Sudden death syndrome (SDS), a disease in soybean plants, quickly spread across the southern United States in the 1970s, eventually reaching most agricultural areas of the US. SDS is caused by multiple Fusarium fungi in the Fusariumsolani complex. Fusarium virguliforme is the sole causal agent in North America. In South America, Fusarium brasiliense, F. cuneirostrum, F. tucumaniae, and F. virguliforme are all causal agents. [1] Losses could exceed hundreds of millions of dollars in US soybean markets alone making it one of the most important diseases found in Soybeans across the US. [2]
Sudden death syndrome (SDS) has become one of the most impactful yield-reducing diseases in North American soybeans. After making its first appearance in Arkansas in 1971 SDS soon spread to the surrounding states of Tennessee and Mississippi, and then traveled up the Mississippi River to Midwestern states. [3] Currently, the disease affects an area stretching from South Dakota to North Carolina, putting the majority of American soybean producers at risk. The disease has the potential to cause up to 80% yield loss, making it a devastating disease for producers if not detected early and managed correctly. [3] Its presence is currently increasing in northern Midwest states and western Corn Belt states including Minnesota, Nebraska, and Wisconsin, and may coincide with the spread of the Soybean Cyst Nematode (SCN). [3]
Most of the SDS symptoms can be confused with other factors like nutrient deficiencies and some other diseases like brown stem rot and stem canker. [4] Usually the first symptom seen is interveinal chlorosis, which is the yellowing of the plant material between the leaf veins. [5] When leaves begin to die, puckering and mottling can also be observed along with the chlorosis. [6] As severity increases, necrosis (death of cells) occurs and eventually these leaves will fall off, leaving only petioles left on the stem. [7] If the conditions are right (cool and wet), these symptoms can appear suddenly, causing large yield reductions. Normally, this is seen in mid or late July around the time of flowering and pod production. [8]
In addition to foliar symptoms, the stem of the soybean plant can show symptoms as well. If a soybean stem with SDS is split, the pith will be visibly white while the cortical tissue around the pith will be tan to light brown in color. [4] [2] If the pith is brown in color (or if the whole stem looks brown on the inside), it is likely that the plant has brown stem rot, rather than SDS. [4]
Along with the above-ground foliar and stem symptoms, the roots usually show some kind of rotting and decrease in vigor compared to other healthy soybean roots. [2] If soil conditions are moist, roots are also likely to show blue masses of spores (macroconidia) around the taproot just below the soil surface. [2] Blue fungal masses, found along with the foliar and stem symptoms, are strong diagnostic indicators for SDS. [2]
F. virguliforme overwinters as asexual macroconidium and chlamydospores and currently, no research has found a successful sexual stage with this pathogen. [2] When conditions are favorable, these spores germinate on seedling roots and infect the plant. From the V1 to R1 stages (seedling to first flower) of soybean growth, the fungus colonizes within the plant cortex and only goes up the stem a few inches above the soil surface. [2] Toxins are produced when the pathogen colonizes the lower parts of the soybean cortex. These toxins travel up the xylem to the leaves, causing leaf chlorosis and necrosis, eventually leading to leaf and pod drop. [5] [2]
Blue Fungal spore masses are produced on the roots of the plant where macroconidia are formed. Macroconidia are one of the overwintering phases of the pathogen and can persist in the soil and plant residue for many years. [2] Between growing seasons, F. virguliforme is also found in the form of chlamydospores in the crop residue and freely in the soil. [2] These thick-walled overwintering structures can withstand large temperature fluctuations within the soil and even resist desiccation. [2]
There is no known sexual reproduction in certain SDS causal agents such as F. virguliforme. [9] However, F. tucumaniae has recently been shown to produce perithecia, a sexual fruiting body, which provides evidence for the existence of a sexual reproduction cycle in that species. [10]
Cool and wet soil is the most ideal condition for F. virguliforme, the pathogen that causes SDS. [11] [3] [12] [13] The presence of the disease is often able to be tracked with storm fronts moving across the country. Symptoms of SDS are usually common 10–14 days after heavy rains. While the disease prefers cool soil, symptoms often do not manifest themselves until July or August after a soaking rain saturates the soil. Early planting can leave seeds susceptible to SDS, as can planting vulnerable varieties. SCN infection of a population of plants also creates a favorable environment for SDS, as the roots of the plants are already under stress from the nematode, leaving them vulnerable to infection from F. virguliforme. The presence of SCN is also one of the most important environmental factors for SDS. Limiting soybean exposure to SCN is much easier in comparison to SDS, so limiting a field's vulnerability to SCN is vital to preventing the introduction of SDS. Additionally, SDS has been shown to be more severe in highly fertile soils, specifically those with high phosphorus, magnesium, and organic matter. [14] Environmental factors are some of the largest variables that will determine both the presence and severity of an SDS infection. The ability to control and react to as many of these factors as possible is key to protecting a soybean crop from SDS.
F. virguliforme is a soil-borne pathogen that starts by infecting the roots of soybean seedlings after germination. The fungus then moves up the plant and infects the vascular tissue, causing a brown color within the cortex around the pith of the plant a few inches above the soil surface. [2] Toxins are produced by the fungus when it colonizes the cortex and are sent up the stem to the leaves, causing the above-ground symptoms around first flower during mid-summer. [2] While infection occurs early in the season, symptoms do not normally appear until mid-summer. [15]
SDS also has a synergistic relationship with Soybean Cyst Nematode (SCN). Fields that have SCN presence have more severe SDS symptoms. [5] While it is not known exactly how the two interact, it is known that symptoms of SDS are more severe when SCN are present in the field and that F. virguliforme can be isolated from an SCN that is found in the same area as this pathogen. [2]
-Plant resistant cultivars: Planting SDS resistant cultivars is likely the most reliable way to prevent SDS infection of a soybean crop. [15] [12] [11] Previously, finding SDS resistant soybean varieties had been fairly difficult to find, and were fairly expensive. However, as the prevalence of SDS in high soybean production areas has increased, seed companies have begun to develop more varieties resistant to F. veruguliforme and SDS. Both resistant and moderately resistant varieties are available. In an informal survey of seed companies showed that about 57% of cultivars are labeled as at least moderately resistant. Individual company lines had a range of 40%-60% of their cultivars labeled as at least moderately resistant. [15] It is important to note that not all seed companies give information regarding the impacts that SDS has on their soybean varieties. It is also recommended to plant a variety that is also resistant to SCN, as the presence of this pathogen can impact the response that a plant has to F. vurguliforme. Because of the symbiotic relationship between these two pathogens, it is important to collect information regarding both when selecting a soybean variety. Most seed companies will release information regarding SCN.
-Plant a week or two later: This is a practice that works well in theory but is hard to put into practice in the field. Due to tight schedules and unpredictable spring weather patterns in the Midwest and Great Plains, it can be hard to not plant soybeans as soon as possible. However, when possible, growers should consider waiting one or two weeks after typical early planting dates to allow soil to warm and dry, which will help protect the seedlings from being infected by F. virugliforme. The pathogen does not prefer to infect seedlings in warmer and drier soil. If planting later is not an option, an extra pass over the field with a soil finisher or other shallow tillage implement will also help to expose soil and dry it out.
-Take active measures to decrease Soybean Cyst Nematode populations: A good way to help prevent and at least slow the spread and onset of F. virugliforme and SDS is to limit the spread and population of SCN. SCN and F. virugliforme have a symbiotic relationship that helps both to spread throughout fields. Limiting the spread of SCN can be a tedious task, as this requires the prevention of soil transferring from field to field. This means washing equipment and tires between fields. While this can be unrealistic for large growers, a recommendation is a quick rinsing of tires and equipment when moving to different areas or farms. While this is still tedious, it is not as time consuming as doing it after every field, and may save growers some yield down the road.
-Limit compaction: While this will not prevent SDS and its spread entirely, limiting soil compaction can help to lessen the severity and yield impact of SDS. When soil becomes compacted, it has less porosity and holds more water. This is very favorable to SDS infection and makes it very hard to control and lessen its severity. Practices that can help to limit compaction include using GPS to run in the same tracks every time you run a pass across the field (tillage, planting, spraying, etc.), using tracks or LSW flotation tires on equipment whenever possible, avoiding driving loaded grain trucks on the field whenever possible, and limiting the travel of loaded grain carts across the field as much as possible.
-Keeping an ideal soil pH: SDS thrives in soils with pH exceeding 7.0. [16] SCN also thrives in high pH and can be controlled by lowering soil pH. [16] It is important to note that lowering soil pH below 6.5 leaves soybeans more vulnerable to brown stem rot. Regular soil sampling and the application of gypsum, lime and sulfur are good practices to help control soil pH.
-Tillage: No-till systems are particularly vulnerable to SDS, [17] [13] as the soil remains cooler and wetter due to not being tilled. While there are benefits to no-till systems, it may be beneficial to consider light tillage prior to planting in cooler and wetter years to help open-up soil to the wind and sun. This will help to dry and warm the soil slightly. Generally, this will require some form of disc or soil finisher, as the coulters on a no-till grain drill generally do not provide enough disturbance to make a measurable difference on soil temperature and moisture by the time of seedling germination. Corn and soybean residue that is left on the field and not tilled under has also been found to maintain inoculum levels of the fungus, which could possibly cause an SDS infection in the next soybean crop. [11] For this reason, a deep tillage that disrupts surface soil is recommended in fields that have been known to have SDS problems in the past. Chisel plows, moldboard plows, field cultivators with v-shoes, and rippers are all effective tillage tools for this type of situation.
Fusarium wilt is a common vascular wilt fungal disease, exhibiting symptoms similar to Verticillium wilt. This disease has been investigated extensively since the early years of this century. The pathogen that causes Fusarium wilt is Fusarium oxysporum. The species is further divided into formae speciales based on host plant.
The soybean cyst nematode (SCN), Heterodera glycines, is the most devastating pest to soybean crop yields in the U.S., targeting the roots of soybean and other legume plants. When infection is severe SCNs cause stunting, yellowing, impaired canopy development, and yield loss. The symptoms caused by SCNs can go easily unrecognized by farmers—in some cases there are no warning symptoms before a loss of 40% of the yield. Due to the slight stunting and yellowing, many farmers may mistake these symptoms as environmental problems when in fact they are SCNs. Another symptom of SCNs that may affect farmers' yields is stunted roots with fewer nitrogen-fixing nodules. Due to the fact that soybean cyst nematodes can only move a few centimeters in the soil by themselves, they mostly are spread via tillage or plant transplants. This area of infection will look patchy and nonuniform making diagnosis more difficult for farmers. They can be seen in the roots of summer soybean plants if the roots are taken out very carefully and gently washed with water. The egg masses should be seen as bright white or yellow "pearls" on the roots. The later the roots are pulled the harder it will be to diagnose due to the SCNs female dying and turning a much darker color, forming a "cyst". The best way to know if a field is infected by soybean cyst nematodes is to take a soil sample to a nematologist.
Phytophthora sojae is an oomycete and a soil-borne plant pathogen that causes stem and root rot of soybean. This is a prevalent disease in most soybean growing regions, and a major cause of crop loss. In wet conditions the pathogen produces zoospores that move in water and are attracted to soybean roots. Zoospores can attach to roots, germinate, and infect the plant tissues. Diseased roots develop lesions that may spread up the stem and eventually kill the entire plant. Phytophthora sojae also produces oospores that can remain dormant in the soil over the winter, or longer, and germinate when conditions are favourable. Oospores may also be spread by animals or machinery.
Fusarium culmorum is a fungal plant pathogen and the causal agent of seedling blight, foot rot, ear blight, stalk rot, common root rot and other diseases of cereals, grasses, and a wide variety of monocots and dicots. In coastal dunegrass, F. culmorum is a nonpathogenic symbiont conferring both salt and drought tolerance to the plant.
Aphanomyces euteiches is a water mould, or oomycete, plant pathogen responsible for the disease Aphanomyces root rot. The species Aphanomyces euteiches can infect a variety of legumes. Symptoms of the disease can differ among hosts but generally include reduced root volume and function, leading to stunting and chlorotic foliage. Aphanomyces root rot is an important agricultural disease in the United States, Europe, Australia, New Zealand, and Japan. Management includes using resistant crop varieties and having good soil drainage, as well as testing soil for the pathogen to avoid infected fields.
Gibberella zeae, also known by the name of its anamorph Fusarium graminearum, is a fungal plant pathogen which causes fusarium head blight (FHB), a devastating disease on wheat and barley. The pathogen is responsible for billions of dollars in economic losses worldwide each year. Infection causes shifts in the amino acid composition of wheat, resulting in shriveled kernels and contaminating the remaining grain with mycotoxins, mainly deoxynivalenol (DON), which inhibits protein biosynthesis; and zearalenone, an estrogenic mycotoxin. These toxins cause vomiting, liver damage, and reproductive defects in livestock, and are harmful to humans through contaminated food. Despite great efforts to find resistance genes against F. graminearum, no completely resistant variety is currently available. Research on the biology of F. graminearum is directed towards gaining insight into more details about the infection process and reveal weak spots in the life cycle of this pathogen to develop fungicides that can protect wheat from scab infection.
Crown rot of wheat is caused by the fungal pathogen Fusarium pseudograminearum. F. pseudograminearum is a member of the fungal phylum Ascomycota and is also known as Gibberella coronicola (teleomorph). It is a monoecious fungus, meaning it does not require another host other than wheat to complete its life cycle. Although F. pseudograminearum can produce both anamorphic and teleomorphic states, the teleomorph is usually not present for crown rot of wheat. This Fusarium species has, until recently, been considered to be the same as the species known as Fusarium graminearum due to many similar characteristics. One of the only differences between the two species is that F. pseudograminearum lacks its sexual stage on the wheat host.
Macrophomina phaseolina is a Botryosphaeriaceae plant pathogen fungus that causes damping off, seedling blight, collar rot, stem rot, charcoal rot, basal stem rot, and root rot on many plant species.
Sclerotinia sclerotiorum is a plant pathogenic fungus and can cause a disease called white mold if conditions are conducive. S. sclerotiorum can also be known as cottony rot, watery soft rot, stem rot, drop, crown rot and blossom blight. A key characteristic of this pathogen is its ability to produce black resting structures known as sclerotia and white fuzzy growths of mycelium on the plant it infects. These sclerotia give rise to a fruiting body in the spring that produces spores in a sac which is why fungi in this class are called sac fungi (Ascomycota). This pathogen can occur on many continents and has a wide host range of plants. When S. sclerotiorum is onset in the field by favorable environmental conditions, losses can be great and control measures should be considered.
Mycosphaerella berkeleyi is a fungal plant pathogen. It is the causal agent of the peanut foliar disease Late Leaf Spot.
Fusarium oxysporum f.sp. ciceris is a fungal plant pathogen that causes fusarium wilt of chickpea.
Fusarium redolens is a species of fungus in the genus Fusarium and family Nectriaceae. This species is a soil-borne plant pathogen in temperate prairies. It causes diseases such as root, crown, and spear rot, seedling damping-off, and wilting disease. It is a known producer of the alkaloids peimisine and imperialine-3β-d-glucoside, which has implications for traditional Chinese medicine.
Alternaria solani is a fungal pathogen that produces a disease in tomato and potato plants called early blight. The pathogen produces distinctive "bullseye" patterned leaf spots and can also cause stem lesions and fruit rot on tomato and tuber blight on potato. Despite the name "early", foliar symptoms usually occur on older leaves. If uncontrolled, early blight can cause significant yield reductions. Primary methods of controlling this disease include preventing long periods of wetness on leaf surfaces and applying fungicides. Early blight can also be caused by Alternaria tomatophila, which is more virulent on stems and leaves of tomato plants than Alternaria solani.
Phytophthora capsici is an oomycete plant pathogen that causes blight and fruit rot of peppers and other important commercial crops. It was first described by L. Leonian at the New Mexico State University Agricultural Experiment Station in Las Cruces in 1922 on a crop of chili peppers. In 1967, a study by M. M. Satour and E. E. Butler found 45 species of cultivated plants and weeds susceptible to P. capsici In Greek, Phytophthora capsici means "plant destroyer of capsicums". P. capsici has a wide range of hosts including members of the families Solanaceae and Cucurbitaceae as well as Fabaceae.
Ascochyta pisi is a fungal plant pathogen that causes ascochyta blight on pea, causing lesions of stems, leaves, and pods. These same symptoms can also be caused by Ascochyta pinodes, and the two fungi are not easily distinguishable.
Cercospora sojina is a fungal plant pathogen which causes frogeye leaf spot of soybeans. Frog eye leaf spot is a major disease on soybeans in the southern U.S. and has recently started to expand into the northern U.S. where soybeans are grown. The disease is also found in other soybean production areas of the world.
Diaporthe phaseolorum var. caulivora is a fungal plant pathogen which infects soybean, causing soybean stem canker.
Phialophora gregata is a Deuteromycete fungus that is a plant pathogen which causes the disease commonly known as brown stem rot of soybean. P. gregata does not produce survival structures, but has the ability to overwinter as mycelium in decaying soybean residue.
Bean pod mottle virus, or BPMV, is a species of plant pathogenic virus in the family Secoviridae. It is known to infect soybean crops.
Bacterial leaf streak (BLS), also known as black chaff, is a common bacterial disease of wheat. The disease is caused by the bacterial species Xanthomonas translucens pv. undulosa. The pathogen is found globally, but is a primary problem in the US in the lower mid-south and can reduce yields by up to 40 percent.[6] BLS is primarily seed-borne and survives in and on the seed, but may also survive in crop residue in the soil in the off-season. During the growing season, the bacteria may transfer from plant to plant by contact, but it is primarily spread by rain, wind and insect contact. The bacteria thrives in moist environments, and produces a cream to yellow bacterial ooze, which, when dry, appears light colored and scale-like, resulting in a streak on the leaves. The invasion of the head of wheat causes bands of necrotic tissue on the awns, which is called Black Chaff.[14] The disease is not easily managed, as there are no pesticides on the market for treatment of the infection. There are some resistant cultivars available, but no seed treatment exists. Some integrated pest management (IPM) techniques may be used to assist with preventing infection although, none will completely prevent the disease.[2]