Introduction and Historical Overview 



During the early 1920s, growers of perennial ryegrass 

 (Lolium perenne L.) seed in New Zealand were 

 troubled by poor germination of their seed crops. A 

 systematic inquiry initiated in 1923 associated re- 

 duced germination with humid conditions during seed 

 development (Foy 1927), but the cause was unknown. 

 By 1926, germination was as low as 19 percent, and in 

 the southern region of New Zealand 95 percent of the 

 seed lots tested had germination of 90 percent or less 

 (Foy 1927). Ungerminable seed had an abnormal 

 appearance characterized by opacity, roughness, and a 

 reddish caryopsis surface (Hyde 1932). These symp- 

 toms were difficult to see unless the lemma and palea, 

 which cover the caryopsis, were removed. The diffi- 

 culty in visual detection of the ungerminable (dis- 

 eased) seeds led Neill and Hyde (1939) to propose 

 "blind seed" as the common name of the disease. 



By 1932, it was apparent that a conidia-producing 

 fungus was associated with affected seeds (Hyde 

 1932), but it was not until 1937 that pathogenicity of 

 the blind seed fungus (tentatively identified as a 

 Pullularia sp.) was established (Hyde 1937). How- 

 ever, another fungus, distinct from Pullularia, was 

 also found associated with infected seed. After careful 

 study, this second fungus, not Pullularia, was found to 

 cause blind seed disease (Muskett and Calvert 1940, 

 Wilson etal. 1940). 



In 1942, after an investigation of the life history of the 

 blind seed fungus, Neill and Hyde (1942) determined 

 that a fungus called Phialea temulenta Prill. & Delacr. 

 was identical to the blind seed fungus on ryegrass in 

 New Zealand. P. temulenta was previously reported 

 on seed of rye (Seeale cereale L.) in France in 1891 

 (Prillieux and Delacroix 1891, 1892b). In 1945. 

 Wilson et al. (1945) reviewed the taxonomic place- 

 ment of P. temulenta and erected a new genus, 

 Gloeotinia, to accommodate it. Thus the blind seed 

 fungus became Gloeotinia temulenta (Prill. & Delacr.) 

 M. Wilson. Noble. & E.G. Gray. 



The effects of blind seed disease on the production of 

 grass seed can be tremendous. Germination in infected 

 seed samples has been as low as 1 percent in New 

 Zealand (Greenall 1943), 13 percent in the United 

 States (Hardison 1945), and 50 percent in Great 

 Britain (Noble and Gray 1945). Blind seed continues 

 to periodically plague growers in New Zealand (Skipp 

 and Hampton 1996), and its recent reappearance in the 



United States (Alderman 1996) has renewed interest 

 in the disease here. This monograph provides a 

 comprehensive review of our understanding of G. 

 temulenta and blind seed disease, including host and 

 geographical distribution, taxonomy, biology, and 

 control. 



Geographical Distribution and Host 

 Range 



The blind seed fungus was first recorded on infected 

 seeds of rye (Seeale cereale L.) in France in 1891 

 (Prillieux and Delacroix 1891. Neill and Hyde 1942). 

 Although first reported on rye. its subsequent occur- 

 rence on this crop is very rare. Blind seed disease is 

 primarily a problem of forage and turf grasses grown 

 for seed. 



Blind seed disease was unknown in Great Britain until 

 after its discovery in New Zealand. However, the 

 connection between blind seed and low germination in 

 ryegrass (Lolium sp.) was suspected to be of long 

 standing in Great Britain, since low germination in 

 some years was well known (Calvert and Muskett 

 1944, 1945). Proof of the long-standing occurrence of 

 blind seed was established when conidia of G. 

 temulenta were found among stored seeds from a 1 909 

 ryegrass crop grown in Ireland (Lafferty 1948). The 

 identification of blind seed disease in the United 

 States in 1944 established that the fungus was widely 

 distributed on ryegrass grown for seed, a distribution 

 likely established through the international grass seed 

 trade. 



Blind seed has been reported from Australia, includ- 

 ing Tasmania, Victoria, and New South Wales (Neill 

 and Hyde 1939, Wade 1949, Anonymous 1955, Wade 

 1957, Anonymous 1962, McGee 1971a, Munro 1978); 

 Denmark (Noble 1939. Gemmell 1940, Lafferty 1948, 

 Kristensen and Jorgensen 1960); England, including 

 Kent, Sussex, Hereford, and the Isle of Man (Neill and 

 Hyde 1939. Gemmell 1940, Glasscock 1940); Ireland 

 (Gemmell 1940, Lafferty 1948); France (Prillieux and 

 Delacroix 1891. 1892a); The Netherlands (de Tempe 

 1950, 1966); New Zealand (Gorman 1939; Neill and 

 Hyde 1939; Blair 1947. 1948; Latch 1966; Hampton 

 and Scott 1980a); Northern Ireland (Neill and Hyde 

 1939; Gemmell 1940; Calvert and Muskett 1944, 

 1945); Scotland, including Ayrshire and the Shetland 

 Islands (Neill and Hyde 1939. Gemmell 1940. Noble 

 and Gray 1945, Dennis and Gray 1954); Sweden 

 (Neill and Hyde 1939); United States, including 



