Identification and Control of Seedling Diseases, Root Rot, and Rhizomania on SugarbeetPP-1142, BU-7192-S, February 1998 Carol E. Windels, Plant Pathologist, Northwest Experiment Station, University of Minnesota,
Crookston
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 and in one field in the RRV in 1997. 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.
Seedling DiseasesSugarbeet 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 it 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 plantsSeedlings 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 sometimes are inconclusive that is, no pathogens are 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 samplesWhen 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. Field historyFamiliarity 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. For instance, 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. Pythium speciesThis "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 are pathogenic to sugarbeet, P. ultimum var. sporangiiferum and P. aphanidermatum predominate in the RRV and in southern Minnesota. Symptoms caused by P. ultimum are indistinguishable from those produced by P. aphanidermatum. 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 degrees Fahrenheit). 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. Aphanomyces cochlioidesDamping-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 tissue 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. Excessive production of lateral roots is a general plant response to loss of a root tip and can be caused by disease or other damage.
If Aphanomyces-infected seedlings survive and the soil remains dry, adult roots are malformed and scarred (Figure 6). Yields are significantly reduced.
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, inoculum of A. cochlioides likely increased on roots of susceptible weeds before a sugarbeet crop was planted. Rhizoctonia solaniThis 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 girdling 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 strain of R. solani on sugarbeet seedlings 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). Corn is susceptible to AG-2-2 in Georgia but it is unknown if corn is infected by AG-2-2 in Minnesota and North Dakota.
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