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ARS Home » Pacific West Area » Logan, Utah » Poisonous Plant Research » Research » Publications at this Location » Publication #298899

Title: The effect of low larkspur (Delphinium spp.) co-administration on the acute toxicity of death camas (Zigadenus spp.) in sheep

Author
item Welch, Kevin
item Green, Benedict - Ben
item Gardner, Dale
item Stonecipher, Clinton - Clint
item Panter, Kip
item Pfister, James
item Cook, Daniel

Submitted to: Toxicon
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/9/2013
Publication Date: 12/15/2013
Publication URL: http://handle.nal.usda.gov/10113/58439
Citation: Welch, K.D., Green, B.T., Gardner, D.R., Stonecipher, C.A., Panter, K.E., Pfister, J.A., Cook, D. 2013. The effect of low larkspur (Delphinium spp.) co-administration on the acute toxicity of death camas (Zigadenus spp.) in sheep. Toxicon. 76:50-58.

Interpretive Summary: In most cases where livestock are poisoned by plants in a range setting, there are multiple poisonous plants in the area. Two poisonous plants that are often found growing simultaneously in the same location are death camas (Zigadenus spp.) and low larkspur (Delphinium spp.). Both plants emerge early in the spring and exhibit similar phenological growth stages. Poisonings generally occur during the spring when these plants are abundant, while other forage species have little growth. Livestock losses to death camas have been reported in numerous species with the largest losses generally occurring in sheep. Sheep are primarily affected because of their tendency to select forbs, particularly in the early spring when there is little other plant growth. Low larkspur poisonings cause large economic losses to cattle producers in the western United States and Canada. The primary result of larkspur intoxication is neuromuscular paralysis. However, larkspurs are five times more toxic to cattle than sheep. Sheep might be less susceptible to larkspur because the binding affinity of alkaloids to nAChRs is lower in sheep than in cattle. Consequently low larkspur is not regarded as a high risk poisonous plant for sheep. However, there is potential that consumption of low larkspur by sheep may exacerbate the acute toxic effects of plants such as death camas. It has been demonstrated that co-treatment of mice with the primary toxins from death camas and low larkspur has an additive effect. Therefore, the objective of this study was to determine if the co-administration of low larkspur will exacerbate the acute toxicity of death camas in sheep. The results from this study demonstrate that low larkspur co-treatment has no effect on the toxicity of death camas in sheep. Treatment of sheep with death camas caused clear signs of cardiovascular deficiencies and muscle fatigue. However, co-treatment with low larkspur did not exacerbate those deficiencies. The results from this study also confirmed previous findings that sheep are refractory to the acute toxicity of larkspur. The results from this study provide an increased knowledge and understanding regarding the acute toxicity of death camas in sheep, one of the more susceptible livestock species. This information will be useful in further developing livestock management recommendations for ranchers and in designing additional experiments to study the toxicity of death camas in other livestock species.

Technical Abstract: In most cases where livestock are poisoned by plants in a range setting, there is more than one potential poisonous plant in the same area. Two poisonous plants that are often found growing simultaneously in the same location are death camas (Zigadenus spp.) and low larkspur (Delphinium spp.). Sheep are known to be susceptible to death camas poisoning while they are thought to be resistant to larkspur. The objective of this study was to determine if co-administration of low larkspur would exacerbate the toxicity of death camas in sheep. A dose finding study was performed to find a dose of death camas that caused minimal clinical signs of poisoning. Sheep were observed for clinical signs of poisoning as well as changes in heart rate and muscle fatigue. Sheep dosed with 1.14 g of death camas per kg BW showed slight frothing and lethargy, whereas sheep dosed with death camas and low larkspur showed slightly more noticeable clinical signs of poisoning. Sheep dosed with only low larkspur, at 7.8 g/kg BW, showed no signs of poisoning. Although we observed a qualitative difference in clinical signs of intoxication in sheep co-treated with death camas and low larkspur we did not detect any quantitative differences in heart rate, exercise-induced muscle fatigue, or differences in serum zygacine kinetics. Consequently, the results from this study suggest that low larkspur does not affect the toxicity of death camas in sheep. The results from this study increase knowledge and understanding regarding the acute toxicity of death camas and low larkspur in sheep. As combined intoxications are most likely common, this information will be useful in further developing management recommendations for ranchers and in designing additional experiments to study the toxicity of death camas to other livestock species.