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FUNGICIDE RESISTANCE IN ASCOCHYTA RABIEI IN THE PACIFIC NORTHWEST
Ascochyta blight, caused by the fungal pathogen Ascochyta rabiei, is a major disease of chickpea (Cicer arietinum L) in the Pacific Northwest and 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 sensitivity of 171 A. rabiei isolates collected from symptomatic chickpeas from Washington, Idaho, Oregon and California to the QoI fungicides azoxystrobin (AZO) and pyraclostrobin (PYR). Isolates included both historic collections from 1984 to 1996 (prior to widespread use of systemic fungicide) and contemporary collections from 2020 and 2022. In vitro conidial germination assays were conducted on a subset of 35 and 32 A. rabiei isolates for AZO and PYR, respectively, representing both historic and contemporary collection years. Results showed markedly reduced sensitivity among contemporary isolates, with EC[subscript 50] values (the effective fungicide concentration required to inhibit fungal growth or germination by 50%) for AZO and PYR, 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 the two fungicides was then applied to assess 127 and 92 A. rabiei isolates for sensitivity to AZO and PYR, respectively. Isolates with >60% conidial germination at this dose were classified as resistant, while isolates with 60% conidial germination, indicating widespread QoI resistance. Greenhouse trials confirmed that resistant isolates caused significantly more Ascochyta blight on AZO-treated chickpea plants, with even the highest concentration of AZO (100 μg/ml) proving ineffective at controlling disease caused by QoI resistant isolates. Molecular assays revealed 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, further validating the QoI fungicide resistance among the isolates. In contrast, mycelial growth inhibition assays with the SDHI fungicide fluxapyroxad (FLU) and the DMI fungicide mefentrifluconazole (MEF) on a subset of 60 isolates from contemporary and historic collections showed a narrow range of low EC[subscript 50] values (FLU: 0.0092 – 0.0795 μg/ml; MEF: 0.0115 – 0.0913 μg/ml) and no significant decreases in sensitivity between historic and contemporary collections. These results suggest that while the two tested QoI fungicides may no longer be effective against A. rabiei in the PNW, SDHI and DMI fungicides remain viable options for disease management
CloverGram, February 2025
In this issue: Starlight Beach Walk; Intro to Beekeeping for Kids; Goat Projects Workshop; Train Show 2025; 4-H/FFA Night at the Silvertip
PHARMACOKINETICS AND SAFETY OF A SINGLE SUBCUTANEOUS OR INTRAMUSCULAR DOSE OF KETAMINE IN HEALTHY HORSES
Background: Pharmacokinetics (PK) of intramuscular (IM) and subcutaneous (SC) administration of ketamine in horses have not been described.Objectives: To describe the PK and safety of ketamine and its metabolites after a single SC or IM administration in horses.Study design: Single-arm, experimental study.Methods: In phase 1, two horses received 0.5 or 1 mg/kg of ketamine via SC and IM routes. In phase 2, eight horses received ketamine at 0.5 mg/kg IM. Plasma or serum concentrations of ketamine and its major metabolites were determined by liquid chromatography-mass spectrometry at baseline and selected intervals post-administration. Pharmacokinetic parameters were calculated using both non-compartmental and compartmental analysis.Results: Plasma drug concentrations after SC administration were extremely low (< 5 ng/mL); thus, only IM administration was investigated in phase 2. Median peak serum ketamine concentration after IM administration was 20.9 ng/mL (IQR 15.2 – 35.9) with time to peak drug concentration of 1.4 h (IQR = 0.8 – 1.9 h) and terminal half-life of 1.8 h (IQR = 1.3 – 2.6 h). No changes in physical examination data (heart rate, respiratory rate, rectal temperature, gastrointestinal sounds, and injection site reactions) or laboratory variables were observed after IM drug administration. Ketamine metabolites were detected within 5 min after IM drug administration. Norketamine was the predominant metabolite.Main limitations: Small sample size, unknown therapeutic plasma concentrations of ketamine and metabolites, large inter-individual variability.Conclusion: Single IM administration of ketamine to healthy horses resulted in rapid drug absorption but highly variable inter-individual ketamine and metabolite concentrations without significant adverse effects. Future studies should evaluate PK of ketamine after repeated IM dosing and determine therapeutic plasma concentrations in horses
Veterinary Medicine Extension Newsletter, January 2025
Included in this newsletter: Chickens and cows and cougars, oh HPA-I; The association between periparturient body condition score and body condition score change and subsequent performance of dairy cows; Immunity in transition cow
Fourth of July Creek - Storage Selection Function, Travel Time, and Residence Time data
This compressed tarball archive contains the datasets and scripts necessary to visualize the residence time distributions, travel time distributions, and storage selection functions for the Fourth of July Creek transient simulations. The scripts and datasets are formatted as Matlab m-file scripts and MAT archives.</p