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Crop yellowing (IRRI).
Gibberella fujikuroi Sawada Wollenworth (teleomorph)
Fusarium fujikuroi Nirenberg (anamorph)
F. moniliforme J. Sheld. (synonym)
White powdery growth of conidiophores can be seen at the base or on the lower portions of the diseased plants. Not all infected seedlings exhibit the visible bakanae symptoms; sometimes they may be stunted or appear normal. Under a stereobinocular microscope, infected seeds on a blotter paper show moderate to heavy growth of white, fluffy mycelia, often covering the entire seed. Later, growth appears powdery due to microconidia formation.
There is no other disease with similar symptoms as the bakanae disease of rice.
Bakanae is primarily a seedborne disease. Sowing ungerminated seeds in infested soil gives rise to infected seedlings. Soil temperature of 35ºC is most favorable for infection.
Application of nitrogen favors the development of the disease. Wind or water easily carries the spores from one plant to another. High temperature, ranging from 30 to 35ºC favors the development of the disease. Wind or water easily carries the conidia from one plant to another.
The bakanae disease is primarily seedborne and the fungus survives under adverse conditions in infected seeds and other diseased plant parts.
The pathogen sexually produces ascospores that are formed within a sac known as ascus. Asci are contained in fruiting bodies called ascocarps which are referred to as perithecia. The perithecia are dark blue and measure 250-330 x 220-280 µm. They are spherical to ovate and somewhat roughened outside. The asci are cylindrical, piston-shaped, flattened above, and are 90-102 x 7-9 µm. They are 4- to 6-spored but seldom 8-spored. The spores are one-septate and about 15 x 5.2 µm. They are occasionally larger, measuring 27-45 x 6-7 µm.
The anamorph form produces gibberellin and fusaric acid. Biological studies of the two substances showed that fusaric acid cause stunting and giberrellin causes elongation.
Hyphae are branched and septate. The fungus has micro- and macroconidiophores bearing micro- and macroconidia, respectively.
The microconidiophores are single, lateral, and subulate phialides. They are formed from aerial hyphae. The microconidia are more or less agglutinated in chains and remain joined or cut off in false heads. They are later scattered in clear yellowish to rosy white aerial mycelia as a dull, colorless powder. They are 1-2-celled and fusiform-ovate.
The macroconidiophores have basal cells with 2-3 apical phialides, which produce macroconidia. The macroconidia are delicate, awl-shaped, slightly sickle-shaped, or almost straight. They narrow at both ends and are occasionally somewhat bent into a hook at the apex and distinctly or slightly foot-celled at the base.
The sclerotia are 80 x 100 µm. They are dark blue and spherical. The stroma are more or less plectenchymatous and yellowish, brownish, or violet.
In Japan, the disease is found to develop in Panicum miliaceum L., barley, maize, sorghum, and sugarcane. Other alternate hosts of the disease include Leucaena leucocephala, Lycopersicon esculentum Mill. (tomato), Musa sp. (banana), Saccharum officinarum L. (sugarcane), Vigna unguiculata (cowpea), and Zea mays L. (maize).
The seeds are usually infected during the flowering stage of the crop. Severely infected seeds are discolored because of the conidia of the pathogen. Seed infectrion occurs via airborne ascospores and also from conidia that contaminate the seed during harvesting. Discolored seeds give rise to stunted seedlings, whereas infected seeds without discoloration produce seedlings with typical bakanae symptoms. Infection may also take place through spores and mycelium, which are left in the water used for soaking seeds.
The fungus infects plants through roots or crowns. It later becomes systemic, i.e., it grows within the plant but does systemically infect the panicle. The microconidia and mycelium of the pathogen are found to be concentrated in the vascular bundles, particularly the large pitted vessels and lacunae of the xylem vessels.
Infection usually occurs during seedling and tillering stages of the rice crop.
Crop losses caused by the disease may reach up to 20% in outbreak cases. For example, in Japan, a 20% to 50% loss was observed. Yield losses of 15% and 3.7% were reported in India and Thailand, respectively.
Clean seeds should be used to minimize the occurrence of the disease. Salt water can be used to separate lightweight, infected seeds from seed lots and thereby reduce seedborne inoculum. Seed treatment using fungicides such as thiram, thiophanate-methyl, or benomyl is effective before planting. Benomyl or benomyl-t at 1-2% of seed weight should be used for dry seed coating. However, rapid development of resistance against benomyl and carbendazim have been observed which may be caused by successive applications as a seed disinfectant. Triflumizole, propiconazole and prochloraz were found to be effective against strains that are resistant to benomyl and combination of thiram and benomyl.
Suparyono, JLA Catindig, NP Castilla, and F Elazegui