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 reduced 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 symptoms were difficult to see unless the lemma and palea, which cover the caryopsis, were removed. The difficulty in visual detection of the ungerminable (diseased) 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). However, 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 et al. 1940).
In 1942, after an investigation of the life history of the blind seed fungus, Neill and Hyde (1942) determined that a fungus called Phialeatemulenta Prill. & Delacr. was identical to the blind seed fungus on ryegrass in New Zealand. P. temulenta was previously reported on seed of rye (Secale cereale L.) in France in 1891 (Prillieux and Delacroix 1891, 1892b). In 1945, Wilson et al. (1945) reviewed the taxonomic placement 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.
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Original posting: October 2001.