Soybean Sudden Death Syndrome- (Andreas Westphal and Gregory Shaner)
- Heavy rains may trigger SDS
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Sudden death syndrome has been a problem in many Indiana soybean fields in recent years. Since the disease was first identified in the southwest corner of Indiana in the mid 1980s, it has spread to affect fields in nearly all of the state. Surveys in Illinois show that SDS has increased steadily over the last 5 to 6 years, with the exception of 2002. The distribution of past outbreaks suggests that the disease may show up in virtually any area of Indiana, where conditions are favorable.
Sudden death syndrome is caused by the soil-borne fungus Fusarium solani f. sp. glycines. This fungus can be isolated from roots of soybean seedlings as early as 1 week after emergence. It colonizes the root systems of susceptible plants. While the fungus can colonize soybean root tissue early on, it is only at mid-season and thereafter that aboveground symptoms of SDS occur. Leaf symptoms usually do not appear until pods are starting to develop, any time from mid July through mid August. Heavy rains during reproductive stages seem to be a critical predisposing factor for SDS. Under these conditions the fungus starts producing toxins in the root system that are translocated within the plant and lead to foliar symptoms.
In affected plants, leaf tissue between the major veins turns yellow, then brown. Soon, the leaflets die and shrivel. In severe cases they drop off, leaving the petioles (leaf stalks) attached. Brown stem rot may cause similar foliar symptoms, but the leaflets tend to remain attached to the petioles. Brown stem rot can be distinguished from SDS by symptoms in the plant stem. When split, the lower stem and taproot will exhibit a dark cortex, but white pith in plants with SDS. In brown stem rot, the pith is dark, but the cortex is not much discolored. If a symptomatic plant is dug up when soil is moist, there may be small, light-blue patches on the surface of the taproot. These are spore masses of the SDS fungus. As the plant dries, this color will fade, but when it is seen, in conjunction with the other symptoms mentioned above, a diagnosis of SDS is strongly indicated.
Some confusion still exists as to the importance of the soybean cyst nematode in the development of SDS. Often in SDS-affected fields, the soybean cyst nematode is also found. However, infection by the nematode is not required for SDS development. There is some indication that the cyst nematode increases the severity of SDS, but details of the interaction are still not understood. Cyst nematodes are most easily seen on the root surface when they first emerge as white females. These females turn yellow, and eventually turn into brown cysts, at which time they are more difficult to see without magnification. The females or cysts are smaller than a pinhead and are easily distinguished from the much bigger Rhizobium nodules. As of this week in test plots at the Purdue Diagnostic Training Center near Lafayette, female nematodes are well developed and easy to see.
Management of SDS should include use of less susceptible soybean cultivars. Cultural practices, e.g., any operations that reduce the time of soil saturation (pretty difficult this year!) have shown some reduction of SDS. The involuntary late planting of much of Indiana’s soybean in 2003 might reduce the risk for SDS since early planting into cold soils increases the risk for SDS. The soybean crop of 2003 is delayed in its development, but beans are now starting to set pods at lower nodes. In addition, some fields were planted early. While some fields are flooded entirely, many more have saturated soil. The SDS fungus is present in many Indiana fields and with this year’s highly disease-conducive conditions; we may see symptoms of SDS in soybean fields over the next 2 weeks.
It is always good practice to keep field records of soil-borne diseases. Fields severely impacted with SDS in 2003 should be earmarked for a late planting date when they are schedule for soybean planting in the future. Such fields also lend themselves for planting soybean cultivars with field resistance or tolerance to SDS as they hopefully become available.
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Phytophthora Root Rot of Soybean- (Andreas Westphal, Gregory Shaner, and Scott Abney)
- Some plant pathogens like to swim.
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Current weather patterns increase the risk for soil-borne diseases of soybean. The accompanying article discusses sudden death syndrome, but the wet conditions are also favorable for another culprit. We will probably see more Phytophthora root rot than in recent years.
The causal organism, Phytophthora sojae, is a fungus-like plant pathogen that thrives in wet soil conditions. This plant pathogen has a unique life history. Although direct infection of the soybean root can occur from vegetative growth of the pathogen, the more typical inoculum is a motile spore, the zoospore. When free water is available in the soil these spores are released by the pathogen and can swim to seek out host plant tissue. The active swimming distance is probably less than 1 inch. However, once in suspension these spores can be passively transported with the soil water and remain infective for some time. The pathogen can infect different plant parts. Frequently, spores will remain in soil and infect soybean roots.
Soybean plants are hosts to infection by P. sojae at any stage of development. Much earlier in the season, right after planting, the pathogen can lead to damping-off and seed rots. Most soybean fields in Indiana have probably grown out of this critical phase. The plants do remain susceptible to the pathogen. At later developmental stages, root rot develops when the pathogen is present and the soil is saturated. When roots of older plants are infected, the first indication of a problem is often leaf yellowing between the veins and along the leaf margin. The plant has an overall wilted, “droopy”, appearance. When lifted from the soil root systems will show a watery decay and be dark in color. Lateral roots, and in severe cases taproots, are destroyed by the time foliar symptoms call attention to a problem. While less severe cases might not result in plant death there still might be yield loss due to a compromised root system. Depending on when the disease develops yield losses can be limited or severe, the latter being the case when disease develops early.
The pathogen survives as robust spores, thick-walled oospores, which are either imbedded in host tissue or released to the soil environment as the plant tissue withers away. The life history of this pathogen makes management with crop rotation impractical, since spores can easily survive several years without a soybean crop. Purdue research has shown the presence of this pathogen in virtually all Indiana soybean fields. Chemical controls are available but do not provide full season protection as pesticides decompose while exposed to the soil environment and lose activity as the growing season progresses. The more practical management of the disease is host plant resistance. Two types of resistance are recognized: partial resistance is slowing down disease development; race specific resistance is effective against particular populations of the pathogen. Under current extreme weather conditions partial resistance might not provide sufficient protection from the disease. To take advantage of race specific host plant resistance it is critical to know the race of P. sojae present in a particular field. Once the race is determined a soybean background that is resistant to this particular race can be identified. Care needs to be taken because the pathogen can adapt to resistance, particularly when soybeans with the same resistance gene are grown repeatedly in a field. Less than 50% of currently available commercial cultivars in northern states have this type of resistance.
In 2003, some plant death, tentatively called “water damage” might turn out to be the result of Phytophthora root rot instead.
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Leaf Blights and Rust of Corn- (Andreas Westphal and Gregory Shaner)
- Warm wet weather promotes activity of corn leaf pathogens.
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We are approaching the time of year when corn leaf diseases start to develop. Several leaf blights are common in corn: gray leaf spot, northern corn leaf blight, northern corn leaf spot, and eyespot are often seen in Indiana fields.
The fungi that cause these leaf blights survive the winter on corn residue. They produce spores on this residue the following summer. Wind and rain disperse these spores; those that happen to land on corn leaves can infect and initiate disease. Leaf wetness is necessary for infection, so the persistently wet weather of recent days has probably allowed a lot of infection to occur. Once infection occurs, a lesion will develop. As the lesion matures, the fungus will produce spores on the necrotic tissue; these spores can cause more infections. If weather continues to be favorable for disease, these infection cycles will repeat several times, leading to premature death of much of the plant’s leaf area.
Fortunately, most hybrids have fair to good resistance to leaf blights. The resistance of most hybrids is partial, meaning that the pathogens can infect, but the resulting lesion is smaller than on a susceptible variety and fewer spores are produced. This is important because spores produced on lesions provide the secondary inoculum that drives an epidemic. Even under favorable weather conditions, the rate of blight development on a partially resistant variety is slow enough to allow the plant the time to produce grain before leaves are severely blighted. Some hybrids, however, may be susceptible to one or more leaf blights, and may sustain enough leaf damage to reduce yield and grain quality. Of the leaf blights mentioned above, gray leaf spot is the one most likely to cause problems on field corn, because breeders have not been dealing with it as long as they have with the other leaf blights.
Gray leaf spot emerged as major leaf blight in the corn belt in the early 1990s and caused extensive damage because most hybrids grown at that time were susceptible (or very susceptible). Since then, corn breeders have made progress in improving resistance to gray leaf spot and now many hybrids are rated in seed company catalogs as having partial resistance.
Indiana is a major producer of seed corn. Inbreds used in these seed fields are particularly at risk. Many of them are more susceptible to leaf blights than are the hybrids they produce. For this reason, disease often shows up earlier and is more severe on inbreds than on hybrids. Accordingly, disease activity in seed corn fields is a good indicator of what may be in store for the less susceptible hybrids. We have already seen mature gray leaf spot and northern corn leaf spot lesions on lower leaves in seed corn fields. There are also numerous flecks on upper leaves, which are probably young lesions. This indicates that weather has been favorable for some time for leaf blight development.
We have also seen a few rust pustules on lower leaves of seed corn. These appear to be pustules of common rust, not southern rust. At this stage, the pustules have erupted on only one surface of the leaf, which is normally an indication of southern rust, but microscopic examination of the spores indicates the pathogen is the common rust fungus (Puccinia sorghi).
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