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Both pre- and post-emergence blights occur with a fungal collar, containing sclerotia, around the stem.
Leaf spot occurs.
A salmon-pink fungal growth develops on the ear and later turns dull grey. Seeds are bleached and rotten. Ahmad et al. (1984) observed a mouldy growth of white mycelium, intermixed with a large number of sclerotia.
Infection usually occurs at or just below the soil surface on isolated plants scattered throughout a field. Light-brown lesions, which quickly darken, enlarge until the hypocotyl or stem is girdled. A white mat of fungal mycelia may extend several centimetres up the stem above the soil line. A sudden yellowing or wilting of plants is usually the first symptom. Leaves of infected plants turn brown, dry, and often cling to the dead stem. A leaf spot phase is characterized by circular, tan to brown, zonate lesions with dark-brown margins. Twin-stem abnormality is associated with seedling infection.
Seedlings die or turn white in patches or in short strips along a drill row. Fluffy white mycelium and small, round, tan sclerotia may be present on the soil surface at the base of affected seedlings. Blighting is severe under warm, cloudy, humid conditions either in irrigated upland rice nurseries or in dry seeded (drill seeded or dry broadcast) rice.
Early symptoms are observed as a slight yellowing of the lower leaves and water-soaking and slight darkening of the stem just below the soil line. Upper leaves subsequently become yellow and drop from the plant.
Stem and roots
The fungus invades the stem and roots, destroying the cortex. Occasionally, the pathogen attacks the vascular tissues and grows systemically upwards into the lower branches, causing a dark discoloration of the tissue. The stem is girdled at the soil line, resulting in wilting and death of the plant. A weft of coarse mycelium may form on the stem and spread into the surrounding soil organic matter and pods in contact with the soil. Spherical, brown sclerotia form on the mycelium and the base of the plant.
Early symptoms are unthrifty top growth and wilting, which later become permanent.
Infected roots become covered with thick, white strands of cottony mycelium bearing numerous spherical sclerotia. Sclerotia are white at first, later becoming tan to dark-brown. Roots decompose with a watery rot.
Symptoms are usually observed approximately 40 days following planting. Lower stem infection results in discoloured, rotten tissues, followed by the appearance of white, cottony mycelium. Spherical, brown sclerotia may be seen on the mycelia. Stem girdling by the fungus results in wilting and death of the plant. Affected plants may be dispersed throughout a row or in groups.
A white, cottony mycelial growth occurs over the surface of bases of stems and crown branches. Plant tissues above the affected area bleach to a tan colour and die. Small, light-brown, spherical sclerotia which look like mustard seeds develop on the stems and crown. Sclerotia may also be found on mycelial mats growing on debris on the soil surface.
Early symptoms include the yellowing and wilting of branches (or the entire plant if the main stem is attacked). Leaves turn dark brown and sometimes fall from the plant prematurely. Sheaths of white mycelium can be seen at or near the soil line around affected plants. Under favourable environmental conditions, mycelial growth rapidly spreads to other branches and plants.
Spherical sclerotia are produced abundantly on affected plant parts and on the soil surface. They are initially white in colour, later becoming dark brown.
Lesions produced on branches and pegs are initially light brown, becoming dark brown as the disease progresses. Infected pods are usually rotten and may be seen on plants without visible above-ground symptoms. In advanced stages of disease development, adventitious roots occasionally form on affected plants.
Cankers girdle the stem or root. If the lower stem or upper taproot is girdled, the host-plant suddenly wilts and dies. Under moist, shady conditions at the base of the dead plant, the fungus may ascend the outside of the stem 2.5 cm or more, producing a conspicuous, superficial collar of cottony-white mycelium containing several or many round-to-irregular sclerotia. The mycelium may flare out from the stem lesion, growing over the surface of the moist soil for 7.5-10.0 cm, forming successive concentric rings of sclerotia. Sclerotia appear white at first, and then turn tan to dark-brown.
Cultural Control and Sanitary Methods
Crop rotation has a strong influence on survival of A. rolfsii. Populations of viable sclerotia were highest in soil in a field in which tomatoes were planted for 3 successive years before sampling and in one in which tomatoes followed groundnut in the 2 years prior to the study. Lowest sclerotial numbers were recorded in fields in which groundnut followed maize or in which maize or sorghum was the last crop before sampling (Chima Wokocha, 1988). In another study, no sclerotia were detected in fields under maize which had been under groundnut the previous year, while 3.33 sclerotia/250 ml soil were found in groundnut fields which had been under maize the previous year (Rodriguez Kabana et al., 1974). Other crop rotation studies on groundnut have shown that the incidence of A. rolfsii infection was lower in rotation with crops such as cotton or soyabean than in goundnut monoculture (Rodriguez Kabana, 1991a, b).
In pot experiments, reduction in pre- and post-emergence death of seedlings infected by A. rolfsii was given by amendments of safflower oil cake and sunn hemp, which also increased the activity of antagonistic microorganisms (Kulkarni et al., 1995). Oat straw, castor cake and neem cake consistently reduced the disease incidence of sclerotium wilt of sunflower in soil infested with A. rolfsii. Castor cake and oat straw inhibited the formation of sclerotia in soil, while rice husk and sawdust stimulated sclerotial formation (Gautam and Kolte, 1979).
In a 2-year field experiment in India, application of nitrogen significantly controlled the disease and increased root yields of beet (Thakur and Mukhopadhyay, 1972). Covering soil with polyethylene sheets controlled A. rolfsii in Phaseolus vulgaris by 71-100% in Mexico (Esqueda Valle and Zenteno Zevada, 1991). The use of black plastic mulch also reduced the severity of the disease on bell peppers (Brown et al., 1989) and in tomato (Tu et al., 1991). Piper betle cuttings planted in plots after 5 days' solarization were free from collar rot caused by A. rolfsii (Deshpande and Tiwari, 1991). Solarization for a 6-week period during the warmest months of the summer between a spring- and autumn-grown vegetable crop could provide an additional management alternative for southern blight of tomatoes in the coastal plains of North Carolina (Ristaino et al., 1991).
Considerable work has been done on screening genotypes and cultivars of a range of crops for resistance to A. rolfsii. Resistance to A. rolfsii has been described for cultivars of alfalfa (Inami, 1988), groundnut (Branch, 1994), sweet potato (Jones et al., 1983) and tomato (Leeper et al., 1992). Other crops in which resistant lines have been detected include sugarbeet (Coe and O'Neill, 1983), cowpea (Nwakpa and Ikotun, 1988), finger millet (Eleusine coracana) (Tabosa et al., 1989), rice (Mathur, 1973) and wheat (Mishra et al., 1992).
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:
Disease caused by A. rolfsii occurs on a broad range of crops and can be of economic importance in tropical and subtropical regions of the world.
Stem and pod rots caused by A. rolfsii affect groundnut in many countries, reducing yields by 10-25%. Pod yield losses may reach more than 80% in heavily infested fields (Mehan et al., 1995). A yield-loss study of groundnut in Alabama, USA, during 1983-89, showed that yield yield was increased by an average of 10.6% and disease incidence was reduced by 52.6% in plots protected by fungicide compared with untreated plots (Bowen et al., 1992). In a survey of betel gardens in different localities in India, A. rolfsii was found to be responsible for plant losses of 42-62% (Singh and Chand, 1972).
In August 1990, soyabean plants with characteristic symptoms of southern blight caused by A. rolfsii were found in south-eastern Kansas, USA; the disease affected 10-50% of plants in localized areas (Appel and Jardine, 1992). In southern regions of the USA, losses in soyabean of 20-30% have been reported, but the disease is generally considered to be minor (Aycock, 1966). The disease has been reported as a minor problem in soyabean in Zimbabwe (Smartt, 1960).
A. rolfsii ear rot has been reported on maize only in the Himachal Pradesh region of India, and in Pakistan, where it has causes significant losses (Sharma et al., 1976, 1977). A sunflower disease survey in the mid-west of the USA during 1989 detected A. rolfsii wilt in 6% of surveyed fields (Gulya et al., 1991).