PHYTOPHTHORA ROT [ Symptoms ] [ Disease Development ] [ Control ]
PYTHIUM ROOT ROT, DAMPING-OFF, SEED DECAY [ Symptoms ] [ Disease Development ] [ Control ]
BROWN STEM ROT [ Symptoms ] [ Disease Development ] [ Control ]
RHIZOCTONIA ROOT AND STEM ROT [ Symptoms ] [ Disease Development ] [ Control ]
STEM CANKER [ Symptoms ] [ Disease Development ] [ Control ]
POD AND STEM BLIGHT AND PHOMOPSIS SEED DECAY [ Symptoms ] [ Disease Development ] [ Control ]
CHARCOAL ROT [ Symptoms ] [ Disease Development ] [ Control ]
SCLEROTINIA STEM ROT [ Symptoms ] [ Disease Development ] [ Control ]
SUDDEN DEATH SYNDROME [ Symptoms ] [ Disease Development ] [ Control ]
The Phytophthora fungus overseasons primarily as dormant, thick-walled oospores in crop debris or soil. Large numbers of oospores are formed in infected roots and stems of susceptible and tolerant soybean cultivars. Oospores are thought to germinate in the spring in wet soils, forming sporangia which contain numerous motile zoospores. Optimal temperature for oospore germination is 75 F (24 C). Zoospores are released into soil water where they swim about and are attracted to soybean roots by normal plant exudates. Optimum temperature for zoospore production is 68 F (20 C) with a minimum of 41 F (5 C). Zoospores adhere to roots, form a cyst, and germinate. Under less ideal conditions, oospores and sporangia in the soil may germinate and infect roots directly (optimum 77 F or 25 C) without forming zoospores.
Leaf infection may result when soil particles containing the Phytophthora fungus are deposited on the leaves during wind or rainstorms. If the weather remains cloudy and damp, severe leaf infection occurs and the fungus grows internally toward the petiole and then the stem.
The severity of Phytophthora rot of soybeans may increase if there are high populations of other root-rotting fungi in the soil (e.g. Pythium or Fusarium spp. and Rhizoctonia solani), because damaged roots are more susceptible to infection. Infection of soybean roots by the nematodes also increases the severity of Phytophthora root rot.
There are many races of Phytophthora sojae, which greatly complicates the development of resistant cultivars by conventional breeding methods. The races can be distinguished on eight soybean differential cultivars. Resistant cultivars are resistant to only certain races. However, this resistance is high and is effective from planting to plant maturity. Tolerant cultivars are susceptible in the seedling stage but are not susceptible to any race past this growth stage. The level of tolerance may vary from high to low.
PYTHIUM ROOT ROT, DAMPING-OFF, SEED DECAY
Figure 2. Soybean seedlings wilting and drying in the field from Pythium, root rot, caused by Pythium spp. (Courtesy H.J. Walters).
Pythium rot is caused by at least five species of the cosmopolitan
soilborne fungus Pythium. Species of Pythium generally
cause seedling diseases that may induce seed decay and damping-off
(seedlings fail to emerge or they emerge then wilt and collapse),
especially in wet seasons with high levels of rainfall before and
after planting. Pythium rot is most severe in poorly drained soils.
Infected plants have dark areas extending up the stem several inches
from the soil line. The diseased areas usually become translucent,
soft, and watery. These areas tear away when the plants are pulled
from the soil.
If dry weather sets in, the plants appear dry and shredded (Figure 2). Usually, the roots are badly decayed. Infected plants normally occur singly or in small groups scattered throughout a field. Pythium usually causes little reduction in yields. Infection by Pythium species is often followed by infection by other root- and crown-rotting microorganisms which can mask typical symptoms.
Pythium fungi are common inhabitants of the soil that colonize crop residues and attack a wide range of crop plants. The fungi survive in soil and plant residue as dormant, thick-walled oospores and as mycelium in crop residues. When the soil is cool (50 to 59 F, 10 to 15 C) and wet, the oospores commonly germinate and produce a sporangium in which zoospores are formed. After escaping from the sporangium, the zoospores swim about in the soil water and are attracted to seeds or to the roots of seedlings where they encyst and later form a germ tube that penetrates and causes infection. At higher temperatures (77 to 97 F, 25 to 36 C), the oospores may germinate directly and form one or more germ tubes that penetrate the seed coat or the root and stem tissues directly. Seedlings up to 10 days old are more susceptible to damping-off than older plants.
Figure 3a. Brown stem rot.
Brown stem rot, caused by the fungus Phialophora gregata (synonym Cephalosporium gregatum), enters plants through the roots and lower stem. Losses are greatest when cool weather occurs during the pod-filling stage (late July and first half of August) followed by hot, dry weather. Losses of 17 to 25 percent may result from lodging, premature death, or from the production of fewer and smaller seeds.
Brown stem rot is difficult to recognize before pod set because it has no external symptoms. When the stems of infected plants about mid-season are split longitudinally, however, a characteristic, dark reddish brown discoloration of the vascular elements and pith is evident (Figure 3a), extending upward from the roots or crown. Occasionally during hot, dry weather in late August or early September, wilting occurs followed by a "scorching" (browning and dying) of the leaf tissue between the veins. The leaves blight and dry rapidly. Infected plants often look "frosted" (Figure 3b). The brown stem rot fungus reduces the efficiency of the water-conducting tissues in the stem. However, leaf symptoms may vary and should not be considered in diagnosis without splitting stems.
Disease development is optimum at air temperatures of 59 to 81 F (15 to 27 C). Little or no disease develops at temperatures above 90 F (32 C). Cool weather leads to more internal stem browning.
The brown stem rot fungus survives in soybean debris and in soil to a depth of about one foot. The fungus produces spores on all types of soybean residue except pods. Infection occurs through main and lateral roots and the pathogen moves into the lower stem early in the growing season. The fungus spreads slowly upward in the water-conducting vessels. The pathogen may plug vessels partially or completely, interfering with the flow of water and nutrients. The fungus has been reported to be seedborne, surviving as mycelium within the seed coat.
Figure 3b. Brown stem rot.
1. Grow soybeans in the same field only once in 3 or 4 years. Rotate with corn, sorghum, small grains, forage grasses, legumes, or other crops.
2. Plant resistant cultivars in fields where brown rot is a severe problem. Cultivars that mature early tend to escape severe infection, but generally yield less than later-maturing ones in the absence of the disease.
Figure 4. Rhizoctonia root and stem rot.
Rhizoctonia root and stem rot is caused by the cosmopolitan, soilborne fungus Rhizoctonia solani and is primarily a seedling disease that attacks the basal stem and roots of young plants during May and June causing pre-and postemergence damping-off. The disease is found sometimes in conjunction with Pythium or Phytophthora rot. Rhizoctonia infection typically produces a sunken, reddish brown to dark brown decay of the outer layer of the main root and stem at the soil line and below (Figure 4). In contrast with Pythium root rot, Rhizoctonia-infected stems remain firm and dry. Phytophthora-infected roots are a dull, dark brown; those infected with Rhizoctonia are usually reddish brown. Rhizoctonia-diseased plants commonly wilt in more or less circular patches 4 to 10 feet in diameter, distributed irregularly throughout a field. Damping-off of seedlings and stem and root decay can reduce stands and yield losses.
The Rhizoctonia fungus is a very common one which infects most field crops, vegetables, ornamentals, and fruits. The fungus survives in soil and plant residue as small, chestnut brown to black bodies (sclerotia) or as resting mycelium. Many strains of the fungus can colonize essentially any dead plant tissue. During moist soil conditions, sclerotia germinate to form mycelium; or, the resting mycelium grows from all types of plant debris to infect seeds, roots, and stem tissue.
The optimum temperature for disease development is between 77 and 85 F (25 and 29 C); but occasionally, severe losses may occur at 59 to 76 F (15 to 24 C). Rainfall followed by cool and then warm, humid weather is most favorable for disease development. Growth of the Rhizoctonia fungus in soil depends on nutrient supply; soil moisture, temperature and pH; and competition from other soil microorganisms.
The severity of Rhizoctonia root and stem rot increases when plants are grown in soils that are deficient in calcium, iron, magnesium, nitrogen, phosphorus, sulfur, or any combination of these elements. There is evidence that some herbicides reduce the number of microbial antagonists in the soil, which favor Rhizoctonia solani.
1. The same as for Pythium Rot.
2. Ridge the soil around the base of plants during cultivation. This practice often stimulates the production of new lateral roots above the rotted basal portion of the taproot. Affected plants commonly recover, at least partially.
3. Apply a recommended seed treatment. See the chapter, "Condensed Plant Disease Management Guide for Field Crops", in the current Illinois Pest Control Handbook for a list of seed protectant materials.
Stem canker is caused by the fungus Diaporthe phaseolorum var. caulivora. It occurs throughout Illinois. Enlarging cankers that are reddish brown to black, slightly sunken, and girdling develop on the lower part of the stem, causing the plants to wilt, wither, and die because the flow of water and nutrients to the foliage is reduced or stopped completely. The lesions usually occur at the fourth or fifth node (joint) or in the region of the second and third trifoliolate leaves (Figure 5). Infected stems are brittle, and the plants break over easily at the center. The symptoms of stem canker usually appear in late July or early August, when the pods are starting to fill out, and persist until the crop matures. The plant withers and dies during the latter half of the growing season. The dead, dried leaves remain attached, instead of dropping off as they normally would at maturity.
An often overlooked symptom of stem canker is the appearance of small, reddish brown lesions on one or both cotyledons. Infection may spread into the stem, causing seedlings to wither and die. Seedlings may also die before emergence. Yield losses of 20 to 50 percent have been recorded when infection occurs soon after the pods begin to develop.
Figure 5. Stem canker
The stem-canker fungus overseasons in soybean residue in or on the soil, and in infected seed. For the stem canker fungus, infected seeds may serve as an important source of long range dissemination. The fungus survives as mycelium and as clusters of long necked, black fruiting bodies (perithecia) on infected tissue. The perithecia are capable of remaining viable up to 14 months at temperatures of 4 to 65 F (-15 to 18 C). Perithecia, containing large numbers of microscopic ascospores, are also produced in lesions on infected cotyledons. The wind- and waterborne ascospores provide inoculum for secondary infections. Most infections occur on the lower leaves. The fungus grows from the leaf blade through the petiole to the stem, where a typical canker results. A daily mean temperature of 70 F (21 C) during wet weather is optimum for disease development.
1. Plant high-quality, certified seed that is disease-free and will germinate more than 80 to 85% in a warm germination test or over 70% in a cold germination test.
2. Plant thoroughly cleaned seed in a warm, fertile, well-prepared seedbed. Treat the seed with a protective fungicide. See the chapter "Condensed Plant Disease Management Guide for Field Crops" in the current Illinois Pest Control Handbook for details.
3. Bury infected crop residue after harvest, where soil erosion
is not a problem.
4. Where feasible, rotate soybeans for 1 or 2 years with corn, sorghum, small grains, alfalfa, or forage legumes.
5. Make a foliar application of a labeled fungicide. This
is suggested for seed-production fields. For details, see the "Condensed
Plant Disease Management Guide for Field Crops" chapter. Spraying
increases seed size, quality, and germination. The proper and timely application
of a fungicide not only controls stem canker, but also pod and stem blight,
Septoria brown spot, anthracnose, Cercospora leaf spot or blight, target
spot, and purple seed stain. Yield increases are not unusual in Illinois
when August and September are very rainy and the harvest is delayed after
full maturity. If these conditions are not present, however, yield increases
may be minimal.
6. Harvest as soon as the crop is mature. When harvest is delayed under wet conditions, seeds may be infected throughout the plant.
7. Maintain adequate potash based on a soil test.
Pod and stem blight, caused by Diaporthe phaseolorum var. sojae (the asexual state is Phomopsis sojae), is similar to stem canker but is spread more widely over the entire state of Illinois. Another involved fungus is Phomopsis longicolla. The relative presence of the two fungal species varies with location and season. Pod and stem blight occurs primarily on plants nearing maturity. Damage is most severe in wet seasons when harvest is delayed. Seed infection is greater in densely populated fields, due to lodging of plants.
Numerous, small black "pimples" (pycnidia, the fungus fruiting bodies) appear on the stems and pods. These "pimples" are first detected on petioles of abscised leaves. They are commonly arranged in straight rows along the stem and are scattered on the pods (Figure 6a). The causal fungus may produce seed rot as the plants mature. Infected seeds (Figure 6b) are often discolored, moldy, cracked, shriveled, lightweight, and often fail to germinate when the soil is cool (59 to 68 F, 15 to 20 C) and wet. The infected seeds that do germinate often give rise to infected seedlings, which may serve as a source of inoculum. Pod and stem blight is a prime factor in reducing seed quality in seed-production fields. Infected seeds produce low quality oil and flour.
Figure 6a. Pod and stem blight.
Figure 6b. Soybean seeds infected with the pod and stem blight fungus, Diaporthe phaseolorum vsr. Sojae (Phomopsis sojae).
The pod and stem blight fungus is seedborne. Most seed infection occurs during or after the yellow pod stage (R7). Insect injury, such as stinkbug feeding wounds on pods, may increase disease levels. The fungus also overseasons in the residue of soybeans or other host plants (e.g. cowpea, garlic, green bean, lespedeza, lima bean, lupines, okra, onion, peanut, pepper, and tomato) as dormant mycelium. Pycnidia of the Phomopsis state may be found in dead soybean tissue such as Phytophthora - induced lesions, tissues damaged by hail, or plants killed by other diseases. In wet seasons latent infections produce tremendous members of pycnidia simultaneously over entire plants as they mature.
Charcoal rot, summer, or dry weather wilt is caused by the widespread soilborne fungus Macrophomina phaseolina (synonyms: Rhizoctonia batiticola, Sclerotium batiticols). The disease attacks the roots and basal portion of the plant throughout the season. Charcoal rot is favored by hot, dry weather especially in combination with fertility deficient soils or other unfavorable growing conditions. Charcoal rot is usually found in plants of low vigor or in a weakened condition after midseason, mostly in the southern two-thirds of Illinois or other parts of the state. In an advanced stage, the leaves on affected plants turn yellow, wilt, wither, but remain attached. After flowering the lower stem and taproot may appear light gray or silvery in color. When the outer "bark" is peeled from the roots and stem base, small black specks can be seen the microsclerotia (propagating bodies) of the causal fungus. These specks may be so numerous that they give a grayish black color to the tissues; hence, the name "charcoal rot" (Figure 7). When split open, the taproot and base of the stem show black streaks in the woody portion. The causal fungus is a weak parasite of soybeans that attacks and may kill seedlings and young plants when their growth is retarded by hot, dry conditions.
Seedling infestations can mimic those of Rhizoctonia producing a reddish superficial lesion on the hypocotyl. Charcoal rot lesions do not cause a shrinking of tissues as does Rhizoctonia. Lesions can often be scraped off with a fingernail where charcoal rot is present.
Figure 7. Charcoal rot.
The charcoal rot fungus overseasons as jet black, round to oblong
or irregular microsclerotia and resting mycelium in dry soils and
embedded in plant residues. The sclerotia germinate on the surface
of roots. The resulting germ tubes penetrate and cause infection.
The fungus is also seedborne. The Macrophomina fungus restricts
water movement in the plant by mechanical plugging of the water-conducting
vessels with mycelium and microsclerotia and by secreting toxins
and enzymes that kill host tissues. Disease development and symptom
expression are most rapid at temperatures of 82 to 95 F (28 to 35
1. Plant high-quality, certified seed that is disease-free. (Same as No. 1 for Stem Canker.)
2. Plant soybeans at the recommended rate. Crowding of seedlings
makes them more subject to infection.
3. Fertilize, based on a soil test.
4. Rotate soybeans with non-host crops (cereals) for one or two years.
5. Where possible, irrigate during extended periods of hot, dry weather.
6. Plow down cleanly infected crop residue, where erosion is not a problem. This places the sclerotia mostly into moist soil where they are more subject to attack by other soil microorganisms.
Sclerotinia stem rot is caused by the soilborne fungus Sclerotinia sclerotiorum. The disease is usually a minor one in Illinois, except for local outbreaks (usually where snap beans, canola, or sunflowers have recently been grown) during prolonged wet periods. The disease is most common in areas of fields where air circulation is poor, e.g. near woods. The first symptoms, often observed on older plants, are the wilting and withering of the upper leaves. A white, cottony growth appears on the branches, pods, and stems of the soybeans, usually near the soil line and originating at stem nodes. Large survival bodies (sclerotia) that are round to irregular and eventually hard and black are formed on and inside the stem; occasionally, in the pods (Figure 8). These sclerotia may be partly covered with the dense cottony fungus growth. Plants die prematurely when the stems are girdled by the fungus. The withered leaves remain attached to the stem for some time. Pod development and pod fill above the girdling stem lesions are greatly reduced. Soybean seedlings may be killed before or after emergence from a watery, soft rot. Seeds may become infected within diseased pods. Infected seeds are discolored, flattened, and smaller than healthy seeds and sometimes replaced by black sclerotia.
Figure 8. Sclerotinia stem rot. Note sclerotia (lower left); also, those forming on the stem (center) and inside the stem (right).
Sclerotia of the Sclerotinia fungus can survive in the soil for long periods and are highly resistant to most fungicides. The sclerotia germinate within 2 inches (5 cm) of the soil surface by producing one to many light tan to brown, funnel-shaped structures (apothecia) during prolonged periods of cool (40 to 59 F, 5 to 15 C), wet weather. Large numbers of asci are formed in the apothecia, which literally eject "clouds" of ascospores under proper conditions. The windborne ascospores germinate and infect soybean blossoms, stems, branches, and pods under very damp conditions.
1. Do not rotate soybeans with garden, snap beans (Phaseolus spp), canola or sunflowers. Control broadleaf weeds which may serve as hosts.
2. Thoroughly clean contaminated seed lots to screen out some of the sclerotia. At a foreign port of entry, even a few sclerotia in a shipment intended for human consumption are grounds for rejection.
3. Grow soybean cultivars that do not lodge readily.
4. Avoid planting soybeans in narrow rows (less than 30 inches or 76 cm) in fields with a history of Sclerotinia stem rot.
5. Avoid irrigation at flowering. High humidity in the canopy at this time increases disease levels.
Figure 9. Sudden death syndrome. A. early symptoms showing small yellow blotching; B. late symptoms, note distinctive green vein pattern; C. defoliation (courtesy S.B. Belmar)
Sudden death syndrome (SDS), caused by a strain of the soilborne fungus Fusarium solani, generally appears about midsummer in soybeans with high yield potential usually after blooming. The disease can result in minor or severe yield loss, depending on when it develops. SDS is identified by the appearance of small, scattered yellow spots or blotches usually on the upper leaves (Figure 9a). These spots enlarge, merge, and the tissues turn brown between the veins; however, the veinal tissues remain green (Figure 9b). Leaflets may curl upward or drop prematurely, leaving the petioles firmly attached (Figure 9c). Severe foliar symptoms give affected areas in a field a tan to brown cast and may be the first evidence of the disease. Flowers and pods may abort and pods drop or not fill. The first pods to set may have a few beans in them which remain small. Later pods may not fill or may have immature green seed. One characteristic of SDS is that the interior of the stem (pith region) remains white. There may be a slight gray-brown discoloration of the vascular system just inside the outer "bark" of the stem but the pith remains white. If the pith is discolored, it may indicate the presence of brown stem rot. Root symptoms preclude foliar symptoms and result in deterioration of the topmost, lateral roots, and nitrogen-fixing nodules. Fields in which the disease is present are likely to develop SDS in subsequent years, although there are no accurate methods of assessing possible disease levels.
The Fusarium fungus overseasons as thick-walled chlamydospores or mycelium in crop debris or in soil. SDS is affected by weather conditions. The disease is more severe during cool, wet growing seasons. It is commonly found in association with soybean cyst nematodes (SCN) and in lower areas of fields. Nematodes are believed to act as a stress factor rather than being directly involved with the disease. However, work in Mississippi has shown that SCN can act to spread the fungus. This research demonstrated that the Fusarium fungus was present both on and in the cysts of soybean cyst nematode. Therefore, direct or indirect movement of the nematode could spread the fungus to new areas. The disease tends to be most severe on well managed soybeans with a high yield potential. However, tillage and rotation practices seem to have little impact on this disease.
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1. Grow well-adapted, high-yielding varieties in a warm, well drained, fertile soil. Maintain balanced soil fertility based on a soil test.
2. Control other diseases, weeds and insects.
3. Although SDS is not seed-transmitted, seeds from infected plants are small in size and tend to produce weaker seedlings than those from healthy plants. Therefore, do NOT save seed from SDS-infected areas.
4. Crop rotation, although not consistent in greatly reducing levels of the Fusarium fungus, is definitely beneficial in reducing the buildup of other pathogens (especially nematodes) that may weaken the plant.
5. Sanitation (e.g., cleaning tires, combines and other equipment of soil and crop debris), although time consuming, will help to reduce spread of the SDS fungus as well as other soybean pathogens.
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For further information concerning diseases of crucifers and other vegetables, contact Mohammad Babadoost, Extension Specialist in Fruit and Vegetable Diseases, Department of Crop Sciences, University of Illinois at Urbana-Champaign.
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