DISEASES OF SUNFLOWER AND CASTOR

SivaK66 9,631 views 113 slides Mar 07, 2019
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About This Presentation

EPIDEMIOLOGY AND MANAGEMENT


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SYMPTOMS ,ETIOLOGY,EPIDEMIOLOGY AND MANAGEMENT OF SUNFLOWER & CASTOR DISEASES PAT-607 DISEASES OF FIELD CROPS (2+1) SIVAGNANAPAZHAM K 2018601508

FUNGAL DISEASES POWDERY MILDEW- Erysiphe cichoracearum DOWNY MILDEW - Plasmopara halstedii RUST - Puccinia helianthi HEAD ROT - Rhizopus sp CHARCOAL ROT - Macrophomina phaseolina FUSARIUM ROOT ROT- Fusarium sp PHOMA BLACK STEM- Phoma macdonaldii PHOMOPSIS STEM CANKER- D.helianthi SCLEROTINIA STEM ROT/WILT- S.sclerotiorum VERTICILLIUM WILT - V.dahliae SUNFLOWER DISEASES

WHITE RUST – Albugo tragopogonis LEAF BLIGHT- Alternaria helianthi / zinniae SEPTORIA LEAF BLIGHT- S.helianthi BACTERIAL DISEASES BACTERIAL HEAD ROT- Pectobacterium carotovorum sub sp carotovorum APICAL CHLOROSIS- P. syringae pv . tagetis BACTERIAL LEAF SPOT- P. syringae pv . helianthi Contd …

VIRAL DISEASES SUNFLOWER MOSAIC - Sunflower mosaic virus. SUNFLOWER NECROSIS- Tobacco streak virus. SUNFLOWER RING SPOT- SRV ( Illar virus). PHANEROGAMIC PARASITE BROOM RAPE – Orobanche cumana

Alternaria Leaf Blight Downy Mildew Rust Sclerotium Wilt and Collar Rot Charcoal Rot Sclerotinia Wilt and Rot Disease Powdery Mildew Head Rot Sunflower Necrosis Disease MAJOR DISEASES OF SUNFLOWER

In areas of tropical and subtropical climates. Prevalent in Brazil. Damage - great reduction in photosynthetic area of the plant. Severely attacked plants show early maturation, with reduced production and seed weight. Seed yield by 27 to 80% and oil yield by 17 to 33%. Affects the seed germination and vigor of seedlings.  ( Leite et al., 2006). 1. ALTERNARIA LEAF BLIGHT

Young leaf spots are small, dark, angular Leaf spots usually are found between major leaf veins, along leaf margins and tips and will coalesce. Extensive yellowing ( chlorosis ) occurs, followed by browning and leaf death. Defoliation occurs from the ground up Stem lesions are dark, narrow, elliptical and about ½ to 1½ inches long. SYMPTOMS

Conidia are cylindrical to ellipsoidal. 5 transverse septa, no tail, and are formed singly in cylindrical conidiophores. Mycelium olive brown, septate , branched. Fungus grow slowly on PDA forming greyish colonies. Also pathogenic to chrysanthemum ( Davet et al., 1991) PATHOGEN - Alternaria helianthi

Favorable conditions – produces large number of conidia that are spread by rain and wind. Conidial germination – High RH & Temp - 25-27° C temperature and 12 hrs of wet foliage. Optimum conditions for infection by A. helianthi are leaf wetness for 24 h at 25°C The disease spreads rapidly in rainy season. Disease progresses rapidly from the lower leaves to upper leaves. ( Leite & Amorim , 2002). EPIDEMIOLOGY

The fungus overwinters as mycelium on infected plant residues and in dry conditions survives for 20 weeks in soil The fungus is seed borne with 22.9% seed transmissible nature. A. alternata infects only in Rabi season. SURVIVAL AND SPREAD .

Crop rotation for atleast four years. Destruction or removal of infected crop debris. Adjustment of sowing dates. Late sowing is favorable to high Alternaria disease severity in sunflower crop Minimize the occurrence of disease, it should avoid when the flowering coincides with periods of heavy rain. ( Gadhave et al., 2011). MANAGEMENT

Seed treatment with Carbendazim (12%) + Mancozeb (63%) formulation @3g/kg seed. Followed by two sprays of Propiconazole @ 1ml/L at 45 and 60 DAS.  Intercropping sunflower with groundnut in the ratio of 6 : 2 reduces the disease incidence. Early planting of sunflower during kharif season results in low occurrence of leaf blight. Spacing of 60 x 30 cm or 45 x 30. ( ICAR- IIOR-Hyderabad) Contd …

Seed treatment with carbendazim+iprodione at 0.3% in water along with foliar spray of hexaconazole was found most effective in managing Alternaria blight. seed treatment with Pseudomonas fluorescens (0.8%) in jelly+hexaconazole foliar spray. (UAS Dharward ) Contd …

Temperate, tropical or subtropical climates Losses - the fungus, which can infect roots, stem or sunflower head. Quickly kills the infected plants at seedling stage, resulting in stand failures. Oil quality is lower due to seeds infected by the fungus. (40DAS after sowing) Indirect losses occur due to contamination of seeds with sclerotia . Persists in the soil for many years. ( Leite et al., 2000). 2. HEAD ROT / WILT - Sclerotinia sclerotiorum

Fungi develops internally and destroys the internal tissues. Infection occurs on leaves wounds and proceeds toward the petiole, ending the stem. Initial symptoms are characterized by light brown and soft lesions on the dorsal side of the head. (Zimmer & Hoes, 1978) Contd …

Basal rot may occur from the seedling stage to maturity. Infection is mostly observed near flowering Rot starts when the mycelium originating from sclerotia in the soil, comes in contact with the lateral roots Sudden wilting of the plant. Infected plant - turgidity at night after a rainfall, but within a few days this symptom becomes irreversible, and the disease is named Sclerotinia wilt SYMPTOMS

Hyaline multicellular hyphae Sclerotium germination occurs in myceliogenic - hyphae and carpogenic –apothecia Myceliogenic germination of sclerotia - root rot, stem rot and wilting. The apothecium is a flat or cup-shaped structure that produces sexual spores of S.sclerotiorum . Asexual – hyphae and sclerotia Sexual - ascospore ( Mordue & Holliday, 1976) PATHOGEN

The fungus survives as sclerotia or mycelium in infected plant residue and soil Secondary contamination is possible through direct contact of the diseased tissue with healthy tissue from neighboring plant Seeds - dissemination of S. sclerotiorum , as sclerotia mixed with the seeds or fungus mycelium colonizing the internal tissues ( Davet et al., 1991) SURVIVAL AND SPREAD

High RH above 70% a mature apothecium can produce up to 2 x 108 ascospores over a period of several weeks. The ascospores are released at temperatures of 3ºC to 22ºC,with greater intensity between 19ºC and 20ºC. Temperatures above 25ºC and relative humidity below 35% are limiting for ascospore survival. Optimum temperature for development of the mycelium is between 18ºC and 25ºC. ( Gulya et al., 1997) EPIDEMIOLOGY

Crop rotation of 3-4 years helps to reduce disease.  Elimination of infected plant residue Deep ploughing of soil. Moisture stress and water logging conditions should be avoided in the field Seed dressing with thiram + carboxin (2:1) at 3-6 g/kg of seed is found to be effective control of the seedling phase of the plant. MANAGEMENT

Occurs in greater intensity in tropical areas In temperate areas, powdery mildew is usually not observed until flowering and rarely has economic importance In India, the disease was first reported in Bombay (Patel et al., 1949) Rajastan ( Prasada et al., 1968), West Bengal ( Goswami and Dasgupta , 1981) Punjab ( Bains et al., 1996) Causing a significant yield reduction. 3.POWDERY MILDEW- Golovinomyces cichoracearum

White to grey powdery patches appear on upper surface of older leaves which are still green. Occassionally the symptoms appear on stem and bracts. White to grey areas enlarge, coalesce and cover most plant parts. As the season progresses, the mildewed leaves take on a dusty, powdery appearance. SYMPTOMS

This powder is easily rubbed off. Small black dots, cleistothecia become visible as black pinpoints over the white mildew areas late in the season. Severely infected areas lose luster, curls, become permanently yellow and may dry up. Normally the lower leaves are more heavily infected than the upper leaves (Zimmer & Hoes, 1978; Almeida et al., 1981) Contd …

Obligate parasite Mycelium is usually well developed. Spores are formed in long chains, have ellipsoid shape and size ranging from 25- 45 μm x 14-26 μm. Produces cleistotecia , which are black structures responsible for survival of the pathogen,containing asci with two ascospores ( Kapoor , 1967) PATHOGEN

Transmission is primarily through cleistotecia that survive from one growing season to another Conidia can also survive Conidia are disseminated primarily by wind, which can reach long distances ( Kapoor , 1967) SURVIVAL AND SPREAD

Optimum conditions for infection are temperatures around 25ºC and relative humidity of 95%. Conidia do not germinate when there is a water film on the leaf surface. Disease is favored by hot and dry periods ( Kapoor , 1967; Zimmer & Hoes, 1978) EPIDEMIOLOGY

Fungicides azoxistrobin + ciproconazole and difenoconazole are registered for control powdery mildew in sunflower ( Ministério , 2012) Clone, Aerosil , Kumulus and Sulfex Gold at 0.02% concentration effective ( Nagaraja, 2000, Singh et al., 2000 ) Application of wettable sulphur 0.2% or karathane 0.2% or propiconazole 0.1% or difenoconazole 0.05% three times at 15 days interval effectively controls the disease. MANAGEMENT

Spray propiconazole / Difenoconozole @ 1ml /L at 45 and 60 DAS. Spraying wettable sulphur @ 3g/L or Calixin 1 ml/L is also effective reducing the disease incidence. (ICAR-IIOR – Hyderabad) Contd …

The disease was recorded for the first time in 1984 in Latur and Beed districts of Marathwada region of Maharashtra in India with an intensity ranging from 5 to 60%. Later the disease has spread to other areas of Maharashtra, Andhra Pradesh and Karnataka. The losses in yield were reported to be 2-25%.  4.Downy mildew – Plasmopara halstedi

The fungus causes different types of symptoms as damping off of seedlings, systemic infection, Local foliar lesions and root galls. Damping off Symptoms appear as yellowing of the first pair of true leaves. Under conditions of cool temperature and high humidity, whitish growth of downy appear on the cotyledonary leaves of young seedlings. SYMPTOMS

As the plant grows, the fungus spreads to younger tissue, the chlorotic area expands and chlorosis appears on leaves and also on stem. Affected plants bear abnormally thick, downward curled leaves showing prominent yellow and green mottling. Stem – brittle & flower heads of the affected plant - sterile, stiff and face upwards and seeds are not produced. Systemic infection

Increases -transpiration rate and respiration Decrease in level of carbohydrates and accumulation of potassium and phosphorus in leaves of infected sunflower plants. Foliar lesions Greenish yellow small angular spots appear on leaves. The spots may enlarge and coalesce to infect a larger part of the leaf.

The galls are formed at the base of plants on primary roots that took discoloured , scurfy and hypertrophied with reduced development of secondary roots. Such plants are less vigorous and subject to lodging. (NIPHM – Hyderabad) Root galls

Obligate parasite Produces intercellular mycelium with globular haustoria and sporangia that arise through the stomata. Sporangia are thin and branched monopodially to form zoosporangia at the ends of the branches. The zoosporangia break up, release biflagellate zoospores (Zimmer & Hoes, 1978). PATHOGEN

The pathogen survives through oospores in this residue of the preceding sunflower crop in soil. Seed borne infection also occurs. After the winter, the oospores germinate, especially in moist conditions of spring. Some oospores, however, remain dormant for up to 14 year (Zimmer & Hoes, 1978). SURVIVAL AND SPREAD

Cool weather with 16-18 temperature, cloudy weather with winds and drizzle or High RH favours infection and disease development. The disease is favored by high rainfall conditions (relative humidity higher than 95%) and temperature between 15ºC to 18ºC (Davet et al., 1991). EPIDEMIOLOGY

Combinations including metalaxyl or oxadixyl gave good control of P. halstedii . Fungicides gave total protection, without phytotoxicity , at 2.5 g commercial product/kg seed for 10% metalaxyl + 48% mancozeb , and at 3 g/kg seed for the combinations 10% oxadixyl + 56% propineb and 8% oxadixyl + 56% mancozeb + 3.2% cymoxanil ( Achbani et al., 1999). MANAGEMENT

Treatment of sunflower seeds with 1×108cfu/ml of PGPR strain INR7 - decreased disease severity and offered 51 and 54% protection under green house and field conditions. Treatment of sunflower seeds with 5% chitosan - decreased disease severity an offered 46 and 52% protection under greenhouse and field conditions. ( Nandeesh Kumar et al., 2008). Contd..

Trifloxystrobin as a foliar spray shows the effective against the disease. ( Sudisha et al., 2010). Crop rotation of three years with ground nut/castor/sorghum/maize; grow Resistant variety hybrids like DRSH-1 and seed treatment with Metalayxl 35SD @ 6g/kg seed. (ICAR-IIOR – Hyderabad)

High yielding hybrids such as BSH-1, KBSH-1, ICI-302, PKVSH- 27, DSH-1, NSH-22, ITC-601, MSFH-17, SPIC-105, Jwalamukhi , NARF- 114 and PKVSF-9, Sidheswar are resistant to downy mildew. RESISTANT VARIETIES

Important yield limiting disease in Great plains of US Severity and incidence increased from 2002 & 2011  More severe in the rabi season and causes a considerable yield reduction whenever it appears in early stages of crop growth. Under severe rust conditions, the seed yield loss of 11-33% has been reported. 5.RUST- Puccinia helianthi

Small round powdery pustules, with 1 to 2 mm diameter, pale orange to black, distributed randomly over the entire surface of the plant Common in lower leaves than to the top. Pustules- small yellow halos. At high levels of infection, stem, petiole and floral parts may exhibit symptoms. The coalescence of pustules entire leaf surface- premature leaf senescence, which causes reduced yield & low seed quality. ( Pereyra & Escande , 1994) SYMPTOMS

Autocieous and macrocyclic rust 5 spore stages during its life cycle, four of which are visible with the unaided eye. The earliest visible stage is the pycnial stage, which has been observed as early as the first week of June Stage is not seen often, but it occurs as a small (1/4 inch or less) yellow-orange spot on the top side of cotyledons or lower leaves PATHOGEN

Aecia -the underside of the leaf, immediately opposite the pycnia . Aecia appear in clusters of orange cups similar in size to the pycnia Uredinia pustules are small (1/16 inch) and can occur on upper or undersides of leaves (Pustules are filled with cinnamon-brown spores ( urediniospores ) that may by surrounded by a chlorotic halo and can be rubbed off easily.

Uredinia pustules are small (1/16 inch) and can occur on upper or undersides of leaves (Pustules are filled with cinnamon-brown spores ( urediniospores ) that may by surrounded by a chlorotic halo and can be rubbed off easily. At season’s end, the uredinia are converted to telia a black structure that does not rub off.

pycnial stage Uredinial stage Telial stage

Inoculum - overwintered as telia on sunflower residue (previous crop residue or wild sunflowers) Aecia produce aeciospores (disseminated by wind) that infect the sunflower The disease spreads by wind-borne uredospores from infected crop. SURVIVAL AND SPREAD

Pathogen is favored by temperatures of 18ºC to 22ºC , under these conditions, can cause epidemics  86-92% relative humidity favoures high rust intensity ( Pereyra & Escande , 1994). EPIDEMIOLOGY

Removal and burning of infected crop residues minimizes initial inoculum . Deep ploughing Crop rotation with non-host crops for 3 years reduces the inoculum load in the soil Avoid high nitrogen rates and high plant populations. Spraying of mancozeb or zineb at 0.25% two to three times at 10 days interval is very effective in control of the disease MANAGEMENT

Application of sulphur fungicides, sulphur dust (15 kg/ ha) or wettable sulphur 0.2% or mixture of sulphur + zineb also gives good control of the disease. Spraying of oxycarboxin 20 EC and benodanil 50WP at 0.4% two times at 30 days interval also effectively control the disease. Application of boron to soil reduces the rust incidence. Contd …

 DL-3-amino-n- butanoic acid (DL-b- aminobutyric acid [BABA]) was the most effective & sodium salicylate ( NaSA ) was the least effective in protecting against rust BABA did not affect urediospores germination, germ tube growth, appresorial formation or initial ingress of P. helianthi , but strongly suppressed mycelial colonization in the mesophyll and consequently pustule and urediospore formation. Amzalek and Cohen (2007)  Contd …

FRAC 3 products ( Tebuconazole ) and FRAC 11 products ( Pyraclostrobin and Azoxystrobin ), will reduce rust. (USDA 2011) Contd …

First reported from Sri Lanka in 1927 The fungus is reported to be soil, seed and stubble borne The disease is more prevalent and economically important in regions with hot, dry growing seasons. It can cause 30-46% reduction in seed weight. The disease also causes lodging that incurs indirect loss. 6.CHARCOAL ROT – M.phaseolina

Epidermis is removed, minute black microsclerotia may be as to give a greyish black look to the tissue (Hoes, 1985; Kolte , 1985) Contd …

Progressive wilting, premature dying, loss of vigor, and reduced yield Responsible for seedling blight, damping off, root rot, basal stem rot and early maturing of sunflower crop After flowering are grey black discoloration and shredding of plant tissue at the stem and top of the taproot with getting hollowing of the stem SYMPTOMS

Root inhibiting fungus and produces tuber or cushion shaped 1-8 mm diameter black sclerotia . The fungus is reported to be soil, seed and stubble borne. Pycnidial stage:  Macrophomina phaseolina Sclerotial stage :   Rhizoctonia bataticola Affects the fibrovascular system of the roots and basal internodes, impends the transport of nutrients and water to the upper parts of the plant. (Sinclair, 1982) PATHOGEN

Sclerotia serve as a primary means of survival The sclerotia float freely on soil surface when field is flooded for irrigation and become primary inoculum for emerging seedlings. Survive for more than 10 months under dry soil conditions. Severity of the disease is directly related to the population of viable sclerotia in the soil ( Kaisar , et al., 1988) SURVIVAL AND SPREAD

 Plants at seed development stage are stressed and most vulnerable to infection. The disease is favoured by higher salt concentration in irrigation water, higher temperature (25-35°C) and moisture stress. EPIDEMIOLOGY

Removal and destruction of diseased plants Deep summer ploughing   Early season planting or choosing an early maturing variety High incidence of the disease may be due to high nitrogen and low phosphorus and potassium Seed treatment with thiram 3-4 g/kg seed reduces the seed borne inoculum . MANAGEMENT

Nitrogen applied as ammonium sulphate or calcium nitrate and phosphorus as single super phosphate is reported to be effective in decreasing the incidence of the disease Plant crude extracts of Occimum,E.globules (15%) were effective against charcoal rot BCA- Bacillus strains, T.harzianum are also found to be effective Fungicide Rizolex-3g/L ( Elaigwu et al.,2017) Contd …

In India SND - Bagepally region of Kolar district and around Bangalore in Karnataka during 1997. Later reported in Andhra Pradesh, Karnataka, Tamil Nadu and Maharashtra. The intensity of disease ranges from 2 to 100%. The disease greatly reduces the growth and seed yield. 7.NECROSIS

Field symptoms of the disease include mosaic on leaves that leads to extensive necrosis of leaf lamina, petiole, stem, floral calyx and complete death of seedlings eventually Causes severe stunting with malformed head filled with chaffy seeds Necrosis at bud formation stage makes the capitulum to bend and twist resulting into complete failure of seed setting and maturation. SYMPTOMS

SND Causative Tobacco streak virus (TSV) was first described by Johnson et al., Species of the genus Ilarvirus , of the family Bromoviridae Viruses having tripartite quasi isometric particles of size 27 to 35 nm PATHOGEN

Weeds such as Trianthema portulacastrum , Priva leptostachya , Digeria arvensis , Clitoria ternata , Solanum nigrum , Vernonia cineraria, Trichodesma indicum and some other species were found to serve as hosts for sunflower necrosis virus Virus spreads through transmission by thrips Frankliniella schultzii . The main source of inoculum - pollen grains of infected crop plants or weeds. ( Lavanya et al.,) SURVIVAL AND SPREAD

Single thrip was enough to acquire and transmit the virus from an infected to healthy sunflower plant Acquisition Access Period (AAP) of 3 days Inoculation Access Period (IAP) of 6 days was necessary for successful transmission of the virus ( Pankaja et al., 2007) TRANSMISSION

Sowing 7-11 rows of fast growing cereals (pearl millet, sorghum or maize) as border crop around fields which obstruct the movement of thrips from landing on crop plants were found to reduce disease incidence in sunflower Intercropping with red gram or castor was found to reduce disease intensity MANAGEMENT

Seed treatment either with imidacloprid at 5g/ kg seed or thiomethoxam at 4g/ kg seed followed by two sprays at 30 and 45 days found to reduce necrosis disease. (IIOR-Hyderabad) Anti viral compounds: Use of various anti viral materials such as Prosopis , goatmilk and Bougainvillea in combinations were used to induce the resistance in sunflower against TSV-SF Contd …

CASTOR Important non edible oilseed crop of arid and semi arid regions Ricinus communis – Euphorbiaceae In india - Gujarat, AP,Orissa,Tamil Nadu The seeds contain between 40% and 60% oil that is rich in triglyceride, mainly ricinolein . The seed contains ricin , a toxin, which is also present in lower concentrations throughout the plant.

SEEDLING BLIGHT-   Phytophthora parasitica LEAF SPOT- Cercospora ricinella ALTERNARIA BLIGHT - Alternaria ricini POWDERY MILDEW- Leveillula taurica RUST- Melampsora ricini WILT- Fusarium oxysporum fsp . ricini MAJOR DISEASES

First reported pusa Bihar -1909 Occurs – Rainy season Severe in low lying areas & badly irrigated regions Destroys the seedlings about 30 – 40% Hyderabad – 1947 Uttra pradesh - 1948 1. SEEDLING BLIGHT

Seedling death First makes its appearance on both the surfaces of the cotyledonary leaves Form of roundish patch of dull green colour which soon spreads to the point of attachment causing the leaf to rot and hang down. SYMPTOMS

The pathogen produces non- septate and hyaline mycelium Inter and intra cellular mycelium Single colourless ovoid sporangium borne at the tip Sporangia – zoospores Forms two germ tubes The fungus also produces oospores and chlamydospores in adverse seasons. PATHOGEN

The pathogen survives in soil or collateral or alternative hosts. Survive as soil borne oospores. Fungus also survives on other hosts like potato, tomato, brinjal , sesamum etc. The secondary spread takes place through wind borne sporangia. SURVIVAL AND SPREAD

Continuous rainy weather. Low temperature (20-25°C). Low lying and ill drained soils. EPIDEMIOLOGY

Seed dressing with T.viride or Metalaxyl @4g /kg of seed Soil drenching with COC 3g/ L Avoid ill drained, damp and low lying place for raising castor Growing resistant varieties DCS-9, Jwala (48-1), Harita , GCH-4, GCH-5, DCH-177, and GCH-7 ( IIOR – Hyderabad) MANAGEMENT

All the aerial parts of the plant, i.e., stem, leaves, inflorescence and capsules are liable to be attacked. Portion of the leaf and are irregular, scattered, and have concentric rings. These are brown and later become covered with bluish-green or sooty growth. Severe- spots coalesce and form big patches resulting in premature defoliation of the plant which gradually wilts away 2.LEAF BLIGHT- A.ricini

The pathogen produces erect or slightly curved, light grey to brown conidiophores, which are occasionally in groups. Conidia are produced in long chains. Conidia are obclavate , light olive in colour with 5-16 cells having transverse and longitudinal septa with a beak at the tip. PATHOGEN

Seed borne both internally as well as externally Causes pre & post emergence D.off and foliage blight Survives on hosts like J.pandurifolia & Bridelia hamiltoniana Primary infection- seed Secondary infection – air borne conidia ( Pawar & Patel 1957) SURVIVAL AND SPREAD

High RH 85 -90 Low Temp 16 – 20 degree celcius MANAGEMENT Removal of weed host Foliar application of 0.2 % @ 15 days interval control the disease Proper dose of Nitrogen fertilizer EPIDEMIOLOGY

Appears as minute brown specks surrounded by a pale green halo. The spots enlarge to greyish white centre portion with deep brown margin. The spots may be 2-4 mm in diameter and when several spots coalesce, large brown patches appear but restricted by veins. Infected tissues often drop off leaving shot-hole symptoms. In severe infections, the older leaves may be blighted and withered 3.LEAF SPOT – C.ricinella

The pathogen hyphae collect beneath the epidermis and form a hymenial layer. Clusters of conidiophores emerge through stomata or epidermis. They are septate and un branched with deep brown base and light brown tip. The conidia are elongated, colourless , straight or slightly curved, truncate at the base and narrow at the tip with 2-7 septa. PATHOGEN

The pathogen remains as dormant mycelium in the plant debris. The disease mainly spreads through wind borne conidia. MANAGEMENT Spraying twice with mancozeb 0.25% & Carbendazim 500 g @ 10-15 days interval Seed treatment with captan or Thiram 2g/kg of seed SURVIVAL & SPREAD

Prevalent during November to March at Coimbatore in India SYMPTOMS Typical mildew growth which is generally confined to the under-surface of the leaf. When the infection is severe the upper-surface is also covered by the whitish growth of the fungus 4.POWDERY MILDEW- L.taurica

Endophytic Intercellular hyphae Condia hyaline borne at tip Sexual fruiting body chasmothecium Produces spongy cell Haustoria SURVIVAL & SPREAD Survive on infected plant debris Secondary infection through air borne conidia PATHOGEN

Wettable Sulphur 2g/lit at 15 days interval, starting from 3 months after sowing Spray 1ml hexaconazole or 2ml dinocap / litre of water at fortnight intervals. The variety Jwala is resistant to this disease. MANAGEMENT

Minute, orange-yellow coloured , raised pustules appear with powdery masses on the lower surface of the leaves and the corresponding areas on the upper surface of the leaves are yellow. Often the pustules are grouped in concentric rings and coalesce together to for drying of leaves. 5.RUST- Melampsora ricini

The pathogen produces only uredosori in castor plants and other stages of the life cycle are unknown. Uredospores are two kinds, one is thick walled and other is thin walled. They are elliptical to round, orange-yellow coloured and finely warty. Survival & spread Survive in self sown crops Spreads through airborne uredospores . PATHOGEN

Rogue out the self-sown castor crops and other weed hosts. Spray Mancozeb at 2kg/ha or Propioconazole 1l/ha. MANAGEMENT

Necrosis of leaves starts from margins spreading to interveinal areas and finally to the whole leaf. Spilt open stem shows brownish discolouration and white cottony growth of mycelia much prominently in the pith of the stem

Leaves droop and drop off leaving behind only top leaves. Diseased plants are sickly in appearance. Wilting of plants, root degeneration, collar rot, drooping of leaves and necrosis of affected tissue and finally leading to death of plants. 6.WILT – Fusarium oxysporum f sp ricini

The fungus is soil-borne and remains in the soil as saprophyte for 2-3 years. The disease is primarily transmitted through infected seed pieces. The secondary spread is aided by wind, rain and irrigation water. EPIDEMIOLOGY High day temperature (30-35˚C). Low humidity (50-60%). Low soil moisture and alkaline soils SURVIVAL & SPREAD

Selection of disease free seeds. Grow tolerant and resistant varieties like Jyothi , Jwala , GCH-4 DCH-30 and SHB 145. Avoid water logging Burning of crop debris Green manuring and intercropping with red gram Treat the seeds with thiram @ 2g/ kg or carbendiazim @ 2g/ kg seed. MANAGEMENT

Seed treatment with 4g of Trichoderma viride talc formulation. Multiplication of 2kg of T.viride formulation by mixing in 50kg farm yard manure Sprinkling water and covering with polythene sheet for 15days and then applying between rows of the crops is helpful in reducing the incidence.

Seed treatment with captan / Thiram @3 kg or Carbendazim 2g/kg seed or T. viride 10g/kg for control of seed borne diseases Soil application of T. viride (2.5 kg mixed with 125kg FYM /ha) Resistant varieties- Jwala,Haritha,DCS107,GCH-7,GCH-4,DCH-177,519- Tolerate wilt Crop rotation with milets and inter cropping with Red gram 1:1 ratio. ICAR IIOR - HYDERABAD
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