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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.
Individual countries have established regulatory limits, including import restrictions and grading standards for ergot in grain, flour, or feed products.
Cultural Control and Sanitary Methods
Bretag (1981) found that sclerotia buried deeper than 5 cm could not extend their stromata above the soil surface: he discussed ploughing and burial of sclerotia for control. Brown (1947) reported similar observations when sclerotia with rye seed were planted 3 inches [7.6 cm] deep.
Burning of stubble and residues reduced ergot viability and was advocated by Hardison (1980), Bretag (1985) and Johnston et al. (1991). Bretag (1985) discussed a control programme that included burning, burial of sclerotia, and planting resistant cultivars. Bretag and Merriman (1981) considered clean cultivation and planting of cultivars which have glumes that only remain open for a short time.
In pastures, cutting after grazing may control ergot (Jenkinson, 1958); cutting before heading, and cutting and removal of infected heads, may also provide control (Chester and Lefebvre, 1942).
Effect of Soil Fertility
With increased nitrogenous fertilization, the severity of ergot increases in rye (Ruokola, 1962; Golcz and Zalecki, 1977; Pandotra et al., 1986) and in triticale (Naylor and Munro, 1992). In Canada, ergot severity on wheat increased with copper deficiency (Evans et al., 1993; Solberg et al., 1995). In Finland, boron deficiency was reported to increase ergot severity (Simojoki, 1991).
Alternative Hosts as a Source of Infection
Because of the broad host range of C. purpurea, infected weed grasses, within or surrounding a field can serve as a source of inoculum. In Australia, infected ryegrass [Lolium] has provided inoculum for wheat (Bretag and Merriman, 1981). In Canada, inoculum has come from grasses surrounding grain fields (Campbell and Freisin, 1959) and all indigenous and forage grasses have been found to constitute a reservoir of ergot inoculum for rye, wheat, and barley (Campbell, 1957). In England, blackgrass [Alopecurus myosuroides] became infected and produced honeydew before anthesis in wheat (Mantle and Shaw, 1976), which increased the risk of infection in wheat (Mantle and Shaw, 1977). Weed grasses which could (A. myosuroides, A. pratensis) and could not (Arrhenatherum elatius, Dactylis glomerata, Holcus lanatus, Lolium perenne) support infection in wheat and barley were identified by Mantle and Shaw (1977). In Israel, ergot was passed from local grasses to wheat (Minz et al., 1960). In New Zealand (Latch, 1966) and the USA (Sprague, 1950), ergot is common on indigenous and forage grasses. Removing weeds may thus aid ergot control.
Resistance to ergot was reported in barley (Cunfer et al., 1974; Pageau et al., 1994a), triticale (Pandotra et al., 1988; Mellado, 1987; Pageau et al., 1994b), wheat (Platford and Bernier, 1970; Platford and Bernier, 1976; Busch et al., 1990) and Kentucky bluegrass [Poa pratensis] (Brede and Willard, 1993). Compared with traditional varieties, hybrid rye has an enhanced susceptibility to ergot (Mielke, 1993).
Control of ergot by Fusarium was reported by Cunfer (1974) and Mower et al. (1975). Hardison (1987) used monocarbamide dihydrogen sulfate (N-TAC) on the soil surface to stimulate microbial decomposition of sclerotia.
Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:
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).