in 2003 and 2004, SDS developed later in nonfumigated than fumigated plots. In 2006 in the greenhouse, nondisturbed or disturbed soil cores (10-cm diameter, 30-cm depth) from field plots received two two-level factors: (i) nonfumigated or fumigated (1,070 kg/ha MB); and (ii) noninoculated or inoculated with 9,000 second-stage juveniles of SCN. At harvest, nonfumigated cores from nonfumigated plots had fewer nematodes and less SDS regardless of disturbance or inoculation than the corresponding fumigated cores and any cores from fumigated plots. In the second field, SCN became detectable after 2003 during the monoculture in nonfumigated plots and lagged in fumigated plots; both treatments had low levels of SDS. Exploiting the suppressiveness of the first field could allow for biological control of SDS and SCN in soybean production.


2019 ◽  
Vol 113 (2) ◽  
pp. 770-778
Author(s):  
Kaushalya G Amarasekare ◽  
Peter W Shearer

Abstract Deraeocoris brevis (Uhler) is a key predatory natural enemy of insects and mites in pear orchards in the United States. Insecticides used for crop protection in pear orchards and their residues can negatively affect populations of D. brevis. The focus of this study was to investigate the field-aged residual effects of lambda-cyhalothrin, spinetoram, and chlorantraniliprole insecticides on D. brevis through contact exposure. An airblast sprayer was used to apply the high label rate of insecticides on pear trees. Leaves were collected from the experimental trees at 1 d after treatment (DAT) and then at 7-d intervals up to 21 DAT. Adults and nymphs were exposed to leaves with insecticide residues or untreated control for 72 h in the laboratory. The nymphs that survived the treatments were reared until they emerged as adults. The surviving paired adults were reared until death. The treated nymphs were assessed for acute mortality, survival, developmental time, and the sex ratio if they emerged as adults. The treated adults were assessed for acute and chronic mortality, fecundity, fertility, and longevity. Both nymphs and adults exposed to leaf residues of lambda-cyhalothrin had significantly higher acute mortality compared with the insects exposed to the control. When compared with the control treatment, the toxicity of field-aged residues of lambda-cyhalothrin, chlorantraniliprole, and spinetoram can persist over a longer period of time. Similar patterns were observed in previous laboratory and field experiments on D. brevis. We discuss the residual effects of three insecticides through contact exposure of D. brevis.


Plant Disease ◽  
2019 ◽  
Vol 103 (6) ◽  
pp. 1234-1243 ◽  
Author(s):  
Jie Wang ◽  
Hyunkyu Sang ◽  
Janette L. Jacobs ◽  
Kjersten A. Oudman ◽  
Linda E. Hanson ◽  
...  

Sudden death syndrome (SDS), caused by members of Fusarium solani species complex (FSSC) clade 2, is a major and economically important disease in soybean worldwide. The primary causal agent of SDS isolated to date in North America has been F. virguliforme. In 2014 and 2016, SDS symptoms were found in two soybean fields located on the same farm in Michigan. Seventy Fusarium strains were isolated from roots of the SDS-symptomatic soybeans in two fields. Phylogenetic analysis of partial sequences of elongation factor-1α, the nuclear ribosomal DNA intergenic spacer region, and the RNA polymerase II beta subunit revealed that the primary FSSC species isolated was F. brasiliense (58 and 36% in each field) and the remaining Fusarium strains were identified as F. cuneirostrum, F. phaseoli, an undescribed Fusarium sp. from FSSC clade 2, and strains in FSSC clade 5 and FSSC clade 11. Molecular identification was supported with morphological analysis and a pathogenicity assay. The soybean seedling pathogenicity assay indicated that F. brasiliense was capable of causing typical foliar SDS symptoms. Both root rot and foliar disease severity were variable by strain, just as they are in F. virguliforme. Both FSSC 5 and FSSC 11 strains were also capable of causing root rot, but SDS foliar symptoms were not detected. To our knowledge, this is the first report of F. brasiliense causing SDS in soybean in the United States and the first report of F. cuneirostrum, F. phaseoli, an as-yet-unnamed Fusarium sp., and strains in FSSC clade 5 and FSSC clade 11 associated with or causing root rot of soybean in Michigan.


Plant Disease ◽  
1998 ◽  
Vol 82 (4) ◽  
pp. 448-448 ◽  
Author(s):  
T. R. Anderson ◽  
A. U. Tenuta

Sudden death syndrome (SDS), caused by Fusarium solani (Mart.) Sacc. f. sp. glycines, is a disease of soybean (Glycine max (L.) Merr.) in several central and southern states of the United States. In Ontario, Canada, individual soybean plants with typical foliar symptoms of SDS (1) have been observed annually in Kent County since 1993 but the causal organism was not isolated or identified. In 1996, plants with symptoms of SDS were observed in six fields located in Essex, Kent, and Lambton counties. Interveinal chlorosis and necrosis occurred on top leaves of affected plants and a pale brown discoloration occurred in the vascular system in lower stems and upper tap roots. Slow-growing isolates of F. solani f. sp. glycines with typical blue sporodochia were isolated from symptomatic plants on acidified potato dextrose agar (1). Root inoculation of 15 2-week-old seedlings with colonized oat kernals with each of five single-spore isolates caused typical SDS symptoms on 5-week-old soybean plants of cvs. Conrad, A2540, S19-90, and Ripley in the greenhouse. The severity and incidence of symptoms varied with cultivar and isolate. Of 125 plants inoculated, 6% of Conrad, 10% of A2540, 14% of S19-90, and 17% of Ripley plants developed foliar symptoms. Symptoms did not develop on noninoculated controls. F. solani f. sp. glycines was reisolated from roots of symptomatic plants. Although Ripley is known to have resistance to SDS (2), foliar and root symptoms developed following inoculation with each Ontario isolate of F. solani f. sp. glycines. Yield losses in 1996 were difficult to assess because of the scattered distribution of diseased plants in most fields. Diseased plants had few and poorly filled pods. In two fields, soybean growth was severely restricted in large areas covering 2 ha each; however, soybean cyst nematode (SCN) was present in both fields. SCN was present at all locations. Although total yield losses are currently low, it is evident that F. solani f. sp. glycines causing SDS has become widely distributed in southwest Ontario and disease severity is increasing. References: (1) K. W. Roy et al. Phytopathology 79:191, 1989. (2) P. A. Stevens et al. Crop Sci. 33:929, 1993.


Plant Disease ◽  
2010 ◽  
Vol 94 (9) ◽  
pp. 1164-1164 ◽  
Author(s):  
M. I. Chilvers ◽  
D. E. Brown-Rytlewski

Leaf lesions and root rot symptoms typical of soybean sudden death syndrome (SDS) caused by Fusarium virguliforme O'Donnell & T. Aoki were observed in commercial soybeans (Glycine max (L.) Merr.) in southern Michigan. Leaf symptoms ranged from chlorotic spots to severe interveinal chlorosis and necrosis, no foliar pathogens were noted. In 2008, isolates were collected from Berrien and St. Joseph counties. In 2009, isolates were collected from Cass, St. Joseph, Van Buren, Allegan, and Monroe counties. Pieces of roots with root rot symptoms were washed prior to surface disinfestation with 70% ethanol for 30 s and 0.5% NaOCl for 1 min and incubated on water agar (WA) in petri plates amended with 50 μg/ml of chloramphenicol for the production of sporodochia. Alternatively, spores were collected directly from nondisinfested roots expressing blue sporodochia. Single-spore cultures were derived by streaking macroconidia with a bacterial loop onto 3% WA + chloramphenicol and incubated overnight. With a dissecting microscope, single germinated macroconidia were collected with a sterile 0.2-mm-diameter insect pin and transferred to potato dextrose agar (PDA). Cultures on PDA grew slowly and developed blue-to-purple masses of sporodochia typical of F. virguliforme descriptions and similar to a representative isolate, Mont-1, grown alongside (1,2). Size of macroconidia from the six representative isolates, one from each county (including isolates derived from surface-disinfested and nondisinfested roots), and Mont-1 were determined to be within the range for F. virguliforme (42 to 56 × 5 to 6 μm), with an average of four septa per macroconidia. Identity of the representative isolates was confirmed by partial DNA sequencing of both strands of the internal transcribed spacer (ITS) region of the ribosomal RNA gene, translation elongation factor 1-α, and β-tubulin loci. All six representative isolates were identical in each of the three loci and matched with 100% similarity F. virguliforme accessions in GenBank and Fusarium-ID database searches, except for the β-tubulin locus in which a single nucleotide insertion was noted (Accession Nos. HM453328–HM453330). Sequences were 98 to 99% similar to other SDS Fusarium spp. not yet recorded in the United States. Koch's postulates were performed in the greenhouse according to Malvick and Bussey (3). Infested sorghum seed (~20 g) was placed 2 cm below soybean seed of susceptible cv. Williams 82 in plastic pots. Noninfested sorghum seed was used as a negative control and sorghum infested with Mont-1 as a positive control. Chlorotic spots developed 2 weeks after establishing the trial, and 3 to 4 weeks postinoculation, severe SDS symptoms of foliar interveinal chlorosis and necrosis and severe root rot developed. Koch's postulates were completed by reisolating F. virguliforme from a subset of infected plants. In addition, an isolate of F. virguliforme collected in 2008 was used to inoculate a 2009 field trial in East Lansing, MI with no history of SDS. Typical SDS symptoms developed in the field trial and F. virguliforme was isolated from a symptomatic plant that was identified as described above. Despite being reported across the majority of soybean-producing states, to our knowledge, this is the first confirmation and distribution report for SDS in Michigan. References: (1) T. Aoki et al. Mycoscience 46:162, 2005. (2) G. L. Hartman et al. Plant Dis. 81:515, 1997. (3) D. K. Malvick and K. E. Bussey. Can. J. Plant Pathol. 30:467, 2008.


2019 ◽  
Vol 109 (10) ◽  
pp. 1710-1719 ◽  
Author(s):  
Mitchell G. Roth ◽  
Zachary A. Noel ◽  
Jie Wang ◽  
Fred Warner ◽  
Adam M. Byrne ◽  
...  

In the United States, sudden death syndrome (SDS) of soybean is caused by the fungal pathogen Fusarium virguliforme and is responsible for important yield losses each year. Understanding the risk of SDS development and subsequent yield loss could provide growers with valuable information for management of this challenging disease. Current management strategies for F. virguliforme use partially resistant cultivars, fungicide seed treatments, and extended crop rotations with diverse crops. The aim of this study was to develop models to predict SDS severity and soybean yield loss using at-planting risk factors to integrate with current SDS management strategies. In 2014 and 2015, field studies were conducted in adjacent fields in Decatur, MI, which were intensively monitored for F. virguliforme and nematode quantities at-planting, plant health throughout the growing season, end-of-season SDS severity, and yield using an unbiased grid sampling scheme. In both years, F. virguliforme and soybean cyst nematode (SCN) quantities were unevenly distributed throughout the field. The distribution of F. virguliforme at-planting had a significant correlation with end-of-season SDS severity in 2015, and a significant correlation to yield in 2014 (P < 0.05). SCN distributions at-planting were significantly correlated with end-of-season SDS severity and yield in 2015 (P < 0.05). Prediction models developed through multiple linear regression showed that F. virguliforme abundance (P < 0.001), SCN egg quantity (P < 0.001), and year (P < 0.01) explained the most variation in end-of-season SDS (R2 = 0.32), whereas end-of-season SDS (P < 0.001) and end-of-season root dry weight (P < 0.001) explained the most variation in soybean yield (R2 = 0.53). Further, multivariate analyses support a synergistic relationship between F. virguliforme and SCN, enhancing the severity of foliar SDS. These models indicate that it is possible to predict patches of SDS severity using at-planting risk factors. Verifying these models and incorporating additional data types may help improve SDS management and forecast soybean markets in response to SDS threats.


Plant Disease ◽  
2015 ◽  
Vol 99 (3) ◽  
pp. 347-354 ◽  
Author(s):  
Yuba R. Kandel ◽  
Carl A. Bradley ◽  
Kiersten A. Wise ◽  
Martin I. Chilvers ◽  
Albert U. Tenuta ◽  
...  

Sudden death syndrome (SDS), caused by Fusarium virguliforme, is an important yield limiting disease of soybean. Glyphosate is used to control weeds in soybean; however, its effect on SDS is not clearly understood. The objective of this study was to examine the impact of glyphosate on SDS, yield, and plant nutrition under field conditions. Fourteen field experiments were conducted in Iowa, Illinois, Indiana, Michigan, Wisconsin, and Ontario, Canada during 2011 to 2013. The experiment consisted of six treatment combinations of glyphosate and herbicides not containing glyphosate. Disease index was significantly different across the location–years, ranging from 0 to 65. The highest disease was noted in locations with irrigation, indicating that high soil moisture favors development of SDS. There were no effects of herbicide treatments or interactions on disease. The foliar disease index among the treatments over all years ranged from 9 to 13. Glyphosate-treatments also tended to yield more than treatments of herbicides not containing glyphosate. There were no interactions between glyphosate-treatments and total manganese in plant tissue. The interaction of glyphosate with other nutrients in plant tissue was inconclusive. This 14 location–year study demonstrated that glyphosate application did not increase SDS severity or adversely affect soybean yield under field conditions.


Plant Disease ◽  
2019 ◽  
Vol 103 (7) ◽  
pp. 1712-1720 ◽  
Author(s):  
Yuba R. Kandel ◽  
Carl A. Bradley ◽  
Martin I. Chilvers ◽  
Febina M. Mathew ◽  
Albert U. Tenuta ◽  
...  

Sudden death syndrome (SDS), caused by Fusarium virguliforme, is an important soilborne disease of soybean. Risk of SDS increases when cool and wet conditions occur soon after planting. Recently, multiple seed treatment and foliar products have been registered and advertised for management of SDS but not all have been tested side by side in the same field experiment at multiple field locations. In 2015 and 2016, seed treatment fungicides fluopyram and thiabendazole; seed treatment biochemical pesticides citric acid and saponins extract of Chenopodium quinoa; foliar fungicides fluoxastrobin + flutriafol; and an herbicide, lactofen, were evaluated in Illinois, Indiana, Iowa, Michigan, South Dakota, Wisconsin, and Ontario for SDS management. Treatments were tested on SDS-resistant and -susceptible cultivars at each location. Overall, fluopyram provided the highest level of control of root rot and foliar symptoms of SDS among all the treatments. Foliar application of lactofen reduced foliar symptoms in some cases but produced the lowest yield. In 2015, fluopyram reduced the foliar disease index (FDX) by over 50% in both resistant and susceptible cultivars and provided 8.9% yield benefit in susceptible cultivars and 3.5% yield benefit in resistant cultivars compared with the base seed treatment (control). In 2016, fluopyram reduced FDX in both cultivars by over 40% compared with the base seed treatment. For yield in 2016, treatment effect was not significant in the susceptible cultivar while, in the resistant cultivar, fluopyram provided 3.5% greater yield than the base seed treatment. In this study, planting resistant cultivars and using fluopyram seed treatment were the most effective tools for SDS management. However, plant resistance provided an overall better yield-advantage than using fluopyram seed treatment alone. Effective seed treatments can be an economically viable consideration to complement resistant cultivars for managing SDS.


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