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Beet (Beta vulgaris L.) includes red beet, sugarbeet, fodder beet andswiss chard. During cultivation several diseases of fungal, bacterial and viral

nature attack these crops, which not only reduce the quantity of the produce

but also the quality.

Seedling diseases such as damping-off, seedling blight, collar rot, root

rot etc. are caused by pathogens such as Sclerotium rolfsii, Rhizoctoniasolani, R. bataticola and species ofPythium and Fusarium in India. Of these

S. rolfsii, R. solani and Pythium spp. cause acute mortality. Pythium spp.produce pre and post -emergence damping-off, while others mostly produce

post-emergence damping-off. High temperature alongwith high moistureconditions favour these diseases.

Management

The pathogens associated with this disease are soil and seed borne in

nature. Use of cultural practices, chemical methods and biological control can

provide effective management of these diseases.

Cultural practices

Cultural practices like collection and destruction of infected plant debris,

deep ploughing during summer months, long crop rotations and use of

healthy seed are important and effective methods for the management of

these diseases. Dimov et al. (1988) reported that when beet crop was rotatedwith alfalfa, the occurrence of Trichoderma, Fusarium, Phytophthora,Pythium, Rhizoctonia and Alternaria varied with the rotation and buildup ofpathogenic fungi did not occur in such soils.

Chemical control

Plant base application of Pencycuron (0.2%) .decreased root rot (R.

solani) considerably (Uchino et al., 1987). Tolclofos methyl + hydroxyisoxazole (hymexol) when mixed with nursery soil and also applied on the soil

surface, effectively controlled damping-off (R. solani) better than PCNB and

hymexazol (Fuji et al., 1987). While seed treatment with hymexazole aloneprovided protection against seedling disease caused by Pythium spp. andAphanomyces cochlioides (Payne and Williams, 1990). Thiabendazoleeffectively controlled pre-emergence damping-off and root rot (Epicoccum

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important in cold stored roots but can cause heavy losses at ordinary

temperatures.

Geographical distribution

The occurrence of the disease has been reported from U.S.A., erstwhile

USSR, New Zealand, Italy, Romania, Venezuella, Egypt, Poland, New

Zealand and India (Rodriguez et al., 2002).

The disease initially appears on the lower part of roots as small, water-

soaked, brown spots. Later, these spots develop rapidly and spread into the

core of the root from where they progress from inside to outside. In theadvanced stage of the disease, infected part becomes soft due to maceration of

tissues, which emit foul smell. Sometimes plants show wilting symptoms.

The disease is caused byErwinia carotovora sub.sp. carotovora (Jones)Bergey et al. . It is a weak parasite and facultative anaerobe. The bacterium

is Gram-negative rod, with peritrichous flagella. It produces grayish whitecolonies on nutrient agar medium and cloudy growth in nutrient broth. It

produces gas in the nutrient medium utilizing several carbohydrates as

carbon source.

Disease cycle

Bacteria survive on plant debris in the soil and may infect the growing

crop especially after heavy rains or in badly drained fields. Roots may be

contaminated at the time of harvesting or during storage.

Management

Improvement in drainage can reduce the field infection. Contamination

of harvested roots can be reduced by washing in chlorinated water that

should be renewed frequently and checked regularly for its disinfectant

capacity. If the roots are subsequently to be stored at ambient temperature,

dry the surface of roots thoroughly because the bacterium is sensitive todesiccation. If roots are stored at temperatures close to OCthen soft rot may

be controlled without recourse to chlorination or surface drying. Cultivar Rola

was found least susceptible to the disease (Kozak, 1990).

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nigrum, Fusarium solani, Pythium spp. and R. solani) under in vivoconditions when applied as seed treatment (Abdel- Rehim et al., 1992).Srivastava and Tripathi (1998) have reported effective management of

sugarbeet seedling disease complex by combination of fungicides. The

effectiveness of five combinations of 4 compatible fungicides, PCNB

(Brassicol), TMTD (Thiram), carboxin (Vitavax) and carbendazim (Bavistin)@ 2.5 g/kg seed (mixed in .equal proportion) incorporated in seed pellets of

sugarbeet was evaluated against seedling diseases complex caused by 4 soil

borne pathogens, namely, Pythium aphanidermatum, Rhizoctonia solani, R.bataticola and Sclerotium rolfsii. Seed pelleted with all combinations offungicides provided better protection to seedlings as against steeping of seeds

in aqueous suspension of a combination of fungicides. Of various

combinations used, a mixture of Bavistin + Thiram was most efficacious in

reducing seedling mortality as compared to other treatments.

The causal fungi responsible for damping-off of seedlings are soil borne

in nature. The use of resident antagonists in reducing this disease can be an

effective approach. Seed pelleting of sugar beet seeds with oospores of

Pythium oligandrum reduced damping-off of sugarbeet in soils naturallyinfested with Aphanomyces cochlioides and Pythium spp. and control was

equivalent to that achieved with hymexazol seed coating (McQuilken et al.,1990). P. oligandrum oospores produced by liquid fermentation in canemollases medium and pelleted on sugarbeet seeds resulted in significant

control of damping-off caused by P. ultimum (Whipps et al., 1993).

This is a disease of considerable importance and in warm temperate

areas, Cercospora beticola is the most devastating foliar pathogen of beet cropand causing significant yield reductions.

Geographical distribution

This is a common disease of Central and Southern Europe, Italy, Poland,

Belgium, Greece, Japan, Russia and certain parts of North America (Walczak

et al., 2002). In India, it was first observed in the tarai region of Uttaranchal

(Mukhopadhyay, 1968). Now the disease is prevalent in Kashmir valley,

Kalpa (Himachal Pradesh), Sriganganagar (Rajasthan) and Punjab.

Symptoms

The symptoms of the disease appear mostly on the leaves and rarely on

the petioles. The characteristic symptoms include discrete circular lesions, 3-

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5 mm in diameter, with a necrotic center and reddish to dark brown margin

during damp and cool weather. In case of severe infection, the petioles are

also infected. The spots are scattered at first but in case of severe attack they

coalesce and cover the entire leaf blade and affect the quality and yield of

seeds. In seed crop, all above ground parts including seed clusters are

affected.

The Pathogen

The disease is caused by Cercospora beticola Sacco The mycelim of the

fungus is septate, dark coloured and intracellular. Small sclerotial masses

are formed on the host tissue from which dark coloured conidiophores arise in

clusters. Conidiophores are 4-6 JlIIl in diameter at the apex and 60-19 ILm

long. The conidia are borne on the tip of the conidiophores. These are hyaline,

elongated, filiform, multiseptate, broadly rounded at the point of attachment

to the conidiophore, measuring 78 - 228 JlIIl in length, being 4.4-6.3 JlIIl wide

at the base and 1.6- 3.2 lAm in size and tapering slightly toward the opposite

end.

Host range

The pathogen infects only beet plants and its close relatives like mangel

wurzel, Swiss chard, spinach and certain closely related weeds.

Disease cycle

The fungus chiefly overwinters in infected plant debris as mycelium or

on the seed. The infected seeds result in diseased seedlings. In the spring

season, overwintering mycelim in plant refuse starts producing conidia which

are disseminated by wind currents, rain splashes and insects to the leaves.

The disease mostly appears in the month of November-December but

severe attacks occur in the month of March -April in the plains. In the hills,

it appears during summer months. High relative humidity is an essential

pre-requisite for sporulation. The conidial germination is best in the presence

offree water and moderate temperatures i.e. in between 15-32 C.

Management

Cultural practices

The inoculum for the annual recurrence of the disease comes frominfected leaf debris, cultural controls are therefore aimed at the destruction of

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infected debris by burning and deep ploughing and use of long rotations to

prevent an accumulation of the soil borne inoculum. Sowing of cereals

(sorghum, wheat) and lucerne before sugarbeet crop alongwith weed free

cultivation reduced the disease (Rajpurohit and Singh, 1996).

The resistance to Cercospora leaf spot has been found to be correlated

with the 3-hydroxytyramine content of the leaves (Rautela and Payne, 1970).

Rjpurohit and Singh (1992) screened 35 varieties of sugarbeet and none was

found-free but variety Desperzpoly RC showed low incidence (3.2%) and also

gave highest tuber yield as well as sucrose content.

The disease can be kept under check by elaborate chemical sprayprogramme including both systemic and non-systemic fungicides. Three

sprays of fentin hydroxide @ 0.75 kglha were found best followed by

mancozeb, zineb, captafol and copper oxychloride@ 2 kg! ha (Rajpurohit and

Singh, 1993). Systemic fungicides such as benomyl, carbendazim and

thiophanate methyl derivatives were found superior to non-systemics

(Mukhopadhyay and Upadhyay, 1977). Rajpurohit and Singh (1993) reported

that two sprays of carbendazim, benomyl or thiophanate methyl @ 0.5 kg! ha

at 20 days interval were found to be best for controlling this disease and

increasing the root and foliage yield as well as sucrose content. Good efficacy

of recently available strobilurin fungicide (pyraclostrobin) has been reported

against this pathogen (Manaresi et ai., 2002). This compound has afavourable toxicological and environmental profile and it is safe to users.

The exclusive use of benomyl or carbendazim should be restricted as the

pathogen may develop resistance (Dixon, 1981). In those areas where this

disease is of common occurrence and the resistance has not been noticed,these fungicides should be used carefully and in combination with protect ant

fungicides like mancozeb. This strategy can prolong the effectiveness ofbenzimidazole fungicides.

This is a widely distributed disease of beet crop and sometimes appears

in severe dimensions.

The disease is widely distributed in several countries of the globe

wherever beet is grown with the possible exception of South America,

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Diseases of Carrot and Sugarbeet

Australia' and Eastern Asia (Dixon, 1981). In India this disease was first

recorded in Pantnagar (Mukhopadhyay, 1969) and later it was observed

extensively in Phaltan and Ahmednagar (Maharashtra) areas under warm

and dry weather.

Symptoms

The disease initially appears on the lower leaves and gradually spreads

towards the top. The formation offirst white and later grey-tan mildew areas

on both the sides of the leaf characterize the disease. In general, infection is

more on the upper surface of the leaf. In advanced stages of the disease

development, mildew patches enlarge and coalesce and the leaf appears as if

dusted with wheat flour. Severely affected leaves turn pale and ultimately

dry up. Under favourable climatic conditions, cleistothecia develop as small

dark round structures on the infected surface of the leaf.

The Pathogen

The disease is caused byErysiphe betae (Vanha) Weltzien. Mycelium issuperficial and persistent. Conidiophores are unbranched and erect. Conidia

arise singly, are hyaline, ovoid, 30-50 x 15-20 IJ.II1 in size. Cleistothecia are

globose, dark brown to black, 80-120 IJ.II1 in diameter with 4-8 asci per

cleistothecium. There are generally 2-3 ascospore~ per ascus.

Host range

The pathogen is specialized to Beta spp., and infects only B. cicla, B.diffusa, B. maritime, B. patellaris, B. patula, B. rapa, B. trigyma and B.

vulgaris.

Management

The disease can be managed by dusting sulphur or spraying wettable

sulphur, benomyl, carbendazim, thiophanate-methyl, tridemorph,thiabendazole lactate (Asher, 1986). Ergosterol biosynthesis inhibitors like

triadimefon, hexaconazole, penconazole, propiconazole, flusilazole,

cyproconazole, carbendazim + flusilazole etc. can be effectively used in

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reducing the intensity of this disease (Asher, 2000). Efficacy of recently

available strobilurin fungicide (pyraclostrobin) has been reported against this

pathogen (Manaresi et al., 2002).

This is a very common and destructive disease of sugarbeet and under

favourable weather conditions reduces yields up to 55 per cent in certain

varieties (Mukhopadhyay and Thakur, 1971).

The disease is characterized by sudden rotting of mature roots below the

soil surface. The affected root is usually covered with white mycelium that

contains numerous brown sclerotia which is the most conspicuous sign of this

disease. The fungal growth and sclerotia can also be seen in the soil around

such roots. Later, when enough damage has been done to the roots, the leaves

show yellowing and wilting and such plants can be easily pulled out.

The Pathogen

The pathogen responsible for this disease is Sclerotium rolfsii SaccoThe

basidial stage of this fungus falls in the species of Athelia. Initially, themycelium of the fungus in pure culture is at first silky white but gradually it

loses its luster and becomes somewhat dull in appearance. The hyphae are

hyaline, thin walled, sparsely septate when young. The cells are 60-350 JLID

long and 2-8 JLID wide. The broader hyphae show clamp connections, which

are absent in thin hyphae. The number of nuclei! cell is highly variable.

Mostly there are 2 nuclei in cells of secondary and tertiary branches.

Sclerotial initials are formed from hyphal strands that consist of 3-12 hyphae

lying parallel. A spherical shape is soon assumed even if it is only a loosemass of hyphae. With further hardening, differentiation takes place and the

sclerotium shows an outer layer of polyhedral cells, 3-4 JLID in diameter,

surrounding the compacted hyphae. Mature sclerotia are dark brown but

variation from lighter brown to darker colour may be found. These are small,

about the size of radish seed, hard and usually round.

The basidial stage grows as a spreading white hymenium on the host

surface or on the surface of the culture medium. Although the hymenia may

be pure white in culture, on the host they may be grey, yellow or buff

coloured. The basidia are obvoid, 7-9 JLID long and 4-5 #lm wide. Each

basidium bears 2-4 parallel or divergent sterigma, which are 2.5-4 #lm long.

Basidiospores are unicellular, elliptical to obvate, sometimes rounded or

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pyriform, smooth walled, hyaline and epiculate at the base measuring 6-7 x

3.5-5 #LII1 in size.

Host range

The pathogen is polyphagous in nature and has a very wide host range.Sclerotium rolfsii infects more than 500 species of plants belonging to 100families and causes economically important diseases in Wa@l moist climates

throughout the world (Aycock, 1966). Roy (1977) also observed this fungus in

Assam, on vegetables like chilli (Capsicum annuum L.), French bean(Phaseolus vulgaris L.), carrot (Daucus carota L. cv. Nantes), Pea (Pisumsativum L.), cauliflower (Brassica oleraceavar. botrytis L.), cabbage (Brassicaoleraceavar. capitata), potato (Solanum tuberosum) and arum (Colocasia sp.).

Disease cycle

The fungus is soil borne in nature and can survive as saprophyte on crop

debris. The fungus also produces sclerotia that are left in the field. These

germinate under favourable weather conditions and cause infections.

Epidemiology

The pathogen is soil borne in the form of sclerotia. High temperature

and humidity favour the disease development. In the plains of India,

sugarbeet is usually grown on ridges and this practice is likely to stimulate

disease incidence because the lower leaves become covered with soil resulting

in a 'bridge' of dead tissue which furnishes an ideal medium for initiating

pathogenesis.

Since the fungus survives in infected plant debris as a saprophyte or by

forming sclerotia, destruction of infected plant debris, crop rotation, deep

summer ploughing, flooding, solarization during summer months etc. can be

helpful in reducing the initi~ inoculum load in the field. Reduction in the

incidence of root rot has also been recorded through the use of nitrogenous

fertilizers including calcium nitrate, anhydrous ammonia, urea, ammonium

sulphate and calcium ammonium nitrate (Thakur and Mukhopadhyay, 1972).

Chemical control

Carboxin and chlomeb significantly reduced fungal growth in vitro atlow concentrations and completely inhibited sclerotia formation. Under field

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conditions ridge soil drenching with carboxin and chlorneb at 2 and" 15 kg!

3000 1 waterlha, respectively, significantly reduced root rot and increased

yields (Mukhopadhyay and Thakur, 1971).

Recently, Das and Raj (2004) suggested the control of this disease

through seed soaking with non-conventional chemicals like 2,3,5-trichloro-

phenoxy acetic acid (10.4 M), chitosan and zinc chloride (10.4 M). Thetreatment not only reduced the disease but also increased root yield, foliage

yield and sugar yield as compared to other tested chemicals.

The methanol extract of leaves ofAegle marmelos decreased the growthand sclerotia production by S. rolfsii and no sclerotia were formed in the

presence of extract at 150 ppm even after 21 days of incubation (Prithiviraj et

al., 1996).

Application ofTrichoderma harzianum inoculum was found effective in

reducing the disease caused by S. rolfsii in sugarbeet (Ciccarese et al., 1992).Correa et al., (1995) tested a metabolite trichorzianines A and B obtainedfrom T. harzianum on the mycelium ofS. rolfsii and produced a change in the

morphogenetic pattern of mycelia. Papavizas and Collins (1990) showed theassociation of Gliocladium virens with sclerotia of S. rolfsii in naturallyinfested soil. When sclerotia were incubated in soil infested with G. virens,

sclerotial viability and capability for infection of host tissue was reduced. G.

virens was found to colonize, penetrate and sporulate inside the sclerotia ofS.rolfsii.

Rhizomania is an economically important disease of sugar beet and

causes severe yield losses. From the infected crop, only 2-3 t sugarl ha is

obtained instead of 8-10 t in the healthy crop (Putz et al., 1990).

Rhizomania has been reported from most of the sugar beet growingareas of Europe, Asia and the U.S.A. (Putz et al., 1990).

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Leaves may show flabbiness, wilting and mild yellowing on the infected

sugarbeet plants in the field. The most characteristic symptoms found in beet

leaves are a pattern of yellowing areas along the veins. However, the virus

mostly remains confined to roots and rarely moves to the foliage. Symptomson roots are characterized by root stunting and a proliferation of lateral

rootlets on the main tap root, giving it bearded appearance.

The virus responsible for this disease is Beet Necrosis Yellow Vein Virus

(BNYVV) which is a probable member of the furovirus (fungus borne rod

shaped virus) group (Shirako and Brakke, 1984). Dilution end point of thisvirus ranged in between 10-4 and 10-5 The infectivity of BNYVV is usually

abolished when sap is heated for 10 min. to 65-700 C or frozen to -200 C.

illtrathin sections of BNYVV- infected tissue show the virus particles

scattered in the cytoplasm and in angled layer aggregates. The virus is not

seen in large aggregates but shows an erratic distribution in the mesophyll

cells of systemic plants (Russoet al., 1981).

Host rangeThis virus infects all cultivars of sugarbeet, fodder beet, red beet, swiss

chard (Beta vulgaris L. var. cycla), spinach (Spinacia oleracea L.), and several

other species of Chenopodiaceae serving as hosts of the Plasmodiopho-

romycete fungus Polymyxa betae. It can also be mechanically inoculated to

other herbaceous species such as Tetragonia expansa Murr. (Aizoaceae),

Gomphrena globosa L. (Amaranthaceae) and Nicotiana clevelandii Gray

(Solanaceae ).

Alopecurus myosuroides, Lolium multiflorum, Sorghum halepense, S.

vulgare, Convolvulus arvensis, Matricaria indora, Stellaria media,

Calystegria sepium, Capsella bursa-pastoris, Centaurea cyan us and

Galinosorga parviflora have reported to act as alternate hosts of BNYVV

(Mouhanna,2000).

Polymyxa betae has been considered to be the vector of BNYVVand wasalso shown to transmit soil borne virus (Ivanovic, 1983). This fungus has

worldwide distribution. The abnormal proliferation of the root lets,

characteristic of rhizomania was found in the presence of non-viruliferous P.

betae but zoospores transmit rhizomania symptoms to whole sugarbcct

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plants, in the absence of detectable virus in the infected plants, indicating

that BNYVV is not requisite to the etiology of the disease. The infectivity of

BNYVV was retained with P. betae in dry soil for atleast 15 years. ELISAdetected BNYVV in extracts of resting spore clusters of a viruliferous P. betaeisolate (Abe and Tamada, 1986).

The control of rhizomania disease is presently based on the development

of varieties resistant to the vector since field trials with fungicides failed to

show any yield benefits (Blunt and Asher, 1989).

Varieties Laetitia and Nagano have been reported to possess resistanceto this disease in Belgium (Anonymous, 2003).

Soil disinfection with dicloropropene was recommended for the control of

fungal vector P. betae (Hess and Schlosser, 1984). Preplant application offumigants like dichloropropene, tolone 11 (1,3- dichloropropene), Vorled (1,3-

dichloropropene + methyl isothiocya-nate), Vorlex 201 (1,3- dichloropropene +chloropicrin +. methyl isothiocyanate) and Pichlor 60 reduced diseaseincidence and significantly increased yields (Martin and Whitney, 1990).

I

Some studies have also been carried out on the biological control of

vector P. betae with Trichoderma spp. Soil inoculation with T. harzianumreduced infection by vector, P. betae upto 25 per cent and the Trichoderma

population introduced remained high throughout experimental period(D1Ambra et al., 1987).

Abdel-Rehim, M.A., Aziza, KD., Tarabeih, A.M. and Hassan, A.A.M.1992. Damping-off and root rot of okra and table beet with reference to chemical control.

Assiut. J. Agrie. Sci. 23(4): 19-36.

Abe, H. and Tamade, T. 1986. Association of best necrotic yellow vein virus withisolates ofPolymyxa betaeKeskin. Ann. Phytopathol. Soc. Jpn. 52: 235-247.

Anonymous, 2003. The choice of varieties for2003. Betteravier-Bruxelles 37: 391.

Asher, M.2000. Control offoliar diseases. Brit. Sugarbeet Rev. 68(2): 32-33.