8/12/2019 Beetroot 0001
1/11
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
8/12/2019 Beetroot 0001
2/11
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).
8/12/2019 Beetroot 0001
3/11
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-
8/12/2019 Beetroot 0001
4/11
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
8/12/2019 Beetroot 0001
5/11
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,
8/12/2019 Beetroot 0001
6/11
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
8/12/2019 Beetroot 0001
7/11
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
8/12/2019 Beetroot 0001
8/11
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
8/12/2019 Beetroot 0001
9/11
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).
8/12/2019 Beetroot 0001
10/11
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
8/12/2019 Beetroot 0001
11/11
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.
Top Related