Agriculture Reference
In-Depth Information
transport costs. With low value, high volume cereal seed, isolating seed production
may not be practical or economic and healthy crops may become infected during
seed production if high levels of inoculum are present in neighbouring crops. Rennie
and Cockerell (in Yarham and Jones, 1992) have shown how barley seed may
become infected with P . graminea 200 m from an inoculum source.
13.3 CASE STUDIES
13.3.1 Bunt of wheat ( causal agent Tilletia tritici )
Teliospores of the pathogen are present on the surface of contaminated wheat grains.
Many lodge in the dorsal crease. When the seed is sown, the teliospores germinate to
produce a promycelium. Infection hyphae then penetrate between and through the
cells of the coleoptile in the germinating seedling, eventually reaching and invading
the young growing point. Mycelium of the fungus is then carried upwards in the
inflorescence as the wheat plant grows and, at flowering, the fungus multiplies
rapidly to produce a mass of teliospores within the pericarp. The resulting
teliospores are protected by the pericarp which is usually broken when the crop is
harvested, releasing spores over other healthy seeds to complete the cycle of
infection.
Establishment of bunt disease within wheat fields from contaminated seeds
depends on the number of spores per seed, the susceptibility of the cultivar to
coleoptile infection and environmental conditions during seed germination. Heald
(1921) found that the cultivar Marquis needed 542-5000 spores per grain to transmit
the disease, compared with only around 100 spores per grain in the susceptible
cultivar Jenkins Club. Oxley and Cockerell (1996) also recorded bunt symptoms in
the field when the level of contamination exceeded 100 spores per seed.
Seed contamination was generally considered to be the only way in which the
pathogen survived between cereal crops and, since seed infection was in the form of
seed surface contamination, control of the disease was relatively easily achieved by
the application of appropriate seed treatment chemicals. From the 1950s to the
1980s, when almost all UK wheat seed was routinely treated with organomercury
seed treatment fungicides, bunt was very rare. There were occasional reports of the
disease in wheat crops in England in the 1980s and these were usually associated
with the sowing of untreated farm-saved seed. However, Yarham (1993) reported
bunt in crops where soilborne inoculum seemed to be the source of infection and this
was associated with dry soil conditions occurring in the short period between the
harvesting of a heavily diseased crop and sowing a following winter wheat crop. The
teliospores appeared to survive between harvest and sowing in the dry soil
conditions. Similar reports of occasional soilborne infection of wheat by T. tritici
have been made in Denmark (Nielsen and Jorgensen, 1994). In conditions
favourable for spore germination, teliospores of T. tritici are thought to be relatively
short-lived (Weltzein, 1957). In these conditions, seedborne inoculum will be of
greatest epidemiological significance but spore balls shed by heavily diseased crops
can probably protect spores at least until a following wheat crop is sown (Paveley
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