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The following points highlight the two major diseases of rice. The diseases are: 1. Nigrospora Disease of Rice 2. Brown Spot of Rice.
Disease # 1. Nigrospora Disease of Rice:
The disease of rice has widespread occurrence in the rice-growing tracts of the world. The occurrence of the disease in India has been reported by Thomas (1937), Padwick (1938), Padmanabhan (1949), Chattopadhyay and Sen Gupta (1952) and Kar (1966). A similar condition of rice plants has been recorded from other countries; Thompson from Malaya, Kimura from Martin from the Unites States.
Symptoms:
Dark streaks and powdery spots of variable dimensions are visible on the surface of leaf blades, sheathing leaf petioles, and the glumes of grains (Fig. 376A—C). A similar diseased condition is also seen on young leaves which remain partly enclosed within the sheathing petioles, and on immature grains of rice.
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Closer examination reveals that the streaks are minute dark pustules developed in linear series and coalescent pustules form the powdery spots (Fig. 376B). The pustules are more prevalent along furrows than the ridges of the host surface. The dark pustules are powdery masses of conidia developed by the mycelium of the pathogen that has already gained entrance in the host tissue.
Causal Organism:
The disease is caused by the fungus Nigrospora oryzae (Berk, and Br.) Petch, 1924. The fungus possesses characteristic septate mycelium which is hyaline when young, becoming dark with age. The ultimate branches of the mycelium bear conidiophores either laterally or terminally.
The conidiophores are short, simple, and inflated below the tip; exhibiting a jar-shaped appearance (Fig. 376F). Each conidiophore produces apically a solitary conidium. The conidia are dark, one-celled, globose to sub-spherical, and smooth-walled with distinct dark pigment. Dimensions of conidia range from 10.5 to 14µ, by 11.5 to 15µ.
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Behaviour of pathogen within the host:
The infection is very superficial, specific, and localized. The pathogen gains entrance through stomata. The activity of the pathogen is restricted particularly along the outer layers of the parenchyma with very little tendency to penetrate deeper (Fig. 376D). The mycelium ramifies along the parenchymatous tissue and produces sporodcchium-like bodies after rupturing the host tissue (Fig. 376E).
The sclerenchyma adjoining the parenchyma remains unaffected. The pathogen induces mild infection resulting little damage to the host tissue. The conidia, conidiophores, and the myceliim produce an unsightly appearance of the host surface.
Control:
Since the disease causes very little damage to the rice crop one can get by without taking any notice of it. Still it is always advisable to use disease-free seeds.
Disease # 2. Brown Spot of Rice:
Brown spot of rice (Oryza sativa L.), also known as Helminthosporium disease of rice is distributed in almost all the rice-growing tracts of the world. But it occurs most severely in South-East Asia, Japan, the Philippines, and the Southern parts of the United States.
In India, the disease was first reported in 1922 and since then it has been recorded to cause damage to rice crop in eastern and southern rice-growing regions of the country. It occurs in an epiphytotic form in States of Andhra Pradesh, Assam, parts of Kerala and Mysore, and West Bengal.
Besides causing heavy leaf spotting, the severity of the disease may reduce yield when ears may be sterile and grain formation may be stopped. The infected seeds have very poor germination rate.
Symptoms:
The disease attacks all parts of the host, usually excepting the roots, in all stages of development.
There may be complete failure of seed germination or the seedlings may succumb to the disease before they emerge out of the soil. In emerged disease affected seedlings, necrotic lesions appear in the coleoptile when its tip turns brown to dark-brown and the infection spreads to the mesocotyl and ultimately the seedlings are completely destroyed.
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It has been reported that in infected rice seedlings, the pathogen produces a toxin (Cochliobolin) which inhibits the growth of the roots and affects respiration of leaves.
The most conspicuous symptom of the disease is the appearance of discrete, dark-brown, ellipsoidal to eye-shaped spots on the upper surface of the leaves (Fig. 377A). The spots often vary in size and shape. They appear in the form of very small brown areas surrounded by a yellowish halo and gradually increase in size turning dark-brown.
Along with the increase in size, the spots also increase in number very rapidly. A fully developed spot has a greyish-brown central portion surrounded by a deep, reddish-brown margin and may be as big as 4-6 mm in dimension.
Some of the spots coalesce to form irregular patches of brown discolouration. When the infection is severe, the affected leaves become greyish-brown and show considerable drying and wilting causing severe damage to rice crop. The symptoms also develop on leaf sheath and culm which turn dark-brown with velvety surface for being covered with the conidiophores of the pathogen.
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In case of severe attack the ears fa.il to emerge from the sheaths and perish without further development. Again in cases where the ears have already emerged from the sheaths become distorted.
The disease may also cause damage to the grains. Lesions on the glumes first appear close to margins of the outer and inner glumes and gradually dark-brown spotting spreads over the entire surface (Fig. 377B) causing brown discolouration of the kernels inside. The quality of grain is also affected.
Depending on the stage of development of the grains, there may be complete sterility or partial filling up of the grains. In case of severe infection no grain formation takes place and the ears become sterile.
Causal Organism:
The disease is caused by Helminthosporium oryzae Breda de Haan, the conidial stage of Cochliobolus miyabeanus (Ito and Kuribay) Drechsler ex Dastur.
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The fungus produces septate mycelium which ramifies inter- and intracellularly in the host tissue. It produces erect rigid conidiophores which arise in tufts through the stomata and at times through the ruptured epidermis or wounds. The conidiophores are short or long, septate, simple or branched, dark-brown to olivaceous at the base and somewhat paler at the growing tip.
Under suitable atmospheric condition, mycelial mat may be developed externally over the surface of the spots, and conidiophores may also arise from such mycelial mat. The conidiophores produce conidia successively on new growing points (Fig. 377C). The points of attachment of successive conidia are marked by scars at regular intervals on the conidiophores.
Conidia are slightly curved tapering towards the rounded ends and are only transversely septate. They are olivaceous brown and are extremely variable in size and number of septation (Fig. 377C & D).
The perfect stage of the causal organism has been obtained under cultural conditions in Japan and in the diseased stubbles in Mexico, but has not yet been found in India.
Disease Cycle:
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The pathogen perennates both externally and internally in the seeds (as conidia externally and internally as mycelium), as well as in straw and stubble. It has also been reported .that two graminaceous plants Leersia hexandra and Echinochloa colona are the collateral hosts. Besides these, some of the rice field weeds (Cyanodon dactylon and Setaria italica) often help in the perennation of the pathogen.
The source of primary inoculum is conidia on the surface of the seeds and mycelium inside the seed. Along with the germination of the diseased seeds the perennating organs (conidia and mycelium) of the causal organism become active and cause infection on the seedlings.
This is the starting point of the disease. Continuous rainy days accompanied with cloudy weather and temperature range of 28- 30°C. are ideal for the development and spread of the disease.
The disease is disseminated by wind and rain. Entrance of the pathogen in the host tissue may be by direct penetration of host epidermis or through stomata. Conidia on germination produce germ tube which is surrounded by a thick mucilaginous substance which enables the germinating conidia to remain adhered to the host surface.
The germ tube then swells to produce an aspersorium from which infection hyphae are developed. The infection hyphae then enter the host tissue either through stomata or by rupturing through epidermis. Immediately after the entrance in the host tissue, the infection hyphae produce more hyphae which ramify along the intercellular spaces of the mesophyll.
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Disease symptoms usually appear within 24 hours of infection.
Maximum development of spots is in shade and with relative humidity of 92 per cent, or more. Sunlight retards the growth of the spots. Under favourable condition, hyphae produce conidiophores which emerge out through stomata of the host tissue.
The emerging conidiophores produce a succession of conidia which are disseminated by wind and rain and on coming in contact with susceptible host induce infection. The air-borne conidia arising from primary infection produce secondary infection of the leaves and grains. Host plants become more susceptible to infection.
Deep sowing resulting in slow emergence of seedlings favours high pre-emergence loss and good seedling infection. Plants growing under conditions of deficiency of nitrogen are extremely susceptible to infection. Susceptibility of infection of the plants also increases when grown in potash deficient soil. Rice plants are most susceptible to tire disease at the flowering stage.
Disease cycle of Brown Spot of rice is presented in Figure 378.
Control:
Since the pathogen is both internally and externally seed-borne, it is very difficult to make the seeds absolutely disease-free.
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The rate of disease incidence can, however, be reduced by the following control measures:
1. Destruction of diseased stubbles and other plant parts by burning.
2. Eradication of collateral graminaceous and rice field weed hosts.
3. Seeds should be obtained from an area where no disease incidence has been reported.
4. Seed treatment with fungicides like Agrosan GN (3 gm. in 1 kg. seeds) or Ceresan or with Aureofungin followed by foliar sprays with copper sulphate.
5. Soaking seeds for 48 hours in 1: 1000 dilution of Uspulan reduces disease incidence.
6. As the pathogen is sometimes internally seed-borne, hot water treatment at 55°C. for ten minutes pre-soaking in cold water for 8 hrs. gives better control than chemical seed disinfectants.
7. Seeds germinated in antibiotics Nystatin and Griseofulvin gives some resistance to the seedlings though these antibiotics are often toxic to the seedlings.
8. Cultural practices like the application of optimum nitrogen fertilizer and sowing and transplanting at optimum dates reduce the intensity of the disease.
9. Dissemination of secondary inoculum can be controlled by spraying fungicides like Bordeaux mixture (5:5: 50) or 0.2 per cent. Dithane Z-78 at regular intervals. Dusting with organo-mercuric dusts containing 0.1 per cent, mercury often produces effective results. Spraying or dusting operation has to be done 3 to 4 times between tillering and emergence of inflorescence.
10. The use of resistant varieties is by far the best way to control the disease incidence. As resistance is controlled by a larger number of genes, it is difficult to obtain completely resistant varieties.
