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Beet necrotic yellow vein virus


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Host plants / species affected

Main hosts

show all species affected
Beta vulgaris (beetroot)
Beta vulgaris var. cicla
Beta vulgaris var. rubra
Beta vulgaris var. saccharifera (sugarbeet)
Chenopodium (Goosefoot)
Spinacia oleracea (spinach)

List of symptoms / signs

Leaves - abnormal colours
Leaves - abnormal forms
Leaves - abnormal patterns
Leaves - necrotic areas
Leaves - wilting
Leaves - yellowed or dead
Roots - 'dirty' roots
Roots - galls along length
Roots - hairy root
Roots - necrotic streaks or lesions
Roots - proliferation roots in ball
Roots - reduced root system
Roots - rot of wood
Roots - stubby roots
Stems - internal red necrosis
Stems - stunting or rosetting
Stems - witches broom
Whole plant - damping off
Whole plant - dwarfing
Whole plant - early senescence
Whole plant - plant dead; dieback


- Foliage: pale-yellowing, long petioles, upright growth, crinkling, necrotic yellow vein.
- Roots: stunting, rootlet proliferation, necrosis of vascular bundle, turnip-like shape, root beard.
- Whole plants: yellowing, stunting, wilting, necrosis, death.

The disease is usually distributed as foci (patches) in the field. The most useful leaf symptom is visible at the end of the growing season. Leaves become pale-yellow in colour, with long petioles and upright growth. Infected plants wilt during the day due to insufficient water uptake by damaged roots, but they recover overnight. Symptoms of BNYVV are characterized by root stunting and proliferation on lateral rootlets on the main tap root and yellow-brown colouring of vascular bundles.

In early and severe infection, the plants are stunted, wilted and eventually die. The tap roots are very small and lateral roots and rootlets proliferate extensively. In this condition, the bright yellow followed by necrosis along veins, after which the virus was named, is very rarely seen. This symptom only results from virus movement to leaves. Slight and later infection leads to a more developed taproot, often showing a turnip-like shape along with rootlet proliferation. Virus infection may infect only one lateral root. Leaves become slightly chlorotic and pale-yellow. Very slight infection may produce no obvious symptoms.

Prevention and control


Control in diseased fields is unlikely to be successful by adopting cultural or agronomic practice. Some chemicals, especially soil fumigants, have been partially effective in reducing yield losses but are generally not economic. The search for tolerant or resistant cultivars has been actively carried out since 1978: the results obtained have been very encouraging. Forecasting or estimating the level of infestation which corresponds to yield losses would be helpful for selection (adaptation) of resistant varieties and other control measures.

Phytosanitary Measures

Precautionary measures should be taken to avoid contamination of healthy areas and to limit the spread of the disease in areas already infested. Areas in which beet seeds and beet stecklings are produced should be kept under constant phytosanitary observation. Any imported seed or stecklings should come from a field (or preferable region) where BNYVV does not occur. Beet seed from infested areas should be kept particularly free from impurities (soil) and should contain not more than 0.5% inert matter (other than pelleting material) in the case of certified seed and 1% in the case of basic seed (OEPP/EPPO, 1990).

Countries where BNYVV does not occur would be well advised to recommend importers of vegetables from infested countries to take special precautions when disposing of waste vegetable matter, soil waste and liquid waste (MAFF, 1985).

Cultural Control

The effects of several agronomic factors and cultural practices on disease development and spread have been tested (Schlosser, 1988; Asher, 1993). The former include the soil type and pH, flooding, the level of the ground water table and the influence of ploughed meadows. The latter include crop rotation, the application of organic manure, the depth of ploughing, the date of sowing, herbicide or lime application and sprinkler irrigation. None of these factors had a significant effect, but the disease appeared to be slowed down by early sowing (Blunt et al., 1992), transplanting in paper pots (Richard-Molard, 1985: Abe, 1987) and decreasing soil pH (Abe, 1987).

In moderately or heavily infested areas, agronomic factors and cultural practices appear to be of minor, if any, importance as far as disease management is concerned. However, in areas where BNYVV is still absent or the inoculum potential is low, measures such as wider crop rotation, controlled irrigation and effective drainage can delay the spread and incidence of the disease.

Chemical Control

Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:

This information is part of a full datasheet available in the Crop Protection Compendium (CPC); For information on how to access the CPC, click here.


BNYVV causes severe damage wherever it occurs. Yield losses depend greatly on the inoculum level in the soil, the weather conditions during the season and the timing of infection. Severe infections can cause reduction in yields of 50% or more while sugar contents are reduced from 16-18% to less than 10%. Changes in physiology can lead to difficulties in extracting sugar and reduce beet value as a sugar source. BNYVV can survive in the soil for many years without any decrease in intensity. It is therefore necessary to avoid growing sugarbeet in heavily infested soils.

BNYVV has shown a great capacity for local dispersal from infested fields and for spread to previously uninfested regions. For example, although the exact origin of the epidemic which has arisen since the 1970s is obscure, it is certain that large areas of beet cultivation in Europe, the USA and China were, until recently, free from BNYVV. There has been considerable spread within European countries and also in China and the USA. Its absence from certain countries and regions has been confirmed by intensive surveys. It is thus only in the last 20 years that rhizomania has developed into a serious problem in many sugarbeet-growing regions of the world (Asher, 1983).

BNYVV content and/or symptom intensity have been correlated with sugar yield and polarization, leaf limpness, leaf temperature and leaf calcium content (Ahrens, 1987). Biaggi et al. (1986) reported that in eight sugarbeet genotypes, the content of BNYVV in the main storage roots (assessing glasshouse-grown material) was negatively correlated with sugar content, sucrose yield/ha, juice purity and amino nitrogen content and was positively correlated with sodium content in the same genotypes grown in the field. The disease has also been shown to reduce P and Na contents (Asher, 1993). Significant decreases in the fresh root weight of infected plants have been recorded. Root sugar content is also consistently lower in infected plants than in healthy plants (Henry, 1996).

In field trials in Yugoslavia in 1989-91, rhizomania reduced sugar and alpha-amino N contents but increased P and Na contents. In the same trials, plant density and N rate had little effect on rhizomania infection (Skrbic, 1995). Nowakowska (1944) reported that in glasshouse experiments, correlations were found between nitrogen, phosphorus and calcium contents, soil acidity and sugarbeet root infection with BNYVV transmitted by Polymyxa betae. Disease resulted in a 68% weight decrease in sugarbeet seedlings.

In 120 sugarbeet trials carried out in north-central Italy in 1986-90, rhizomania incidence increased with increasing soil pH (Biancardi et al., 1994). Harada et al. (1990) also reported that higher rates of infestation with BNYVV were associated with high soil pH. Uchino and Kanzawa (1995) examined the effect of reducing soil pH on rhizomania over a 6-year period. Soil pH was maintained at pH 6-6.5 in one field and at pH 5-5.5 in another. Rhizomania was not suppressed in the field of soil pH <5.5 in the first 2 years although the number of tap roots in which BNYVV was detected decreased compared with the control field (pH 7.4). After 3 years yellowing, caused by rhizomania, was suppressed in the field of soil pH <6 and sugar yield was higher than in the non-treatment field. After 6 consecutive years of sugarbeet crops, the population of viruliferous P. betae infected with BNYVV was estimated. Inoculum density was lower than in the control when the soil was below pH 5.5. In fields where the soil was above pH 6.5, inoculum density appeared to be intensified by continuous cultivation and higher soil pH.

Other factors have also been reported to influence the spread and severity of BNYVV infection. In Belgium, rhizomania first appeared in 1984. Spread was initially slow, but appeared to accelerate from 1992. The factors affecting the increasingly rapid spread included the intensification of sugarbeet cultivation and two exceptionally hot, dry summers (Wauters et al., 1996). Hofmeester and Tuitert (1981) studied the effect of irrigation on the development of rhizomania in an artificially inoculated field. More infected plants occurred in irrigated than non-irrigated plots. At harvest, sugar content was significantly reduced in plants grown in heavily infested plots, of which irrigated plots had lower yields than non-irrigated ones. In the UK, isolates of P. betae, the vector of BNYVV, have been shown to have high temperature requirements. It has been suggested that yield losses from rhizomania may be reduced by sowing crops several weeks earlier than is usual (Blunt and Asher, 1989).

Yield losses and disease incidence vary from year to year and from country to country in addition to the factors already mentioned. The following represents some of the data which is available with respect to BNYVV.

In Hokkaido, Japan, sugarbeet rootlets were collected from fields from 307 growers during the period 1986-92. In three trial areas, 28.9, 56 and 93.5% of growers had infested fields. The yearly mean percentages of fields in which BNYVV was detected, that of infested fields and that of fields with disease symptoms were 22.6, 18.8 and 9.5%, respectively. A positive correlation was found between the yearly rate of infested fields and air temperature (Uchino et al., 1994). In the years 1985-89, 25% of the fields in Niseko Town, Hokkaido, were affected by rhizomania and nearly 50% of the farmers had infested fields. It was estimated that 9% of the soil used for pot tubes and 7% of the bed soils under the pots were contaminated with BNYVV, providing a source of infection (Harada, 1990).

Rhizomania was first detailed in the UK in 1987. In 1997, a partially resistant cultivar recommended for growing on affected farms showed a 24% yield loss on severely infested plots in UK trials (Asher, 1998).

In the UK, estimates have suggested that an average yield loss of 67% can be caused by rhizomania (Henry, 1996). In 1984, 40 fields were found to be contaminated with BNYVV (Asher and Dewar, 1995). Evidence has also been obtained that sugar yield reductions approaching 50% could result from infection under English climatic conditions (Asher and Beck, 1990). The authors also indicated that BNYVV can be present in plants without producing obvious symptoms and that even very small amounts of heavily infested soil can transmit the disease, causing measurable yield reductions within a single growing season. Buttner and Burcky (1990) have also reported that levels of infestation in soil samples correlated well with yield losses in succeeding crops.

In Croatia, the yield of 18 sugarbeet varieties was assessed in relation to various levels of rhizomania infection. The yield of all varieties decreased with increased infection levels (Dumancic and Novokmet, 1991).

In Hungary, soil from an area of ca 7000 ha was tested for the presence of BNYVV. Twenty per cent of the area was infested with the virus (Nemeth et al., 1992).

In the Netherlands, annual sugar yields from individual farms known to be infected with BNYVV were compared with figures for the whole of the Netherlands in order to estimate the year in which the farms first suffered crop losses due to rhizomania. In one farm, this was found to be 1967. Analysis of sugarbeet root samples from infested and virus-free fields showed negative correlations between sugar and sodium contents and between sugar content and the occurrence of rhizomania. The quotient Na mmol per kg of beet/sucrose % = 0.5 was considered to be the threshold for rhizomania infection (Heijbroek,1989).

Using a susceptible sugarbeet cultivar, Tuitert and Hofmeester (1994) studied the epidemiology of BNYVV, at different inoculum levels over the 3-year period. In 1989, 90-100% of plants were infected in plots with the highest inoculum level. In 1990, all plots had high disease levels. In 1988, root weight at harvest was unaffected by infection, but a 10% reduction in sugar yield was observed at the highest inoculum level. Both root weight and sugar content decreased progressively with increasing inoculum level in 1989 and 1990. Buttner et al. (1995) also showed that the quantity of BNYVV in young plant roots was significantly and negatively correlated with final yield under disease conditions in the field.

In 1979, regression analysis of data from different locations showed a close relation between the percentage at disease-free sugarbeets and sugar yield/ha. From the infection-yield loss relation, it was concluded that 10% more disease-free sugarbeets corresponded to an average increase in sugar yield of ca 8 dt/ha. Control of the vector also lead to reduced infection and increased sugar yield (Hess and Schlosser, 1984).

The optimum temperature for transmission of BNYVV is reported as 25°C by Horak and Schlosser (1980). No infection occurred in plants kept below 15°C. Therefore, the earlier sugarbeets are planted, the longer is the period with soil temperatures below 15°C and plants escape early infection and yield losses due to rhizomania are reduced.