FUNGICIDE RESISTANCE IN ASCOCHYTA RABIEI IN THE PACIFIC NORTHWEST

Alexandra Zvenigorodsky

Ascochyta blight, caused by the fungal pathogen Ascochyta rabiei, is a major disease of chickpea (Cicer arietinum L) worldwide. Management of this disease relies heavily on fungicide applications, namely demethylation inhibitors (DMI), succinate dehydrogenase inhibitors (SDHI) and quinone outside inhibitors (QoI). However, repeated use of fungicides over time can select for resistant pathogen populations, diminishing the efficacy of these fungicides and threatening disease control. This study evaluated the QoI fungicide sensitivity of 171 A. rabiei isolates collected from symptomatic chickpeas in major chickpea-growing regions across California, Oregon, Washington, and Idaho. Isolates included both historic collections from 1984–1996 (prior to widespread fungicide use) and contemporary collections from 2020 and 2022. In vitro conidial germination assays were conducted on a subset of 35 A. rabiei isolates for azoxystrobin (QoI) and 32 isolates for pyraclostrobin (QoI), representing both historic and contemporary collection years. Results showed markedly reduced sensitivity among contemporary isolates, with EC₅₀ values (the effective fungicide concentration required to inhibit conidial germination by 50%) for azoxystrobin and pyraclostrobin indicating a 331-fold and 978-fold decrease in sensitivity, respectively, compared to historic baseline isolates. A discriminatory dose assay using 1 µg/ml of QoI fungicide was then applied to assess a broader group of isolates. Isolates with >60% conidial germination at this dose were classified as resistant, while isolates with <10% conidial germination at this dose were classified as sensitive. All isolates collected in 2020 and 2022 demonstrated >60% conidial germination, indicating widespread QoI resistance. Greenhouse trials confirmed that resistant isolates caused significantly more disease on azoxystrobin-treated plants, with even the highest concentration of azoxystrobin proving ineffective at controlling disease caused by QoI resistant isolates. Molecular assays further validated these findings, revealing that all resistant A. rabiei isolates carried the G143A mutation in the cytochrome b gene, which is known to confer total QoI resistance to fungal pathogens. In contrast, mycelial growth inhibition assays with the SDHI fungicide fluxapyroxad and the DMI fungicide mefentrifluconazole on 60 isolates from contemporary and historic collections showed a narrow range of small EC₅₀ values and no significant shifts in sensitivity between historic and contemporary collection years. These results suggest that while QoI fungicides are no longer effective against A. rabiei in the PNW, SDHI and DMI fungicides remain viable options for disease management.

FUNGICIDE RESISTANCE IN ASCOCHYTA RABIEI IN THE PACIFIC NORTHWEST

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