The Morphology and Disease Cycle of Ergot Caused byClaviceps fusiformisin Pearl Millet

Publisher Website
Google Scholar
Abstract
Sclerotia of the pearl millet ergot pathogen, C. fusiformis, germinated in moist sand in the laboratory, in potted soil in the screenhouse, and in the field. Germinaing sclerotia produced 1-16 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 .times. 0.5 .mu.m. Macroconidia contained in fresh honeydew were hyaline, unicellular, fusiform, and averaged 15.9 .times. 3.9 .mu.m. Microconidia produced in chains from the tips of the germ tubes of macroconidia were globular, unicellular, hyaline, and averaged 5.9 .times. 2.5 .mu.m. 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.