Ascochyta rabiei, the causal agent of Ascochyta blight (AB) in chickpea, is a stubble-borne pathogen that significantly reduces grain yield and quality globally. In Australia, splash-dispersed conidiospores serve as the primary inoculum source, unlike other chickpea-growing regions where windborne ascospores play a major role, but the key factors influencing development and persistence of stubble-borne A. rabiei inoculum during off-season is lacking. Field and laboratory tests were undertaken to identify various factors, including host genetics, fungicides, environment, and non-host plants, that contribute to inoculum persistence and carryover. Understanding these factors is essential to inform sustainable disease management strategies.
AB inoculum load declined rapidly between harvest and the subsequent sowing period but persisted at low levels thereafter. The severity of in-season AB epidemics did not reliably predict post-harvest inoculum levels on chickpea stubble. Fungicide application during the growing season effectively reduced inoculum loads, whereas varietal resistance had no measurable effect, as both resistant and susceptible cultivars generally exhibited similar inoculum levels. Field experiments in 2022 at Wagga Wagga, Tamworth, and Horsham provided stubble from five chickpea cultivars with varying genetic resistance. Post-harvest, stubble was collected to assess cultivar and environmental effects on AB inoculum carryover and decay. Trials were conducted on-site, with additional testing in a common garden in Canberra. Environmental factors significantly influenced inoculum persistence, with higher loads in Canberra than in Wagga Wagga, despite identical conditions.
Beyond chickpea, A. rabiei was detected in multiple non-host species. It was detected in 9 of 11 sampled weeds species from AB hotspots within chickpea crops and in canola crops after chickpea rotations, with 12 - 38% of sampled canola leaves testing positive during the season. Canola stubble at season-end also carried A. rabiei, though transmission to chickpea plants via conidiospores was inconclusive. Glasshouse experiments confirmed non-host species could harbor A. rabiei. While AB symptoms appeared exclusively on chickpea, PCR detected the pathogen in various pasture and crop species. Chickpea seedlings developed symptoms when inoculated with A. rabiei-exposed stubble from non-host species, including wheat, canola, pea, and vetch. Some weed species, such as prickly lettuce, facilitated AB transmission despite no prior PCR detection, while other species, like wild mustard, showed atypical symptoms, requiring further investigation.
These findings highlight the complexity of A. rabiei epidemiology in Australian chickpea systems. While inoculum levels decline significantly post-harvest, low-level persistence may still pose a disease risk. Additionally, the ability of A. rabiei to survive in non-host species suggests a potential alternative inoculum source and a reservoir for genetic variation, underscoring its role in adaptation and the need for integrated disease management strategies beyond fungicide application. Future research should focus on further characterising the role of non-host reservoirs and developing targeted approaches to disrupt the inoculum cycle in chickpea production systems.
Keywords: Conidiospore survival, Stubble-borne pathogens, Non-host reservoirs, Epidemiology, Fungicide management