The role of seedling infection in epiphytotics of ascochyta blight on chickpea

Abstract

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; R 2 > 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.

Integrated disease management of ascochyta blight in pulse crops

“…Seed to seedling transmission Seed transmission rates for A. rabiei have been reported as 5% in field conditions (Kimber et al 2007) to 20-30% in glasshouse conditions Maden 1983). The production of diseasefree seed is seen as an important strategy in Pakistan, in areas free from A. rabiei infection (Mitsueda et al 1997).…”

“…The production of diseasefree seed is seen as an important strategy in Pakistan, in areas free from A. rabiei infection (Mitsueda et al 1997). The use of disease-free seed is crucial for susceptible chickpea cultivars as seedling foci rapidly develop into epidemics in conditions conducive to disease development (Kimber et al 2007). The rapid spread of ascochyta blight from primary infections in susceptible chickpea cultivars led to the development of a more rigorous PCR-based seed test in Australia.…”

“…The original seed test (400 seeds on culture medium) was based on a procedure recommended by the International Seed Testing Association (ISTA 1996) and was able to detect as low as 0.25% infection levels. However, even lower levels of infected seed (0.01-0.1%) are sufficient to initiate epidemics when weather conditions are favourable (Kaiser 1992;Kimber et al 2007). The PCR test uses DNA primers specific to A. rabiei, based on sequencing of the internal transcribed spacer region of the ribosomal gene complex.…”

Advances in winter pulse pathology research in Australia

“…Infected seed may have reduced germination while seed to seedling transmission rates of up to 15% were recorded in field studies (Kimber et al 2006a). Infection on less than 1% of seedlings can lead to serious epidemics (Kimber et al 2007b). An overseas report (Kaiser and Hannan 1988) indicated that thiabendazole was amongst the most effective fungicides tested against seed-borne A. rabiei but Kimber and Ramsey (2001) found that a seed dressing of thiram plus thiabendazole (P-Pickel T®) was superior to thiram.…”

A Mechanistic Weather-Driven Model for Ascochyta rabiei Infection and Disease Development in Chickpea

“…The regular seasonal occurrences of Ascochyta blight epidemics suggest that the fungus has efficient mechanisms for overwintering from one season to the next. The main sources of primary inoculum are infected seeds that cause seedling infection [12,13] and air-borne ascospores produced in pseudothecia formed on chickpea infected debris [14,15]. During the growing season, secondary spread of the disease is driven by splash-borne pycnidiospores (conidia) produced in pycnidia that develop on Ascochyta lesions [11].…”