scholarly journals Recent Outbreak of Soybean Sudden Death Syndrome in Iowa

Plant Disease ◽  
1999 ◽  
Vol 83 (6) ◽  
pp. 590-590
Author(s):  
S. Sanogo ◽  
X. B. Yang

Sudden death syndrome (SDS) of soybean, caused by Fusarium solani f. sp. glycines, was first found in four Iowa counties in 1993 at low intensities. Following the first report of the disease, a statewide survey in 1994 and 1995 showed an overall low prevalence of the disease, mainly in eastern Iowa (2). In 1998, an epidemic of the disease occurred with drastic increases in prevalence and severity at regional, local, and field levels. The disease was found in 31 Iowa counties covering five out of the nine Iowa crop-reporting districts, with expansion in occurrence northward and westward. There were 12 SDS-affected counties in the North Central and Central districts, and 19 in the East Central, Southeast, and Northeast districts. To assess the extent of SDS increase at the local level, extensive surveys were conducted in 1998 in three areas where previous surveys were made in 1994 or 1995. In Washington County (Southeast District), the frequency of infestation has increased from 5% (2 of 40 fields surveyed) in 1995 to 30% in 1998. In Black Hawk County (East Central District), 26% of the fields examined had SDS, compared with 4.5% in 1995 (2 of 44 fields). In Story County (Central District), 35% of soybean fields were found with SDS in 1998, as opposed to 3% (2 of 62 fields) in 1994. In previous surveys (2), large disease patches (about 1 ha) were not found in central Iowa and were mainly limited to eastern counties along the Mississippi River. However, approximately 30% of the infested fields surveyed in 1998 had two to five patches with areas from 0.5 to 2.5 ha. The remaining 70% of the fields had several patches of diseased soybean plants with areas ranging from 3 m2 to 0.5 ha. The largest disease patch observed was about 10 ha, covering half of a field in Black Hawk County. Percentage of field area affected by SDS varied from 3 to 15% in 60% of the fields where the disease was found, and from about 20 to 60% in the remainder. In all fields surveyed, SDS was confirmed based on the presence of bluish sporulation or isolation from taproots of representative plants. The outbreak supports the 1996 risk assessment (1) that SDS would become a major production concern in Iowa. References: (1) H. Scherm and X. B. Yang. Phytopathology 87:S86, 1997. (2) X. B. Yang and P. Lundeen. Plant Dis. 81:719, 1997.

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.


Plant Disease ◽  
1997 ◽  
Vol 81 (7) ◽  
pp. 719-722 ◽  
Author(s):  
X. B. Yang ◽  
P. Lundeen

Soybean sudden death syndrome (SDS), caused by blue-pigmented, slow-growing strains of Fusarium solani, is a disease recently reported in Iowa. In 1994 and 1995 the geographic distribution and status of the disease was determined at the state, local, and field levels. An east-to-west decreasing trend of SDS prevalence was found at the state level. No SDS was found in the western part of Iowa. The disease was found in commercial production fields in 4 Iowa crop reporting districts — central, north-central, east-central, and southeastern — with the greatest severity and the most frequent occurrence of SDS found in the east-central district. In two counties along the Mississippi River, disease prevalence was high; more than 50% of soybean fields had SDS in locations where surveys were conducted. Intensive surveys on a local scale were conducted in areas around the fields where the disease was first noticed. In areas where disease prevalence was low, all detected infested fields belonged to the same owners. In areas where disease prevalence was high, no such pattern was found. Disease incidence varied from field to field. Information on SDS occurrence at different geographic scales serves as baseline information to monitor the future development of the disease in Iowa.


Plant Disease ◽  
2003 ◽  
Vol 87 (4) ◽  
pp. 449-449 ◽  
Author(s):  
J. E. Kurle ◽  
S. L. Gould ◽  
S. M. Lewandowski ◽  
S. Li ◽  
X. B. Yang

In August 2002, soybean (Glycine max (L.) Merr.) plants exhibiting foliar and root symptoms typical of sudden death syndrome were observed in Blue Earth and Steele counties in south-central Minnesota. Leaf symptoms ranging from small chlorotic spots to prominent interveinal necrosis were present on soybean plants at the R6 to R7 growth stage. As plants matured, complete defoliation took place with only petioles remaining. Symptomatic plants had necrotic secondary roots, truncated taproots, and discolored cortical tissue at the soil line. Blue sporodochia containing macroconidia were observed on the taproot of affected plants at both locations (3,4). Multiple cultures from both locations were obtained by transferring macroconidia from the sporodochia to potato dextrose agar (PDA) and modified Nash-Snyder Medium (NSM) (3). After 14 days, isolations were made from fungal colonies exhibiting bluish pigmentation and masses of bluish macroconidia (4). The isolates grew slowly, developed a bluish color, and formed sporodochia containing abundant macroconidia on NSM. These isolates were identified as Fusarium solani (Mart.) Sacc. f. sp. glycines based on colony characteristics and morphology of macroconidia (2). Pathogenicity tests were conducted with a single isolate from each location. The isolate from Blue Earth County was inoculated as mycelia in a plug of media onto taproots of plants of susceptible cvs. Williams 82 and Spencer at the V2 growth stage. Chlorotic spots appeared on leaves after 12 days of growth at 22 to 25°C in the greenhouse. Interveinal necrosis appeared after 15 days (4). The isolate from Steele County was used to inoculate the susceptible cv. Great Lakes 3202. Sorghum seed (3 cm3) infested with mycelia of the isolate were placed 2 to 3 cm below soybean seed planted in Cone-Tainers. Noninfested sorghum seed was used as a control. Plants were maintained for 21 days at 22 to 28°C in the greenhouse. Chlorotic spots appeared on leaves of inoculated plants within 21 days after planting followed by the development of interveinal chlorosis and necrosis (1). Molecular analysis further supported the identification of the Steele County isolate as F. solani f. sp. glycines. Polymerase chain reaction with specific primers Fsg1 and Fsg2 of total genomic DNA extracted from the Steele County isolate amplified a 438-bp DNA fragment identical with that extracted from previously identified isolates of F. solani f. sp. glycines (1). In 2002, symptoms of sudden death syndrome were also reported in Olmsted, Freeborn, and Mower counties. Although studies are needed to determine the distribution of sudden death syndrome in the state, the occurrence of the symptoms at multiple locations suggests that F. solani f. sp. glycines is widely distributed in southeast and south-central Minnesota. The counties where sudden death syndrome symptoms were reported are located in the most productive soybean-growing region of Minnesota. Sudden death syndrome could be a serious threat to soybean production in this area since poorly drained, heavy, clay soils are common, and soil temperatures 18°C or less are normal before the end of May. References: (1) S. Li et al. Phytopathology 90:491, 2000. (2) K. W. Roy. Plant Dis. 81:566, 1997. (3) K. W. Roy et al. Plant Dis. 81:1100, 1997. (4) K. W. Roy. Plant Dis. 81:259, 1997.


Plant Disease ◽  
2011 ◽  
Vol 95 (4) ◽  
pp. 436-440 ◽  
Author(s):  
C. C. Gongora-Canul ◽  
L. F. S. Leandro

Sudden death syndrome (SDS) of soybean is favored by planting in cool soil but epidemics can be severe even when planting occurs later in the season into warmer soil. Our objective was to determine how soil temperature affects susceptibility of plants exposed to Fusarium virguliforme at different ages. Soybean plants were grown in rhizotrons in water baths at 17, 23, and 29°C. Subsets of plants were inoculated 0, 3, 7, and 13 days after planting (DAP) by drenching soil with a conidial suspension. Root rot developed in all inoculated plants but severity decreased with increasing temperature and plant age at inoculation. Severity of foliar symptoms also decreased with increasing plant age. Whereas plants inoculated 0 DAP developed severe foliar symptoms at all temperatures, plants inoculated 3 and 7 DAP developed symptoms only at 17 and 23°C, and those inoculated 13 DAP never developed foliar symptoms at any temperature. Root length at inoculation was negatively correlated with disease severity. Our findings suggest that roots are most susceptible to infection during the first days after seed germination and that accelerated root growth in warmer temperatures reduces susceptibility to root infection conducive to foliar symptoms. However, soil temperature may not affect infections that occur as soon as seeds germinate.


Plant Disease ◽  
1997 ◽  
Vol 81 (6) ◽  
pp. 566-569 ◽  
Author(s):  
K. W. Roy

Production of macroconidia by the causal agent of sudden death syndrome, Fusarium solani f. sp. glycines, occurred on lower stems and roots of soybean plants symptomatic for the disease in Illinois, Indiana, Kentucky, Mississippi, and Tennessee. Most of the sporulation was light to dark blue to blue-green in color. Microscopically (15×) visible sporulation occurred on plants in 26, and macroscopically visible sporulation occurred on plants in 15, of 32 fields inspected. In some fields, the incidence of plants with microscopically visible sporulation was as high as 70%, and the incidence of plants with macroscopically visible sporulation reached 50%. Sporulation varied from pinpoint microscopic areas to macroscopically visible masses 4 to 6 cm2 or larger. Areas of microscopically visible sporulation occurred on lower stems and roots within 2.5 cm above and below the soil line on about 50% of the plants, and areas of macroscopically visible sporulation occurred within the same region on about 60% of the plants. Both microscopic and macroscopic sporulation also occurred on taproots as far as 10 cm or more below the soil line. Severe foliar symptoms and root decay were associated with a greater incidence of plants with sporulation. The occurrence of sporulation should help distinguish sudden death syndrome from other diseases of like foliar symptomatology and help confirm its diagnosis. It is presumed from the results that sporulation eventually contributes to the inoculum density of F. solani f. sp. glycines in soybean fields.


Plant Disease ◽  
1997 ◽  
Vol 81 (3) ◽  
pp. 259-266 ◽  
Author(s):  
K. W. Roy

Two morphological forms of Fusarium solani pathogenic on soybean, forms A and B, were further characterized and distinguished from other fungi. Questions regarding their identity were addressed. Soybean plants grown in the field and in a growth chamber were inoculated with Fusarium solani form A and F. solani f. sp. phaseoli. F. solani form A incited leaf symptoms typical of sudden death syndrome; F. solani f. sp. phaseoli did not. It was concluded that the two fungi are different and distinguishable on the basis of host specialization and the types of symptoms they incite on soybean. F. solani form A, the causal agent of sudden death syndrome, was designated F. solani (Mart.) Sacc. f. sp. glycines form. nov. Cultural and morphological characteristics of F. solani form B, the cause of seedling disease and root rot of soybean, and Plectosphaerella cucumerina were compared to determine the validity of a report indicating that they were conspecific. Results demonstrated that F. solani form B and P. cucumerina are distinctly different and not conspecific. The relevance of identifying and recognizing the two F. solani forms as separate and distinct members of the F. solani pathogen complex on soybean is discussed.


2012 ◽  
Vol 25 (6) ◽  
pp. 817-824 ◽  
Author(s):  
Hargeet K. Brar ◽  
Madan K. Bhattacharyya

Plants do not produce antibodies. However, plants can correctly assemble functional antibody molecules encoded by mammalian antibody genes. Many plant diseases are caused by pathogen toxins. One such disease is the soybean sudden death syndrome (SDS). SDS is a serious disease caused by the fungal pathogen Fusarium virguliforme. The pathogen, however, has never been isolated from diseased foliar tissues. Thus, one or more toxins produced by the pathogen have been considered to cause foliar SDS. One of these possible toxins, FvTox1, was recently identified. We investigated whether expression of anti-FvTox1 single-chain variable-fragment (scFv) antibody in transgenic soybean can confer resistance to foliar SDS. We have created two scFv antibody genes, Anti-FvTox1-1 and Anti-FvTox1-2, encoding anti-FvTox1 scFv antibodies from RNAs of a hybridoma cell line that expresses mouse monoclonal anti-FvTox1 7E8 antibody. Both anti-FvTox1 scFv antibodies interacted with an antigenic site of FvTox1 that binds to mouse monoclonal anti-FvTox1 7E8 antibody. Binding of FvTox1 by the anti-FvTox1 scFv antibodies, expressed in either Escherichia coli or transgenic soybean roots, was initially verified on nitrocellulose membranes. Expression of anti-FvTox1-1 in stable transgenic soybean plants resulted in enhanced foliar SDS resistance compared with that in nontransgenic control plants. Our results suggest that i) FvTox1 is an important pathogenicity factor for foliar SDS development and ii) expression of scFv antibodies against pathogen toxins could be a suitable biotechnology approach for protecting crop plants from toxin-induced diseases.


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