|Spraker, Terry - COLORADO STATE UNIV|
Submitted to: Veterinary Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 10, 2005
Publication Date: September 1, 2005
Repository URL: http://naldc.nal.usda.gov/download/31601/PDF
Citation: Stegelmeier, B.L., James, L.F., Gardner, D.R., Panter, K.E., Lee, S.T., Ralphs, M.H., Pfister, J.A., Spraker, T.R. 2005. LOCOWEED (OXYTROPIS SERICEA) INDUCED LESIONS IN MULE DEER (ODOCOILEIUS HEMIONUS). Veterinary Pathology. 42(5): 566-78. Interpretive Summary: Locoweed poisoning is common in livestock and has been reported in wildlife, but it is unknown if mule deer (Odocoileius hemionus) are susceptible. In many locoweed areas, deer and elk have also contracted chronic wasting disease (CWD). The purpose of this study was to induce and describe chronic locoweed poisoning in deer and compare those with CWD. Two groups of four mule deer were fed alfalfa pellets or alfalfa pellets containing 15% Oxytropis sericea formulated to obtain a swainsonine dose of 1.5 mg swainsonine/kg bw/day. Locoweed poisoned deer lost weight and developed a scruffy, dull coat. After 180 exposure days they developed reluctance to move and when they were forced to move, subtle intention tremors were apparent. Poisoned deer had extensive neuronal swelling and cytoplasmic vacuolation typical of locoweed poisoning in other species. Neuronal vacuolation was severe in cerebellar Purkinje cells and there were fewer Purkinje cells. Axonal swelling and dystrophy was found in many white tracts but was most severe in the cerebeller peduncles and the gracilis and cuneate fasciculi. These findings indicate that deer are susceptible to locoweed poisoning and they develop lesions similar to those seen in other species. These histologic changes are distinct from those of CWD in deer. However, the clinical presentation of locoweed poisoning in deer are very similar to CWD suggesting histologic and immunohistochemical studies are required for a definitive diagnosis.
Technical Abstract: Locoweeds are plants of the Astragalus and Oxytropis genera that induce a storage disease similar to genetic mannosidaosis. Toxicosis is attributed to swainsonine, an endophyte-produced indolizidine alkaloid. Swainsonine inhibits lysosomal '-mannosidase and Golgi mannosidase II resulting in cellular vacuolation and degeneration. Animals must ingest locoweed for several weeks before they become depressed, anorexic, and lethargic with muscular weakness, intention tremors, proprioceptive deficits, and obvious behavioral change. Reported histologic lesions include widespread neuronal vacuolation and axonal dystrophy as well as vacuolation of the kidney, liver and various endocrine cells. Some tissues appear to be more susceptible to locoweed-induced lesions as changes are first seen in the proximal convoluted tubules of the kidney, transitional epithelium of the urinary bladder, reticular cells or macrophages of the lymph nodes, liver, and spleen and finally neurons of the cerebellum, cerebrum, basal ganglia, hippocampus, thalamus, midbrain, and autonomic ganglia. This cellular vacuolation is probably better described as micro-vesiculation as the vacuoles are small and often gives affected cells a swollen granular appearance. Initially vacuolation is confined to the neurophil, but with longer durations of poisoning, both glia and neurons are affected. Poisoning-induced lethargy and anorexia combined with malabsorption and decreased feed efficiency results in wasting and cachexia. Locoweed poisoning is relatively common in cattle, horses, sheep and goats; and the annual economic losses in those species have been estimated at over 20 million dollars. Less is known of the impact of locoweed poisoning in wildlife. Sp9ontaneous poisoning has been reported in elk (Cervus elaphus nelsoni) and there are anecdotal reports of poisoning of pronghorn antelope (Antilocapra Americana), but it is unknown if mule deer (Odocoileius hemionus) are susceptible. Although there are minor differences in species susceptibility to locoweed poisoning, swainsonine’s remarkable solubility and method of action through enzyme inhibition suggest that all species including wildlife will be affected. The relatively recent emergence of chronic wasting disease (CWS) in deer and elk in locoweed endemic areas in Wyoming and Colorado raises questions as to the effects of locoweed poisoning in confounding CWD diagnosis, the spread of CWD and potential interactions of locoweed poisoning in CWD progression. Though spongiform diseases and locoweed poisoning produce distinct clinical signs and histologic lesions, no comparative studies documenting these differences are available. The purpose of this study was to induce and describe the clinical and histologic lesions of chronic locoweed poisoning in deer.