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On leaves, elliptical or spindle-shaped lesions (0.5-1.5 x 0.3-0.5 cm), with pointed ends and grey or white centres; dark-green to reddish-brown margins, sometimes with a yellow halo. Under humid conditions, abundant conidia are produced on lesions. In cases of severe infection, lesions coalesce, killing the leaves. Leaf sheaths dry up and whole plants may be killed. Severely infected fields have a scorched appearance.
On resistant rice cultivars, hypersensitive spots or small, round to elliptical, brown lesions are formed.
On leaf collars, rotting may result in premature leaf fall. On lower nodes, rotting causes 'white heads'.
On panicles, all parts of the rachis, rachilla and grains may be infected. Most often, the basal node of the panicle is infected, resulting in 'neck rot' or 'rotten-neck' and 'white heads'. Bluish-grey fungal growth and sporulation occurs over infected regions. Early infection results in white heads or partially filled heads; late infection after grain filling, in 'broken necks'.
Control of rice blast is usually necessary to prevent crop losses or total failure of susceptible cultivars grown under conditions that are favourable to the pathogen.
Resistant Crop Cultivars
Host cultivars that are resistant against leaf and panicle blast have been the most widely used method of disease control (Bonman et al., 1992), but resistance (mainly race-specific resistance) has tended to be ephemeral because of pathogen adaptation. Forms of 'partial resistance' (Marchetti, 1994; Roumen, 1994) have been identified but are little understood or used. Cultivars with multiple genes for blast resistance (Marchetti et al., 1996) and 'durable' forms of resistance in hybrid rice (Zhou-ShaoChuan et al., 1999) have been described as offering better hopes of sustained activity against the pathogen.
Advances in understanding the molecular genetics of the pathogen (e.g. Leung and Taga, 1988; Shi-ZhiXin et al., 1998; Talbot, 2003; Wilson and Talbot, 2009; Yi and Valent, 2013), the increasing availability of fertile lines, and advances in mapping resistance genes in the host (McCough et al., 1994; Chen et al., 1999; Ballini et al., 2008) together with knowledge of virulence and avirulence genes in the pathogen (Leong et al., 1994; Liu et al., 2010; Huang et al., 2014) and pathogen population structures (Chin, 1985; Zeigler et al., 1994; Zeigler, 1998; Saleh et al., 2014) have improved our understanding of interactions between the rice host and the blast pathogen and should lead to the development of more durable forms of resistance. Marker-aided selection of resistance from recombinant populations have provided new tools for rice breeding and resulted in improved genetic analysis of resistance (Inukai et al., 1996).
Host resistance is likely to be more durable when deployed in appropriate rice cultivar mixtures (Chin and Husin, 1982; Mundt, 1994; Zhu et al., 2000), as a result of the 'mixture effect', consisting of reduced inoculum, barrier and induced resistance (Chin and Wolfe, 1984). Nakajima et al. (1996a, b) regarded the same effects as being responsible for effectiveness of multilines for the control of blast.
Note that cultural methods are unlikely to be implemented in isolation from other agronomic considerations.
Avoid excessive levels of nitrogenous fertilizer (Prabhu et al., 1996) and moisture stress to crops in order to help reduce disease severity. Field sanitation and synchronized planting reduce carryover and/or spread of disease (see Biology and Ecology). The effects of plant density are variable: although closer planting favours the microclimate for disease, plants have less available nitrogen for the fungus. Silicon soil amendments (Kozaka, 1965; Thiagalingam and Chin, 1976; Seebold et al., 2001) are known to increase host resistance to attack. In Madagascar, disease severity was significantly lower in a no-tillage cropping system than in the conventional tillage system (Sester et al., 2014).
Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:
Rice blast, because of its capacity to reduce yields, is currently the most important disease of rice worldwide and threatens food security (Pennisi, 2010). Pinnschmidt et al. (1994) reviewed knowledge on the relationship between blast infection and yield losses.
Severe attack can completely destroy rice nurseries and crops at the tillering stage. Later leaf attack stunts plants and reduces the number of bearing panicles and the weight of individual grains. Infection of stem nodes results in barren panicles; late neck infection (after grain filling) results in 'broken necks'. Losses of up to 70% have been recorded in fields attacked by neck blast (Chin, 1975). In the same manner, infection of the panicle results in chalky kernels, sterile grains or losses at harvesting. Panicle and neck blast also reduces head rice milling yield, bulk density of the grain and increases fissured kernels (Candole et al., 1999). Additionally, attack of leaf collars results in premature leaf death and loss of photosynthetic capacity. Other studies have revealed that leaf blast increases plant respiration and reduces the maximum photosynthetic rate at light saturation and the initial light use efficiency (Pinnschmidt et al., 1994).
Formerly, rice blast was recognized in relation to the rice growth stage affected: seedling blast, leaf blast and neck and node blast. Seedling blast occurs in seedbeds. Infected leaves have many small, brown, oval lesions. At advanced stages, leaves and leaf sheaths are dead. Severe infections results in the death of large patches of seedlings. In leaf blast, lesions appear on the leaves, particularly near the upper end. Collar blast is commonly found and leaves may break from the sheath as a result of rotting at the junction of leaf and sheath. Collar blasted leaves also seem to have a shorter lifespan than unaffected leaves (Pinnschmidt et al., 1994). Neck and node blast occur in nearly mature plants. No grain is formed when these lesions develop early. Later development of lesions results in the production of poorly developed grain. These are the most destructive forms of disease (Disthaporn, 1994).
In China during 1980-1990, between 6 and 12% of the rice crop was annually infected by blast (Shen and Lin, 1994). Countrywide annual losses ranged from 0.1-2.2%. Changes in cultural practice in China were the cause of the development of rice blast from being a regional disease in 1950-1960 to one that threatened China with nationwide disaster in the 1970s. By the late 1970s and early 1980s, epidemics began occurring nationwide. In 1985, leaf blast affected 12% of national rice acreage and neck blast another 12%. In 1984 and 1985, rice blast was widespread in the prefectures which consisted about 40% of China's rice area. The average loss of early season rice due to blast in 1981-1990 was 27.2 kg/ha (ca 0.53% of average yields in those years). Late season loss was ca 0.23% of average yields in this period. The greatest loss was recorded in 1985 and amounted to 130 kg/ha or ca 2.2% of the average yield in China (Shen and Lin, 1994).
In Japan, annual losses averaged 2.5% over the period 1967-1987 (Kushibuchi, 1987); in 1994, leaf and panicle blast occurred in over 900,000 ha of rice (Anon, 1994). Previous losses due to blast were recorded for 1953, 1960 and 1962; 1953 was an epidemic year in which ca 800,000 tonnes were lost. Annual losses during 1953 to 1960 varied from 1.4% to 7.3% (average 2.98%). In 1960 the estimated loss in yield was 273,000 tonnes. In 1962, panicle blast developed on 721,000 of the 909,000 hectares sprayed with chemicals; leaf blast occurred over an area of 865,000 ha, of which 847,000 had been sprayed (Ou, 1985).
In Korea Republic between 1983 and 1992, major outbreaks of leaf blast occurred on 62,000-193,000 ha annually. Yield loss due to blast was estimated as 5.6% in 1960, 4.2% in 1970, 3.9% in 1980 and 0.02% in 1990 (Kim, 1994).
Blast is a major disease in Bangladesh on dry seedbeds and sandy soils (Miah et al., 1985).
Padmanabhan (1965) reported that 266,000 tonnes (0.8% of total yield) of rice were lost in India in 1960/61. Field experiments conducted in Madhya Pradesh in 1991-92 revealed that disease incidence increased with increasing nitrogen levels but decreased with increasing potash applications (Sangar and Singh, 1998). Experiments in Himachal Pradesh revealed that fungicide applications reduced leaf and neck blast and increased yields by ca 43% compared with the untreated controls (Sood and Kapoor, 1997). In Tamil Nadu, Murugesan et al. (1995) reported that application of potash significantly reduced disease incidence and resulted in higher yields in Eleusine coracana. In Karnataka an increase of 1% infection in neck and finger infection in E. coracana resulted in an increase of 0.32 and 0.084% in yield losses. Grain yield losses ranged from 6.75 to 87.5% in the period 1976-1985 (Rao, 1990). In Uttar Pradesh, losses in E. coracana were drastic when the disease appeared within 10 days of ear emergence. Considerable losses incurred even when infection took place up to 20 days after ear emergence (Bisht et al., 1988). In Bangalore, a field experiment revealed that the yield of infected E. coracana plants was ca 54% that of healthy plants. Grain from infected plants was small and shrivelled, which accounted for a further 21% loss during processing. The total crop loss was 64% (Rao and Hegde, 1986). Other field tests reported that estimated yield losses due to blast were ca 29% (Rao and Hegde, 1985).
During the 1992 epidemic in Thailand, over 200,000 ha of rice were damaged. Over 60% of plants had panicle blast. Subsequently, 60% of total yield was confirmed to be lost due to the disease, equivalent to ca 650 000 tonnes of paddy rice. In addition, the government allocated US$10 million for paddy seeds and fertilizers to be given to farmers whose crops had been damaged (Disthaporn, 1994).
Blast is also considered to be the most serious disease of rice in West Africa, where losses of 3-14% (Sierra Leone) and over 77% (Liberia) have been recorded. In Cote d'Ivoire, grain yield losses of 0.5 to 58.5% have been recorded in farm trials (Fomba and Taylor, 1994). Blast incidence and damage vary according to the different rice environments in West Africa. It is particularly common and destructive in upland environments and is far less severe in inland valley swamp (IVS)/paddy. Seedling blast can, however, cause major problems in IVS/paddy. Complete desiccation and total loss have been recorded in drybed nurseries established on uplands for transplanting in mangrove swamps. In riverain grassland, blast incidence is low because the land consists of wide expanses of open land allowing free air movement. In the Sahel, blast is rarely a problem because of the low relative humidity, lack of prolonged wetness on aerial surfaces and temperature extremes (Fomba and Taylor, 1994). In Uganda, losses on E. coracana were studied over two seasons. Significant losses were recorded on susceptible lines during the first and second rainy seasons and averaged 55% (Bua and Adipala, 1995). In western Kenya, blast is the major rainfed rice disease, giving grain yield losses of up to 50% (Ombakho, 1995).
In the USA, observations have indicated a significant reduction in bulk density and head rice yield due to blast. Blast reduced kernel bulk density by 140 kg/cubic m and head rice yield by 12%. The incidences of unfilled, chalky and fissured kernels in diseased samples were higher by 30, 21 and 7%, respectively, than in blast-free samples (Candole et al., 1999). A serious disease outbreak was also recorded on golf course fairways in Pennsylvania. Turfgrass loss due to the disease was over 90% in several golf courses (Uddin et al., 1999). In the first year, ca 16,700 ha of cultivar Newbonnet were damaged, of which 13,000 sustained losses of 25% or less. Yield reductions of 26-50% were sustained over 2350 ha and yield reductions of 50% or more were sustained over 1242 ha. In 1987 and 1988, blast was widespread and an estimated 10% yield reduction occurred state-wide. In spite of these losses, state yields were exceptional for these periods (Lee, 1994). TeBeest and Guerber (1998) report that rice blast is present each year in Arkansas, and can reach epidemic proportions on susceptible cultivars.
Although upland rice is more susceptible than lowland rice, Teng (1994) considered that, overall, rice blast causes more yield loss in cool-season tropical and temperate lowland rice because the latter (lowland rice) is responsible for 93% of world production.
Thresholds and estimates for losses have been calculated. In Thailand, the threshold for leaf blast control is suggested by doing a diagonal sampling of 10 tillers/0.16 ha, recording blast incidence of the top four leaves or on leaf 3. Fungicides are applied when >70% of the leaves are infected (Disthaporn, 1994). In Hokkaido, Japan, a regression model showed that apparent yield loss should not occur when the disease affects <5% of panicles. The author proposes this level as the yield loss threshold (Takeuchi, 1997). Katsube and Koshimuzo (1970) reported that for every 10% of neck blast, there was a 6% yield reduction and a 5% increase in chalky kernels, which lowered the rice quality by one or two classes. The gross income loss was estimated at 7-9%. Other methods for estimating losses and models for predicting losses are described in detail by Luo et al. (1997), Pinnschmidt et al. (1994) and Torres and Teng (1993).