Seedling diseases and root rot of older sugarbeets are important diseases that occur annually in the Red River Valley and southern Minnesota. This fact sheet discusses the pathogens and conditions that favor their activity.Disease management strategies also are included.
Sugarbeets are very susceptible to seedling diseases caused by several soil borne fungi. Stand loss occurs when these fungi cause seed rot, pre-emergence damping-off, and post emergence damping-off during spring months. Postemergence damping-off occurs very quickly (within a day of onset of symptoms), after which infected seedlings can desiccate and blow away. Unless a field is watched carefully, it is difficult to determine whether poor stands occurred because seedlings failed to Merge, or because seedlings merged and then died. Infection of seedlings does not always result in death, but may result in root systems that are stunted or malformed. The severity of these symptoms on "recovered" plants depends upon the extent of the initial infection.
Most seedling pathogens in Minnesota and North Dakota are soil-borne fungi. These include Pythium species, Aphanomyces cochlioides, and Rhizoctonia solani. Phoma betae is a seed borne pathogen that also affects sugarbeets, but this disease has not been a problem in Minnesota and North Dakota in recent years. The 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 can contribute to the seedling disease complex.
The fungi causing seedling diseases produce symptoms that are quite similar. Sometimes a single pathogen may cause disease, but in other cases, two or more pathogens attack simultaneously or successively. Therefore, positive identification of the pathogen(s) causing stand loss often requires verification by laboratory analysis.
Severity and prevalence of seedling diseases varies among regions, between fields, and within a particular field during a single growing season. There also can be variation within the same field from one beet growing season to the next.The severity of seedling disease is determined by the amount of the pathogen(s) in the soil, susceptibility of the variety, and environmental factors such as temperature and soil moisture. Effectiveness of control measures, such as seed treatments, also will directly influence seedling disease severity.
Wind injury, heat and drought, frost, insect damage, misapplication of herbicide, or herbicide carry-over problems can produce symptoms very similar to seedling diseases. Consider the past and present history of climatic and field conditions when evaluating the possible causes of poor seedling establishment.
Among the several Pythium species that infect sugarbeet, P. ultimum is the most common and widespread. It attacks unprotected (non-fungicide treated) seed at temperatures that favor germination of sugarbeet seed. P. ultimum grows over a temperature range of 40-95° F, with an optimum of 61-77° F. Pythium is a "water mold" and requires moist or wet soil to infect germinating seeds and seedlings.
P. ultimum is primarily responsible for seed rot and pre-emergence damping-off.
The disease is characterized by a brown, water-soaked discoloration of the seedling before
it emerges through the soil.Under extended, moist conditions, P. ultimum also
causes postemergence damping-off of young seedlings (Figure 1).
Problems with P.ultimum are most commonly associated with wet seasons, poorly
drained fields, or fields that have been fallowed (which favors moisture buildup).
P. aphanidermatum is a high temperature fungus present in some fields. It attacks seeds and seedlings in wet, warm soils (optimum at 86-95°F). Symptoms caused by P. aphanidermatum are similar to those produced by P. ultimum.
Damping-off caused by A. cochlioides is the most serious seedling disease of sugarbeet in terms of damage to the crop, persistence of the fungus in soil,and difficulty of control. The disease occurs in two phases an early acute phase of short duration on seedlings and a later chronic phase, affecting the taproot, that can continue until harvest.
A. cochlioides causes very little preemergence damping-off, but causes extensive postemergence damping-off in warm (6886°F), wet soil. The fungus seldom infects seedlings growing in soil at temperatures below 59°F. A. cochlioides invades the hypocotyl (region below the seed leaves or cotyledons) near the soil surface, and produces a brown, water soaked area which may extend up to the base of to cotyledons (Figure 2). The infected hypocotyl and root rapidly turn a characteristic black color and then shrink to a dark, slender thread (Figure 3). In extreme cases, entire fields of to 5-week-old plants can be strayed. Severely infected seedlings that survive often are distorted and yield poorly.
Based on surveys conducted since 1984, A. cochlioides is not present in all fields where sugarbeets are grown. The disease occurs in some fields in the southern portion of the Red River Valley, and in southern Minnesota, where it has been particularly severe in Renville county.
Infected seedlings are observed in patches ranging from a few yards in diameter to several acres. Sometimes,entire fields are affected. Disease develops in both heavy-textured soils and in sandy, light-textured soils. The disease usually is a problem in fields that have been in sugarbeet production for many years, but A. cochlioides has seen reported in fields during the first or second season of sugarbeet production. In these cases, it is suspected that the fungus was recently introduced or that it has been present for some time and persisted on roots of susceptible weeds.
This soilborne fungus causes some pre-emergence death of seedlings, but more often, causes postemergence damping-off or stunting of young plants. Infection begins below the soil surface but sometimes extends up the hypocotyl. A sharp margin develops between brown infected tissue and white healthy tissue. On older seedlings, infected roots may appear stunted with brown, sunken lesions on lateral roots and taproots (Figure 4).
R. solani grows over a temperature range of 54-95°F, but is particularly active at 6886° F. The fungus does not require high soil moisture to infect seedlings. Slightly infected seedlings often can survive and produce nearly normal roots. Infected seedlings can be scattered or occur in patches. Usually seedling stand loss does not warrant replanting.
R. solani is a very complex species and is composed of several strains that are referred to as anastomosis groups (AGs). Four AGs of R. solani have been isolated from dead and dying sugarbeet seedlings in fields throughout the Red River Valley. The primary strain involved in seedling disease of sugarbeet is AG-4, although other strains including AG-1, AG-2-2, and AG-5 are present in lower frequencies.
In many fields, Pythium species, A. cochlioides, and R.solani occur together. In such cases, A. cochlioides will cause the most significant damage in the spring if soils are warm and wet. In hot, dry years, stand losses caused by R. solani will be more noticeable and the activity of A. cochlioides will be suppressed. Cold, wet soils favor the development of seedling disease caused by P. ultimum.
Aphanomyces cochlioides and Rhizoctonia solani also cause diseases on taproots of older beets. The symptoms caused by these two fungi can be distinguished on older roots, provided the plant has been infected recently and secondary decay organisms have not destroyed the taproot.
The chronic phase of Aphanomyces root rot appears on older plants in late June and can continue through the remainder of the growing season. Plants that have recovered from seedling infection may show symptoms of chronic root rot at these later growth stages. A. cochlioides also can invade sound, older roots during periods when soils are wet.
Infected plants occur in small to large patches. Above ground symptoms include undersized plants with considerable yellowing of the lower leaves (Figure 5). Leaves of infected plants wilt during the afternoons of hot sunny days and appear to recover overnight. Below ground, lateral rootlets can be produced in abundance on infected plants, and many appear shriveled, black, and necrotic. These roots are severely stunted in size.
In some cases, brown to black lesions occur at the basal portion of the taproot, a syndrome referred to as taproot tip rot (Figure 6). Later the basal portion of the root may take on a fibrous or tasseled appearance (Figure 7). Many infected beets are too small to be mechanically harvested. Diseased beets that are lifted, usually have a lower than normal sugar content and higher levels of impurities compared to healthy beets.
Rhizoctonia root and crown rot is caused by the AG-2-2 population of R. solani. The disease first starts to appear in fields when plants are at least 8 weeks old (mid- to late-June). The fungus continues to infect plants throughout the rest of the season. Rhizoctonia root rot often appears as randomly scattered plants within a field. Several dead plants may occur successively in a row, especially when soil containing the fungus has been thrown into the crowns of plants during cultivation (Figure 8 and Figure 12).
Above ground symptoms of Rhizoctonia root and crown rot include yellowing and sudden wilting of leaves. Petioles of the outer leaves may be blackened and rotted at the point of attachment to the crown (Figures 8-Figure 10). Below ground, a dark brown-gray rot starts under the crown and spreads over the root surface. This primary symptom may be accompanied by cracking or the presence of slightly sunken lesions scattered over the surface of infected taproots (Figure 9). These lesions differ from the irregular scars produced on root surfaces by the sugarbeet root maggot. Rhizoctonia root and crown rot progresses inward, and secondary microorganisms enhance the total decay of the root. At harvest, completely rotted roots can result in the appearance of "holes in the ground" where an infected beet had decayed earlier in the season.
On young beet roots collected in June and early July, root infections may encircle and sever the root 3 to 4 inches below the soil surface (Figure 10). Thus, it is important to carefully remove the entire taproot from the soil when diagnosing the problem. Pulling a diseased root from soil can leave a portion of the root behind and lead one to confuse symptoms of Rhizoctonia root and crown rot with Aphanomyces root rot.
Seed treatment with protective fungicides is the most convenient and economical method of controlling fungi that cause seed decay and pre-emergence damping-off. Commercial sugarbeet seed is always pretreated with at least one seed treatment fungicide.Combinations of materials sometimes are used to broaden the spectrum of activity of seed treatments against anticipated pathogens. The chemical(s) used to treat the seed will
The most effective seed treatment fungicides are quite selective against particular fungi (Table 1), so a knowledge of which pathogens occur in a field can be important in obtaining the best results. Since Pythium ultimum is present in all field soils and is active at the same temperatures that favor beet seed germination, fungicides that have specific activity against Pythium are particularly important in protecting seed that is germinating in wet or moist soils.
Currently, there are no effective seed treatment fungicides registered for control of Aphanomyces on sugarbeet. Fenaminosulf (also known as Axons or LesanŽ) was widely used on sugarbeet seed before 1984 because it is effective against both Pythium species and Aphanomyces cochlioides. The fungicide no longer is manufactured, but use of shell stock of fenaminosulf is permitted. Many sugarbeet seed companies purchased the remaining stock of fenaminosulf and have been applying it to seed sold in regions known to have A. cochlioides. Seed treated with fenaminosulf may still be available, but reserves of the fungicide are nearly exhausted.
Seed treatment fungicides provide only limited protection of seedling stands beyond a week or two after emergence. The greater the plant population emerging, the greater the number of seedlings that survive. However, overseeding will not necessarily compensate for stand losses.
In 1985, a seed treatment study showed that seedling emergence was better when seeds were treated with metalaxyl (which is sold under the trade name Aprons and has specific activity against Pythium species) compared to thiram (a general seed treatment fungicide with fair activity against Pythium species and Rhizoctonia solani). Non-fungicide-treated seed (control) resulted in the poorest stands (Figure 11). Pythium ultimum was responsible for disease during seed germination, but postemergence stand loss was caused by both Aphanomyces cochlioides and Rhizoctonia solani.
Pythium aphanidermatum Aphanomyces cochlioides, and Rhizoctonia solani do not grow well at low temperatures. In some areas, it is possible to avoid severe infection by these pathogens by planting early ,into cool soils. Early planting fosters good emergence and early vigorous growth. This enables plants to advance beyond the extremely susceptible stage before soils warm up and pathogen activity increases. Little possibility exists of avoiding infection by P.ultimum by altering planting date since the fungus is favored by the same temperature range that favors beet seed germination. However, seed treatment with fungicides having specific activity against Pythium species (e.g., Aprons) will effectively control P. ultimum even in soils that are cool and wet.
Pythium species and A. cochlioides require wet soil to allow movement and infection by swimming zoospores. The severity of damping-off can be minimized by shallow planting of seed and by managing soil moisture, where possible, to encourage rapid emergence and drying of soil. R. solani has a lower requirement for soil moisture and is less affected by planting depth
Crop sequence can affect the severity of seedling diseases and root rots. However, the relationship of crop sequence and disease severity is not the sale for all sugarbeet pathogens.
Pythium species attack roots of many crops 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 fungi then attacks young, succulent tissues and increases its inoculum level. Thus, populations of Pythium species are as closer tied to environmental factors the soil as they are to previous crops. Rhizoctonia solani parasitizes many species of crops and weeds, and also survives in dead organic matter in soil. A3-year rotation between sugarbeet crops is the minimum duration recommended to allow the fungus population to decrease.
There are no studies showing exactly how long R. solani survives in sugarbeet fields of the Upper Midwest. When growing a susceptible crop during the rotation, such legumes (which are susceptible AG-2-2 and AG-4 of R.solani), much of the root rot control benefits derived from crop rotation are lost. Residues from legume crops have been shown to increase severity of disease. Cereal crops are less likely to result in a buildup or maintenance of populations of R. solani.
Evidence for the effect of previous crops on Aphanomyces cochlioides is conflicting.Research in Michigan found that the incorporation of residue from corn tended to reduce damping-off. However, severe damping-off caused by A.cochlioides has been observed in sugarbeet fields in southern Minnesota where the previous crop was corn.
The duration of rotation may have a limited effect on replacing populations of A. cochlioides. Thick-walled oospores are produced in diseased tissue but limits of oospore survival are unknown. The effectiveness of rotation may depend upon the initial population of the fungus. Some fields have low populations of A. cochlioides, but little or no disease occurs, particularly if fields are well drained. On the other hand,severe Aphanomyces root rot has been observed in some fields rotated out of sugarbeet for up to 10 years.
Tillage and fertilization practices that promote good crop growth and adequate soil drainage will help to reduce, but not entirely prevent, diseases caused by soilborne pathogens. Rhizoctonia solani (AG-2-2) commonly enters roots of adult sugarbeet plants through petioles and crowns. "Hilling up" of soil around crowns of plants during cultivation encourages root and crown rot (Figure 12). This practice should be avoided whenever possible.
Some common weeds, including pigweed, kochia, and lambsquarters, are hosts of Aphanomyces cochlioides and Rhizoctonia solani. Controlling these weeds, both in-season and between crops, will help discourage the buildup and maintenance of these pathogens.
To retard movement and spread of A. cochlioides and R. solani, field equipment should be thoroughly washed with a high pressure sprayer before it is moved from a diseased to a healthy field. Used machinery purchased from other beet growing areas should be washed before being used in local sugarbeet fields. Avoid introducing soil from diseased to healthy fields via boots, tools, trucks, etc., and by dumping tare soil.
In general, varieties with rapid seed germination and vigorous seedling growth suffer less from seedling diseases than slower-growing varieties. Little effort has been made to develop varieties tolerant or resistant to damping-off fungi.
There are a limited number of commercial varieties with tolerance to Aphanomyces root rot or Rhizoctonia root and crown rot. However, no single variety has tolerance to both diseases. The root rot tolerant varieties yield better than other varieties under conditions favorable for disease development and when the pathogen population is high. Tolerant varieties are not widely grown because under disease-free conditions, they have a lower yield potential than other commercial varieties.
Chemical control of root rot diseases of sugarbeet is not feasible at present. Currently, there are no chemical compounds registered for use in the United States to control Rhizoctonia root and crown root although some experimental fungicides show promise. Also, there are no compounds available to control Aphanomyces root rot of older plants, nor are there any experimental fungicides for control of this disease on the immediate horizon.
Figures 3 and 7: photos by C.M .Rush, Texas Agricultural Experiment
Station, Bushland, TX
Figures 8 and 12: photos by E.G. Ruppel, USDA-ARS Crops Research Lab, Fort Collins, CO
Figures 1, 2, 4-6 and 9-11 photos by C.E. Windels, NW Experiment Station, Crookston, MN.
The information in this publication is for educational purposes only. Reference to commercial products or trade names is made with the understanding that no discrimination is intended and no endorsement by the Minnesota Extension Service is implied.
Issued in furtherance of cooperative extension work in agriculture and home economics, acts of May 8 and June 30, 1914, in cooper with the U.S. Department of Agriculture, Patrick J. Borich, Dean and Director of Minnesota Extension Service, University of Minnesota St. Paul, Minnesota 55108. The University of Minnesota, including the Minnesota Extension Service, is committed to the policy thrown persons shall have equal access to its programs, facilities, and employment without regard to race, religion, color, sex, national origin, handicap, age, veteran status, or sexual orientation.
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