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The spread of Karnal bunt has been closely monitored since it was discovered near the city of Karnal in Punjab, India in 1931. The disease reached the Western Hemisphere in 1972 when it was discovered in the Mexican state of Sonora. The first report of Karnal bunt in the United States came from Arizona in March of 1996. A significant reduction in yield and quality is seldom associated with this disease. However, due to its mode of dissemination and control difficulties many countries have imposed strict quarantines on the importation of infected seed. In many cases, any seed produced from an area where the disease has been identified cannot be imported. The potential for economic losses as a result of import restrictions has led to an extensive Karnal bunt survey in the U.S. The causal organism is Tilletia indica Mitra = Neovossia indica (Mitra) Mundk. Common or bread wheat is the host most affected by the pathogen but durham wheat and triticale are also susceptible. There is a great deal of genetic variability within the species but researchers do not agree on the designation of specific races. The fungus survives between crops as teliospores. The spores are soil or seed-borne and can survive up to 5 years on either medium. Spores are disseminated on or in infected seed as well as on transportation vehicles and harvesting and threshing equipment. They are also windblown. Teliospores require a dormant period before they will germinate. Poor germination may last up to 9 months. After the dormancy period spores on the soil surface germinate at an optimum temperature range of 15o to 25oC. Moisture is the most critical factor in germination requiring a relative humidity of 82% or higher, preferable with the presence of free water. A basidium (promycelium) emerges from the teliospore and basidiospores (primary sporidia) are produced on this structure. Primary sporidia germinate on the soil or are wind blown to lower leaf leaves and germinate to form secondary sporidia which are forcibly ejected. Secondary sporidia can germinate and form more spores or invade host tissue. They are also wind disseminated. Infection of host plants occurs during a two- to three week period near or at anthesis. Secondary sporidia invade glumes through stomata. The fungus grows intercellularly down to the base of the glume and into developing kernels. It may or may not invade the embryo and mycelial growth is restricted by the pericarp. Infection commonly occurs in a few kernels per head and a few heads per plant. Mycelium splits and develops into teliospores in much the same way as common bunt. The mass of spores that are produced is referred to as a sorus. The sorus commonly replaces part but not the entire kernel. Teliospores remain encased in the pericarp until it is ruptures during harvest and they are released.

Bonde, M.R., peterson, G.L., Schaad, N.W. and Smilanick, J.L. 1997. Karnal bunt of wheat. Plant Dis. 81:1370-1377.
Bowden, B., McCluskey, P. and Sim. T. 1996. Karnal bunt, questions and answers. Cooperative Extension Service, Kansas State University, Manhattan, KS. MF-2220.
Mathur, S.B. and Cunfer, B.M. eds. 1993. Seed-borne diseases and seed health testing of wheat. Jordbrugsforlaget. Frederiksberg, Denmark. 168 pp.
Wiese, M.V. ed. 1987. Compendium of wheat diseases, 2nd ed. APS Press. St. Paul, MN 112 pp.
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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

Questions, Comments, Complaints and Complements?
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.