The role of seedling infection in epiphytotics of ascochyta blight on chickpea
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Didymella rabiei, the causal agent of ascochyta blight, survives on infected seeds and seedlings. Diseased seedlings originating from infected seeds occasionally serve as the source for primary infection in chickpea crops. Experiments carried out independently in Australia and in Israel provided quantitative information on the temporal and spatial distribution of ascochyta blight from initial infections and on the relationship between the amount of initial infection and the intensity of subsequent epiphytotics for cultivars differing in susceptibility to the pathogen. Disease spread over short distances (<10 m) from individual primary infections, was governed by rain and wind, and was up to five times greater down-wind than up-wind. Cultivar response to D. rabiei significantly affected the distance and area over which disease spread and the intensity of the disease on infected plants. At onset of the epiphytotic, the relationship between disease spread and time was exponential (P < 0.05; R2 > 0.95) and the area of the resulting foci was over 10 times greater in susceptible cultivars than in resistant cultivars. Regression equations showed the relationship between disease severity and the distance from the focus-plants was inverse-linear for all cultivars tested (P < 0.05). A simulation model based on the experimental data revealed that even if primary infection is infrequent (less than 1% of plants), the consequences are potentially devastating when susceptible cultivars are used. The epidemiological information and simulation model generated by this study provide an increased understanding of the development of an epiphytotic in which the primary foci of disease originate from infected chickpea seedlings.
KeywordsAscochyta rabiei Gram blight Quantitative epidemiology
The assistance of Haim Vintal and Judith Lichtenzveig in the study conducted in Israel is acknowledged. We also thank: Larn McMurray and staff of the Field Crop Evaluation and Agronomy, SARDI for sowing and maintaining the Australian trial; Dr Mark Sosnowski and Ms Jenny Davidson for scientific and technical support; Mr Ross Ballard for assistance in revision of this manuscript; and Ms Debra Partington (BiometricsSA) for assistance with statistical analyses. Seed was tested for DNA of D. rabiei by SARDI—Root Disease Testing Service. The Australian component of this study was part of the Honours research of R.B.E. Kimber, with support from the Grains Research and Development Corporation (GRDC), SARDI and the University of Adelaide.
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