Pathogen Profile : Fusarium virguliforme (a.k.a F. solani f. sp. glycines)

By Kevin Bugg

PP728 Class Project Fall 2010


Fusarium virguliforme (formerly F. solani f. sp. glycines) is the causal agent of Soybean Sudden Death Syndrome (SDS). This pathogen/disease was first detected in Arkansas in 1971 and has since been reported not only across the southern U.S. but also throughout the north central U.S. as well as other countries including Brazil , Argentina , and Canada . SDS is commonly diagnosed by somewhat characteristic foliar symptoms (Figure 1.) but these may at times be confused with other diseases such as Brown Stem Rot (caused by Phialophora gregat). SDS is an economically significant disease annually responsible for losses potentially reaching hundreds of millions in the U.S. soybean market alone.   Like many soilborne pathogens, disease severity may be increased by planting in cool wet soils but the negative impact of this particular pathogen is also intensified in the presence of Heterodera glycines (commonly known as Soybean Cyst Nematodes or SCN). Management strategies are limited and currently the best option seems to be to take steps to control the factors which may contribute to increased disease severity rather than attempting to control the actual disease


FIGURE 1. - A. Control Plant; B. Chlorosis/early foliar symptoms; C. Increased chlorosis begin of decay on leaf periphery; D. Classical foliar symptoms including interveinal chlorosis and periphery necrosis (All photos courtesy of Bayer CropScience; Reseach Triangle Park, NC)

Infection/Disease Cycle

It is believed that Fusarium virguliforme primarily overwinters as chlamydospores both free in the soil and in crop debris. Germinating soybeans plus warming temperatures lead to the germination of the chlamydospores allowing for the infection cycle to begin. The roots of the newly emerging seedlings are particularly susceptible to the invading pathogen however the foliar symptoms as shown above are not typically seen until later in the season around the flowering stage. The fungus itself does not invade much further than a few inches above the soil line colonizing the vascular tissue. Once established in the xylem, the pathogen produces toxins which are systemically transferred throughout the plant leading to the foliar symptoms Toxin production and subsequent transport is increased under wet conditions and other diseases associated with said conditions as well as invading Heterodera glycines may increase the infection potential and consequently disease severity. Cooler temperatures may also intensify disease severity as Fusarium virguliforme is a cortical rotter which are typically known to cause more damage at temperatures not optimum for normal host growth and development.


The initial symptoms of Fusarium virguliforme occur at the infection site and are therefore not observable above the soil line. Preliminary root symptoms may include discoloration and rotting in the tap root and lower stem and an overall reduction in the development of the lateral root system (Figure 2.). More commonly “observable” early symptoms are seen with yellowing/chlorosis spotting of upper leaves which may then progress to a molting/mosaic appearance and ultimately to interveinal chlorosis and necrosis along the periphery of chlorotic areas as well as the periphery of the leaf itself. As the disease progresses, premature defoliation may occur along with pod abortion. For diagnostic purposes it is also important to examine the stem interior as some of the foliar symptoms of SDS may be confused with symptoms of other causal agents. For example Brown Stem Rot (a.k.a BSR caused by Phialophora gregata) causes similar foliar symptoms. With SDS the cortex of infected plants exhibit a light tan discoloration while the pith remains essentially white. Alternatively with BSR most of the interior stem de-coloration occurs within the central pith region instead of the cortex. Also diagnostic of SDS is the occasional observation of characteristic blue spore masses along the surface of the tap root.


FIGURE 2. - E. Root system of non-infected control plant as compared to; F. SDS infected root system


Fusarium virguliforme can be isolated from infected plants using standard isolation procedures. For example a section of infected tap root/stem near the upper most progression of the disease (as determined by the exterior lesion/de-colorization) can be surface sterilized and split and placed on Potato Dextrose Agar (PDA). Then a pure culture may be obtained using a hyphal tip isolation procedure. Alternatively, the surface sterilized infected tissue may be ground (ex. using a mortar/pestle) in sterile water and then a pure isolate of the target organism obtained through spread plate? dilutions of the ground material. Fusarium virguliforme will grow on a standard non-selective/non-differential agar plate (ex. PDA) more slowly than most Fusarium species but within two weeks should spread across the entire surface of the plate with characteristic blue spore masses near the center (Figure 3.)


FIGURE 3. – Pure cultrure of Fusarium virguliforme grown on PDA from wheat inoculum


Management options for Fusarium virguliforme are limited at this time. For example while certain cultivars appear to be less sensitive to SDS, to date there has been very little success in developing highly resistant cultivars. As for fungicides, some success has been achieved through in furrow applications and seed treatments but foliar applied fungicides are largely ineffective as they fail to reach the true site of the infection. Studies have also shown crop rotation to have little impact on SDS incidence and severity. Currently the best management for SDS is trying to limit external factors which may lead to increased disease severity. Planting under cool wet conditions may ultimately increase SDS disease potential because of the effect on the normal germination and development of the host and the increased incidence of other soilborne pathogens which may serve to weaken the host defenses. In fields known to have a history of SDS it is advisable to delay planting until conditions are more optimal for the host and less optimal for other potential pathogens. There have been definite correlations made between Heterodera glycines infection and SDS severity. By taking steps to control Heterodera glycines (resistant cultivars, nematicides) it is possible to help control SDS or at least manage its potential impact if not the disease itself.


 Farias Neto, A. L. de; Schmidt, M.; Hartman, G. L.; Li, S. X.; Diers, B. W. 2008. Inoculation methods under greenhouse conditions for evaluating soybean resistance to sudden death syndrome.  Pesquisa Agropecuária Brasileira; 43 (11):1475-1482,  Brasília: Empresa Brasileira de Pesquisa Agropecuária.

Navi, S. S. and Yang, X. B. 2008. Foliar symptom expression in association with early infection and xylem colonization by Fusarium virguliforme (formerly F. solani f. sp. glycines), the causal agent of soybean sudden death syndrome. Plant Health Progress doi:10.1094/PHP-2008-0222-01-RS.

Westphal, A., Xing, L., Abney, T. S., and Shaner, G. Diseases of Soybean: Sudden Death Syndrone. Purdue Extension. BP-58-W. online

Xing, L.J., Westphal, A., 2006. Interaction of Fusarium solanif. sp. glycinesand Heterodera glycines in sudden death syndrome of soybean. Phytopathology 96: 763–770.

Xing, L. J.; Westphal, A. 2009. Effects of crop rotation of soybean with corn on severity of sudden death syndrome and population densities of Heterodera glycines in naturally infested soil.  Field Crops Research; 112: 107-117 .