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Brown Spot

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Crop infected with brown spot (IRRI).

Diagnostic summary

  • seedling mortality
  • quality and number of grains affected

  • seedlings manifest seedling blight
  • infected seedlings become stunted or die
  • infected leaves with numerous oval spots and witheryoung or underdeveloped spots are small, circular, dark brown or purplish brown dots
  • fully developed spots are brown with gray or whitish centers
  • infected panicles with brown spots
  • infected young roots with blackish lesions

  • presence of infected seeds, volunteer rice, rice debris, and several weeds
  • poorly drained or nutrient deficient soils
  • abnormal soils, which are deficient in nutrient elements
  • temperature ranging from 25-30oC
  • water stress and high humidity
  • maximum tillering up to the ripening stages of the crop

 

Full fact sheet

Brown spot

Bipolaris oryzae (Breda de Haan) Shoemaker (anamorph) Drechslera oryzae (Breda de Haan)

Subramanian & P. C. Jain (synonym) Helminthosporium oryzae Breda de Haan (synonym)

Cochliobolus miyabeanus (Ito & Kuribayashi) Drechsler ex Dastur (teleomorph)

  • Infected seedlings have small, circular or oval, brown lesions, which may girdle the coleoptile and cause distortion of the primary and secondary leaves (symptom is called seedling blight)

  • Infected seedlings become stunted or die

  • Young or underdeveloped lesions on older leaves are small and circular, dark brown or purplish brown

  • A fully developed lesion on older leaves is oval, brown with gray or whitish center with reddish brown margin

  • Lesions on older leaves of moderately susceptible cultivars are tiny and dark

  • When infection is severe, the lesions may coalesce, killing large areas of affected leaves.

  • Infected glumes with black or dark brown spots

  • Velvety appearance of lesions on infected glumes under severe conditions

  • Infected grains with black discoloration or with brown lesions

  • Infected young roots with black discoloration

 

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Brown spots on leaves

 

Brownish, circular to oval spots lesions that have a light brown to gray center surrounded by a reddish brown margin. are the most common identifying features to confirm the disease. Mycelial mats, which are black and velvety, are visible on the glumes of affected spikelets.

The lesions can be similar to blast lesions in certain rice varieties.

The fungus can survive in the seed for more than 4 years. Infected seeds, volunteer rice, infected rice debris, and several weeds are the major sources of inoculums in the field. Infected seeds give rise to infected seedlings. The fungus can spread from plant to plant and in the field by airborne spores.

The disease is common in nutrient-deficient soils and unflooded soil but rare on rice grown on fertile soils.

Abnormal soils, which are deficient in nutrient elements, or soils in a much-reduced condition in which toxic substances accumulate favor the development of the disease.

Disease development is favored by high relative humidity (86-100%) and optimum temperature between 16 and 36°C. Leaves must be wet for 8-24 hours for infection to occur. Yield losses due to brown spot epidemic in Bengal in 1942 was attributed to continuous temperature of 20-30°C for two months, unusually cloudy weather, and higher-than-normal temperature and rainfall at the time of flowering and grain-filling stages.

The fungi causing the disease occur in two states or stages. These are the asexual stage, which is called anamorph or imperfect stage and the sexual stage, which is called teleomorph or the perfect stage.

The somatic structures of the fungus consist of black velvety mycelial mats which are made up of prostrate hyphae and erect sporophores. The hyphae are abundant, branching, and anastomosing. They are dark brown or olivaceous and measure 8-15 µm or more in diameter. The sporophores arise as lateral branches from the hyphae. They change from olivaceous at the base to light ferruginous and the tip to subhyaline. The sporophores are 150-600 x 4-8 µm. Their geniculations are not always well defined. The conidia measure 35-170 x 11-17 µm. Typical conidia are slightly curved, widest at the middle and tapering toward the hemispherical apex, where their width approximates half the median width. Mature conidia are brownish with a moderately thin peripheral wall.

Aside from the rice plant, the disease also infects barley, oats, Cynodon dactylon (L.) Pers., Digitaria sanguinalis (L.) Scop., Eleusine coracana (L.) Gaertn., Leersia hexandra Sw., Panicum colonum (L.) Link, Setaria italica (L.) P. Beauv., Triticum aestivum L. em. Thell. (wheat), Zea mays L. (maize), and Zizania aquatica (wild rice).

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The infection processes start at the formation of appressoria. During this time, there is an increase in protoplasmic streaming in the host cells and the cell nuclei moved near the appressorium. It is followed by the hyphae attacking the middle lamella and penetrating the cells. The middle lamella started to separate and caused the formation of yellowish granules. Then, 2 or 3 cells died and mycelia developed in the cells. Appearance of minute spots followed.

Another observation showed that the spores or conidia germinate by germ tubes from the apical and basal cells. Germ tube is covered with mucilaginous sheath and at its tip, an appressorium is formed. The fungus directly penetrates the epidermis by the infection pegs formed under the appressoria. The germ tubes also penetrate the leaf through the stomata without producing any appressorium.

It is observed during the maximum tillering up to the ripening stages of the crop. Damage is important when infection occurs in the seed, causing the formation of either unfilled grains or spotted or discolored seeds giving rise to infected seedlings. Numerous spots or big spots on a leaf may result in blight, thus killing the whole leaf.

The disease causes blight on seedlings, which are grown from heavily infected seeds, and can cause 10-58% seedling mortality. It also affects the quality and the number of grains per panicle and reduces the kernel weight. The reduction in yield can be as high as 45% in severe infection and 12% in moderate infection. There is no loss in yield in light infection. The disease was considered to be the major factor contributing to the “Great Bengal Famine” in 1942 resulting to yield losses of 50% to 90% and caused the death of 2 million people. Epidemics in India have resulted in 14-41% losses in high yielding varieties. Under favorable environment, yield loss estimates ranging from 16 to 40% in Florida, USA was reported.

The use of resistant varieties is the most economical means of control. There are cultivars in Thailand, which are found to be resistant to the disease. Proper management of fertilizer by using silicon fertilizers (e.g., calcium silicate slag) in poor soil conditions can be used to reduce disease intensity.

Since the fungus is seed transmitted, a hot water seed treatment (53-54°C) for 10-12 minutes may be effective before sowing. This treatment controls primary infection at the seedling stage. Presoaking the seed in cold water for 8 hours increases effectivity of the treatment.

Seed treatment with captan, thiram, chitosan, carbendazim, or mancozeb has been found to reduce seedling infection. Seed treatment with tricyclazole followed by spraying of mancozeb + tricyclazole at tillering and late booting stages gave good control of the disease. Application of edifenphos, chitosan, iprodione, or carbendazim in the field is also advisable.

Selected references:

  • International Rice Research Institute (IRRI). 1983. Field problems of tropical rice. Manila (Philippines): IRRI. 172 p.
  • Nyvall RF. 1999. Field crop diseases. Iowa State University Press, USA. 1,021 p.
  • Ou SH. 1985. Rice diseases. Great Britain (UK): Commonwealth Mycological Institute. 380 p.
  • Reissig WH, Heinrichs EA, Litsinger JA, Moody K, Fiedler L, Mew TW, Barrion AT. 1986. Illustrated guide to integrated pest management in rice in tropical Asia. Manila (Philippines): International Rice Research Institute. 411 p.
  • Webster RK, Gunnell PS. 1992. Compendium of rice diseases. St. Paul, Minnesota (USA): The American Phytopathological Society. 62 p.

Contributors:

Suparyono, JLA Catindig, NP Castilla, FA Elazequi, and FA dela Peña