Cochliobolus lunatus (head mould of grasses, rice and sorghum)
Identity
- Preferred Scientific Name
- Cochliobolus lunatus R.R. Nelson & Haasis
- Preferred Common Name
- head mould of grasses, rice and sorghum
- Other Scientific Names
- Acrothecium lunatum Wakker
- Curvularia lunata (Wakker) Boedjin
- Pseudocochliobolus lunatus (R.R. Nelson & Haasis) Tsuda et al.
- International Common Names
- Englishblack kernel of riceblack point of wheatblack smudge of ricebrown spot of asparaguscurvularia blight of turfcurvularia cotyledon spot of soyabeancurvularia cotyledon spot of soybeancurvularia leaf spotcurvularia leaf spot of maizefalse maize blastglume mould of riceglume spots disease of ricegrain mould of sorghumkernel rot of grasses, rice and sorghumleaf blight of Job's tearsleaf blight of riceleaf mould of grasses, rice and sorghumleaf spot of maizepecky kernel of ricered stripe of riceseedling blight of sugarcanestem disease of cassava
- Local Common Names
- GermanyStengelfaeule: Mais
- EPPO code
- COCHLU (Cochliobolus lunatus)
Pictures
Distribution
Host Plants and Other Plants Affected
Symptoms
LeafOn sorghum, leaf spots may occur that are diffuse and reddish with greyish centres.On rice, leaf spots are circular to elongate, centrally grey with dark-brown periphery within a yellow halo.On maize, small, necrotic or chlorotic leaf spots occur with a pale halo, that reach 0.5 cm diameter when fully developed.On soyabean, necrotic lesions appear on the cotyledons.SeedsC. lunata appears on sorghum grain or seeds as shiny, velvety black, fluffy growth on the surface.Infection of rice seeds by C. lunata is characterized by discoloration of the aleurone and starch layer, with the hulls becoming brown. A close association occurs between discoloration of glumes, empty glumes and discoloration of kernels. In severe infections, the rice kernel shows a black discoloration.
List of Symptoms/Signs
Symptom or sign | Life stages | Sign or diagnosis |
---|---|---|
Plants/Inflorescence/distortion (non-graminaceous plants) | ||
Plants/Leaves/abnormal colours | ||
Plants/Leaves/necrotic areas | ||
Plants/Seeds/discolorations | ||
Plants/Seeds/empty grains | ||
Plants/Seeds/lesions on seeds | ||
Plants/Seeds/mould | ||
Plants/Seeds/rot |
Prevention and Control
Cultural Control and Sanitary Methods
Disease escape is a traditional approach to controlling grain mould in sorghum. Harvesting earlier can reduce the amount of grain mould. In areas where photosensitive cultivars have been grown, grain mould is avoided when flowering and grain fill occur in the dry season. Production of sorghum seed in arid regions under irrigation also minimizes the development of grain moulds (Forbes et al., 1992).
Storing bananas at 10 or 30°C with low humidity reduced storage rot caused by C. lunatus (Ram and Vir, 1996).
Avoiding high nitrogen rates and drought stress on centipedegrass (Eremochloa ophiuroides) turf can reduce Curvularia blight (Wilson and Hanna, 1999).
Host-Plant Resistance
Extensive efforts have been made in the past 15 years to obtain genetic resistance to grain mould of sorghum. In a recent study, 66 guinea-based sorghum accessions of diverse geographical origin (Nigeria, Tanzania, Malawi, Botswana, Burkina Faso, Sierra Leone and India), comprising a range of eight races, together with controls IS9471 (red grain, resistant) and SPV104 (white grain, susceptible), were evaluated against Fusarium moniliforme, F. pallidoroseum and C. lunata using an in vitro screening technique. Fourteen accessions showed a moderate to high degree of resistance to all three pathogens, compared to SP104 (>50% mould). Seedlings of these resistant genotypes were transplanted into pots during 1992, maintained at 80% humidity and spray-inoculated with a mixed spore suspension at 50% anthesis. Genotypes IS7173, IS23773, IS23783 and IS34219 were completely resistant to mould 55 days after inoculation and a further six developed moderate to low mould growth (Singh et al., 1993).
Understanding of resistance mechanisms to grain mould is complicated because the disease is caused by a complex of pathogens. Two of the major pathogens, Fusarium moniliforme and C. lunata, infect seeds in different ways, which partially explains that resistance to the two occasionally differs (Forbes et al., 1992). A generation-means analysis of resistance to C. lunata and F. moniliforme was carried out in the parental, F1, F2 and backcross generations of eight crosses representing different combinations of susceptibility (high x high, high x low and low x low). The results indicated large dominance effects and significant epistatic effects for resistance to both pathogens. In a majority of crosses duplicate epistasis governed resistance to F. moniliforme. Additive and additive x additive effects were less important than dominance effects. It was suggested that intercrossing of early segregating material followed by selective inbreeding could improve resistance to both pathogens (Murty and House, 1984). In another study, four parental cultivars with distinct characteristics and gene markers for caryopsis traits were used as a base population to generate F1, F2 and BC1 populations at College Station, Texas, USA. These populations were evaluated for resistance to grain mould, mainly caused by F. moniliforme and C. lunata, at College Station, Texas in 1990, and at Namulonge and Serere Research Stations in Uganda in 1991. The presence of a pigmented testa (B1-B2-), a red pericarp (R-Y-), a thin mesocarp (Z-) and an intensifier gene (I-) were all dominantly inherited. A pigmented testa was the single most important trait conferring grain mould resistance. The red pericarp trait also conferred grain mould resistance, though not as much. The effect of a red pericarp was enhanced by the presence of the intensifier gene. The effects of both a pigmented testa and a red pericarp were additive. Mesocarp thickness did not play a significant role in grain mould resistance. College Station and Serere were suitable locations for grain mold evaluation (Esele et al., 1993).
Extensive resistance studies have also been made on rice. A new sheath rot disease of rice incited by C. lunata was first observed on rice cultivars in Tamil Nadu, India, at the end of the dry season (April and May) in 1990. Nearly 70% of rice plants at the boot leaf stage showed typical sheath rot symptoms. Panicles emerging from diseased plants were mostly black. In subsequent evaluations of genetic resistance, six improved cultivars (IR 50, ADT 36, ADT 38, ASD 7, ASD 8 and ASD 17) and five breeding lines (WC 8953, WC 9082, WC 9189, WC 9212 and WC 9213) derived from Oryza officinalis were completely free of the disease under both natural and artificial infection conditions. It is suggested that these genetic stocks with resistance to C. lunata can be utilized in breeding programmes (Lakshmanan, 1993). In 3 years of trials in Cuba, ears of five varieties were inoculated with a conidial suspension. At harvest ripeness the percentage of grain surface area damaged by C. lunata was measured in 20 ears of each variety. No variety showed strong resistance, but Bluebonnet and Cuba C58 were less susceptible than the others (Hermida-Laffitte and Gonzalez-Barrios, 1980).
Disease escape is a traditional approach to controlling grain mould in sorghum. Harvesting earlier can reduce the amount of grain mould. In areas where photosensitive cultivars have been grown, grain mould is avoided when flowering and grain fill occur in the dry season. Production of sorghum seed in arid regions under irrigation also minimizes the development of grain moulds (Forbes et al., 1992).
Storing bananas at 10 or 30°C with low humidity reduced storage rot caused by C. lunatus (Ram and Vir, 1996).
Avoiding high nitrogen rates and drought stress on centipedegrass (Eremochloa ophiuroides) turf can reduce Curvularia blight (Wilson and Hanna, 1999).
Host-Plant Resistance
Extensive efforts have been made in the past 15 years to obtain genetic resistance to grain mould of sorghum. In a recent study, 66 guinea-based sorghum accessions of diverse geographical origin (Nigeria, Tanzania, Malawi, Botswana, Burkina Faso, Sierra Leone and India), comprising a range of eight races, together with controls IS9471 (red grain, resistant) and SPV104 (white grain, susceptible), were evaluated against Fusarium moniliforme, F. pallidoroseum and C. lunata using an in vitro screening technique. Fourteen accessions showed a moderate to high degree of resistance to all three pathogens, compared to SP104 (>50% mould). Seedlings of these resistant genotypes were transplanted into pots during 1992, maintained at 80% humidity and spray-inoculated with a mixed spore suspension at 50% anthesis. Genotypes IS7173, IS23773, IS23783 and IS34219 were completely resistant to mould 55 days after inoculation and a further six developed moderate to low mould growth (Singh et al., 1993).
Understanding of resistance mechanisms to grain mould is complicated because the disease is caused by a complex of pathogens. Two of the major pathogens, Fusarium moniliforme and C. lunata, infect seeds in different ways, which partially explains that resistance to the two occasionally differs (Forbes et al., 1992). A generation-means analysis of resistance to C. lunata and F. moniliforme was carried out in the parental, F1, F2 and backcross generations of eight crosses representing different combinations of susceptibility (high x high, high x low and low x low). The results indicated large dominance effects and significant epistatic effects for resistance to both pathogens. In a majority of crosses duplicate epistasis governed resistance to F. moniliforme. Additive and additive x additive effects were less important than dominance effects. It was suggested that intercrossing of early segregating material followed by selective inbreeding could improve resistance to both pathogens (Murty and House, 1984). In another study, four parental cultivars with distinct characteristics and gene markers for caryopsis traits were used as a base population to generate F1, F2 and BC1 populations at College Station, Texas, USA. These populations were evaluated for resistance to grain mould, mainly caused by F. moniliforme and C. lunata, at College Station, Texas in 1990, and at Namulonge and Serere Research Stations in Uganda in 1991. The presence of a pigmented testa (B1-B2-), a red pericarp (R-Y-), a thin mesocarp (Z-) and an intensifier gene (I-) were all dominantly inherited. A pigmented testa was the single most important trait conferring grain mould resistance. The red pericarp trait also conferred grain mould resistance, though not as much. The effect of a red pericarp was enhanced by the presence of the intensifier gene. The effects of both a pigmented testa and a red pericarp were additive. Mesocarp thickness did not play a significant role in grain mould resistance. College Station and Serere were suitable locations for grain mold evaluation (Esele et al., 1993).
Extensive resistance studies have also been made on rice. A new sheath rot disease of rice incited by C. lunata was first observed on rice cultivars in Tamil Nadu, India, at the end of the dry season (April and May) in 1990. Nearly 70% of rice plants at the boot leaf stage showed typical sheath rot symptoms. Panicles emerging from diseased plants were mostly black. In subsequent evaluations of genetic resistance, six improved cultivars (IR 50, ADT 36, ADT 38, ASD 7, ASD 8 and ASD 17) and five breeding lines (WC 8953, WC 9082, WC 9189, WC 9212 and WC 9213) derived from Oryza officinalis were completely free of the disease under both natural and artificial infection conditions. It is suggested that these genetic stocks with resistance to C. lunata can be utilized in breeding programmes (Lakshmanan, 1993). In 3 years of trials in Cuba, ears of five varieties were inoculated with a conidial suspension. At harvest ripeness the percentage of grain surface area damaged by C. lunata was measured in 20 ears of each variety. No variety showed strong resistance, but Bluebonnet and Cuba C58 were less susceptible than the others (Hermida-Laffitte and Gonzalez-Barrios, 1980).
Chemical Control
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:
•
EU pesticides database (http://ec.europa.eu/food/plant/pesticides/eu-pesticides-database/)
•
PAN pesticide database (www.pesticideinfo.org)
•
Your national pesticide guide
Impact
C. lunatus is part of a complex of fungi, including Fusarium moniliforme and Phoma sorghina, and some other fungi that produce grain mould of sorghum under conditions of high rainfall and high relative humidity (Forbes et al., 1992). Grain mould has been classed as a high priority disease of sorghum in East Africa (Hulluka et al., 1992), a severe disease in Venezuela and Argentina (Teyssandier, 1992) and an occasionally important disease in the USA (Frederiksen and Duncan, 1992).Martin (1939) and Martin and Alstatt (1940) reported a new disease of rice in the USA characterized by the presence of a small percentage of jet black grains in the polished product. The primary fungus most commonly associated with the problem was C. lunata, although other fungi were also present. As the affected kernels could not be seen prior to milling it was assumed that considerable expense might be involved in removing these black grains before marketing. Three types of damage were found in commercial long-grain rice kernels: hull spotting caused by Cochliobolus miyabeanus, hull discoloration caused by insect damage and/or C. lunata; and kernels with chalky areas due to insect damage. Losses from 3.4-12.7% were associated with sustained pressure from these combined causes (Lee and Tugwell, 1980). Seed infection levels as high as 86% have been reported on rice (Ribeiro, 1980).C. lunata is also part of the complex of fungi that cause black point of wheat (Fakir et al., 1989) and discoloration of okra seeds (Kumkum-Gupta et al., 1989). Curvularia leaf spot, caused by several Curvularia species including C. lunata, is a late-season disease of maize that can cause serious losses in tropical regions. Up to 60% loss has occurred in inoculated plots (Fajemisin and Okuyemi, 1976; Grewal and Payak, 1976; Mabadeje, 1969; Mandokhot and Basu Chaudhary, 1972). It is a minor disease in temperate regions (McKeen, 1952; Nelson, 1956).
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History
Published online: 9 October 2023
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