Bacteria were isolated from internal tissues of surface sterilized healthy tubers of Solanum tuberosum cv. Maris Piper (8 different isolates) and from tubers inoculated with Erwinia carotovora ssp. carotovora showing soft-rot symptoms (3 different isolates), and identified by fatty acid profiling. Bacillus polymyxa and an Arthrobacter sp. were isolated from both sources, E. carotovora only from the soft-rotted tubers. The volatile organic compounds (VOCs) generated by tubers inoculated with E. carotovora, B. polymyxa and the Arthrobacter sp. were identified. Inoculated tubers of cv. Maris Piper were incubated under controlled humidity (95% relative humidity) and temperature (10ЊC) to simulate typical storage conditions. B. polymyxa and Arthrobacter sp. did not cause symptoms, whilst E. carotovora caused limited soft-rot infections after 4 weeks at the low temperatures typically associated with potatoes in storage. The VOCs released to the headspace around these tubers were collected using an adsorbent system and analysed by Gas Chromatography-Mass Spectrometry (GC-MS). Twenty-two volatiles unique to E. carotovora infection of potato tubers were found, including 10 alkanes, four alkenes, two aldehydes, one sulphide, one ketone, one alcohol, one aromatic, one acid and one heterocyclic compound. B. polymyxa generated three unique volatiles: N,Ndimethylformamide, 1-pentadecene and 1-hexadecane. Only one volatile, 2,3-dihydrofuran, was unique to the Arthrobacter infection. Production of volatile nitrogen species from E. carotovora-infected tubers increased with time, whereas none were detected in the headspace above uninfected tubers. Further analysis using a modified GC-MS method established that ammonia, trimethylamine and several volatile sulphides were evolved from tubers infected by E. carotovora. No specific volatile was useful as a marker associated with any of the three bacterial species but in the case of E. carotovora-infected potato tubers a significant increase in the volume of compounds evolved was clearly observed. The results are discussed in relation to the use of sensors to detect VOCs evolved from infected tubers in order to provide an early warning system for the control of soft rot in potato stores.

In the UK, conidia of Pseudocercosporella capsellae, the anamorph of Mycosphaerella capsellae, were observed on white leaf spot lesions on leaves throughout the growing season. Ascomata were not observed on lesions on either green or senescent leaves, although stromatic knots and spermogonia were occasionally seen in summer. However, spermogonia and protoascomata were produced in white leaf spot pod and stem lesions in early summer. Protoascomata continued to mature after harvest in these lesions on the debris. Mature ascomata subsequently developed by early autumn, but were exhausted by early January and did not overwinter. A diurnal periodicity in numbers of air-borne M. capsellae ascospores discharged from infected debris was observed with a Burkard spore sampler, with greatest numbers of ascospores collected near the middle of the day; the records also suggested that ascospores were released in response to wetting by dew or rain. Studies of natural white leaf spot epidemics in winter oilseed rape provided evidence that air-borne ascospores are the primary inoculum for initiating epidemics in the autumn in the UK. White leaf spot disease gradients over 100 m across a winter oilseed rape crop at Rothamsted were fitted by both negative exponential and inverse power-law models, with gradient slopes suggesting the deposition of air-borne spores dispersed from a single local source of inoculum. In comparison, no obvious white leaf spot gradients were observed over 250 m in a severely diseased crop near North Petherton, Somerset, suggesting that the air-borne spores were dispersed from a number of more distant sources in the area. Both patterns of disease were unlikely to have been initiated by P. capsellae conidia, which are dispersed only very short distances by rain-splash. However, once epidemics have been initiated by air-borne ascospores in the autumn, subsequent disease spread within an infected crop is dependent only on splash-dispersed conidia. A revised disease cycle of the pathogen is proposed.