( 1957) concluded that blind seed in Oregon was not 

 present in inflorescences formed in fields after the 

 regular harvest because postharvest conditions in 

 Oregon are typically dry with little precipitation. 



Large numbers of apothecia can appear during wet 

 weather. Blair ( 1948) counted 20 apothecia per square 

 foot and observed subsequent severe disease develop- 

 ment during a wet season in New Zealand. Under the 

 dry conditions of 1947, no apothecia were found, and 

 subsequent disease development did not occur. 

 Hardison (1963) estimated that under favorable 

 conditions in Oregon, 100 pounds of severely infected 

 seed dispersed per acre would be expected to yield 

 10-50 apothecia per square foot. 



Wet seasons, combined with low temperatures, extend 

 the period of apothecial production and spore release. 

 However, not all apothecia are produced at the same 

 time. Some apothecia develop early, others late. 

 Under cool (13 °C), wet conditions, apothecia can be 

 produced over a 2-month time frame (Wright 1956). 

 The expected lifespan of an individual apothecium is 

 about 8-14 days, although they shrivel within a few 

 hours in a dry atmosphere (Neill and Hyde 1939). 



Temperatures of 10-16 °C and high humidity are 

 considered ideal for blind seed development (Anony- 

 mous 1948, Alderman 1992). Infection does not occur 

 under very warm (30 °C) temperatures (Alderman 

 1992). 



Calvert and Muskett (1944, 1945) were the first to 

 suggest that blind seed disease could spread from 

 infested areas to noninfested areas, based on observa- 

 tions of commercial fields and field plots planted with 

 pathogen-free seed. Additional sources of infection 

 include seed for pastures (Hardison 1945), hedgerows 

 with susceptible grasses, and waste ground (Calvert 

 and Muskett 1945). Direct observations of spore 

 movement were made by Neill and Armstrong (1955), 

 who trapped spores of G. temulenta 18 m high and at 

 ground level 1.6 km from the nearest infected field. 



The highest rate of infection occurs while florets are 

 open. The potential for infection reduces greatly 

 after flowering (Calvert and Muskett 1944, 1945; 

 Blair 1947). Corkill (1952) reported 90 percent 

 infected seed when florets were open during inocula- 

 tion, compared with 33 percent when florets were 

 closed. Cool, moist weather conditions aid dispersal, 



prolong the period of pollination (Calvert and Muskett 

 1945), and extend the period of greatest susceptibility 

 of the plant. 



Flowering in a ryegrass spike begins at the top and 

 progresses downward over about 10 days (Noble and 

 Gray 1945). Production of conidia begins within 6 

 days of infection and increases for about 16 days 

 (Alderman 1992). Consequently, infection of upper 

 florets by windborne ascospores may result in the 

 spread of subsequently produced conidia to lower 

 florets (Noble and Gray 1945) under rainy conditions. 

 Rain dissolves the slime in which conidia are embed- 

 ded and provides a vehicle for their secondary spread 

 (Neill and Hyde 1939, Calvert and Muskett 1945. 

 Hyde 1945). 



Calvert and Muskett (1945) speculated that insects 

 may be involved with transmission of the condidial 

 slime. However, no observations or data on associa- 

 tion of Gloeotinia with insects or their ability to vector 

 G. temulenta has been published. 



Infections occurring at flowering or prior to en- 

 dosperm formation resulted in seeds that are thin and 

 light in weight (Neill and Hyde 1939, Hyde 1945). 

 These infected seeds may not be capable of supporting 

 apothecial production (Wilson et al. 1945), although 

 they may support development of macroconidia (Hyde 

 1945). Abundant production of macroconidia during 

 early flowering or seed development provides inocu- 

 lum for secondary spread and subsequent disease 

 development. 



Seeds infected during the early to middle stages of 

 development are approximately normal size and 

 weight (Neill and Hyde 1939, Hyde 1945, Wilson et 

 al. 1945), and a large quantity of spores are produced 

 (Hyde 1945). Seeds infected late in development may 

 be capable of germination (Wilson et al. 1940, Calvert 

 and Muskett 1945. Hyde 1945, de Tempe 1950). 

 Fewer spores are produced from late infections than 

 from early ones (Hyde 1945). 



The potential for rapid increase in blind seed severity 

 was emphasized by Hardison (1948, 1957), who 

 noticed a rapid increase in disease over a 1- to 3-year 

 period. De Tempe ( 1966) noted that seed with a 6.3 

 percent infection rate produced a crop with 26.7 

 percent seed infection. 



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