Claviceps purpurea (ergot)

Ergot disease, caused by C. purpurea, is characterized by the presence of elongated, straight to curved, black to purplish-black bodies emerging from the glumes. Each ergot is one to several times longer than the host seed. The honeydew stage precedes the sclerotial stage and is characterized by the appearance of drops of clear to amber or tan liquid (honeydew) which exude from the infected flower.

Losses from ergot can occur through direct seed replacement, increased sterility of neighbouring spikelets (Seymour and McFarland, 1921; Kossobutzky, 1929) and reduced kernel weight (Brentzel, 1947; Harper and Seaman, 1980) due to diversion of host nutrients at the expense of adjacent florets (Corbett et al., 1974; Bacon and Luttrell, 1981). Alderman et al., (1998) showed that during 1991-1993, ergot (caused by C. purpurea) was detected in 36, 44 and 62%, respectively, of fields of Kentucky bluegrass (Poa pratensis) grown for seed in central Oregon, USA. Relatively few fields (2 to 13%) had a high (more than 20 sclerotia/g seed) level of ergot. Ergot severity (percentage sclerotia by weight) in 1991-1993 was estimated at 0.85, 0.07, and 0.34%, respectively. Percentage seed replaced by ergot in 1991-1993 was estimated at 0.22, 0.02 and 0.08, respectively. Recleaning of seed to reduce ergot contamination and to meet purity standards resulted in a 7.8% reduction in marketable seed weight. Estimated value of seed replaced by ergot in 1991, 1992 and 1993, was US $75,625, $4758 and $17,076, respectively. Estimated value of seed lost during recleaning in 1991, 1992 and 1993 was US $37,669, $8171 and $21,964, respectively. Weed grasses supporting ergot at the time of harvest of P. pratensis were species of Bromus, Secale, Festuca and Poa. However, very few seed heads of weed grasses were infected and they appeared to contribute little to ergot development in central Oregon. Most infested fields (with more than 1 sclerotium/g seed prior to recleaning) or weed grass sites with ergot were located in the southern range of the area of study.In Canada, yield losses due to ergot in 1972-1976 were less than 0.1% (Harper and Seaman, 1980). Trace levels of ergot were reported in wheat in 1992 (Bailey et al., 1993) and in 1994 (Alain, 1995).In England, UK, rye, wheat and barley samples from 1918 to 1941 were examined and, in 16 out of 23 years, ergot contamination in rye exceeded 10% (Weston and Taylor, 1942). In samples of rye, wheat and barley from 1918 to 1957, ergot content varied in all years, but Marshall (1960) did not consider it as an important problem.In Brazil (Lucca-Filho et al., 1999) 100 samples of seed lots of Lolium multiflorum from 26 seed-producing counties in Rio Grande do Sul, Brazil, were examined for the presence of C. purpurea sclerotia. The results indicate that the pathogen is widely spread in the seed-producing counties. Ninety-two percent of the examined seed samples were contaminated with sclerotia, ranging from 0.001 to 0.314% of the seed sample weight.The sclerotia (ergots) of C. purpurea contain numerous alkaloids that are toxic to animals and humans. Cases of ergot poisoning (ergotism) in animals and humans have been well documented (Mantle, 1969; Bové, 1970; Lorenz, 1979). Ergotism can occur through consumption of ergot-contaminated feed or grain products or during grazing of infested pastures.Standards for ergot levels in grains or flour for human consumption are established in all countries, and the inspection and grading standards are designed to protect consumers from ergot toxins. Commercial wheat and rye flour may contain low concentrations of alkaloids but do not pose a health risk (Scott and Lawrence, 1980). Risk may be associated with infested locally grown grains, especially rye, where grading standards are not enforced (Lorenz, 1979). Alkaloids are stable during processing, cooking or baking (Fajardo et al., 1995).