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Common bunt has been recognized as an infectious disease since the 1700's. The disease is also referred to as stinking smut or covered smut. Despite advances in control measures the disease continues to be a threat to wheat producers, especially in areas where seed treatment is not practiced. Bunt can reduce the quantity and quality grain. It also poses a health and safety hazard to field workers. The spores are an allergen to many people and large masses of spores easily become ignited causing explosions in harvesting and threshing equipment and storage units. Two fungi serve as causal organisms of the disease: Tilletia caries (DC.) Tul. & C. Tul. = T. tritici (Bjerk.) G. Wint. in Rabenh. and Tilletia laevis Kuhn in Rabenh. = T. foetida (Wallr.) Liro. Wheat is the primary host but triticale, barley, rye and several grasses may occasionally serve as hosts. The process of genetic recombination leads to a great deal of variability in virulence within these fungal species. A few races of the fungi have been identified but it is almost impossible to keep track of all the different races because they are constantly changing. This fact also makes breeding for plant resistance nearly impossible. The fungi overwinter as teliospores on seed and may also survive in the soil. Soil survival is most important when winter wheat is produced in an area with arid summers. Teliospores germinate and form a basidium (promycelium) in cool moist soil. The basidium gives rise to haploid (1n) basidiospores, also known as primary sporidia. These spores exist in different mating types that fuse via lateral conjugation hyphae. An H-shaped structure called a dikaryon (2n) is formed. Infectious hyphae or secondary sporidia are produced from the dikaryon. Secondary sporidia are forcibly ejected and germinate to form infectious hyphae or form more sporidia. Infectious hyphae invade coleoptile tissue directly through the cuticle before they emerge from the ground. Teliospore germination, production of infectious hyphae and host penetration occur at a soil temperature range of 40-60oF and soil moisture at 15 to 60% field holding capacity. The fungus invades the terminal meristem (growing point) and grows systemically in the host both inter- and intracellularly. Mycelia invade the developing ovary and replace the tissue that would normally form in the pericarp. The mycelium then splits off into dark, thick-walled fragments that develop into teliospores and a bunt ball is created. Each bunt ball may contain 1-4 million teliospores. These structures are easily ruptured during harvest and release spores that infest soil, seed, and harvesting equipment. Storage facilities also become contaminated when filled with infected seed. One cycle of bunt occurs per season. Fall seeded wheat may become infected from soil-borne teliospores if soil conditions have r emained dry during the summer and are cool at the time the seed is germinating. If viable teliospores are not present in the soil, seed borne spores are the primary source inoculum. Common bunt also occurs on spring seeded wheat but infection is less frequent and less damaging than it is on fall seeded crops. Infection with common bunt increases susceptibility to winter injury and other diseases including yellow stripe rust and seedling blights while it increases resistance to powdery mildew.

Agrios, G. N. 1978. Plant Pahtology, 2nd ed. Academic Press, New York. 703 pp.
Holton, C.S. and Tapke, V.F. 1953. The smuts of wheat, oats, barley. Pages 360-368 in Plant diseases, the yearbook of agriculture 1953. U. S. Dept. of Agriculture, Washington, D.C. House Document No. 122.
Mathur, S.B. and Cunfer, B.M. eds. 1993. Seed-borne diseases and seed health testing of wheat. Jordbrugsforlaget. Frederiksberg, Denmark. 168 pp.
Watkins, J.E. and Prentice, L.J. 1997. Diseases affecting grain and seed quality in wheat. Cooperative Extension Service, Institute of Agriculture and Natural Resources, University of Nebraska - Lincoln. EC97-1874.
Wiese, M.V. ed. 1987. Compendium of wheat diseases, 2nd ed. APS Press. St. Paul, MN. 112 pp.
The most obvious symptoms of common bunt are visible on the head. Most people are on the lookout for bunt galls and may miss the more subtle symptoms that occur on the flowers. Several changes take place in the appearance of floral structures when they become infected by these fungi. Pistils are longer while stamens are shorter than normal. Stamens also fail to extrude at flowering time. The anthers change in color from a healthy green to pale yellow. Infected ovaries, the site of teliospore production, are longer and wider than normal and are green instead of white.
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This page was researched and drafted by: Jane Christensen, Department of Plant Pathology, University of Nebraska-Lincoln
Disease images were provided by: Dr. David Wysong, Department of Plant Pathology, University of Nebraska-Lincoln

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This page is authored and maintained by:
Dr. J.E. Partridge, Department of Plant Pathology, University of Nebraska-Lincoln
Copyright (C) 2003 J.E. Partridge, University of Nebraska-Lincoln. All Rights Reserved.