scholarly journals First Report of Sudden Death Syndrome (Fusarium solani f. sp. glycines) of Soybean in Minnesota

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 ◽  
2000 ◽  
Vol 84 (8) ◽  
pp. 914-920 ◽  
Author(s):  
Y. Luo ◽  
K. Hildebrand ◽  
S. K. Chong ◽  
O. Myers ◽  
J. S. Russin

Field studies were conducted to determine the relationships between soybean yield and foliar disease index (FDX) of sudden death syndrome (SDS) as well as root colonization by Fusarium solani f. sp. glycines, the causal agent. Single-row plots in a soybean field with relatively uniform SDS incidence and severity were identified at growth stage R6 on cultivar Pioneer 9492 in DeSoto, IL, in 1997 and 1998. For each plot, foliar disease index (FDX), yield, and yield components were determined. In 1997, linear relationships between yield (Y, grams per meter of row) and FDX were obtained from the wide-row (Y = 207.84 - 1.09 FDX) and narrow-row (Y = 126.66 - 0.745 FDX) plots, respectively. A linear relationship (Y = 124.23 - 1.11 FDX) also was observed in 1998. Increase in each FDX unit caused yield loss from 18 to 29 kg/ha (0.7 – 1.1 g/m of row). FDX was negatively correlated with seed weight (grams per plant) in both years and with seed size (grams per 100 seeds) in 1997. A no-tilled field at Southern Illinois University planted to soybean cultivar Asgrow 5403 was divided into 25 plots in 1997 and 40 plots in 1998. Root samples were taken from each plot at five or six sampling times during the seasons. Roots were used to isolate and enumerate F. solani f. sp. glycines on a selective medium to obtain the CFU. FDX was assessed and soybean yield was obtained from each plot. Soybean yield correlated negatively with FDX in both years. Both yield and FDX correlated significantly with CFU from slightly before growth stage R1 to R2 in both years, and with area under the pathogen population curve (AUPC) in 1997. An increase in one unit of AUPC or CFU per gram of root at R6 was associated with yield loss of 0.19 or 0.014%, respectively.


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.


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 ◽  
2006 ◽  
Vol 90 (1) ◽  
pp. 109-109 ◽  
Author(s):  
A. D. Ziems ◽  
L. J. Giesler ◽  
G. Y. Yuen

During August of 2004, soybean (Glycine max (L.) Merr.) plants exhibiting symptoms typical of sudden death syndrome (SDS) caused by Fusarium solani (Mart.) Sacc. f. sp. glycines (= Fusarium virguliforme Akoi, O'Donnell, Homma, & Lattanzi) (1) were observed in Nemaha and Pierce counties in eastern Nebraska. Leaf symptoms ranged from small chlorotic spots to prominent interveinal necrosis on plants at R5-R6 growth stages. Taproots of symptomatic plants were plated on potato dextrose agar (PDA) amended with hymexazol, ampicillin, and rifampicin (HAR). Resulting fungal isolates grew slowly and developed masses of blue macroconidia, characteristic of F. solani f. sp. glycines. Sorghum seed infested with the isolates were placed 1.5 cm below soybean seeds of the susceptible cv. Sloan planted in clay pots (3). Noninfested sorghum seed and sorghum seed infested with F. oxysporum were controls. Plants were maintained for 32 days at 27.5 ± 2.5°C in the greenhouse. Small cholorotic spots were observed on leaves of F. solani f. sp. glycines-inoculated plants within 21 days followed by the development of interveinal chlorosis. Roots of symptomatic plants were plated on PDA with HAR and F. solani f. sp. glycines was recovered. Identification of the fungal cultures was further confirmed as F. solani f. sp. glycines by a real-time quantitative polymerase chain reaction (qPCR) assay described by Gao et al. (2). During 2005, SDS symptoms were also reported in early planted soybeans from Jefferson and Seward counties and the presence of SDS was confirmed by qPCR. The confirmation of SDS at multiple locations suggests that the pathogen is widely distributed in the eastern one-third of Nebraska. SDS could be a serious threat to soybean production in this area since spring weather conditions favor SDS infection and many producers plant soybean early in cool soils. References: (1) T. Akoi et al. Mycologia 95:660, 2003. (2) X. Gao et al. Plant Dis. 88:1372, 2004. (3) K. W. Roy et al. Plant Dis. 81:259, 1997.


Plant Disease ◽  
1999 ◽  
Vol 83 (9) ◽  
pp. 879-879 ◽  
Author(s):  
B. W. Pennypacker

A small, circular patch of soybean (Glycine max) showing symptoms consistent with sudden death syndrome (SDS) (2) was noted on July 25, 1998, in a producer's field in Jersey Shore, PA. Foliar symptoms included interveinal chlorosis and necrosis, leaf cupping, and leaf abscission. The vascular cylinder of roots and stems had areas of reddish-brown discoloration. A slow-growing Fusarium sp., which produced a bluish-purple color on potato dextrose agar, was isolated from the roots of several symptomatic plants. The fungus was identified as Fusarium solani by The Fusarium Research Center, The Pennsylvania State University. Koch's postulates were tested on soybean cultivars A2506, Stine 3171, Pioneer 9305 and 9306, and Jack. Five plants per cultivar were inoculated at growth stage V1 by pouring 35 ml of a 4 × 107 spores per ml suspension on the growth mix in each pot. Five plants per cultivar were treated similarly with sterile water. Foliar symptoms of SDS began to appear 3 weeks after inoculation. Seven weeks after inoculation, symptoms of interveinal chlorosis and/or necrosis, leaf cupping, and occasional leaf abscission were apparent on the inoculated plants and on several noninoculated plants. The percentage of the plant showing symptoms was recorded and converted to the 0 to 5 scale (in which 0 = 0%, 1 = 1–10%, 2 = 11–30%, 3 = 31–40%, 4 = 41–90%, and 5= 91–100% of the leaf area affected) used by Rupe (3). Regardless of the rating method, there was a significant difference (P = 0.0001) between inoculated and noninoculated plants. There were no significant differences among cultivars. Roots of the inoculated plants were frequently discolored, in contrast to those of the noninoculated plants. F. solani was isolated from the roots of 97% of the inoculated plants and 23% of the noninoculated plants. Fungus gnats were suspected of spreading the pathogen to the noninoculated plants (1). F. solani f. sp. glycines causes SDS in soybean and its identity is confirmed by the symptoms produced on soybean (2). The symptoms produced when soybean plants were inoculated in the greenhouse were consistent with those of SDS (2) and indicate that the F. solani isolate recovered from symptomatic plants in the field was F. solani f. sp. glycines. This is the first documented occurrence of SDS on soybean in Pennsylvania. References: (1) D. W. Kalb and R. L. Millar. Plant Dis. 70:752, 1986. (2) K. W. Roy et al. Plant Dis. 81:1100, 1997. (3) J. C. Rupe. Plant Dis. 73:581, 1989.


2018 ◽  
pp. 583-591
Author(s):  
Yi Chen Lee ◽  
M Javed Iqbal ◽  
Victor N Njiti ◽  
Stella Kantartzi ◽  
David A. Lightfoot

Soybean (Glycine max (L.) Merr.) cultivars differ in their resistance to sudden death syndrome (SDS), caused by Fusarium virguliforme. Breeding for improving SDS response has been challenging, due to interactions among the 18-42 known resistance loci. Four quantitative trait loci (QTL) for resistance to SDS (cqRfs–cqRfs3) were clustered within 20 cM of the rhg1 locus underlying resistance to soybean cyst nematode (SCN) on Chromosome (Chr.) 18. Another locus on Chr. 20 (cqRfs5) was reported to interact with this cluster. The aims here were to compare the inheritance of resistance to SDS in a near isogenic line (NIL) population that was fixed for resistance to SCN but segregated at two of the four loci (cqRfs1 and cqRfs) for SDS resistance; to examine the interaction with the locus on Chr. 20; and to identify candidate genes underlying QTL. Used were; a NIL population derived from residual heterozygosity in an F5:7 recombinant inbred line EF60 (lines 1-38); SDS response data from two locations and years; four segregating microsatellite and 1,500 SNP markers. Polymorphic regions were found from 2,788 Kbp to 8,938 Kbp on Chr. 18 and 33,100 Kbp to 34,943 Kbp on Chr. 20 that were significantly (0.005 < P > 0.0001) associated with resistance to SDS. The QTL fine maps suggested that the two loci on Chr. 18 were three loci (cqRfs1, cqRfs, and cqRfs19). Candidate genes were inferred.  An epistatic interaction was inferred between Chr. 18 and Chr. 20 loci. Therefore, SDS resistance QTL were both complex and interacting.


Crop Science ◽  
1998 ◽  
Vol 38 (2) ◽  
pp. 472-477 ◽  
Author(s):  
V. N. Njiti ◽  
T. W. Doubler ◽  
R. J. Suttner ◽  
L. E. Gray ◽  
P. T. Gibson ◽  
...  

2018 ◽  
Vol 19 (1) ◽  
pp. 46-53 ◽  
Author(s):  
David A. Marburger ◽  
Jaime F. Willbur ◽  
Maria E. Weber ◽  
Jean-Michel Ané ◽  
Medhi Kabbage ◽  
...  

Lipo-chitooligosaccharides (LCOs) are signal molecules produced by plant root endosymbionts and have been identified, formulated, and marketed as growth-promoting adjuvants for soybean (Glycine max [L.] Merr.). Experiments were conducted under controlled environmental conditions to characterize the effects of foliar LCO applications on early symptom development of sudden death syndrome (SDS), caused by Fusarium virguliforme, and Sclerotinia stem rot (SSR), caused by Sclerotinia sclerotiorum. Treatment factors for the SDS experiment included two soybean cultivars (Sloan and CH2105R2), two inoculation levels (noninoculated control and inoculated), and two LCO applications (control and foliar LCO application), whereas two experimental soybean lines (91-38 and 91-44) and two LCO applications (water control and foliar LCO application) were used in the SSR experiment. The LCO application did not significantly influence SDS root symptom severity or early-season growth characteristics. However, on the susceptible line (P = 0.01) and with LCO application (P = 0.03), significantly larger SSR lesions developed compared with the nontreated control and resistant line. These results suggest foliar-applied LCOs have a limited effect on early root symptom development caused by F. virguliforme but increase stem symptom development caused by S. sclerotiorum.


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