ADAS Arthur Rickwood, Mepal, Ely, Cambs CB6 2BA, UK

Background and objectives
Grey mould (Botrytis cinerea) is a major cause of stem rot and premature plant death in crops of long-season protected tomatoes in the UK. In recent years some greenhouses have by early autumn lost up to 40% of plants from the disease, and in 1994 stem botrytis was estimated to have caused a loss of 1.5 million out of marketed home production valued at 61.8 million [1]. Fungicides are now used infrequently for grey mould control, particularly where a crop is grown for supermarket production. Instead, the disease is usually managed by hygiene measures, manipulation of the glasshouse environment and crop management practices. Leaf and leaf scar infections are widely recognized as important routes by which stem lesions arise [2]. More recently, fruit stalks which die back after fruit picking have also been identified as a cause of stem rot. Some growers now routinely remove old fruit trusses as they occur in an attempt to minimize stem botrytis. It is a difficult and time-consuming task. The objective of this work was to determine the effect of regularly removing fruit stalks, soon after fruit picking is completed on a truss, on the incidence of stem rot.

Materials and methods
Methods of fruit truss removal were compared in a hydroponic (rockwool) crop of cv. Saporo grown in a heated glasshouse on a nursery in Norfolk, England. There was a history of severe stem botrytis in tomato crops at the site. The crop was planted (slab contact) on 15 February 1996 and empty fruit trusses were (i) left on, (ii) pulled off, (iii) pulled off as they turned brown or (iv) cut off with secateurs every 2 weeks from 21 June to 10 September. In two further treatments, a programme of six fungicide sprays (dichlofluanid, chlorothalonil and iprodione each applied twice) was applied at 14-day intervals (v) to plants with empty fruit trusses left on and (vi) to plants with fruit trusses pulled off. Fungicides were applied immediately after fruit truss removal. Treatments were applied to rows of 60 adjacent plants and there were four replicates in a randomized block design.

Results and conclusions
Botrytis occurred naturally in the crop in April, and by June the disease was widespread with infection of leaves and fruit trusses and also of stubs left on the stem after leaf and fruit truss removal. A high incidence of stem lesions developed. On 10 September 1996, the mean number of stem lesions per plant was greatest where fruit trusses had been left on (0.98) and least where fruit trusses had been removed as they turned brown (0.40). Infection arising from leaves and leaf scars accounted for around 30% of stem lesions and was not affected by fruit truss removal or fungicide treatment. The mean number of stem lesions per plant arising from fruit truss infection on plants with the trusses left on and not sprayed with fungicide was 0.63. Where green trusses were pulled off or cut off, this was reduced to 0.29 and 0.50 lesions, respectively; pulling off part-brown trusses was even more effective (0.11 lesions). Examination of stems at positions where fruit trusses had been removed revealed an association between occurrence of truss stubs (3-10 mm in length) and development of stem botrytis. Cutting off trusses with secateurs left the greatest number of stubs and 31% of them developed botrytis. Pulling off part-brown trusses left few stubs and only 17% of them developed botrytis. Application of fungicides to fruit trusses and to wound sites left after truss removal resulted in temporary reductions of around 25% in the incidence of stem botrytis, although there was no statistically significant effect at the end of cropping. A high incidence of stem lesions often results in a high incidence of dead plants. This crop was pulled out early, and on 10 September none of the treatments affected the incidence of dead plants, which ranged from 1.6 to 6.3%. It appears that pulling off decaying fruit trusses, the most effective control method in this experiment, both removed decaying trusses before infection had reached the stem and also left few stubs for B. cinerea to colonize.

1. O'Neill TM, Shtienberg D, Elad Y, 1997. Plant Disease 81, 36-40.
2. Verhoeff K, 1967. Netherlands Journal of Plant Pathology 74, 184-194.