Rice Diseases PDF

Course Title: DISEASES OF FIELD AND HORTICULTURAL CROPS AND THEIR MANAGEMENT-I COURSE CODE: PP-353; COURSE CREDIT: 3(2+1)  Lecture topic: Symptoms, etiology, disease cycle and management of major diseases of Rice. Course Instructor:...

Course Title: DISEASES OF FIELD AND HORTICULTURAL CROPS AND THEIR MANAGEMENT-I COURSE CODE: PP-353; COURSE CREDIT: 3(2+1)  Lecture topic: Symptoms, etiology, disease cycle and management of major diseases of Rice. Course Instructor: Dr. Lourembam Sanajaoba Singh Assistant Professor, CoA, CAU-I, Kyrdemkulai, Meghalaya- 795105  Diseases of Rice Disease Casual organism 1. Blast Pyricularia oryzae 2. Brown spot Helminthosporium oryzae 3. Bacterial blight Xanthomonas oryzae pv. oryzae 4. Shealth blight Rhizoctonia solani 5. Flase smut Ustilaginoidea virens 6. Khaira Zn deficiency 7. Tungro Rice tungro bacilliform virus (RTBV) and Rice tungro spherical virus (RTSV)  FUNGAL DISEASES OF RICE 1. Blast - Pyricularia oryzae (Syn: P. grisea) (Sexual stage: Magnaporthe grisea) Symptoms:  attacks the crop at all stages of crop growth. Symptoms appear on leaves, nodes, rachis, and glumes.  On the leaves, the lesions appear as small bluish green flecks, which enlarge under moist weather to form the characteristic leaf Blast spindle shaped spots with grey centre and dark brown margin (leaf blast)  Black lesions appear on nodes girdling them. The affected nodes may break up and all the plant parts above the infected nodes may die (nodal blast). Nodal Blast  During flower emergence, the fungus attacks the peduncle and the lesion turns to brownish-black which is referred to as rotten neck / neck rot / panicle blast (neck blast). Neck Blast Etiology: The determination and study of the cause of the disease PATHOGEN:  The mycelium is hyaline to olivaceous and septate.  Conidia are produced in clusters on long septate, olivaceous conidiophores.  Conidia are pyriform to ellipsoid, attached at the broader base by a hilum.  Conidia are hyaline to pale olive green, usually 3 celled.  The perfect state of the fungus is Magnaporthe grisea producing perithecia. The ascospores are hyaline, fusiform, 4 celled and slightly curved. Favourable conditions:  Intermittent drizzles, cloudy weather, more of rainy days, longer duration of dew  high relative humidity (93-99 per cent).  Low night temperature (between 15-20°C or less than 26°C).  Availability of collateral hosts and excess dose of nitrogen  Forecast for rice blast can be made on the basis of minimum night temperature range of 20-26°C in association with a high relative humidity of 90 % and above lasting for a period of a week or more during any of the three susceptible phases of crop growth, viz., seedling stage, post transplanting tillering stage and neck emergence stage.  In Japan, the first leaf blast forecasting model was developed named as BLAST. Later several other models have also been developed namely, PYRICULARIA, PYRIVIEW, BLASTAM, EPIBLA and PBLAST. Disease cycle:  Mycelium and conidia in the infected straw and seeds are major sources of inoculum.  The disease spreads primarily through airborne conidia  Irrigation water may carry the conidia to different fields.  The fungus also survives on collateral hosts viz., Panicum repens, Digitaria marginata, Brachiaria mutica, Leersia hexandra and Echinochloa crusgalli.  Spores land on leaves, germinate, penetrate the leaf, and cause a lesion 4 days later; more spores are produced in as little as 6 days.  Spores arising from the primary infections are capable of causing many more infections. This cycling is called secondary spread.  Secondary spread is responsible for the severe epidemics of blast in fields and localized areas. Disease cycle of Rice blast  Management:  Grow resistant to moderately resistant varieties CO47, IR 20, ADT36, ADT39, ASD 18 and IR64. Avoid cultivation of highly susceptible varieties viz., IR50 and TKM6 in disease favourable season.  Remove and destroy the weed hosts in the field bunds and channels.  Treat the seeds with Captan or Thiram or Carbendazim or Tricyclazole at 2 g/kg. or Pseudomonas fluorescens @ 10g/kg of seed. Spray the nursery with carbendazim 500mg/L or tricyclazole 300mg/L.  Spray the main field with Edifenphos 500 ml or Carbendazim 500 g or Tricyclazole 500 g or Iprobenphos (IBP) 500 ml /ha. 2. Brown Spot - Helminthosporium oryzae (Syn: Drechslera oryzae; Bipolaris oryzae) (Sexual stage: Cochliobolus miyabeanus) Symptoms:  attacks the crop from seedling to milky stage in main field.  Symptoms appear as minute spots on the coleoptile, leaf blade, leaf sheath, and glume, being most prominent on the leaf blade and glumes.  Later the spots become cylindrical or oval, dark brown with yellow halo later becoming circular.  Several spots coalesce and the leaf dries up.  The seedlings die and affected nurseries can be often recognised from a distance by scorched appearance.  Dark brown or black spots also appear on glumes leading to grain discoloration.  It causes failure of seed germination, seedling mortality and reduces the grain quality and weight. Pathogen: Helminthosporium oryzae (Syn: Drechslera oryzae; Bipolaris oryzae) ; (Sexual stage: Cochliobolus miyabeanus)  produces brown septate mycelium.  Conidiophores arise singly or in small groups.  Conidia are usually curved with a bulged center and tapered ends.  They are pale to golden brown in colour and are 6-14 septate.  The perfect stage of the fungus is C. miyabeanus.  It produces perithecia with asci containing 6-15 septate, filamentous or long cylinderical, hyaline to pale olive green ascospores.  The fungus produces terpenoid phytotoxins called ophiobolin A (or Cochliobolin A), ophiobolin B (or cochliobolin B) and ophiobolin I Favourable Conditions:  Temperature of 25-30°C with relative humidity above 80 per cent are highly favourable.  Excess of nitrogen aggravates the disease severity. Disease cycle:  Infected seeds and stubbles are the most common source of primary infection.  The conidia present on infected grain and mycelium in the infected tissue are viable for 2 to 3 years.  Airborne conidia infect the plants both in nursery and in main field.  Collateral host: Leersia hexandra and Echinochloa colonum.  Airborne spores that are capable of causing infection are produced in infested debris and older lesions. Figure: Disease cycle of rice brown spot.  Management:  Field sanitation-removal of collateral hosts and infected debris from the field.  Use of slow release nitrogenous fertilizers is advisable.  Grow tolerant varieties viz., Co44 and Bhavani.  Use disease free seeds.  Treat the seeds with Thiram or Captan at 4 g/kg. Spray the nursery with Edifenphos 40 ml or Mancozeb 80 g for 20 cent nursery.  Spray the crop in the main field with Edifenphos 500 ml or Mancozeb 2 kg/ha when grade reaches 3. If needed repeat after 15 days. 3. Sheath blight - Rhizoctonia solani (Sexual stage: Thanetophorus cucumeris) Symptoms:  The fungus affects the crop from tillering to heading stage.  Initial symptoms are noticed on leaf sheaths near water level.  On the leaf sheath oval or elliptical or irregular greenish grey spots are formed later it turn into greyish white with an irregular blackish brown or purple brown border.  Lesions on the upper parts of plants extend rapidly coalescing with each other to cover entire tillers from the water line to the flag leaf.  The infection extends to the inner sheaths resulting in death of the entire plant.  Older plants are highly susceptible.  Plants heavily infected in the early heading and grain filling growth stages produce poorly filled grain, especially in the lower part of the panicle. Pathogen:  The fungus produces septate mycelium which are hyaline when young, yellowish brown  when old. It produces large number of spherical brown sclerotia. Favourable conditions:  High relative humidity (96-97 per cent), high temperature (30-32°C).  Closer planting.  Heavy doses of nitrogenous fertilizers. Disease cycle:  The pathogen can survive as sclerotia or mycelium in dry soil for about 20 months but for 5-8 months in moist soil.  Sclerotia spread through irrigation water. The fungus has a wide host range. Management:  Grow resistant varieties like Mansarovar, Swarau Dhan, Pankaj etc.  Apply organic amendments viz., neem cake @ 150Kg/ha or FYM 12.5 tons/ha. Avoid flow of irrigation water from infected fields to healthy fields.  Deep ploughing in summer and burning of stubbles.  Spray Carbendazim 500 g/ha  Soil application of P.fluorescens @ of 2.5 kg/ha after 30 days of transplanting (product should be mixed with 50 kg of FYM/Sand and applied).  Foliar spray P.fluorescens at 0.2% at boot leaf stage and 10 days later. 4. False smut or Green smut - Ustilaginoidea virens (Sexual stage: Claviceps oryzae - sativa) Symptoms:  The disease appears on the ears, where individual ovaries are transformed into large, velvety green masses.  These irregular round or oval sclerotial bodies attain a size of about 8 x 10 mm.  Only a few spikelets in a panicle are affected.  The glumes are not affected but are covered superficially by the green mass of spores.  They are slightly flattened, smooth and yellow and are covered by a membrane. The membrane burst as a result of further growth and colour of the ball become yellowish green. Pathogen: Ustilaginoidea virens (Sexual stage: Claviceps oryzae - sativa)  The fungus infects the young ovary, which transformed into a mass of closely united, fine, colourless hyphae. The growth of the fungus expert pressure on the glumes and cause them to burst.  It continues to grow and develop spores, the immature orange colour becoming brownish green at maturity.  The spore are formed laterally or rarely terminally on short sterigmata on radial hyphae.  The young spore are almost round and smooth, but when mature they have a rough, olive green, granular coating and measured 4-6 µ in diameter. They germinate and produced pear shaped secondary conidia on branched and septate germ tubes.  The sclerotia overwinter in the field and produce stalked stromata in the following season.  The stromata form a swelling at the tip of the stalk are more or less globose and contain perithecia around the periphery.  Each perithecium ( flask shaped) contains about 300 asci.  The asci are cylindrical with hemispherical apical appendage, 180-220 x 4 µ and eight spore.  Ascospore are hyaline, filiform, unicellular, 120-180 x 0.5-1 µ.  Chlamydospores are formed as spore balls which are spherical to elliptical, warty and olivaceou Favourable condition: rainfall cloudy weather and high humidity during flowering and maturity soils with high nitrogen content wind for dissemination of the spores from plant to plant overwintering fungus as sclerotia and chlamydospores  Disease cycle:  Grasses / collateral host and wild rice species are alternate hosts. The main source of inoculum is airborne spores.  Ascospores produced from sclerotia act as primary source of infection while chalmydospores are secondary source of infection which is the major part of the disease cycle.  Chlamydospores are airborne and are profusely present at the time heading of rice plant and abundant at heading stage. Management: Preventive methods: Use of disease-free seeds that are selected from healthy crop. Seed treatment with carbendazim 2.0g/kg of seeds. Split application of nitrogen is recommended. Removal and proper disposal of infected plant debris.  Cultural methods Destruction of straw and stubble from infected plants to reduce the disease. Use of resistant or tolerant varieties. Avoid field activities when the plants are wet. Early planted crop has less smut balls than the late planted crop. At the time of harvesting, diseased plants should be removed and destroyed so that sclerotia do not fall in the field. Field bunds and irrigation channels should be kept clean to eliminate alternate hosts. Excess application of nitrogenous fertilizer should be avoided. Regular monitoring of disease incidence during rabi season is very essential. Chemical methods Spraying of copper oxychloride at 2.5 g/litre or Propiconazole at 1.0 ml/litre at boot leaf and milky stages will be more useful to prevent the fungal infection. Seed treatment with carbendazim 2.0g/kg of seeds. At tillering and pre flowering stages, spray Hexaconazole @ 1ml/lit or Chlorothalonil 2g/lit. At tillering and pre flowering stages, spraying of carbendazim fungicide and copper base fungicide can effectively control the disease.  Bacterial Leaf Blight Symptoms:  The disease is usually noticed at the time of heading but it can occur earlier also.  Seedlings in the nursery show circular, yellow spots in the margin, that enlarge, coalesce leading to drying of foliage. “Kresek” symptom is seen in seedlings, 1-2 weeks after transplanting. The bacteria enter through the cut wounds in the leaf tips, become systemic and cause death of entire seedling.  In grown up plants water soaked, translucent lesions appear near the leaf margin. The lesions enlarge both in length and width with a wavy margin and turn straw yellow within a few days, covering the entire leaf. As the disease advances, the lesions cover the entire lamina which turns white or straw coloured.  Milky or opaque dew drops containing bacterial masses are formed on young lesions in the early morning. They dry up on the surface leaving a white encrustation. The affected grains have discoloured spots. If the cut end of leaf is dipped in water, it becomes turbid because of bacterial ooze. Bacterial leaf blight Symptoms: White encrustation  Pathogen / Etiology: Xanthomonas oryzae pv. oryzae  The bacterium is aerobic, gram negative, non-spore forming, rod with size ranging from 1-2 x 0.8-1.0μm with monotrichous polar flagellum.  Bacterial colonies are circular, convex with entire margins, whitish yellow to straw yellow coloured and opaque.  size ranging from 1-2 x 0.8-1.0 μm with monotrichous polar flagellum. Favourable Conditions:  Clipping of tip of the seedling at the time of transplanting.  Heavy rain, heavy dew, flooding, deep irrigation water  Severe wind and temperature of 25-30 ºC  Application of excessive nitrogen, especially late top dressing.  Disease cycle:  The infected seeds as a source of inoculum may not be important since the bacteria decrease rapidly and die in the course of seed soaking.  The pathogen survives in soil and in the infected stubbles and on collateral hosts Leersia spp., Plantago najor, Paspalum dictum, and Cyanodon dactylon.  The pathogen spreads through irrigation water and also through rain storms.  Management:  Remove and destroy of alternative host growing along canals and ridges.  Field sanitation by burning or taking out disease straw from the fields.  Excess of nitrogen and deficiency of potassium should be avoided as these increase the disease incidence.  Crop rotation, late sowing, early thining, good tillage and early irrigation help to reduce the disease incidence.  Grow resistant cultivars IR 20, TKM 6 and Ratna.  Avoid clipping of tip of seedling at the time of transplanting.  Avoid flooded conditions.  Spray Streptomycin sulphate and tetracycline combination 300g + Copper oxychloride1.25 Kg/ha. Rice Tungro Disease (RTD) - Rice tungro bacilliform virus (RTBV) and Rice tungro spherical virus (RTSV) Symptoms:  Infection occurs both in the nursery and main field.  The characteristic symptoms of the disease are discolouration of leaves stunting of the infected plants.  Plants are markedly stunted. Leaves show yellow to orange discoloration and interveinal chlorosis. Young leaves are sometimes mottled while rusty spots appear on older leaves.  Tillering is reduced with poor root system. Panicles not formed in very early infection, if formed, remain small with few, deformed and chaffy grains. Rice tungro disease Symptoms: Pathogen: Rice tungro bacilliform virus (RTBV) and Rice tungro spherical virus (RTSV)  Two morphologically unrelated viruses present in phloem cells.  Rice tungro bacilliform virus (RTBV) bacilliform capsid, circular ds DNA genome and Rice tungro spherical virus (RTSV) isometric capsid ss RNA genome.  RTBV consists of bacilliform particle having circular unipartite ds DNA measuring 110-400 x 30-35 nm  RTSV consists of isometric particles measuring 30 nm in diameter, have ss RNA, unipartite.  Spherical virus particle are attached either along the sides or at the end of the bacilliform particle.  Both the virus are serologically unrelated.  RTBV depends on the RTSV for its transmission by leaf hopper and cause tungro symptoms however, RTSV alone causes mild stunting and enhances the tungro symptoms. Rice tungro bacilliform virus (RTBV) Rice tungro spherical virus (RTSV)  Disease Cycle  Transmission mainly by the leaf hopper vector Nephotettix virescens Males, females and nymphs of the insect can transmit the disease.  Both the particles are transmitted semipersistently, in the vector the particles are noncirculative and nonpropagative.  Plants infected with RTSV alone may be symptomless or exhibit only mild stunting. RTBV enhances the symptoms caused by RTSV.  RTSV can be acquired from the infected plant independently of RTBV, but acquisition of RTBV is dependent on RTSV which acts as a helper virus.  Both the viruses thrive in rice and several weed hosts which serve as source of inoculum for the next. Ratoon from infected rice stubble serve as reservoirs of the virus.  Disease incidence depends on rice cultivars, time of planting, time of infection and presence of vectors and favourable weather conditions.  Management:  Field sanitation, removal of weed hosts of the virus and vectors.  Grow disease tolerant cultivars like Pankhari203, BM66, BM68, Latisail, Ambemohar102, Kamod253, IR50 and Co45.  Control the vectors in the nursery by application of Carbofuran 170 g/cent 10 days after sowing to control hoppers.  Spray Phosphomidan 500 ml or Monocrotophos 1lit/ha (2 ml/litre) or Neem oil 3% or NSKE 5% to control the vector in the main field 15 and 30 days after transplanting.  Set up light traps to monitor the vector population.  Khaira disease of Rice:  The Khaira disease of rice was first reported in 1966 at Pant nagar, Uttrakhand by Y. L. Nene. This is an important physiological disorder of rice plant. The plant disorder has no relation with biological agents. Khaira disease is caused by the deficiency of Zn in soil. Generally, it is a disease of rice seen in nursery stage.  This disease is caused in rice plants due to the deficiency of a very important nutrient in the soil. It is a micro nutrient which known as zinc. So, it is a type of disease in paddy crop which is caused by abiotic factor instead biotic factors. This disease is common in densely or intensively planted rice field. The saline-sodic type of soil is another important factor of khaira disease. Irrigation water having higher bicarbonate concentration. Symptoms:  Symptoms appear after sowing in nursery or field and transplanting in field which is 15 – 30 DAS. Chlorosis starts from the base of leaves. It is common in younger plants. The midribs at the base become chlorotic in younger leaves. Bronzing appears on leaf surface in the form of blotches. It seems like something sprayed over the leaf surface. In advance stage, entire leaf turns into rusty- brown known as Khaira disease. Plant root growth is restricted. Roots also turn brown in colour.  Bronzing symptoms of zinc Note the stained “bronzing” and deficiency on rice leaf. pale yellow mid rib. Zinc Deficiency symptoms Brown colour spots : Growth is stunted, shortening of internodes.  Managements: Grow zinc efficient varieties.  Use of fertilizers that generate acidity. (replace some urea with ammonium sulphate)  Apply organic manure before seeding in nursery or transplanting of rice in rice field.  Monitoring irrigation water quality.  Broadcast ZnSo4 (zinc sulfate) in nursery bed 5 days before pulling out the seedling.  On an average 25 kg Zinc Sulphate per hectare should be applied. It can be done before transplanting or sowing. The next application of zinc sulphate is done after 3 years.  The roots of seedling should be dipped in 2% ZnO (Zinc oxide) suspension.  Spraying of 0.5% zinc sulphate solution 3 times at 15 day’s intervals.