Seedling diseases and root rot of sugarbeet occur annually in the Red River Valley (RRV) and southern Minnesota. Rhizomania, another root disease, was identified in southern Minnesota in 1996. Prevalence and severity of these diseases varies among regions and fields and within fields during a single growing season. Variation within the same field from one sugarbeet-growing season to the next also can occur. Disease severity is determined by: the amount of pathogen in the soil; susceptibility of the sugarbeet variety; environmental factors, especially soil moisture and temperature; and effectiveness of disease control measures in previous seasons.
This bulletin discusses the pathogens that cause seedling diseases, root rot, and rhizomania. A section on "impostors" - some problems that resemble seedling and root rot diseases - also is included.
Sugarbeet seedlings are susceptible to fungi that cause seed rot, damping-off, and root rot. Damping-off occurs quickly (within a day or two after onset of symptoms), after which infected seedlings dry up and blow away. Unless a field is watched carefully, it is difficult to determine if poor stands occurred because seed rotted in the ground, seedlings died before emergence, or if seedlings emerged and then died.
Most seedling diseases in Minnesota and North Dakota are caused by fungi that live in soil (soilborne fungi). These fungi include Pythium species, Aphanomyces cochlioides, and Rhizoctonia solani. Phoma betae is a seedborne fungal pathogen that also infects sugarbeet seedlings, but this disease has not been a problem in Minnesota and North Dakota in recent years. Occurrence of rainy weather in seed production fields in Oregon favors invasion of seed by P. betae at harvest. If present in seed, this fungus causes damping-off of sugarbeet seedlings.
Fungi that cause seedling diseases produce similar symptoms, so positive identification of the pathogen(s) that cause stand loss should be verified. Sometimes only one pathogen causes disease in a field. In other cases, two or more pathogens attack plants in the same field, or even the same plant, and result in a seedling disease "complex." Ways to determine the cause(s) of seedling stand establishment problems include laboratory analysis of symptomatic plants, assay of soil samples, and knowledge of field history.
Laboratory analysis of symptomatic plants
Seedlings displaying the range of symptoms observed should be removed from soil with a spade. Then, soil should be carefully removed and the seedlings gently washed, blotted dry, wrapped in paper towels, and placed in a plastic bag. Samples can be stored in a cooler or refrigerator for 24 hours or transported immediately to a private or university diagnostic laboratory for analysis. Include healthy plants for comparison to unhealthy plants. A competent field advisor also should make an on-site inspection of the field.
Results of a laboratory analysis are sometimes inconclusive - that is, pathogens are not isolated. This can happen even when plants have typical symptoms of disease. Such results occur when plants have been infected for a long time or are in an advanced state of decay. Pathogens are not detected because they cannot grow in the presence of the many secondary microorganisms invading and disintegrating diseased roots.
Assay of soil samples
When a laboratory analysis of plants is inconclusive, or if producers have not confirmed the cause of stand establishment problems or root rot in previous seasons, a soil assay can be helpful. This assay, however, is recommended only when Aphanomyces is suspected. It is not used for Pythium species (they occur in all fields) or Rhizoctonia solani (populations usually are too low to detect). Soil samples should be collected from the portion of the field in question. The assay consists of a four to five week analysis in the greenhouse and laboratory. For information on collection and storage of soil samples and for details on the assay, contact the Plant Disease Clinic, 495 Borlaug Hall, 1991 Upper Buford Circle, University of Minnesota, St. Paul, MN 55108 (612/625-6290) or sugarbeet cooperative.
Familiarity with the history of a field can provide clues important to understanding the cause of stand establishment problems. Consider the past and present climate and production history of the field. A number of factors cause symptoms similar to seedling diseases, including insect damage, wind injury, heat, drought, frost, insecticides, soil fertility, and misapplication, drift, or carryover of herbicides.
Results of previous laboratory analyses of sugarbeet plant or soil samples can be helpful but may be misleading in diagnosing a current problem. Fields with a history of disease problems may have poor stands not because of disease, but because of adverse environmental conditions or injury from pesticides. The amount of soil moisture can favor infection by one fungus and not another, although two or more fungal pathogens are present. Some fungi cause disease even after fields have been out of sugarbeet production for several years. Pythium species and Aphanomyces cochlioides survive in soil for years in the absence of a sugarbeet crop, while populations of Rhizoctonia solani decrease or increase depending upon length of rotation and the crop sequence.
This "water mold" fungus occurs in all fields. Pythium requires moist or wet soil to infect seeds and seedlings. Pythium can infect and rot seeds before or as they geminate. The disease is characterized by a brown, water-soaked discoloration of the seedling before or shortly after emergence (Figure 1). Commercial sugarbeet seed is pretreated with fungicides that usually control Pythium diseases effectively. When conditions slow or delay emergence, Pythium can cause seed rot (even when seed is treated with fungicide). These conditions include deep planting, cold weather, and excessive soil moisture (especially in poorly drained or fallowed fields). Under extremely wet conditions, Pythium also causes damping-off, usually within the first week of emergence (Figure 1).
Among the species of Pythium that infect sugarbeet, P. ultimum var. sporangiiferum and P. aphanidermatum predominate in the Red River Valley and in southern Minnesota. Symptoms caused by P. ultimum are indistinguishable from those produced by P. aphanidermatum. Both species are pathogenic to sugarbeet.
Pythium ultimum is the most common and widespread species. It attacks unprotected seed (no fungicide treatment) at the same temperatures that favor germination of sugarbeet seed (40-95 °F). The fungus grows over a temperature range from 40 to 95 °F and attacks germinating seed most actively at 60-80 °F.
Pythium aphanidermatum is a high temperature fungus. It attacks seeds and seedlings at temperatures from 50 to 105 °F, with most infections occurring at 85-95 °F.
Damping-off caused by A. cochlioides is the most prevalent and serious soilborne fungal disease of sugarbeet in warm, wet seasons, especially in late-planted fields. Many fields in the southern RRV are infested with A. cochlioides; in recent wet years this fungus also has been active in the northern RRV. The fungus is prevalent in sugarbeet fields in southern Minnesota. In 1993, a season with abundant rainfall and warm weather, about 50% of the sugarbeet fields in southern Minnesota had symptoms of Aphanomyces diseases compared to about 15% of the fields in the southern RRV.
Under warm, wet soil conditions, overwintering spores (oospores) of A. cochlioides are stimulated to germinate by exudates from sugarbeet roots. The fungus then produces and releases motile zoospores that swim through water and infect roots. Sugarbeet plants are susceptible to infection throughout the growing season.
Aphanomyces cochlioides rarely causes seed rot, but damping-off occurs frequently in warm (68-86 °F), wet soil. Infection seldom occurs when soil temperatures are less than 60 °F. The fungus infects seedling roots and the hypocotyl (region between the cotyledons and seed). Symptoms include brown, water-soaked regions that can extend up to and include the cotyledons (Figure 2). The infected hypocotyl and root rapidly turn black and shrink to a dark, slender thread (Figure 3).
Pythium causes damping-off most frequently during the first week of emergence while A. cochlioides does not begin to cause damping-off until after the first week of emergence at the earliest (Figure 4). Also, A. cochlioides causes more extensive stand losses than do Pythium species.
Seedlings infected by A. cochlioides occur in patches ranging in size from a few feet in diameter to extreme cases where entire fields of two- to five-week old plants are destroyed. Disease frequently occurs in portions of fields that tend to remain wet - near drainage ditches, on hill sides, in low spots, or in compacted areas. Disease develops in light-textured soils but is favored in heavy-textured soils, which tend to hold water. As soil dries, surviving seedlings resume growth and may produce numerous lateral roots (Figure 5), a symptom sometimes confused with rhizomania. If Aphanomyces-infected seedlings survive and the soil remains dry, adult roots are malformed and scarred (Figure 6) with significantly reduced yields.
Aphanomyces damping-off tends to occur more frequently in fields planted to sugarbeet for many years, especially fields in short rotations. The disease, however, can occur during the first or second season of sugarbeet production. In these cases, A. cochlioides likely survived on roots of susceptible weeds before a sugarbeet crop was planted there.
This fungus can cause seed rot but more often causes damping-off or stunting of young plants. Rhizoctonia solani occurs in most fields, but at low concentrations of inoculum. The damage it causes rarely warrants replanting. Occasionally, a few acres within a field are replanted because of early-season damage caused by R. solani.
Infections occur below the soil surface, but symptoms can extend up the hypocotyl (Figure 7). A sharp margin of demarcation develops between the brown to dark-brown lesions girding the root and white healthy tissue. On older seedlings, infected roots sometimes are stunted, with brown, sunken lesions on lateral roots and taproots (Figure 8). Lightly infected seedlings often survive and produce roots that are nearly normal.
Rhizoctonia solani is active over a temperature range from 54 to 95 °F, but it is particularly active from 68 to 86 °F. Beet seedlings usually escape infection when soil temperatures are less than 60 °F. The fungus infects seedlings when soil moisture conditions range from somewhat dry to wet. In wet soil, R. solani can grow from plant to plant, damaging or killing several adjacent plants. Infected seedlings occur in patches or as scattered plants.
Rhizoctonia solani is composed of several strains referred to as anastomosis groups or AGs. Four strains of R. solani have been isolated from diseased sugarbeet seedlings in fields throughout the RRV and southern Minnesota. The prevalent cause of seedling disease on sugarbeet is AG-4. Other strains, including AG-1, AG-2-2, and AG-5, occur less frequently. Several crops rotated with sugarbeet also are susceptible to AG-1, AG-2-2, AG-4, and AG-5 (Table 1).
In some fields, Pythium species, A. cochlioides, and R. solani occur together. When soil is warm and wet, A. cochlioides causes the most significant damage among these seedling pathogens. When soil temperatures are below 60 °F, P ultimum infects seedlings but P. aphanidermatum, A. cochlioides, and R. solani rarely cause disease. At temperatures above 68 °F, all of these fungi cause disease when soil is wet, but only R. solani causes disease if soil is somewhat dry.
In Minnesota and North Dakota, root rot of sugarbeet is caused by Aphanomyces cochlioides and Rhizoctonia solani. Pythium root rot on older beets is extremely rare. Seedling diseases caused by A. cochlioides and R. solani often are indistinguishable based on symptoms, but root rot on older plants caused by these fungi usually can be distinguished by symptoms. It is important, however, to examine roots of several diseased plants for symptoms before plants are severely rotted or die. Symptoms of both fungi can occur in the same field and, occasionally, on the same root. The cause(s) of root rot also can be identified by laboratory analysis of symptomatic plants, assay of soil samples, and knowledge of field history, as described in the section on seedling diseases.
Pythium root rot is characterized by a black lesion that develops on the root surface (Figure 9). Rot may be extensive in the interior of the beet. In instances where this disease has been observed in the RRV, fields were extremely wet for about 10 to 14 days.
In wet seasons, Aphanomyces root rot occurs throughout the summer until harvest. Root rot can develop in plants that were infected as seedlings or from new infections on sound older roots.
Disease occurs in patches ranging from a few feet in diameter to the entire field. Aboveground symptoms include undersized plants with considerable yellowing of lower leaves (Figure 10). Infected plants wilt during afternoons of hot sunny days and appear to recover overnight and on cool cloudy days. If a crop insurance adjuster will be assessing a field for losses caused by Aphanomyces root rot, schedule the inspection on a hot sunny day when plants are wilted so prevalence of the disease is easy to observe.
Below ground, a brown to black rot develops at the root tip and at junctures of lateral roots (Figure 11). Infected plants can be severely stunted (Figure 12) or the basal portion of the root is fibrous or tasseled (Figure 13). Infected plants often survive, but when foliage is mechanically removed at harvest, rotted roots are easily dislodged or are too small to be harvested. Roots that recover from seedling infections or survive late-season infection have reduced yield and sucrose content and have higher levels of impurities (non-sucrose constituents), which makes sucrose extraction difficult and expensive. If diseased beets are mixed with healthy roots in storage piles, the quality of the entire pile can be reduced.
Rhizoctonia root and crown rot is caused by R. solani AG-2-2. The disease begins to occur when plants are about eight weeks old (mid to late June) and roots can become infected throughout the season. Aboveground symptoms of Rhizoctonia root and crown rot include yellowing and sudden wilting of leaves. Petioles of the outer leaves are blackened at the point of attachment to the crown (Figures 14-17) and often lay flat on the ground. This disease frequently occurs on scattered plants or on several plants successively in a row (Figure 14). A dark brown-gray rot starts near the crown and spreads over the root surface. Symptoms vary from slightly sunken lesions scattered over the root to complete rotting and cracking of the surface (Figure 15). Rhizoctonia root and crown rot is favored when soil containing the fungus is thrown into crowns of plants during cultivation (Figure 16).
Rhizoctonia infections can encircle and sever the root 3 to 4 inches below the soil surface (Figure 17), so it is important to carefully remove the entire taproot with a hand trowel or shovel when diagnosing root diseases. If a diseased root is pulled from the soil, a portion may remain behind, which can result in confusing symptoms of Rhizoctonia root and crown rot with Aphanomyces root rot.
In cool, wet seasons, a superficial dusty growth that is white to gray in color occasionally occurs on petioles near the beet crown (Figure 18). Disease symptoms do not appear on foliage, crowns, or roots of these plants. The dusty growth is the hymenium of Thanatephorus cucumeris, the sexual (spore-forming) phase of Rhizoctonia solani. It is of minor economic importance to sugarbeet, but in the RRV may be a source of genetic recombination in R. solani AG-3 (pathogenic to potato) and AG-5 (pathogenic to potato and soybean). Strains of R. solani (AG-2-2 and AG-4) that cause root rot on sugarbeet also are reported to cause foliar blight as T. cucumeris in other regions of the U.S.A., but this symptom has not been observed in Minnesota or North Dakota.
CONTROL MEASURES FOR SEEDLING DISEASES AND ROOT ROTS
Seed treatment fungicides
These products are a convenient, economic, and effective method of reducing seed rot and damping-off. All commercial sugarbeet seed is pretreated with fungicides, and the products used are listed on the seed package. Some fungicides have activity against one pathogen while others have activity against two or more pathogens. Combinations of fungicides are applied to broaden the spectrum of activity and protect against two or more fungal pathogens. The most effective seed treatment fungicides are active against certain fungi (Table 2), so knowledge of which pathogens occur in a field is important to obtaining the best stands.
Pythium species occur in all fields and are active at the same temperatures favorable for beet seed germination. Thus, fungicides with specific activity against Pythium are particularly important in protecting seed. Excellent control of Pythium is achieved with several fungicides but the most widely used fungicide is Apron (= metalaxyl). If seed has not been treated with a fungicide, Apron Dry Seed Protectant (12.5%) can be applied in the drill box, but thorough mixing of fungicide and seed is essential for good control.
Aphanomyces damping-off is reduced by seed treatment with Tachigaren (hymexazol). It is registered for pelleted seed at rates of 45 to 90 grams per unit of 100,000 seed (approximately 2.2 pounds), but only the 45 and 75 g rates are available for the 1998 season. Tachigaren also is highly effective against Pythium at lower rates than those recommended for control of Aphanomyces. For low to moderate levels of Aphanomyces, a label rate of 45 grams per unit is recommended. The 90 gram rate should be reserved only for use in severely infested fields. Tachigaren loses effectiveness as it decomposes and provides protection to seedlings for about three to four weeks.
Seed treatment fungicides provide limited protection of seedling stands because they decompose from one to four weeks after planting, depending on the fungicide. The greater the plant population that emerges, the greater the number of seedlings that survive. Overseeding may not compensate for stand losses and risks buildup of pathogen populations. Pythium usually is effectively controlled by seed treatment because it is active early in the season. Aphanomyces cochlioides and Rhizoctonia solani, however, can cause problems throughout the season. In fields with a history of disease pressure, particularly with Aphanomyces, use of an appropriate fungicide on varieties with partial resistance is recommended.
Control tips: Aphanomyces
Select varieties with partial resistance
Plant Tachigaren-pelleted seed
Cultivate and keep soil dry
Enhance field drainage
Increase length of rotation
Avoid spread of contaminated soil
Soil treatment fungicides
Various formulations (granule, emulsifiable concentrate, wettable powder) of Ridomil (metalaxyl) are available to supplement Apron (metalaxyl) seed treatment for control of Pythium species. Yield increases are documented in producers fields, but benefits vary among fields and seasons. These variable results are attributed to different populations of Pythium in fields and because cool, wet soil conditions (favorable for Pythium activity) do not occur each spring. Ridomil is beneficial when sugarbeet seeds are planted into cold, wet fields with a history of Pythium disease problems. Check the label for planting restrictions within 12 months of application.
Pythium aphanidermatum, Aphanomyces cochlioides, and Rhizoctonia solani do not grow well at low temperatures, so infection of sugarbeet seedlings by these pathogens can be avoided by planting early, into cool soils. Early planting fosters good emergence and vigorous growth. This enables plants to advance beyond an extremely susceptible stage before soils warm up and pathogen activity increases. Infection by P. ultimum cannot be avoided by altering planting date since the fungus is active at the same temperatures favorable for germination of sugarbeet seed. Seed treatment with fungicides with specific activity against Pythium species are recommended.
Control tips: Pythium
Select seed treated with an appropriate fungicide
Avoid deep planting in wet soil
Cultivate to keep soil dry
Planting depth, soil moisture
Pythium species and A. cochlioides require wet soil to allow swimming zoospores of these fungi to move through soil and infect sugarbeet roots. Shallow planting at a ¾-inch depth encourages maximum emergence and reduces disease in wet, early-seeded fields. Cultivation helps dry out soil and reduces early season losses from Aphanomyces seedling diseases. R. solani has a lower requirement for soil moisture and is less affected by planting depth than Pythium species and A. cochlioides.
Crop sequence affects seedling diseases and root rots. However, the relationship of crop sequence and disease severity is not the same for all sugarbeet pathogens.
Pythium species attack roots of all agricultural crops and weed species and survive in soil for years. Germination of resting spores of Pythium species is stimulated by seed and root exudates, particularly when soils are wet. The fungus then infects young succulent roots, produces resting spores, and increases its population. Populations of Pythium species are as closely tied to environmental factors in soil as they are to previous crops. Duration of rotation has no effect on Pythium species because of their wide host range.
Evidence for the effect of previous crops on Aphanomyces cochlioides is conflicting. Researchers in Michigan reduced damping-off by soil-incorporation of corn residue. Severe damping-off caused by A. cochlioides, however, has been observed in sugarbeet fields in southern Minnesota where the previous crop was corn. Recent data suggest that chisel plowing a green oat crop into the soil in late fall may reduce Aphanomyces disease of sugarbeet the following season, but results are best when disease pressure is low to moderate.
Increasing the number of in years between growing a sugarbeet crop has a limited effect on reducing populations of A. cochlioides because the fungus produces thick-walled oospores that survive in soil for years. Effectiveness of rotation depends on the initial population of the fungus. Long rotations in fields with low populations of A. cochlioides slow down buildup of inoculum. On the other hand, severe Aphanomyces root rot has been observed 20 years after severely infested fields were rotated out of sugarbeet.
Rhizoctonia solani infects many species of crops (Table 1) and weeds and also colonizes organic matter in soil. When a susceptible crop is grown during the rotation, particularly the season before planting beets, benefits of disease control by crop rotation can be lost. This is because some crops (such as soybean and edible bean crops) are susceptible to R. solani AG-1, AG-2-2 and AG-4, which also cause damping-off and root rot on sugarbeet. Cereals are less likely than broadleaf crops to sustain inoculum of R. solani. A three year rotation of nonhost crops is the minimum duration recommended to allow the fungus population to decrease.
Control tips: Rhizoctonia
Select varieties with partial resistance
Plant seed treated with an appropriate fungicide
Cultivate and keep soil dry
Avoid "hilling" soil on beet crowns
Increase length of rotation (minimum of three years)
Rotate with nonhost crops
Avoid spread of contaminated soil
Cultivation to encourage soil drying or deep tillage to promote better water penetration reduces seedling diseases caused by Pythium species, A. cochlioides, and R. solani. Other practices that divert excess moisture, such as drainage ditches or tiling, also reduce seedling diseases and Aphanomyces root rot. Reduction of soil moisture is beneficial in controlling R. solani, but this fungus also infects roots when soil is somewhat dry.
No-till of small grain crops the season before a sugarbeet crop is planted produces environmental conditions favorable for seedling diseases and root rot. The thick layer of straw retains soil moisture and stabilizes soil temperature - environmental conditions optimal for repeated infections of sugarbeet roots by pathogens.
Rhizoctonia solani AG-2-2 usually infects adult sugarbeet roots through petioles and crowns. High speed cultivation deposits "hills" or excess soil around beet crowns (Figure 16). If R. solani is present in soil hilled on the beet crown, the fungus can readily infect. The sugarbeet canopy also provides a moist and warm microclimate favorable for infection by R. solani. Cultivation at moderate speeds results in less soil deposition in the beet crown and consequently, less Rhizoctonia root and crown rot.
Some common weeds, including pigweed, kochia, and lambsquarters, are infected by Aphanomyces cochlioides and Rhizoctonia solani. Control of these weeds during the sugarbeet season as well as during production of other crops discourages buildup and maintenance of these pathogens.
To reduce movement and spread of A. cochlioides and R. solani, equipment used in an infested field should be thoroughly washed in soapy water with a high pressure sprayer before it is moved to a healthy field. Used machinery from other beet-growing areas should be washed before introduction into local sugarbeet fields. Also, soil should be removed from boots, tools, vehicles, and all materials contaminated by Aphanomyces-infested soil. Tare soil should be deposited in areas or fields not planted to sugarbeet.
Commercial varieties with partial resistance to Aphanomyces root rot or Rhizoctonia root and crown rot are available as "specialty varieties." There is no single variety, however, with resistance to both diseases. Nor are there any varieties immune to infection by A. cochlioides or R. solani. When the pathogen is present and weather conditions are favorable for disease, varieties with partial resistance outyield other varieties. Under disease-free conditions, varieties with partial resistance to root rot yield comparably to other varieties.
Root rot fungicides
There are no fungicides registered in the United States to control Rhizoctonia root and crown rot, although some experimental fungicides show promise. There are no fungicides registered to control Aphanomyces root rot of older plants, nor are there any experimental fungicides for control of this disease on the immediate horizon.
Rhizomania occurs in young and adult plants. Expression of symptoms on foliage and roots varies. Some infected plants appear healthy while others have mild to severe symptoms. Early infections can cause severe stunting and yield loss, while late infections may go undetected and cause little or no yield loss. Rhizomania is not related to Rhizoctonia root rot of sugarbeet.
Aboveground symptoms appear as patches of plants with poor growth and light green or yellow-green foliage, similar to nitrogen deficiency. Leaves are narrow, with long and erect petioles (Figure 19). Foliage may become flaccid and wilt without discoloration. Affected plants often occur in lens-shaped patches (Figure 20), and sometimes an entire field shows symptoms. Since rhizomania-infected plants are stunted, weeds tend to be common in the affected portion of the field.
Below ground symptoms of this disease explain the name rhizomania, also known as "crazy root" or "root madness." Symptoms include stunted taproots with masses of hairy, secondary roots along the sides and tip of the root, giving it a "bearded" or "whiskered" appearance (Figure 21). Roots often appear constricted a few inches below the soil surface and have a "wineglass" shape. A pale yellow to dark brown discoloration of the vascular bundles occurs at the tip of the taproot (Figure 22).
Fields severely damaged by rhizomania have greatly reduced tonnage, a low percentage of sucrose, and are low in nitrate-nitrogen. The unusual combination of low sucrose and low nitrate is characteristic of fields with rhizomania.
Rhizomania is difficult to diagnose based on symptoms. Suspect plants should be confirmed by laboratory analysis. Positive identification can be done only by sophisticated laboratory tests using serological techniques. To collect samples, dig up plants suspected of having rhizomania and take care to preserve all secondary roots. Then, ship the plants overnight to a laboratory that specializes in rhizomania identification. Sugarbeet agriculturists can assist in collecting samples and sending them to an appropriate laboratory.
Control tips: Rhizomania
Select resistant varieties (available by 1999)
Cultivate and keep soil dry
Enhance field drainage
Avoid short rotations
Avoid spread of contaminated soil
Clean equipment, tools, and boots of contaminated soil before entering rhizomania-free fields
Plant cover crops to prevent erosion
Biology of Rhizomania
Rhizomania is caused by the beet necrotic yellow vein virus (BNYVV), which is spread by the soil fungus vector Polymyxa betae. The fungus survives in uncultivated soil for 15-20 years as thick-walled resting spores called cystosori. The BNYVV virus survives in the cystosori. Cystosori are stimulated to germinate when in proximity to sugarbeet roots and when soil conditions are warm and wet. If the germinating cystosori contain the BNYVV, the swimming zoospores that are released also contain the virus. BNYVV is introduced into sugarbeet when zoospores infect root hairs. The fungus then invades the lateral roots, which are killed by BNYVV, and more roots form. If wet weather persists, zoospores are liberated from infected roots and additional infection cycles occur. A mass of hairy roots forms following repeated infections, with much of the mass composed of dead roots.
Several conditions must occur simultaneously for rhizomania to develop: P. betae is present in the field; BNYVV is associated with P. betae; soil temperatures are above 59 oF (most infections occur at 77 oF); and the soil is wet (a condition necessary for zoospore production). Rhizomania tends to occur most frequently in lower portions of fields, areas with poor drainage, in compacted soils, and along hillsides where water seeps to the soil surface.
Control measures for rhizomania
There are no seed treatments that control this disease. Every effort should be made to avoid introduction of rhizomania-contaminated soil into geographic areas where it has not been reported. Even small amounts of contaminated soil (such as one teaspoon) can potentially result in a significant rhizomania problem after growing sugarbeet for a few seasons. Equipment from infested areas should not be moved to non-infested areas. If equipment is moved from a rhizomania-infested area, it should be power-washed with soapy water and steam-cleaned. All tools and vehicles employed in infested areas should be thoroughly cleaned before entering rhizomania-free areas. Also, boots worn in infested areas should be thoroughly cleaned or worn only in infested fields.
In geographic areas where rhizomania already exists, all tools and equipment should be cleaned between fields. Infested fields should be harvested last. Prevent wind and water soil erosion by planting cover crops. Cultural practices, such as early planting to avoid early infection, tiling to improve drainage, and deep tillage to improve water penetration, also help avoid serious losses from rhizomania. Tare soil from infested fields should not be returned to noninfested fields. Extending crop rotations is of little benefit, but avoidance of short rotations prevents buildup of inoculum to damaging thresholds.
Soil fumigation has been used in California to reduce rhizomania infections and to delay the onset of infection. At present it is unclear if fumigation is economic in nonirrigated sugarbeets. Research on soil fumigation on nonirrigated sugarbeet land is under way to determine if treatment of severely infested fields or portions of fields is practical.
Varieties with resistance to rhizomania that are adapted for sugarbeet production in Minnesota and North Dakota should be available by 1999. Until resistant varieties are available, producers should not plant a sugarbeet crop in infested fields.
IMPOSTORS: PROBLEMS THAT RESEMBLE SEEDLING AND ROOT DISEASES
Diagnosis of seedling diseases and root rot can be confusing because several other disorders produce symptoms that resemble these diseases. The disorders include a wide variety of problems including wind injury, heat, excess soil moisture, frost, insects, insecticides, soil fertility problems, and herbicide drift and carryover. When evaluating the possible cause of a problem, consider the past and present history of climatic, cropping, and field conditions. Some examples of impostors of seedling and root diseases are illustrated in Figures 23- 32.
Root maggot damage on sugarbeet occurs as larvae feed. Larvae scrape the root surface with their mouth hooks and cause irregular scars, which later darken when sap exudes from the damaged root. Larvae feeding on small tap roots can sever the root (Figure 23, top), causing a sudden and permanent wilting of foliage sometimes confused with root rot. On larger roots, larvae produce irregular scars (Figure 23, bottom). Presence of the root maggot is confirmed by carefully removing and examining soil around the root for small white larvae.
The sugarbeet root aphid sucks sap from roots and reduces the quality and size of beet roots. Heavy infestations result in wilting and death of sugarbeet plants (Figure 24). Affected roots are characterized by a white waxy material secreted by the aphids on the small lateral roots and the lateral grooves of the taproot (Figure 25). This material remains even after aphids have left the root.
Modified in-furrow application of Counter (terbufos) into light-textured soil can result in brown constriction of seedling roots at the point of seed attachment (Figure 26). The root system has a corkscrew or coiled appearance, tips of cotyledons turn brown or black, and severely affected plants die. Careful examination of soil around affected young seedlings will reveal granules of insecticide in close proximity to the seed. Severely affected seedlings may die before emergence.
Aboveground symptoms of Lorsban (chlorpyrifos) injury include wilting similar to root rot. Affected roots are constricted about 1 inch below the soil surface with no rot extending above or below the weakened area (Figure 27). These weakened plants are prone to wind damage.
A herbicide applied at the recommended rate in a previous season may not completely decompose because of weather conditions and soil type. Sugarbeet seedlings are sensitive to residues of certain herbicides in soil. For instance, residues of dinitroaniline herbicides such as Treflan (trifluralin), result in stunted sugarbeet seedlings. Roots turn brown and die starting at the point where the root joins the hypocotyl, about 1 to 1½ inches below the soil surface (Figure 28). Knowledge of herbicides applied at least the previous two seasons, soil type, and soil moisture conditions can help identify herbicide carry-over problems. Herbicide carryover occasionally persists six to seven years after application.
Drift from certain herbicides not only affects sugarbeet foliage but can produce injury that resembles root rot. For example, when sugarbeet plants are exposed to imidazolinone or sulfonylurea herbicides, foliage turns bright yellow and, if severely affected, roots become brown and constricted. Sugarbeet plants shown in (Figure 29) were exposed to Harmony, a sulfonylurea herbicide. Root rot is distinguished from Harmony damage by symptoms on foliage - Harmony damage is characterized by a bright yellow color on young leaves whereas early symptoms of root rot include mild yellowing of lower leaves and wilting.
Sugarbeet seedlings are particularly vulnerable to wind injury. Damage is associated with the back and forth oscillation of plants in wind and exposure to blowing soil, which acts as an abrasive and shears off young plants. On very young seedlings it may be impossible to determine if stands were reduced by wind or disease. If the weather has been hot and dry and accompanied by strong winds, however, wind damage is probable. If weather has been wet, seedling disease is more likely.
On older roots, wind damage produces a sudden wilting and death of foliage similar to aboveground symptoms of root rot. The cause of plant death is revealed by careful examination of the root. Wind damage causes severe root constriction about an inch below the soil surface, but the root appears normal and healthy above and below this point (Figure 30). If the root has a black rot on the petioles or crown, it likely was killed by Rhizoctonia. If the root is thin and threadlike, it likely was killed by Aphanomyces. Wind injury may be confused with root damage caused by the insecticides Lorsban and Counter.
When sugarbeet fields are flooded or heavily saturated for several days, oxygen movement to the root ceases and plants die. Sudden permanent wilting of foliage can be confused with Aphanomyces or Rhizoctonia root rot. Roots affected by excess moisture are characterized by a slimy rot and disintegration of the root by nonpathogenic microorganisms (Figure 31).
During drought conditions, foliage cannot extract enough moisture from soil to meet transpiration needs of the plant. Initially, this condition results in temporary wilting, but if prolonged, older leaves die prematurely (Figure 32). Foliage of plants already affected by root rot or rhizomania wilt more readily than healthy plants. Drought conditions, however, are not favorable for infection by soilborne fungal pathogens.
For additional information on disease and other problems on sugarbeet, see: Compendium of Beet Diseases and Insects, 1986, by E.D. Whitney and J.E. Duffus (available from The American Phytopathological Society, 3340 Pilot Knob Road, St. Paul, MN 55121, $39.00 including shipping; outside of U.S.A., $44.00 surface mail, $48.00 air mail) and Herbicide Mode of Action and Sugarbeet Injury Symptoms - A-1085, 1994, by A.G. Dexter et al. (available from North Dakota State University Extension Service, Fargo, ND 58105, $1.50 including shipping).
Figures 1-3, 5-12, 15, 17, 18, 21, 22, 26, 28 and 29:
photos by C.E. Windels, Northwest Experiment Station, University of Minnesota, Crookston,
Figure 4: data from P. Payne and M. Asher. 1989. British Sugar Beet Review 57:44-47.
Figures 13, 30 and 31: photos by C.M. Rush, Texas Agricultural Experiment Station, Bushland, TX.
Figures 14 and 16: E.G. Ruppel, USDA-ARS, Crops Research Lab, Fort Collins, CO.
Figure 19: H.A. Lamey, Department of Plant Pathology, North Dakota State University, Fargo, ND.
Figures 20 and 32: A.W. Cattanach, Department of Soil Science, North Dakota State University, Fargo, ND.
Figures 23A and 23B: R. Dregseth, Department of Entomology, North Dakota State University, Fargo, ND.
Figures 24 and 25: Chris Campbell, formerly of the Department of Entomology, University of Minnesota, St. Paul, MN.
Figure 27: R.A. Kuznia, formerly of the Northwest Experiment Station, University of Minnesota, Crookston, MN
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