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.
The search for resistance to blind seed began shortly after discovery of the disease. Early investigations in New Zealand compared indigenous grasses to commercial 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 flowering (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 resistance 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) concluded that more than one gene was involved in resistance. Wright and Faulkner (1982) used a backcross 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.
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 establishment 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).
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 obtained in dry years when little disease develops.
Prillieux (1897) reported that in France the disease was scarce on rye (Secale cereale L.), but recommended that, where the disease is present, seed from regions free of contamination be used for planting.
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 minutes 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 2-2½ 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). However, modern systemic fungicides such as benomyl have proven effective as a seed treatment (Hardison 1970, 1972; McGee 1971b). In New Zealand, seed treatment with fungicides has proven effective and is recommended for control of blind seed disease (Rolston and Falloon 1998).
Calvert and Muskett (1944) reported that seed samples from fields sown with a high level of blind seed did not on average show a higher rate of infection than seed from fields sown with disease-free seed. Similarly, de Tempe (1966) found no association between severity of blind-seed-infected seed at planting and subsequent level of infection at harvest. However, the effect of infected seed introduced at the time of planting depends on the method of planting and planting depth. Hardison (1957) observed that maximum production of apothecia occurred when fields too small for drill planting were planted by broadcasting seed over the soil surface. When seeds are planted more than one-half inch deep, apothecia have difficulty reaching the soil surface (Hardison 1949, 1957). Good preparation of the seed bed facilitates planting at the proper depth and good coverage of seed (Hardison 1949, 1963).
Fields with heavy soils or poor drainage may be more favorable for blind seed development because they provide the prolonged moist conditions that are favorable for production of ascospores. Good soil drainage provides conditions that are less favorable for apothecial production (Hardison 1949, 1963).
Infected seed must undergo a cool, moist period for about 8 weeks to induce the reproductive (apothecial) phase of the pathogen. Wright (1956) found that when seed was planted in spring, apothecial production did not occur; the requirement for cold conditioning was not met. Similar results were reported by Fischer (1944), who detected no apothecia when seed was planted in spring but found 75.6 apothecia per square meter in fall-planted seed.
Planting a susceptible first-year companion crop such as L. temulentum is not recommended because of its potential to increase inoculum if seed becomes infected (Hardison 1949, 1957, 1963).
Crops in New Zealand that are closed to grazing very early or very late in the season may yield a crop that escapes peak ascospore dispersal (Blair 1947). Early closing was recommended in New Zealand by Gorman (1940), Lithgow and Cottier (1953), and Lynch (1952).
Numerous studies indicate a reduction in blind seed in response to manure or nitrogen fertilization. Chestnutt (1958) and Rutherford (1956) reported a significant reduction in blind seed in manured plots, compared with unmanured plots of perennial ryegrass. Lynch (1952) and Lithgow and Cottier (1953) observed that nitrogen improved yield and germination, although the effect of nitrogen on blind seed was uncertain. In a paired-plot experiment, Stewart (1963) found blind seed levels decreased in plots treated with nitrogen compared with untreated plots.
Hampton and Scott (1980a) established that a decline in blind seed between 1960 and 1980 in New Zealand correlated with the increased use of nitrogen fertilizer. In field trials, they demonstrated that as nitrogen rate increased, the rate of blind seed infection decreased, a result also reported by Hampton (1987) and de Filippi et al. (1996).
Under laboratory conditions, Hampton and Scott (1980a) observed that urea directly suppressed apothecial formation. However, in field plots, Hampton and Scott (1981) found no significant differences in number of apothecia among field plots treated with various levels of urea, although a reduction in blind seed infection was observed in urea treatments. They concluded that nitrogen fertilization altered the physiology of the plant, enhancing resistance to G. temulenta (Hampton and Scott 1980b).
In subsequent studies de Filippi et al. (1996) examined the level of blind seed in adjacent irrigated and nonirrigated field plots to which various rates of urea had been applied. In irrigated field plots, nitrogen application significantly reduced blind seed disease, but this did not occur in nonirrigated plots. As the inoculum source was external to the trial, they concluded that plants which are able to utilize available nitrogen develop a greater capacity to resist blind seed. The mechanisms associated with this resistance need to be determined.
Hampton (1987) reported there was no advantage to a split application of nitrogen (fall, spring) and recommended that all nitrogen be applied in spring. Blind seed levels in the study were lowest when all of the spring nitrogen was applied at spikelet initiation.
In addition to increasing resistance, nitrogen applications can also increase lodging or increase stand density, providing a physical barrier to restrict spore movement up through the canopy (Gorman 1940, Noble and Gray 1945, Blair 1947).
Movement of ascospores upward through ryegrass stands is believed to be reduced in a dense canopy, in stands that lodge, or where clover is planted with the ryegrass (Gorman 1940, Noble and Gray 1945, Blair 1947). Hampton (1987) reported that as lodging increased, blind seed disease decreased.
Lynch (1952) and Lithgow and Cottier (1953) found no evidence that germination was related to crop density or the extent of bottom growth, although they noticed improved germination in crops that lodged or those with increased percentages of grass in the sward. Wilson et al. (1945) observed that a ryegrass crop which remains standing until harvest was more likely to become infected by G. temulenta than a dense, heavily lodged crop. Noble and Gray (1945) found that acidic soils could contribute to poor stands of ryegrass and recommended replacement of ammonium sulfate with nitro chalk.
Under field conditions, fungicides applied as foliar or inflorescence sprays were not demonstrated effective in blind seed control by Corkill and Rose (1945), Hair (1952), or Hardison (1970). However, recent research from the Foundation for Arable Research (Rolston and Falloon 1998) has established that fungicides such as tebuconazole or carbendizim are effective for blind seed control in New Zealand.
Sprays applied as soil drenches or to the soil surface have been shown effective in reducing the number of apothecia. McGee (1971b) observed that benomyl applied at 2.8 and 5.6 kg/ha reduced apothecia 80 and 90 percent, respectively. Hardison (1970) eliminated apothecia during April and May with a single application of benomyl (4.5 kg/ha) applied the previous November, December, or January. Hardison (1972, 1975) lists other fungicides effective against G. temulenta under greenhouse conditions.
Since the primary source of inoculum is the infected seed, early harvest to avoid excessive seed shatter is recommended. Osborn (1947) suggested early harvest under dry conditions as a source of disease-free seed, since late season disease could develop with a change in the weather to wet conditions. In Oregon, there is a narrow window of time in which swathing can occur to avoid seed shatter and obtain optimum seed yields.
Removal of lightweight or infected seeds during harvest reduces inoculum left in the field. Hardison (1949, 1957, 1963) recommends adjusting combines to retain lightweight seeds for removal from fields.
Since dry soil conditions are unfavorable for apothecial development and spore release, Hardison (1949) recommended removing the straw after harvest to allow the soil surface to dry more rapidly in spring. In Oregon, residue is commonly baled and removed from the field. In some cases the straw is finely chopped with specialized flails. Residues that are not sufficiently chopped decompose slowly and can interfere with crop growth or development and may leave the soil wet for prolonged periods (Young et al. 1992).
Plowing infested fields reduces the area of infestation by burying much of the inoculum source--the infected seeds (Hardison 1963). Hardison (1949) recommended plowing in Oregon before May 15 to prevent emergence of apothecia near the time of flowering in ryegrass. The effectiveness of plowing in control of blind seed in Oregon was demonstrated by Hardison (1949, 1957, 1963).
Blair (1947) reported that less infection occurred in stands following 3-4 years of arable crops, suggesting that rotation with crops not susceptible to blind seed may provide a means to reduce inoculum within a field.
The effectiveness of field burning in control of blind seed was established by Hardison (1949, 1980). Excellent control of blind seed is achieved with postharvest field burning. For optimal control, the entire dry-straw residue should be open burned. Burning by propane flaming after residue removal (baling) is not as effective as open burning, since propane does not achieve the temperatures of open-grass burning (Johnston et al. 1996).
Recleaning of seed lots is not very effective in reducing the level of blind seed (de Tempe 1966). Hampton et al. (1995) reported that cleaning to a higher seed weight by removing infected seeds improved germination for some seed lots with a high level of infection; but in lots with a low level of blind seed, cleaning simply removed small but viable seed. A relationship between seed weight and germination could not be established.
Since infected seed are present in screenings, destroying the screenings destroys the inoculum. Destruction of screenings infested with blind seed was advocated by Hardison (1949).
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Original posting: October 2001.