University of Wyoming

Rhizomania of Sugar Beet

Gary D. Franc, Eric D. Kerr, William Brown, Jr., Jack H. Riesselman1

1 Research and Extension Plant Pathologist, University of Wyoming; Extension Plant Pathologist, University of Nebraska; Extension Plant Pathologist, Colorado State University; Extension Plant Pathologist, Montana State University, respectively.

Quick Facts

* Rhizomania is a disease of sugar beet caused by Beet Necrotic Yellow Vein Virus (BNYVV).

* The Soilborne fungus Polmyxa Betae Keskin is the vector of BNYVV.

* BNYVV can persist in soil for years within resting spores formed by the fungus.

* Rhizomania development is favored by warm, wet soil.

* An accurate diagnosis is done by a serological laboratory test.

* Most control methods involve containing the virus by preventing movement of infested soil.

* Rhizomania is unrelated to the common sugar beet root-rot disease caused by Rhizoctonia.


Rhizomania, "crazy root" or "root madness,'is one of the most serious diseases of sugarbeet. Rhizomania can greatly reduce sugar yield by reducing either the tonnage or sugar content, or both tonnage and sugar content, of harvested roots. Further losses to producers in infested areas can result when movement of agricultural products is restricted by quarantine laws. Rhizomania is not related to root roof sugar beet caused by Rhizoctonia.

Rhizomania first was described in Italy in1952. The causal agent apparently was spread by movement of infested soil. Rhizomania subsequently was reported in Japan in 1969; California in 1983; Texas in 1986; and Idaho, and Nebraska in 1992. The causal agent was not known until 1973, when Japanese plant pathologists showed rhizomania was caused by a virus, and that a common soilborne fungus served as the vector or carrier of the virus.


Symptom expression varies greatly, with some infected plants occasionally appearing healthy. Classical root symptoms following early infection include a mass of fine, hairy secondary roots, mostly dead, that give the taproot a beard-like appearance (Figure 1). With slightly later infection, the storage root often is rotted and constricted, becoming much broader near the crown, thus resembling the shape of a wine glass (Figure 2). Longitudinal sections of infected roots reveal vascular tissue that is visibly darkened (Figure 2). Infected roots occasionally rot. Very late infections may result in no obvious symptoms.

Leaves may become flabby and wilt without discoloration. Sometimes, smaller leaves proliferate at the crown. A general chlorosis (yellowing) of foliage commonly occurs. Because infected roots are inefficient in water and nutrient uptake, general foliar symptoms are similar to water stress or nitrogen deficiency (Figure 3). Rarely, veinal yellowing with associated dead (necrotic) areas of leaf tissue can be seen (Figure 4). This rare symptom occurs when infection becomes systemic, and the virus usually can be recovered from the leaf tissue, otherwise it normally cannot.

Diseased plants usually occur in patches or areas of the field and not as scattered individual plants dispersed throughout the field (Figure 3). Because the fungus vector thrives in moist areas, disease severity usually is greatest in depressions or compacted, poorlly,drained portions of the field that tend to collect water and remain wet. Reduced wateruptake by infected roots increases the tendency for soil around diseased plants to remain water logged, which promotes additional rhizomania development and root decay caused by other fungi.

Disease Cycle

Beet necrotic yellow vein virus (BNYVV) is the causal agent of rhizomania. The soilborne fungus, Polymyxa betae, serves as a vector of BNYVV by carrying the virus to healthy roots.The association of BNYVV with the fungus is an unusual biological relationship that results in rhizomania development when a susceptible host is present and conditions are favorable for infection. Sugar beet serves as a host to both the fungus and the virus. Although some weeds, primarily in the goosefoot family, also serve as hosts, their role in rhizomania development is not clear.

Data from field surveys in Wyoming and Nebraska showed that P. betae is relatively common and, when not carrying BNYVV, usually causes little damage to the sugar beet. Because BNYVV is spread by P. betae, conditions that favor infection of sugar beet by the fungus also favor rhizomania development. Therefore, a greater understanding of rhizomania development and control can be achieved by knowing the life cycle of the virus vector, P. betae (Figure 5).

The fungus forms two types of spores during its life cycle, resting spores and motile zoospores. Clusters of tiny, thick-walled resting spores, also called cystosori, enable the fungus to survive in soil for 15 years or longer in the absence of a suitable host (Figure 6). The virus also can persist in these resting spores forat least 15 years. When soil conditions become favorable for infection, germination of the resting spore is triggered by the presence of a host-plant root. As resting spores germinate, motile zoospores are released that actively swim to the root surface where new infections occur.

Infection of roots by zoospores results in the formation of a fungus body, or plasmodium, inside the root. The plasmodium is able to quickly produce additional zoospores that are released and attracted to new roots. This rapidly repeating infection cycle requires approximately 48 hours for completion at 25 degrees celcius (77 degrees farenheit) and enables a rapid increase of the fungus in soil when soil conditions are favorable for infection. The plasmodium also forms resting spores that infest soil as root tissues degrade, enabling the fungus to persist in soil until conditions once again become favorable for infection of a suitable host. Both spore types can become viruliferous or carriers of BNYVV.

Soil temperature and moisture greatly affect development of rhizomania. Root infection is favored by relatively high soil temperatures, with an optimum of 23 -27 degrees celcius (73 -81 degrees farenheit). Infection is sharply reduced by cooler temperatures, with a minimum temperature of approximately 15 degrees celcius (59 degrees farenheit) required for germination of resting spores and infection of roots. Warm soil temperatures in the spring result in earlier infection and more severe damage from rhizomania. Zoospores require free moisture for movement to roots and infection. Therefore, soil moisture at or near saturation for a prolonged period is necessary for infection and disease development. Short periods of rain in spring and early summer and use of irrigation favors fungus activity and increased rhizomania severity, provided soil temperature is favorable. Soil pH plays a minor role in disease development, with a pH range of 6-8 favoring disease development. Zoospore activity has appeared to be more frequent in coarse-textured soils.

Disease Diagnosis

Because symptom expression varies greatly, diagnosis of rhizomania cannot be based solely on visual inspection. Instead, an accurate diagnosis is done by a serological ELISA test, or enzyme-linked immunosorbent assay. Plant tissue is needed for the test, which requires approximately 36 hours for completion. Apositive ELISA test indicates that BNYVV was detected and rhizomania was present. A negative test merely indicates that BNYVV, if present, was not detected. Marginally (weak) positive ELISA tests may occur when viruses serologically related to BNYVV are present in the tissue being tested. Also, false negativeELISA tests commonly can occur due to anumber of factors, including methods ofsample collection and the stage of disease development. Therefore, all test results mustbe carefully interpreted. To maximize the likelihood of an accurate test, sugar beet samples collected for testing should include new fibrous root growth, occurring immediately after rainfall or irrigation, and samples should arrive at the laboratory within one day after collection. Currently, few laboratories inthe United States test for the presence of BNYVV.

Procedures for rapid detection of BNYVVdirectly from the soil have not been perfected.A bioassay for detection of viruliferous P. betae in field soil samples has been developed for the greenhouse. Susceptible sugar beet is planted in the soil sample being tested and allowed to grow under conditions ideal for rhizomania development. After approximately eight weeks, plants growing in the soil sample are harvested and tested for BNYVV by ELISA. A positive ELISA test, from a properly conducted bioassay sample, indicates that the pathogen was present in the soil sample. Soil samples collected for analysis should not represent more than 40 acres and should consist of 2 quarts of soil composited from at least 20 subsamples of soil-tube cores taken from the upper 6 inches of the soil profile. The laboratory performing the bioassay should be contacted to determine when soil samples should be collected. Quarantine laws may specifically state the maximum field size and other sampling restrictions that must be met before fields qualify as rhizomania-free.

Control Measures

Surveys to locate infested fields will aid incontrol of rhizomania. Because rhizomania can readily spread by movement of infested soil, fields not previously used for sugar beet production are also at risk and may be infested. Results for a properly conducted soil bioassay, or direct testing of suspicious beets by ELISA, will permit growers to identify infested fields and allow them to make more effective management decisions related to cropping practices and containment.

Continuous planting or close rotation of sugar beet increases the risk of loss due to rhizomania. Early planting, when soil temperatures are cooler, and use of production practices that result in the rapid establishment of the plant canopy, will reduce risk of loss. Early planting should be done at slightly greater plant densities to compensate for increased seedling loss in cooler soils.

Early season water management is especially critical for reducing loss from rhizomania. Manage soil moisture to minimize or eliminate the need to irrigate during the first six weeks after seed germination. Because disease development is favored by high soil moisture, avoid over-irrigation and any other practices that result in standing water or excessively wet soil. Proper fertility and irrigation practices for the variety grown always must be followed to reduce plant stress and further reduce the risk of disease development. If possible, run off water from infested fields should be contained to prevent movement of viruliferous spores to downstream sites. Efforts to reduce infection by lowering soil pH are not practical in most situations because ofthe large pH change required (a target pH of 5.6 or less).

Deep tillage to improve drainage also will help to reduce disease risk. However, avoid unnecessary tillage operations that spread infested soil within a field. Compaction associated with tillage operations also decreases drainage and increases disease risk. Minimize soil erosion in an infested field, because it ishighly probable that conditions that permit wind erosion also will spread and redistribute resting spores. Wind erosion can be reduced by maintaining surface residue from the previous crop, maintaining soil surface ridging and roughness, or by growing a cover crop.

Once a field becomes infested, crop rotation will not appreciably reduce disease risk because of the long-term survival of viruliferous cystosori. However, some soil fumigants, suchas Telone II, may kill enough cystosori to reduce disease development to acceptable levels. Fumigation treatments are very expensive, and research is being done to determine their efficacy and conditions under which they should be used. Expenses associated with fumigant application may be justified, because significant sugar beet acreage is routinely treated with Telone II for nematode control. The use of soil-applied fungicides has not been effective for rhizomania control in infested fields.

Currently available tolerant or resistantvarieties perform satisfactorily in the presence of rhizomania in some production areas, especially when used in combination with soil fumigation. However, these varieties must betested in each production area to evaluate their performance under local environmental conditions and production practices. They alsomust be evaluated for performance after exposure to local diseases, insects, and weed pests. Research on the development of resistant varieties is progressing rapidly, with some having dual resistance to both rhizomania and curly top virus.

Because effective, practical control methods are not currently available, most effort to control rhizomania spread is placed on containment, or limiting the movement of infested soil into uninfested fields and production areas. The sharing of farm equipment, migrant labor, and the movement of cattle or other livestock among farms are just several examples of how infested soil may be moved. The practice of returning tare dirt to fields greatly increases the risk of spreading BNYVVand its vector as well as other soilborne disease agents.

Infested fields should be isolated as much as practical to prevent movement of the tiny amounts of soil that are sufficient to spread the pathogen. Traffic in infested fields should belimited only to that which is absolutely necessary. Signs warning against entry may also reduce traffic and subsequent spread of infested soil. Although it may be impossible to prevent eventual spread of infested soil, rigid sanitation practices may delay its movement into uninfested fields.

If entry into an infested field is unavoidable, rubber boots or disposable footwear should be worn to permit easy cleaning and removal of adhering soil at the field site. Also, soil ontractors, machinery, and highway vehicles should be removed. Removal of soil at the field site is necessary because resting sporesare extremely difficult to kill with chemical disinfectants, especially when associated with soil. Therefore, infested soil remoyed fromfootwear and equipment is likely to remain infested and will serve as a potential source of contamination.

Boots should be immediately cleaned to remove adhering soil after leaving the field, sanitized with a general disinfecting agent as a precaution to minimize spread of pathogens,and placed in a disinfested sealed container before reentering the vehicle. If disposable footwear is used, it must be disposed of properly to prevent contamination of the vehicle. Soil is most effectively removed from equipment with soapy hot water applied under pressure. Bleach is relatively ineffective against resting spores because the thick walls provide protection and because it is quickly inactivated by soil and organic matter. Bleach also is corrosive to metal and damaging to clothing. Commercial products for disinfecting machinery, footwear, and use in wheel dips have not been marketed in the United States for control of P. betae.

Sources of Information

Duffus, James E. 1986. Rhizomania (Beet NecroticYellow Vein) Pages 29-30, In: Compendium of Beet Diseases and lnsects. APS Press, St. Paul, MN. (Available from The American Phytopathological Society, 3340 Pilot Knob Rd.,St. Paul, MN 55121, or the Beet Sugar Development Foundation, 90 Madison St., Suite 208, Denver, CO 80206; BSDF price is $15 plus postage).


Appreciation is expressed to the following reviewers: Earl G. Ruppel, research leader and plant pathologist, USDA-ARS Sugar Beet Research, and James Gerik, plant pathologist, Holly Sugar Corporation.

In additon the authors would like to thank the following for their financial contibutions to this project/publication. Western Sugar Company; Holly Hybrids; Big Horn Basin Beet Growers Association; Big Horn County Sugarbeet Growers Association; Colorado Sugarbeet Growers Association; Mountain States Beet Growers Marketing Association of Montana; Nebraska Nonstock Sugarbeet Growers Association.

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