A weather-based disease prediction model for bacterial canker of kiwifruit (known worldwide as Psa; Pseudomonas syringae pv. actinidiae biovar 3) was developed using a new mechanistic scheme for bacterial disease forecasters, the multiplication and dispersal concept. Bacterial multiplication is estimated from a temperature function, the M index, accumulated from hourly air temperature over 3 days for hours when the leaf canopy is wet. Rainfall provides free water to move inoculum to infection sites, and the daily risk indicator, the R index, is the 3-day accumulation of the M index output on days with total rainfall >1 mm; otherwise, R is zero. The model was field-tested using potted kiwifruit trap plants exposed for discrete periods in infected kiwifruit orchards to identify when leaf infection occurred. In a 9-week study during spring, the R index predicted leaf-spot intensity with high accuracy (R = 93%) and, in an 82-week seasonal accuracy study, prediction of infection incidence was most accurate from spring to late summer and lower during other times. To implement the risk model for the New Zealand kiwifruit industry, a modified risk index, R', used relative humidity (RH) >81% instead of wetness, so that 2- and 6-day weather forecasts of RH could be used. Risk index values were affected by the shape of the temperature function and an alternative 'low temperature' function for the M index was identified that could be used in climates in which high temperatures are known to limit Psa development during some parts of the year. This study has shown how infection risk for bacterial diseases can be conceptualized as separate processes for temperature-dependent bacterial multiplication and rain-dependent dispersal and infection. This concept has potentially wide application for bacterial disease prediction in the same way that the infection monocycle concept has had for fungal disease prediction.
Pseudomonas syringae pv actinidiae (Psa) was first identified on kiwifruit (Actinidia spp) in New Zealand in November 2010 and has since caused serious losses particularly in Te Puke The role of fallen leaves and pruning debris in the lifecycle of Psa in New Zealand is unknown Survival of Psa was investigated in fallen leaves and cane prunings over winter 2011 Heavily infected leaves and cane prunings with Psa dieback symptoms were kept on the orchard floor and in the laboratory and assayed weekly for the presence of viable Psa At leaffall all leaves yielded live Psa Although detection frequency declined over time especially after 56 weeks Psa was still isolated from leaf litter 15 weeks after leaffall and cane prunings 11 weeks after winter pruning These results indicate that the pathogen overwinters readily in leaf litter and pruning debris representing a potential inoculum source for infection of new spring growth
Bacterial canker of kiwifruit commonly referred to as Psa is caused by Pseudomonas syringae pv actinidiae and the biovar 3 strain has affected kiwifruit vines in New Zealand since 2010 Psa has had an impact on the management and production of kiwifruit in New Zealand This paper provides a review of the epidemiological risk factors that are associated with Psa disease within orchards The presence of the pathogen rain and a susceptible host are sufficient to cause disease in kiwifruit but there are other risk factors that can increase the amount of disease that develops and the spread of disease including other environmental factors (eg temperature) host factors (eg cultivar) and management factors (eg pruning practices) The aim of this literature review was to describe the current knowledge of a range of known and postulated risk factors for the development of bacterial canker in kiwifruit
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