Toxicity of the lichen secondary metabolite (+)-usnic acid in domestic sheep.

Toxicity following ingestion of the vagrant, foliose lichen Xanthoparmelia chlorochroa was identified as the putative etiology in the death of an estimated 400-500 elk on the Red Rim-Daley Wildlife Habitat Management Area in Wyoming during the winter of 2004. A single, unsubstantiated report in 1939 attributed toxicity of X. chlorochroa in cattle and sheep to usnic acid, a common lichen secondary metabolite. To test the hypothesis that usnic acid is the proximate cause of death in animals poisoned by lichen, domestic sheep were dosed PO with (+)-usnic acid. Clinical signs in symptomatic ewes included lethargy, anorexia, and signs indicative of abdominal discomfort. Serum creatine kinase, aspartate aminotransferase, and lactate dehydrogenase activities were considerably elevated in symptomatic sheep. Similarly, only symptomatic ewes exhibited appreciable postmortem lesions consisting of severe degenerative appendicular skeletal myopathy. The median toxic dose (ED(50)) of (+)-usnic acid in domestic sheep was estimated to be between 485 and 647 mg/kg/day for 7 days.

Lack of relay toxicity in ferret hybrids fed carbaryl-treated prairie dogs.

Carbaryl (1-napthol methylcarbamate) is being considered for control of fleas on prairie dogs (Cynomys spp.) used in black-footed ferret (Mustela nigripes) recovery in the western United States. The potential for relay toxicity in ferrets was determined by feeding carbaryl treated prairie dogs to black-footed ferret x Siberian polecat (M. eversmanni) hybrids. Adult prairie dogs were treated topically with 2.5 g of commercial 5% carbaryl dust sold as flea powder. After 14 days prairie dogs were killed and fed to ferrets. Potential for relay toxicity was evaluated by analyzing ferret blood cholinesterase (CHe), prairie dog brain Che, and hepatic carbamate concentration. There was no difference between pre- and post-exposure blood CHe activity, nor did treated prairie dog brain CHe differ significantly from controls. Post-exposure blood CHe did not exhibit reactivation after dilution in aqueous buffer. Hepatic carbaryl concentrations were less than detection limits (50 ppb). Based on these results, we conclude that short-term use of carbaryl for flea control on prairie dogs does not pose a hazard of relay toxicity in black-footed ferrets.

In vitro ruminal metabolism of larkspur alkaloids.

Larkspur (Delphinium sp) poisoning of range cattle is a serious, recurring problem in the western United States. Numerous stratagems have been recommended to ameliorate larkspur intoxication, but none are completely effective. Previous studies in this laboratory indicated bovine ruminal microflora are capable of chemically modifying Delphinium alkaloids. Research reported herein was undertaken to further evaluate whether differences in ovine and bovine rumen metabolism might explain differences in susceptibility to larkspur intoxication and whether existing metabolic activity can be enhanced by sustained exposure to Delphinium alkaloids. Comparison of ovine and bovine rumen metabolism of Delphinium geyeri alkaloids in vitro failed to demonstrate differences in the rate of alkaloid metabolism. Rumen liquor collected sequentially from a fistulated cow dosed with dried Delphinium geyeri did not vary in ability to metabolize larkspur alkaloids.