—— ae United States Department of Agriculture Agricultural Research Service Miscellaneous Publication Number 1567 November 2001 Blind Seed D Historic, archived document Do not assume content reflects current scientific knowledge, policies, or practices. United States Department of Agriculture Agricultural Research Service Miscellaneous Publication Number 1567 Blind Seed Disease Stephen C. Alderman 5S ow 2D.ClUC SS 2 lw zz 5 OR IH & bf = = ia a ba YU rr = wl [oa] Alderman is a research plant pathologist, U.S. Department of Agriculture, Agricultural Research Service, National Forage Seed Production Research Center, Corvallis, OR. YOV LIVN Vdsn EVE) Of t AE Abstract Alderman, Stephen C. 2001. Blind Seed Disease. United States Department of Agriculture, Agricultural Research Service. Miscellaneous Publication No. 1567. 36 pp. In blind seed disease, unfertilized or developing seed of susceptible grasses are colonized by the fungus Gloeotinia temulenta. Infection results in loss of seed germination. About 56 species of grasses are suscep- tible, including important forage and turf grasses such as ryegrass and tall fescue. The disease occurs in all areas of production of cool season grasses grown for seed. Germination in infected seed samples has been reported as low as | percent in New Zealand, 13 percent in the United States, and 50 percent in Great Britain. Blind seed disease continues to periodically plague growers in New Zealand, and a recent reap- pearance of blind seed in the United States has re- newed interest in the disease. This monograph pro- vides a comprehensive review of our understanding of G. temulenta and blind seed disease, including host and geographical distribution, taxonomy, biology, and control. Keywords: Disease management, disease distribution, Gloeotinia, grass seed, host range, seed production, seed quality This publication reports research involving pesticides. It does not contain recommendations for their use nor does it imply that uses discussed here have been registered. All uses of pesticides must be registered by appropriate state or Federal agencies or both before they can be recommended. Mention of trade names, commercial products, or companies in this publication is solely for the purpose of providing specific information and does not imply recommendation or endorsement by the U.S. Depart- ment of Agriculture over others not recommended. While supplies last, single copies of this publication can be obtained at no cost from USDA-ARS, National Forage Seed Production Research Center, 3450 S.W. Campus Way, Corvallis, OR 97331. November 2001 Copies of this publication may be purchased from the National Technical Information Service, 5285 Port Royal Road, Springfield, VA 22161; telephone (703) 605-6000. 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General life cycle of Gloeotinia temulenta. 14 (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 1s 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 19972), 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 |- 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. Histopathology Detailed infection studies were conducted by Wilson et al. (1945) and Neill and Hyde (1939). Infections occurred at the base of the stigma in ovaries within | week of fertilization (Wilson et al. 1945). Hyphae invaded the inner epidermis, nucellus, and embryo sac. Within 9 days, conidia were produced between inner epidermis and outer integument and appeared on the surface. The endosperm and embryo filled with hyphae. The resulting grains were as long as healthy seeds but thinner. Hyphae invaded the embryo and endosperm when infections occurred after the embryo was differentiated into scutellum, plumule, radicle, and endosperm. Neill and Hyde (1939) observed greater ramification and degradation of endosperm and embryonic tissues than Wilson et al. (1945), who observed extensive invasion of both embryonic and endosperm tissues. Wilson et al. (1945) observed hyphal penetration through the epithelial and aleurone layers, while Neill and Hyde (1939) reported that G. temulenta did not appear to penetrate cells of the aleurone layer. Sys- temic infections beyond the seed were not observed (Cunningham 1940, 1941; Neill and Hyde 1942; Wilson et al. 1945). Fungal Genetics and Physiology G. temulenta is heterothallic—it requires genetic exchange between two different mating types for sexual reproduction and subsequent production of apothecia (Griffiths 1958). G. temulenta has two mating types that are identical in all morphological features. Within each apothecium half of the as- cospores are of each mating type, arbitrarily called “a” and “b.” Apothecia will develop only after mating types a and b come into contact with one another and undergo fusion. Conidia produced following infection from an ascopore of one mating type will produce only conidia of that mating type. Genetic exchange between types can occur through transfer of macroconidia from one infected seed to another or through transfer of micro- conidia, which can develop on the seed in spring after the seed has overwintered. A conjugation tube—a device to exchange genetic information—can form between pairs of macroconidia even before either conidium germinates (Wilson et al. 1945). As ex- 16 pected from the heterothallic requirement of G. temulenta, relatively few infected seeds produce apothecia. The vegetative hyphae are uninucleate. Chromosome number in G. temulenta 1s n=15, and mitotic chromo- somes range in size from 0.25 to 1.0 um. (Griffiths 1959b). In the microconidiophores the nucleolus is lacking, RNA is low, and the level of RNA depends on the level in the subtending cells (Griffiths 1959a). Microconidia have not been observed to germinate and produce a vegetative mycelium but can serve a sexual function (Griffiths 1958). Little is known about variability in virulence of G. temulenta. Sproule and Faulkner (1974) reported variation in aggressiveness among strains of G. temulenta. Wright and Sproule (1969) reported that disease ranking of clones was the same when mixed blind seed isolates from The Netherlands or the British Isles were used. Little is known about the physiology of G. temulenta. A cold conditioning period of about 8 weeks is required to induce the apothecial phase. The metabolic pathways or mechanism associated with the induction have not been investigated. Toxicity Prillieux and Delacroix (1892a) and Prillieux (1897) described toxic properties associated with infection of rye by the asexual stage of the blind seed fungus, Endoconidium temulentum (anamorph of G. temulenta). Consumption of bread made from the flour induced dizzyness, faintness, vertigo, and an intensive stuporous state lasting for several days. Dogs, pigs, and poultry that consumed the bread became depressed, numb, and refused to eat or drink for 24 hours. The symptoms in humans and animals differed from those produced after ingestion of ergot (Claviceps purpurea) or darnal (Lolium temulentum) (Prillieux and Delacroix 1892a, Prillieux 1897). This is the only known report of toxicity from seed infected with G. temulenta. Cunningham (1958) conducted trials in which sheep were fed seed infected with G. temulenta. No abnor- mal symptoms or effects were observed. 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 $24. 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 | 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 2-200 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). Planting 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. Simi- larly, 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 maxi- mum production of apothecia occurred when fields too small for drill planting were planted by broadcast- ing seed over the soil surface. When seeds are planted more than one-half inch deep, apothecia have diffi- culty 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. temlentum is not recommended because of its potential to increase inoculum if seed becomes infected (Hardison 1949, 1957, 1963). Time of Closing (Grazing) Crops in New Zealand that are closed to grazing very early or very late in the season may yield a crop that 18 escapes peak ascospore dispersal (Blair 1947). Early closing was recommended in New Zealand by Gorman (1940), Lithgow and Cottier (1953), and Lynch (1952). Nitrogen Fertilization 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) ob- served 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 apo- thecial 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 con- cluded 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 recom- mended 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 applica- tions 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). Stand Density 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. femulenta 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 ammo- nium sulfate with nitro chalk. Fungicide Sprays 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 applica- tion 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. Harvest 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. Straw Residue Removal Since dry soil conditions are unfavorable for apoth- ecial 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 suffi- ciently chopped decompose slowly and can interfere with crop growth or development and may leave the soil wet for prolonged periods (Young et al. 1992). Postharvest Plowing Plowing infested fields reduces the area of infestation by burying much of the inoculum source—the in- fected 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). Crop Rotation 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. Field Burning The effectiveness of field burning in control of blind seed was established by Hardison (1949, 1980). Excellent control of blind seed 1s 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). Seed Cleaning Recleaning of seed lots is not very effective in reduc- ing 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 germina- tion 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, destroy- ing the screenings destroys the inoculum. Destruction of screenings infested with blind seed was advocated by Hardison (1949). Methods for Detection and Assessment Postharvest Disease Detection and Assessment Early methods of blind seed detection involved the direct observation of seed. Gemmell (1940) detected infection by looking for small pinkish spots on dehusked seed under a binocular microscope illumi- nated by direct light on a white background. At Lincoln College in New Zealand, the usual procedure was to place 100 paled seeds under magnification and examine them for infection (Blair 1947), although removing the lemma or palea to examine the caryopsis can be tedious. Sproule and Wright (1966) developed a manually operated apparatus to facilitate the re- moval of lemma and palea. Infected seeds generally appear more opaque than healthy seeds. A diaphanoscope was used to differen- tiate infected and healthy seeds based on opacity (Noble 1939, Glasscock 1940, Hyde 1945, Muskett 1948). However, opaque seeds can also occur if the seed is weathered before threshing, in which case opacity increases due to pigmentation (Gemmell 1940, Calvert and Muskett 1945, Muskett 1948). For estimation of total infection, Hyde (1945), Blair (1947), and Matthews (1980) believed that direct observations were not as reliable as placing seed in water and looking for spores under the microscope. A magnification of 1003 is suitable for examination for conidia of G. temulenta (Calvert and Muskett 1945). The lemma and palea may be removed (Calvert and 20 Muskett 1945, Hyde 1945, Sproule and Wright 1966) or left intact (Kolk and Rennie 1978). Kolk and Rennie (1978) soaked seed for 4 hours; Matthews (1980) soaked seed for at least 2 hours. The number of seeds considered to provide an accu- rate estimate of rate of infection was reported as 100 (Calvert and Muskett 1945, Blair 1947, de Tempe 1966), 200 (Hyde 1945, Matthews 1980), or 500 (Muskett 1948). Matthews (1980) referred to the soaking and examination of seed as the “soaking test.” Matthews also performed a “droplet test,” in which 100 seeds were individually soaked in drops of water on microscope slides for at least 4 hours. The drops were examined at 1003 and classified subjectively as having light, moderate, or heavy spore concentration. However, Matthews did not find a significant correla- tion between the droplet test and ungerminated seed. Rose (1945) correlated conidial numbers removed through soaking samples of 100 seeds with germina- tion rate, but high variability in the number of conidia prevented accurate prediction of germination. Hardison (1957) mixed 18 ml of seeds and 18 ml of water in 250-ml flasks, soaked the seeds for 20 minutes, then counted conidia in a 0.0063-mm* hemacytometer chamber. The number of conidia per 0.0063 mm? corresponded to five infection classes ranging from trace to heavy. One to three conidia per 0.0063 mm? corresponded to a trace infection level, and more than 30 conidia corresponded to a heavy infection. Alderman (1999) used a similar seed- washing procedure and established a linear relation- ship between the number of conidia washed from a standardized seed sample and the percentage of infected seed. Matthews (1980) described a detection method based on production of apothecia. In this test, 200 seeds were scattered over moist perlite in 14-cm-diameter petri dishes. The dishes were placed in plastic bags and stored at 5 °C for 12 weeks. Normal germinated seeds were removed. Dishes were transferred to 20 °C under a 12 hour light/12 hour dark cycle for a further 4—5 weeks. Seeds with apothecia were recorded. This procedure estimates the potential inoculum from seed, but since many infected seeds do not produce apoth- ecia, the total number of infected seeds is greatly underestimated. The number of seeds infected with viable G. remulenta can be assessed by isolating the pathogen on nutrient media. In this test, the palea are removed from the seeds, the caryoposis is surface sterilized and bisected, and the halves are plated on malt-extract agar (Neill and Hyde 1942, Calvert and Muskett 1945, Muskett 1948). Preharvest Testing Preharvest testing of blind seed was common during the 1940s in New Zealand (Scott 1974) to determine if the ryegrass seed crop should be harvested. Greenall (1943) sampled seed heads 2 weeks before harvest and found good correlation between the percentage of seed not infected (healthy seed) and germination of ma- chine-dressed seed. However, samples should be taken within | week of cutting (Hyde 1942, 1945; Lithgow and Cottier 1953; Munro 1978; Alderman 1988, 1991b). Infection can occur up to the time of cutting, so samples collected too early could underestimate postharvest infection levels. The number of seed heads believed to be representa- tive of the area was reported as 50 (Wade 1949), 300 (Hyde 1945, Osborn 1947), or 400-500 (Lithgow and Cottier 1953; Alderman 1988, 1991b). Outlook The past decade has seen considerable changes in the management of grass seed as growers moved away from open-field burning of postharvest residue. Current management practices generally include baling and removing straw residue followed by flail chopping any remaining residue. In some cases, specialized flail choppers are used on the full straw load. Some growers practice no-till planting. It is not clear what long-term effect these practices will have on development of blind seed disease. Weather’s role is significant. Several consecutive years of wet weather during flowering could be highly favorable for disease development. Surveys of blind seed disease conducted over the past decade have established the presence of a low level in Oregon. The recent appearance of a high level of blind seed in some fields of tall fescue indicates the poten- tial for development of the disease. The greatest risk will come from residue management practices that leave large numbers of seeds in the field. Practices such as field cleaning or late harvesting in which considerable seed shatter occurs will only encourage the disease under favorable conditions. Although significant yield losses are possible, it is important to keep in mind that there can be a signifi- cant drop in seed value at relatively low levels of infection. Germination rates below 90 percent can significantly reduce the value of the crop. Thus, the presence of only 5 to 10 percent blind seed can hurt profits. Table 1. Geographical and host distribution of Gloeotinia temulenta Agropyron cristatum (L.) Gaertn.: United States (Hardison 1962) Agrostis canina L.: Northern Ireland (Calvert and Muskett 1944), United States (Hardison 1962) Agrostis capillaris L. [= A. tenuis Sibth.]: United States (Hardison 1962, Alderman 1991a,b) Agrostis exarata Trin. [= A. exarata Trin. var. monolepsis (Torr.) Hitche.]: United States (Fischer 1944) Agrostis gigantea Roth: New Zealand (Blair 1947) Agrostis stolonifera L. [= A. alba L.; = A. palustris Huds.]: New Zealand (Blair 1947), Northern Ireland (Calvert and Muskett 1944), United States (Hardison 1962, Alderman 199 1a,b) Aira caryophyllea L.: United States (Fischer 1944) Alopecurus geniculatus L.: United States (Fischer 1944) Alopecurus pratensis L.: United States (Hardison 1962) Arrhenatherum elatius (L.) Beauv. ex J. and C. Presl: United States (Hardison 1962) Bromus carinatus Hook. and Arn.: United States (Hardison 1962) Bromus inermis Leyss.: United States (Hardison 1962) Bromus racemosus L.: United States (Fischer 1944) Bromus rubens L.: United States (Hardison 1962) Calamagrostis bolanderi Thurber in S. Watson [= Calamagrostis varia Bol. ex. Thurber]: Germany (Schmid- Heckel 1988) Cynosurus cristatus L.: New Zealand (Blair 1947), Northern Ireland (Calvert and Muskett 1944) Cynosurus echinatus L.: United States (Fischer 1944) Dactylis glomerata L.: United States (Hardison 1962) Danthonia californica Boland: United States (Fischer 1944) Deschampsia cespitosa (L.) P. Beauv.: United States (Fischer 1944, Hardison 1962) Elymus elymoides (Raf.) Swezey [= Sitanion hystrix (Nutt.) J.G. Sm.]: United States (Hardison 1962) Elymus glaucus Buckley: United States (Hardison 1962) Elymus lanceolatus (Scribn. and J.G. Sm.) Gould [= Agropyron dasystachyum (Hook.) Scribn.]: United States (Hardison 1962) Elymus repens (L.) Gould [= Agropyron repens (L.) Beauv.; = Elytrigia repens (L.) Nevski]: Norway (Schumacher 1979), United States (Hardison 1962) Elymus trachycaulus (Link) Gould ex Shinners [= Agropyron trachycaulum (Link) Malte]: United States (Hardison 1962) Festuca idahoensis Elmer: United States (Hardison 1962) Festuca nigrescens Lam. [= F. rubra L. var. commutata Gaud.; = F. fallax auct. non Thuill.; = F. rubra L. subsp. fallax auct. non (Thuill.) Nyman |: New Zealand (Neill and Hyde 1942, Blair 1947), United States (Hardison 1962, Alderman 199 1a,b) Festuca ovina L.: Northern Ireland (Calvert and Muskett 1944), United States (Hardison 1962) Festuca rubra L.: United States (Hardison 1962) Festuca trachyphylla (Hackel) Krajina [= F. ovina var. duriuscula (L.) Koch]: United States (Hardison 1962) Glyceria borealis (Nash) Batsch.: United States (Fischer 1944) Holcus lanatus L.: New Zealand (Blair 1947), Northern Ireland (Calvert and Muskett 1944), United States (Fischer 1944, Hardison 1962) Hordeum marinum Hudson subsp. gussoneanum (Parl.) Thell. [= H. hystrix Roth]: United States (Fischer 1944) Hordeum murinum L. subsp. leporinum (Link) Arcang. [= Hordeum leporinum Link]: United States (Hardison 1962) Hordeum vulgare L.: United States (Hardison 1962) Lolium arundinaceum (Schreber) Darbysh. [= Festuca arundinacea Schreb.; = F. elatior L.]: New Zealand (Neill and Hyde 1942, Blair 1947), United States (Hardison 1962; Alderman 1988, 1991a,b) Lolium giganteum (L.) Darbysh. [= Festuca gigantea (L.) Vill.]: United States (Hardison 1962) Table 1. Geographical and host distribution of Gloeotinia temulenta Continued Lolium multiflorum Lam.: Denmark (Lafferty 1948), Ireland (Lafferty 1948), Scotland (Noble and Gray 1945), New Zealand (Hyde 1938b, Lafferty 1948, Latch 1966), Northern Ireland (Calvert and Muskett 1944, 1945), United States (Hardison1962) Lolium perenne L.: Australia (Anonymous 1955, 1962; Wade 1957; McGee 1971a; Munro 1978), Denmark (Gemmell 1940, Lafferty 1948, Kristensen and Jorgensen 1960), England (Neill and Hyde 1939, Gemmell 1940, Glasscock 1940), Ireland (Gemmell 1940, Lafferty 1948), Netherlands (de Tempe 1950, 1966), New Zealand (Gorman 1939; Hyde 1942; Blair 1947, 1948; Lafferty 1948; Hampton and Scott 1980a; Neill and Hyde 1939, 1942), Northern Ireland (Neill and Hyde 1939, Calvert and Muskett 1944), Scotland (Neill and Hyde 1939, Gemmell 1940, Noble and Gray 1945, Dennis and Gray 1954), Sweden (Neill and Hyde 1939), United States (Fischer 1944; Hardison 1962; Alderman 1988, 1991a,b) and Wales (Neill and Hyde 1939) Lolium pratense (Hudson) Darbysh. [= Festuca pratensis Huds.]: Northern Ireland (Calvert and Muskett 1944), New Zealand (Neill and Hyde 1942) Lolium temulentum L.: New Zealand (Neill and Hyde 1942), United States (Fischer 1944, Hardison 1962) Lolium temulentum L. subsp. remotum (Schrank) A. and D. Love [= Lolium remotum Schrank]: United States (Hardison 1962) Phleum pratense L.: United States (Fischer 1944, Hardison 1962) Poa ampla Merr.: United States (Hardison 1962) Poa arachnifera Torrey in Marcy.: United States (Hardison 1962) Poa compressa L.: United States (Hardison 1962) Poa nemoralis L.: United States (Hardison 1962) Poa pratensis L.: New Zealand (Blair 1947), Northern Ireland (Calvert and Muskett 1944), United States (Hardison 1962, Alderman 1991a,b) Poa secunda J. Pres subsp. juncifolia (Scribner) Soreng [= P. juncifolia Scribn.; = Poa nevadensis Vasey ex Scribn.]: United States (Hardison 1962) Poa trivialis L.: New Zealand (Blair 1947), Northern Ireland (Calvert and Muskett 1944), United States (Hardison 1962) Psathyrostachys juncea (Fisch.) Nevski [= Elymus junceus Fisch.]: United States (Hardison 1962) Pseudoroegneria spicata (Pursh) A. Love [= Agropyron inerme (Scribn. and J.G. Sm.) Rydb.; =A. spicatum (Pursh) Scribn. and J.G. Sm.]: United States (Hardison 1962) Secale cereale L.: France (Prillieux and Delacroix 1891), Germany (Rehm 1900), New Zealand (Neill and Hyde 1942), United States (Hardison 1962) Thinopyrum intermedium (Host) Barkworth and D.R. Dewey [= Agropyron intermedium (Host) P. Beauv.; = A. trichophorum (Link) Richt.; = Elytrigia intermedia (Host) Nevski]: United States (Hardison 1962) Vulpia myuros (L.) C.C. Gmelin [= Festuca myuros L.]: United States (Fischer 1944, Hardison 1962) Table 2. Relative susceptibility of grass species to Gloeotinia temulenta Relative Subfamily Tribe Species Infection Arundinoideae Danthoneae Danthonia californica Boland none Pooideae Aveneae Agrostis canina L. none to light Agrostis capillaris L. [= A. tenuis Sibth. none to heavy Agrostis stolonifera L. [= A. alba L.: =A. none to moderate palustris Huds. ] Aira caryophyllea L. var. capillaris (Host) none Mutel [= Aira elegans Willd. ex. Gaudin] Alopecurus aequalis Sobol. none Alopecurus arundinaceus Poir. in Lam. none Alopecurus pratensis L. none to light Anthoxanthum odoratum L. none Arrhenatherum elatius (L.) Beauv. ex J. none to trace and C. Pres] Avena fatua L. none Avena sativa L. none Deschampsia cespitosa (L.) P. Beauv. none to trace Holcus lanatus L. none to light Phalaris aquatica L. {= Phalaris tuberosa L.] none Phalaris arundinacea L. none Phleum pratense L. none to light Trisetum flavescens (L.) Beauv. none Trisetum spicatum (L.) Richter none Poeae Cynosurus cristatus L. none Dactylis glomerata L. Festuca idahoensis Elmer Festuca ovina L. Festuca rubra L. Festuca rubra subsp. fallax Thuill [= F. rubra L. var. commutata Gaud. | Festuca trachyphylla (Hackel) Krajina (= F.ovina var. duriuscula (L.) Koch) Lolium arundinaceum (Schreber) Darbysh. (= Festuca arundinacea Schreb.; = F. elatior L.) Lolium giganteum (L.) Darbysh. [= Festuca gigantea (L.) Vill.] Lolium multiflorum Lam. Lolium perenne L. Lolium pratense (Hudson) Darbysh. [= Festuca pratensis Huds.) Lolium temulentum L. Lolium temulentum L. subsp. remotum (Schrank) A. and D. Love (= Lolium remotum Schrank) none to trace none to heavy none to heavy none to moderate none to trace light light to heavy none to heavy heavy heavy light heavy heavy Table 2. Relative susceptibility of grass species to Gloeotinia temulenta Continued Relative Subfamily Tribe Species Infection Poa ampla Merr. trace to heavy Poa arachnifera Torrey in Marcy none to heavy Poa compressa L. heavy Poa nemoralis L. heavy Poa palustris L. none Poa pratensis L. none to heavy Poa secunda J. Presl |= P. canbyi (Scribn.) trace to heavy Howell] Poa secunda J. Presl subsp. juncifolia light to heavy (Scribner) Soreng [= P. juncifolia Scribn.; = P. nevadensis Vasey ex Scribn.] Poa trivialis L. none to heavy Vulpia myuros (L.) C.C. Gmelin light to heavy [= Festuca myuros L.]| Triticoideae Bromeae Bromus arvensis L. none Bromus carinatus Hook. and Arn. none to trace Bromus catharticus Vahl none Bromus commutatus Schrad. none Bromus erectus Huds. none Bromus hordaeceus L. {= B. mollis L.} none Bromus inermis Leyss. none to trace Bromus madritensis L. none Bromus marginatus Nees in Steud. none Bromus polyanthus Scribn. in Shear none Bromus rigidus Roth none Bromus rubens L. none to trace Bromus secalinus L. none Bromus squarosus L. none Bromus tectorum L. none Triticeae Aegilops cylindrica Host none Agropyron fragile (Roth) Candargy [= A. none sibiricum (Willd.) P. Beauv.; = A. fragile (Roth) Candargy subsp. sibiricum (Willd.) Melderis] Agropyron cristatum (L.) Gaertn. trace Elymus canadensis L. none Elymus caninus (L.) L. [= Agropyron none caninum (L.) Beauv. ] Elymus elymoides (Raf.) Swezey |= Sitanion trace hystrix (Nutt.) J.G. Sm.] Elymus glaucus Buckley light Elymus lanceolatus (Scribn. and J.G. Sm.) trace to light Gould [= Agropyron dasystachyum (Hook.) Scribn. | Table 2. Relative susceptibility of grass species to Gloeotinia temulenta Continued Relative Subfamily Tribe Species Infection Elymus repens (L.) Gould [= Agropyron trace repens (L.) Beauv.; = Elytrigia repens (L.) Nevski] Elymus sibiricus L. none Elymus trachycaulus (Link) Gould ex trace Shinners [= Agropyron trachycaulum (Link) Malte] Elymus trachycaulus (Link) Gould ex none Shinners subsp. subsecundus (Link) A. and D. Léve[= Agropyron subsecundum (Link) A.S. Hitchce. | Hordeum brachyantherum Nevski none Hordeum bulbosum L. none Hordeum marinum Hudson subsp. none gussoneanum (Parl.) Thell. [= H. hystrix Roth] Hordeum murinum L. subsp. leporinum none to trace (Link) Arcang. [= Hordeum leporinum Link] Hordeum vulgare L. none to trace Leymus triticoides (Buckley) Pilg. none [= Elymus tritcoides Buckley | Pascopyrum smithti (Rydb.) A. Love none [= Agropyron smithiti Rydb.] Psathyrostachys juncea (Fisch.) Nevski none to heavy [= Elymus junceus Fisch. | Pseudoroegneria spicata (Pursh) A. Love trace to moderate [= Agropyron inerme (Scribn. and J.G. Sm.) Rydb.; = Agropyron spicatum (Pursh) Scribn. and J.G. Sm.] Secale cereale L. none to heavy Thinopyrum intermedium (Host) Barkworth trace and D.R. Dewey [= Agropyron inter- medium (Host) P. Beauy.; = A. trich- ophorum (Link) Richt.;= Elytrigia inter- media (Host) Nevsk1] Triticum aestivum L. none Source: Based on data from Hardison (1962). 26 References Alderman, S.C. 1988. Distribution of Gloeotinia temulenta, Claviceps purpurea, and Anguina agrostis among grasses in the Willamette Valley of Oregon in 1988. Journal of Applied Seed Production 6:6—10. Alderman, S.C. 1991a. Assessment of ergot and blind seed diseases of grasses in the Willamette Valley of Oregon. Plant Disease 75:1038—1041. Alderman, S.C. 1991b. Distribution of Claviceps purpurea, Gloeotinia temulenta, and Anguina agrostis among grasses grown for seed in Oregon in 1989. 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