Rice Diseases PDF

Rice Blast This disease is incited by Pyricularia oryzae [teleomorph: Magnaporthe oryzae]. Symptoms The fungus can infect leaves, nodes, and various parts of the panicle. Leaf Blast: Greyish or bluish dots of 1–3 mm diameter appear on the leaf blades. On susceptible cultivars, the spots enlarge quic...

Rice Blast This disease is incited by Pyricularia oryzae [teleomorph: Magnaporthe oryzae]. Symptoms The fungus can infect leaves, nodes, and various parts of the panicle. Leaf Blast: Greyish or bluish dots of 1–3 mm diameter appear on the leaf blades. On susceptible cultivars, the spots enlarge quickly under humid conditions and become elliptical or ‘eye shaped’ with grey or whitish centre and brown or dark brown margin (Fig. 1 b, c). In severe infection, seedlings and plants in the nursery may be completely blasted or killed. Node Blast: The pathogen also infects the nodes that turn black and get weakened due to tissue disintegration, resulting in breakage of stem at the nodal region followed by death of all the plant parts above the infected nodes (Fig. 1 d). Neck and Panicle Blast: At the time of flowering, area near the panicle base is girdled by a greyish brown lesion, and the panicle falls over in the case of severe infection (Fig. 1 e, f). The neck becomes shrivelled and covered with grey mycelium. If neck infection occurs before the milking stage, the entire panicle may die prematurely, leaving it white and completely unfilled. Later, infections may cause incomplete grain filling and poor milling quality. Pathogen Rice blast pathogen, Magnaporthe oryzae (previously M. grisea; anamorph: Pyricularia oryzae), is a filamentous ascomycetous fungus and is classified in the newly erected family Magnaporthaceae (Fig. 1 a). Fig. 1: Symptoms and causal organism of rice blast: (a) Magnaporthe oryzae, causal organism of rice blast disease; (b) minute blast lesions on leaves; (c) characteristic eye-shaped lesions on leaves; (d) node blast; (e) typical panicle blast; (f) severe panicle blast-infected rice field Disease Cycle and Epidemiology In temperate regions, mycelium and conidia on diseased straw and infected seeds are the principal sources of primary infection. The fungus can attack several cereal and grass hosts which could be important source of primary infection. In the tropical climate of South India, where several crops of rice are taken in a year, the pathogen maintains a continuous disease cycle on the rice crop itself. Under favourable conditions, the conidia can produce symptoms within 4–5 days of infection. Conidia are produced on the lesions 6–7 days after infection and disseminated by wind. Disease Management Though chemical control measures for managing the disease have been very successful, a major emphasis has been given to host plant resistance due to increased concern of ill effects of chemical pesticides. Host Plant Resistance Varieties like IR 64, Rasi and IR 36 expressed good level of blast resistance in India and elsewhere. Cultural Control Cultural practices like use of healthy seeds collected from disease-free fields; destruction of weeds, collateral hosts and crop residues; balanced application of fertilizers; application of farm yard manure and rice husk ash; and wider spacing have been found to reduce the disease severity in the fields. Biological Control Reduction of blast disease severity under experimental condition by application of different biocontrol agents like Pseudomonas fluorescens, Bacillus subtilis and B. polymyxa has been reported. Chemical Control Chemical control has been practiced and found to be highly satisfactory at many places. In endemic areas, seed treatment with pyroquilon 50 WP at 1 g/kg or tricyclazole 75 WP at 1 g/kg or carbendazim 50 WP at 2 g/kg has been found to protect the plants from seedling blast. When the leaf blast symptoms appear in fields, the options for chemical control include tricyclazole 75 WP at 0.6 g/l or iprobenphos 48 EC at 2 g/l or isoprothiolane 40 EC at 1.5 ml/l or kasugamycin 3 SL at 2.5 ml/l or carbendazim 50 WP at 1 g/l or azoxystrobin at 1 ml/l or metominostrobin 20 SC at 2 ml/l. However, the farmers are advised to strictly adhere to the use of recommended chemicals, their doses, formulation and time of application for better disease management and to overcome the problem of pesticide residues in rice grains and straw. Brown Spot Causal Organism: Helminthosporium oryzae (Syn: Drechslera oryzae) (Sexual stage: Cochliobolus miyabeanus) Symptoms The fungus 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. The spots become cylindrical or oval, dark brown with yellow halo later becoming circular. The 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 H. oryzae produces brown septate mycelium. Conidiophores may arise singly or in small groups. They are geniculate and brown in colour. Conidia are usually curved with a bulged center and tapered ends. They are pale to golden brown in colour and 6-14 septate. The perfect stage of the fungus is C. miyabeanus. Favourable conditions Minimum temperature of 27–28˚C, Relative humidity of 90-99% and rainfall of 0.4 -14.4 mm favours the dispersal of the conidia to maximum extent. 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. The brown spot fungus is normally present in areas with a long history of rice culture. The fungus survives on stubble and debris from previous rice crops and on seed. Airborne spores that are capable of causing infection are produced in infested debris and older lesions. Airborne conidia infect the plants both in nursery and in main field. The disease occurs naturally on as many as 20 different wild species of oryzae. A few colateral hosts like Digitaria sanguinalis, Leersia hexandra, Echinochloa colona, Pennisetum typhoides, Setaria italic and Cynodon dactylon on which the fungus is recorded through artificial inoculation may serve as sources of primary inoculum. Secondary infection is by the first formed spores on the seedlings, which become wind borne. Management Field sanitation-removal of collateral hosts and infected debris from the field. Crop rotation 2 to 3 years. Use of slow-release nitrogenous fertilizers is advisable. Grow tolerant varieties disease free seeds. Avoid water stress and give balanced nutrition. Treat the seeds with Thiram or Captan @ 4 g/kg. Spray Dithane M 45 @ 600 g / acre in 300 to 400 L of water. If needed repeat after 15 days. Bacterial Blight Causal Organism: Xanthomonas oryzae pv. oryzae Symptoms The bacterium induces either wilting of plants or leaf blight. Wilting syndrome known as “Kresek” symptom occurs sporadically in the fields causing serious damage. It commonly occurs within 3-4 weeks after transplanting of the crop. Kresek results either in the death of whole plant or wilting of only a few leaves. Leaf blight phase is the most predominant form of the disease occurring between tillering and heading stages of the crop. A third type of less conspicuous symptom caused by the bacterium is yellowing of leaves. Such leaves show blighted appearance. The bacterium enters through the cut wounds in the leaf tips, becomes systemic and causes death of entire seedling. The earliest symptom of the blight phase is the appearance of dull greenish water soaked or yellowish spots 5 to 10 mm in length on the leaf towards the tip or margins, leading to tip and marginal drying. The infection soon extends along one or both margins, sometimes to the leaf sheath also. As the disease progresses, several lesions may coalesce to form straw brown large lesions or blighted portions. The inner margin of the blighted patch in contact with the adjoining green portion of the leaf is ragged or wavy. Occasionally, the lesions may extend from the tip downward along the midrib itself, the leaf margins remaining green. Small droplets of bacterial ooze, pale amber in colour is found on the affected portions. When dried, these droplets form minute crusts and impart a rough touch to the leaves when passed between the fingers. The lesions are usually covered by saprophytic fungi, giving them a dark brown colour. In severe infections, all of the leaves are attached and premature drying results. When the affected leaves are cut and immersed in clear water in a test tube a turbid ooze of the bacterium streaming from the vascular bundles can be observed. Pathogen The bacterium is aerobic, gram negative, non-spore forming, rod with size ranging from 1-2 x 0.8-1.0 µm with monotrichous polar flagellum. Bacterial colonies are circular, convex with entire margins, whitish yellow to straw yellow colored and opaque. Favorable conditions Clipping of tip of the seedling at the time of transplanting, heavy rain, heavy dew, flooding, deep irrigation water, severe wind, temperature of 22 to 26℃ and application of excessive nitrogen, especially late top dressing. Disease Cycle Primary infection may result from the inocula overwintering in the seed, being present on the husk as well as in the endosperm. It may also survive in soil or plant stubbles and debris, and the initial inocula may be built up on the nursery seedlings. The bacterium is reported to infect some grasses like Leersia spp. which might play a role in the spread of the disease. It is disseminated through irrigation water and wind-borne rain, and hydathodes and wounds are its portals of entry. Once the bacterium becomes systemic in the vascular bundles thereafter disease symptoms may not show up until a few weeks later in transplanted seedlings and become more severe at the time of flowering. Management Grow resistant cv. HKR 120, HKR 126, IR 64. Use balanced amount of plant nutrients, especially nitrogen. Ensure good drainage of fields (in conventionally flooded crops) and nurseries.  Avoid clipping of tip of seedling at the time of transplanting. Keep fields clean - removing weed hosts and ploughing under rice stubble, straw, rice ratoons and volunteer seedlings, which may constitute sources of inoculum. Allowing fallow fields to dry to suppress inoculum in the soil and plant residues. Soaking of seeds (10-12 Kg) in 10 L of water having 10 g Emisan; 1 g Streptocycline or 2.5 g Agrimycin. False Smut Causal Organism: Ustilaginoidea virens Symptoms The disease appears in sporadic form on the ear, the fungus transforms individual ovaries / grains into greenish spore balls of velvetty appearance. Only a few spikelets in a panicle are affected. Ears individual ovaries are transformed into large velvety green masses. These are round to oval attain a size of 10mm. Glumes are not affected but covered by a membrane. Colour changes when it is exposed by breaking of membrane. Pathogen The fungus infects the young ovary which is transformed into a mass of closely united, fine, colourless hyphae. The growth of the fungus exerts pressure on the glumes and causes them to burst, it continue to grow and develop spores, the immature orange colour of which becomes brownish green at maturity. The spores are formed laterally or rarely terminally on short sterigmata on radial hyphae. The young spores are almost round and smooth but when mature they have a rough, olive green, granular coating and measure 4 to 6 µ in diameter. They germinate and produce pear shaped secondary conidia on branched and septate germ tubes. Some of green spore balls develop into four sclerotia in the centre. The sclerotia overwinter in the field and produce stalked stromata in the following season. Favourable conditions The presence of the disease is believed to be an indication of a year of good crops since environmental conditions favorable for crop production are also favorable for false smut. It is generally believed that fertilizer application at the flowering stage and cloudy days with high relative humidity favor the development of false smut during flowering and maturity. Disease Cycle The primary infection is caused mainly by ascospores produced from sclerotia. Chlamydospores play a important role in the secondary infection which is a major part of the disease cycle. Chlamydospores are air borne and are profesely present at the time of heading of rice plant. Infection of few individual grains only lends support to the presumption that the infection is floral. If the infection takes place in the early stages of flower opening the ovary is destroyed, whereas if the infection is later the grain is set, the mycelium invades the endosperm and produces masses of spores. The disease is not seed borne, but no one has succeeded in obtaining infection by artificial floral inoculation. Management Spray Tilt (propiconazole) @0.1% at boot stage. Spraying copper-oxy-chloride @ 0.25% at late booting to heading stage gave good control of false smut Fungicides used for managing other rice diseases are also effective against false smut. Khaira Due to Zinc deficiency Symptoms Usually in nursery; chlorotic/ yellow patches at leaf base on both sides of the midrib; restricted root growth and usually main roots turn brown. Management Use 25 kg ZnSO4 / ha before transplanting or sowing at time of land preparation. If crop is infected then use 1.5 kg ZnSO4 + 5 kg urea in 600-700 litre water per hectare. Tungro Causal Organism: (Rice Tungro Spherical Virus, Rice Tungro Bacilliform Virus) Symptoms Infection occurs both in the nursery and main field. Plants are markedly stunted. Leaves show yellow to orange discoloration and interveinal chlorosis. Yellow discoloration is commonly seen in “Japonica” varieties, while “Indica” varieties show orange discoloration. Young leaves are mottled while rusty spots appear on older leaves. Tillering is reduced with poor root system. The infected plants have few spikelets and panicles are small. Tungro infected leaves show dark blue streaks. Most panicles are sterile or partially filled grains and covered with dark brown blotches. Pathogen The disease is caused by two morphologically unrelated viruses: rice tungro bacilliform virus (RTBV) and rice tungro spherical virus (RTSV). RTBV has a bacilliform capsid with a circular double - stranded DNA as a genome. RTSV has an isometric capsid with a single - stranded RNA as its genome. Both the particles in plant are restricted to phloem cells. Disease Cycle Wild collateral grasses - Eleusine indica, Echinochloa colonum are the primary sources of inoculum Plants infected with RTBV alone may be symptom less or exhibit only mild stunting. RTSV enhances the symptoms caused by RTBV. Both the particles are transmitted semi-persistently by the leaf hoppers Nephotettix virescens, N. nigropictus, N. parvus, and N. cincticeps. RTSV can be acquired from the infected plant independently of RTBV, but acquisition of RTBV is dependent on RTSV. Leaf hoppers cannot acquire RTBV, unless they feed on plants infected with RTSV. Both the particles are noncirculative and nonpropagative. Both the viruses thrive in rice and several weed hosts. Ratoon from infected rice stubble serve as reservoirs of the virus. Disease incidence depends on rice cultivars, time of planting, time of infection and leaf hopper species present. Green leaf hoppers are the secondary source of infection (female hopper is more efficient over male hopper) Management Summer deep ploughing and burning of stubbles. Destroy weed hosts of the virus and vectors. Effective management, however, is limited by lack of resistant hybrid rice varieties, lack of symptoms during early development of the disease, and vector adaptation to insect resistant varieties. Observe the field diligently and ratoon or cut off infected plants. Stubbles and plant debris should be removed after harvesting by ploughing and harrowing to eliminate the inoculum. Farming communities should be organized so that planting would be synchronous to at most within one month of the general planting schedule of the locality. Detect the presence of GLH as early as possible. Set up light traps to monitor the vector population. No chemicals available to directly control the virus. However, the insect vector can be controlled by use of Carboryl @0.1%.  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.