Direct harvesting, with mechanical removal of the foliage (topping), of onion crops followed by post‐harvest drying at ambient temperatures (c. 18°C) resulted in an increase in the incidence of onion neck rot (Botrytis allii). The disease was substantially reduced if topped onions were dried at 30°C with an airflow of 425 m3 air/h/tonne. The treatment was most effective if the crop was removed from the field for drying within 48 h of topping thus avoiding severe infection of the damaged green tissues of the necks of onions.
Botrytis byssoidea (mycelial neck rot) was more prevalent than B. allii (sclerotial neck rot) on the leaves of field onions and the bulbs of stored onions grown in some of the areas where onions or onions and leeks had previously been grown sequentially. B. byssoidea and B. porri were also isolated from leeks. Spores of B. allii, B. byssoidea (from onions and leeks), B. porri, and B. squamosa caused infection of seedlings of salad (green) and bulb onions. Inoculation with B. squamosa spores caused severe infection of seedling leaves, but inoculation with mycelial discs caused little damage to onion bulb tissue. By comparison, mycelial discs of the remaining species were highly pathogenic to bulbs. The practical implications of disease transfer of certain of these species between onions and leeks are discussed.
Neck rot (Botrytis allii) affected bulbs of onions for 2 successive years when these were grown either in the field in soil from which an infected crop had been cleared 6 months previously or when infected debris was incorporated into field soil 6 months before the first crop was sown. These sources did not continue to cause infection of onion crops grown on the contaminated areas in the four succeeding years. The white storage tissue of onion bulbs (healthy or infected) persisted for less than 6 months in unsterile field soil contained in pots while sclerotia present in similar soil varied in their rate of decay but lost their capacity to produce conidiophores of B. allii after 6 months. In one sample, sclerotia were not recovered after 5 months; Gliocladium roseum, a mycoparasite, was present in this sample and may have affected survival.
SUMMARYIn 1974/75, 13 sprays of 0·2% a.i. thiram applied at 14 day intervals to overwintered salad onions reduced the incidence of Botrytis cinerea and significantly increased onion yields. In 1977/78 both B. cinerea and B. squamosa occurred, and 12 iprodione sprays at 0·1% a.i. applied at 14‐day intervals or 6 sprays at 0·2% a.i. applied at 28‐day intervals gave good control of B. cinerea and B. squamosa and significantly increased onion yields. Benomyl (0·1% a.i. at 14‐day intervals, or 0·2% a.i. at 28‐day intervals) failed to control either pathogen because of the development of carbendazim‐insensitive strains of the fungi. Effective control of both pathogens and increased yields were obtained with an application of 0·4% a.i. thiram in October and November followed by an application of 0·2% a.i. iprodione in December and January.
SUMMARY Experiments on neck rot of onions, caused by Botrytis allii showed that, although the disease only became evident in store, a major source of the pathogen was samples of infected seeds. In 1972 and 1973, 39·5 and 71·4% respectively of commercial onion seed samples tested at Wellesbourne were infected. The pathogen was internal in seed and persisted for 3 ½ yr in infected seeds kept in a seed store at 10°C and 50% r.h. Seedlings raised from diseased seeds became infected by mycelial invasion of the cotyledon leaf tips from seed‐coats many of which remained attached to the cotyledons when seedlings emerged from the soil. The fungus attacked the living tissues of these leaves symptomlessly, producing conidiophores only after the leaf tissue senesced and became necrotic. Because the fungus was symptomless, the rate of spread of the pathogen in onion crops was assessed by incubating successive samples of plants from the field in humid conditions when infected tissues developed conidiophores of the fungus. This method showed that the disease was progressive in onion crops spreading more rapidly in wet humid conditions (e.g. 1972) than in dry ones (e.g. 1973). The principal means of spread were probably fungal spores; conidiophores bearing spores being produced abundantly on plants in the field under high humidity. The fungus invaded the leaves of plants successively, first infecting each leaf at the tip and then growing downwards in the tissues and eventually invading the neck of the onion bulb via the leaves which emerged directly from the top of the neck. By harvest, the fungus was situated deep within the neck tissues of infected maturing onion bulbs.
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