Disease Management 



The survival propagule of G. temulenta is the infected 

 seed. Control measures center around removing as 

 many infected seeds as possible from the field during 

 harvest and avoiding introduction of infected seed by 

 using disease-free or treated seed. Maintaining a 

 healthy stand through good fertilization practices also 

 contributes to control of blind seed. An integrated 

 approach to blind seed control should consider disease 

 resistance, field location, seed source, seed treatments, 

 planting, time of closing, fertilization, stand density, 

 fungicide sprays, methods of harvest, postharvest 

 residue management (straw residue removal, 

 postharvest plowing, crop rotation, field burning), and 

 postharvest seed cleaning. 



Disease Resistance 



The search for resistance to blind seed began shortly 

 after discovery of the disease. Early investigations in 

 New Zealand compared indigenous grasses to com- 

 mercial grasses (Hyde 1932, Calvert and Muskett 

 1944, Corkill and Rose 1945, Blair 1947). Differences 

 in susceptibility were attributed to timing of flowering 

 and favorability of climatic conditions during flower- 

 ing (Gorman 1939, Gemmell 1940, Calvert and 

 Muskett 1945, Corkill 1952, Wright 1956). 



Early attempts at breeding ryegrass for resistance to 

 G. temulenta were confounded by high variability and 

 inconsistent results (Corkill 1952). Corkill and Rose 

 (1945) examined progeny of crosses of resistant and 

 susceptible ryegrass plants and concluded that resis- 

 tance or susceptibility to the disease was inherited. 

 Sproule and Faulkner (1974) reported that resistance 

 was quantitative and repeatable across environmental 

 conditions and fungal strains. Wright (1967) con- 

 cluded that more than one gene was involved in 

 resistance. Wright and Faulkner ( 1982) used a back- 

 cross program to introduce resistance to G. temulenta 

 into S24 perennial ryegrass. Cultivars Calan and 

 Logan were found to have significantly greater 

 resistance than S24. Unfortunately, little resistance is 

 believed to be present in most cultivars of perennial 

 ryegrass and tall fescue now grown commercially for 

 seed. 



Field Location 



Locating fields away from infested fields to avoid the 

 introduction of inoculum from nearby sources is 

 recommended (Blair 1947, 1948, 1952; Hardison 

 1949; Lithgow and Cottier 1953). To prevent estab- 



lishment and persistence of infected seed, grazed areas 

 not kept for seed should be topped when seed heads 

 appear (Blair 1948). Surrounding fields with crops 

 such as cereals or root or forage crops may provide a 

 barrier to movement of spores into a field (Blair 

 1947), although long-distance (more than 1 km) 

 airborne movement of ascospores can occur (Neill and 

 Armstrong 1955). 



Seed Source 



Since infected seed is the source of inoculum, planting 

 disease-free seed is recommended (Calvert and 

 Muskett 1944; Blair 1947, 1948; Hardison 1949). 

 Osborn (1947) and Blair (1948) suggested that in New 

 Zealand supplies of disease-free seed could be ob- 

 tained in dry years when little disease develops. 



Prillieux (1897) reported that in France the disease 

 was scarce on rye (Secale cereale L.), but recom- 

 mended that, where the disease is present, seed from 

 regions free of contamination be used for planting. 



Seed Treatments 



G. temulenta has limited survival in seed stored dry. 

 Seed stored for 18 (Blair 1947), 21 (Calvert and 

 Muskett 1945), or 20-22 months before spring 

 planting (Hardison 1949, 1957) and 24 months before 

 fall planting (Hardison 1949, 1957; Wade 1955) is 

 considered safe to plant. 



Calvert and Muskett (1944, 1945) controlled blind 

 seed with a hot water treatment that included either a 

 4-hour pretreatment with tepid water, then 15 minutes 

 at 50 °C, or no preimmersion treatment and 30 min- 

 utes at 50 °C. The treatments provided full control 

 with little or no reduction in seed germination. After 

 hot water treatment, infected seeds decayed in the soil 

 (Calvert and Muskett 1944). Untreated infected seeds 

 resisted decay. De Tempe (1966) reported complete 

 blind seed control with no effect on germination when 

 seed was treated with water at 45-46 °C for 2-2DD 

 hours. Gorman (1940), however, reported lack of 

 adequate control from hot water treatments. 



Numerous fungicides have been evaluated for their 

 efficacy as seed treatments for blind seed disease. 

 Although Hair ( 1952) reported some success, most of 

 the early research indicated that chemicals applied as 

 seed protectants were not effective against blind seed 

 disease (Gorman 1940; Calvert and Muskett 1944, 

 1945; Blair 1947; de Tempe 1966; Hardison 1975). 



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