ABSTRACT
Claviceps purpurea causes the ubiquitous ergot disease. This phytopathogenic ascomycete parasitizes ~400 species of grasses throughout the world [1], mainly rye, wheat, and barley as well as numerous forage and roadside grasses [2,3]. Such wide host range is unique in the genus, pointing to immense pathogenic potential. The fungus causes harvest losses due to replacement of host ovaries with the parasite’s resting structures, the ergot-called sclerotia. The main problem, however, is not a severe loss in seed quantity but arises from complete ruin of seed quality due to the alkaloid content of the sclerotia. These secondary metabolites induce highly dangerous or even deadly ergotism in animals and man. A contamination of crops with ergots >0.3% by weight spoils the grain even for feeding [4]. Certainly, ergot alkaloids are produced worldwide on a large scale because of their high pharmacological value [5]. For these reasons, C. purpurea has been of interest ever since, and its importance, which peaked at the unfortunate notoriety of several severe epidemics of ergotism, called St. Anthony’s fire, in the Middle Ages [6], will persist as long as cereals as the main nutritional basis to man and herbivorous livestock are affected. Around the turn of the new millennium the ergot disease even quickly increases worldwide owing to the use of highly susceptible malesterile plants [7,8]. Reduction in grain yield and quality causes the permanent necessity for an expensive cleaning of attacked cereals to maintain a minimum of purity standard. Specific measures for reliable control of ergot are limited and closely depend on an overall understanding of host and pathogen biology.
