Abstract

In February and March 2004, 304 elk (Cervus elaphus) developed paresis in the Red Rim habitat area southwest of Rawlins, Wyoming. Elk were found in sternal recumbency, alert and responsive, but unable to rise. Bright red discolored urine was adjacent to many affected elk. Many elk progressed to lateral recumbency followed by dehydration, obtundation, and death. Several elk provided feed and water remained alive and responsive but never became ambulatory. The majority of elk were euthanatized due to the poor prognosis for survival and return to normal function. Postmortem examinations were performed on 12 elk from the field, and at necropsy these animals were in fair to good body condition. Most of the elk that were recumbent for a day or more demonstrated gross evidence of myopathy, with pallor and streaking in skeletal muscles, particularly the semimembranosus, semitendinosus, and gastrocnemius muscles. Microscopic examination of tissues from the majority of elk was unremarkable, with significant lesions most consistently observed in skeletal muscles. In affected muscles, there were degenerative lesions of varying duration, severity, and distribution, some with early mineralization and attempts at regeneration and some associated with degenerating protozoal cysts (Sarcocystis sp.). Sporadic lesions were observed in other tissues from a small number of elk, including mild tubular degeneration/necrosis in kidneys, mild fibrinoid degeneration/change in small blood vessels of adrenal glands and a few other organs, and mild hepatocellular degeneration or less frequently apoptosis/necrosis.

Common infectious, inflammatory, toxic, and traumatic causes of weakness, paresis, and recumbency were ruled out via histopathology, virus isolation and associated tests, bacterial culture, parasitology analyses, and toxicology analyses. During field investigations, large quantities of ground lichen (Xanthoparmelia chlorochroa) were observed in the area where affected elk were found. This lichen was found in the rumen contents of several elk. Approximately 50 kg of lichen was collected and fed to captive research elk. Three elk initially were offered a diet of 100% lichen for 7 days. After 7 days, elk were offered free choice alfalfa hay and lichen. After 7 days on this diet, one elk became sternally recumbent and was unable to rise. After 10 days on the diet, a second elk went down in a similar manner. Both elk were euthanatized and necropsied. Gross and microscopic lesions were consistent with lesions from the affected elk in the field and red discolored urine was noted in the pens where the elk had been housed.

Our preliminary conclusion is that this lichen was responsible for recumbency and death. Interestingly, cattle, horses, mule deer, and pronghorn also were observed on Red Rim habitat area during the elk mortality event, with access to the lichen, but were unaffected. The toxic compound of the lichen has not yet been identified. We plan to analyze the lichen for toxic compounds and analyze the diets of the other herbivores in the area to determine if they ate the lichen.