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Etiology

The Morphology and Disease Cycle of Ergot Caused by Claviceps fusiformis in Pearl Millet. R. P. Thakur, Plant pathologist, Pearl Millet Improvement Program, International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), PO: Patancheru, A.P. 502324, India; V. P. Rao(2), and R. J. Williams(3). (2)(3)Research associate and principal pathologist, respectively, Pearl Millet Improvement Program, International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), PO: Patancheru, A.P. 502324, India. Phytopathology 74:201-205. Accepted for publication 18 August 1983. Copyright 1984 The American Phytopathological Society. DOI: 10.1094/Phyto-74-201.

Sclerotia of the pearl millet ergot pathogen, Claviceps fusiformis, germinated in moist sand in the laboratory, in potted soil in the screenhouse, and in the field. Germinating sclerotia produced one to 16 fleshy stipes each with a globular capitulum which contained pyriform perithecia. Asci contained in perithecia were long with an apical pore. Ascospores trapped on cellophane tape and greased microscope slides averaged 127.7 0.5 μm. Macroconidia contained in fresh honeydew were hyaline, unicellular, fusiform, and averaged 15.9 3.9 μm. Microconidia produced in chains from the tips of the germ tubes of macroconidia were globular, unicellular, hyaline, and averaged 5.9 2.5 μm. The primary disease cycle of ergot was shown to begin with airborne ascospores discharged from the germinating sclerotia and infecting pearl millet at flowering. Honeydew appeared 6- 7 days after inoculation with ascospores and contained numerous macroconidia which play an important role in secondary spread of the disease. Conidia-to-conidia cycle took 4- 6 days, and matured sclerotia were observed 20- 25 days after inoculation.

Additional keywords: Pennisetum americanum.