Biology and Epidemiology
Overwintering and Production of Apothecia
The general life cycle of G. temulenta is illustrated in figure 14. The overwintering, or survival, unit of G. temulenta is the infected seed. Infected seeds reach the soil by shattering, by seed loss during harvest operations, by planting of diseased seeds, and by natural seed dispersal in harvested areas (Hardison 1945). Infected, ungerminable seeds resist attack by bacteria and molds and do not decay as they overwinter (Neill and Hyde 1939; Calvert and Muskett 1944, 1945).
At or near the soil surface, G. temulenta continues to develop within the seed. Moist soil conditions with temperatures near 2 °C for about 8 weeks are required to induce the sexual (apothecial) stage of G. temulenta (Griffiths 1958). The precise biochemical changes that occur or metabolic pathways affected during this conditioning have not been determined.
In spring or early summer, at or prior to flowering of perennial ryegrass, apothecia emerge from the overwintering infected seeds (Calvert and Muskett 1945, Wilson et al. 1945). Usually one to three, but as many as seven, apothecia can emerge from a single infected seed (Gray 1942, Calvert and Muskett 1945). Not all infected seeds will yield apothecia. In fact, only 5-30 percent of ungerminated seed produce apothecia (Calvert and Muskett 1945, Griffiths 1958).
Production and Release of Ascospores
(Primary Inoculum) and Primary Infection
Large numbers of ascospores are ejected from each apothecium in response to slight changes in relative humidity (Calvert and Muskett 1945). In New Zealand, spore release occurs between early November and middle December, with peak numbers coinciding with flowering in perennial ryegrass (Neill and Armstrong 1955). Most spores are airborne between 10:00 a.m. and 2:00 p.m. (Johnston et al. 1965).
Ascospores that land on flowers, including the stigma, ovary, or styles, will germinate and infect the host. However, seeds can be infected up to the time they reach their maximum size (Hyde 1937).
Within about 7 days (Hyde 1937, 1945; Wilson et al. 1945) to 16-17 days (Calvert and Muskett 1945) after inoculation, the conidial stage is manifest--a pinkish slime in which conidia are embedded. These spores are relatively short-lived, about 1 month (Cunningham 1941, Neill and Hyde 1942). However, a few conidia may survive as long as 4-6 months if stored under cool, dry conditions (Calvert and Muskett 1945).
Disease Development and Spread
Wet seasons, especially during anthesis in the grasses, are clearly supportive of blind seed infection (Foy 1927; Gorman 1940; Osborn 1947; Blair 1947, 1948; Lithgow and Cottier 1953; Chestnutt 1958; de Tempe 1966; Grant 1985). Based on field surveys in New Zealand, Lithgow and Cottier (1953) found that districts which produced ryegrass seed with high germination (low blind seed disease) had less than half the rain days during flowering than districts producing seed with low germination. Hardison (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 development 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 is 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 (Anonymous 1948, Alderman 1992). Infection does not occur under very warm (30 °C) temperatures (Alderman 1992).
Calvert and Muskett (1944, 1945) were the first to suggest that blind seed disease could spread from infested areas to noninfested areas, based on observations 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 inoculation, 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 embedded 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 association of Gloeotinia with insects or their ability to vector G. temulenta has been published.
Infections occurring at flowering or prior to endosperm 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 inoculum 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 1- 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.
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Original posting: October 2001.