Between 1948 and 1960, 70 percent of seed samples 

 tested positive for blind seed disease; the average was 

 12 percent (Hampton and Scott 1980a). Levels of 

 infection declined after 1960. During 1976-1978, 27 

 percent of samples tested positive, with a mean of 4 

 percent infected seed. The disease declined between 

 1964 and 1974 to the point that preharvest testing was 

 stopped (Scott 1974). Hampton and Scott (1980a) 

 related decreased levels of blind seed to the increased 

 use of nitrogen fertilizers. In 1980-1990, only low 

 levels of blind seed were detected (Skipp and Hamp- 

 ton 1996). In 1993, environmental conditions were 

 favorable for blind seed development, and 100 percent 

 of seed lots were infested, with a mean of 13.5 percent 

 infected seed (Skipp and Hampton 1996). Low levels 

 of blind seed infection returned in 1995 when condi- 

 tions were again less favorable for blind seed develop- 

 ment (Skipp and Hampton 1996). 



Northern Ireland. By 1944, infection levels ranged 

 from 31 to 55 percent and were as high as 70 percent 

 in perennial ryegrass (Calvert and Muskett 1944). 

 During 1947-1948, 60-70 percent of samples had 

 trace to 60 percent infected seeds (Lafferty 1948). 



United States. In the Willamette Valley of Oregon, 

 low germination in ryegrass was first noticed in 1941 

 (Hardison 1957). Blind seed disease was positively 

 identified in 1943 (Hardison 1948, 1949). By 1944, 

 the disease was found in 85 percent of certified 

 samples (Hardison 1945), and about one-quarter of the 

 seed crop could not be certified (Hardison 1948). 



U.S. levels of infection with blind seed disease 

 declined during the late 1940s after the introduction of 

 field burning to control the disease (Hardison 1976, 

 1980). During the 1950s, blind seed increased as 

 growers explored alternatives to field burning. During 

 the 1960s, when field burning was again widely 

 practiced, blind seed occurrence returned to trace 

 levels. Low levels of the disease were detected during 

 1986-1989 (Alderman 1991a,b). 



In 199L the Oregon State legislature mandated an 

 incremental reduction in postharvest burning of grass 

 fields to a maximum of 16,000 hectares after 1997. 

 The area burned declined from about 80,000 hectares 

 in 1987 to about 28,000 in 1993 (Young et al. 1994). 

 In 1995, a high level of blind seed (20 percent infected 

 seeds) was found in several fields of tall fescue in 

 Oregon (Alderman 1996). However, surveys from 

 1995-1997 (Alderman 1999) indicate that blind seed 

 disease levels in most fields in Oregon remain low. 



Symptoms 



The seed is the only component of the host plant 

 infected by G. temulenta (Wilson et al. 1945). Infected 

 caryopses appear shriveled, rough on the surface, and 

 rusty brown or pinkish in color (Gemmell 1940, 

 Calvert and Muskett 1945, Hyde 1945, Noble and 

 Gray 1945, Wilson et al. 1945, Blair 1947). Conidia 

 accumulate on the seed surface in a spore secretion 

 (slime), which may be waxy and clear or pale pink in 

 color (Hyde 1938a) or may appear as a reddish-brown 

 crust (Calvert and Muskett 1945. Hyde 1945). Healthy 

 caryopses normally appear golden brown, plump, and 

 smooth (Calvert and Muskett 1945). However, 

 infected seeds covered by the lemma and palea are 

 difficult to discern from normal seeds (Gemmell 1940, 

 Neill and Hyde 1942, Hyde 1945). 



A consequence of blind seed infection is reduced 

 germination, and the correlation between percentage 

 of infected seed and percentage germination in 

 ryegrass is well established (Hyde 1932; Gemmell 

 1940; Greenall 1943; Calvert and Muskett 1944. 

 1945; Hyde 1945; Lafferty 1948; Chestnutt 1958; 

 Hardison 1963; de Tempe 1966; Matthews 1980). 

 Germination of infected seed is rarely greater than 10 

 percent (Gemmell 1 940. Lafferty 1948). 



Causal Agent 



The taxonomic placement of Gloeotinia is not clearly 

 established. Wilson et al. ( 1954) placed G. temulenta 

 within the family Sclerotiniaceae, based on its occur- 

 rence as a plant pathogen, presence of spermatia and 

 macroconidia, and formation of a fleshy cupulate 

 apothecium from a stroma. Although G. temulenta 

 shares many features of the Sclerotiniaceae. it devel- 

 ops only an interwoven mycelium within the infected 

 seed and does not form the true sclerotium that is 

 characteristic of the Sclerotiniaceae. Ellis (1956) 

 described Gloeotinia as structurally similar to 

 Symphyosirinia, a member of the family Leotiaceae. 

 Similar views were stated by Baral ( 1994) who 

 considered Gloeotinia and Symphyosirinia related and 

 members of the Leotiaceae, subfamily 

 Hymenoscyphoideae. In 1997, Hoist-Jensen et al. 

 ( 1997) provided data from DNA analysis that 

 Gloeotinia was distinct from other fungi within the 

 Sclerotiniaceae. These studies support the concept that 

 Gloeotina should be considered a member of the 

 Leotiaceae, subfamily Hymenoscyphoideae. 



Schumacher (1979) reported that a specimen de- 

 scribed on Bromus erectus by Quelet ( 1 883) as 



