Author(s): Sushan Han and Kristin Mansfield
Free-ranging Roosevelt elk (Cervus elaphus roosevelti) in South Western Washington state are presenting with severely overgrown and deformed claws, and often marked emaciation, the etiology of which has not yet been elucidated. Although reports of deformed hooves in elk have occurred sporadically in SW Washington for over a decade, the number and geographical distribution of these reports increased dramatically in 2008. During the winter of 2009 we undertook an investigation to better characterize the lesions and examine possible etiologies. Agency biologists surveyed groups of elk and interviewed landowners to estimate the prevalence and distribution of affected elk and to plot locations of positive cases on maps. Findings during the winter of 2008-2009 showed that approximately 80% of all herds observed had between 30 to 90% of animals affected with a wide variation in the severity of each case. Affected animals represented all age and sex classes. In this study five affected cow elk from three locations, and three apparently unaffected cow elk from one location were euthanized by gunshot. In all elk complete necropsies were performed and lower limbs were collected. On specimens we performed distal limb radiology, routine histopathology, hepatic trace mineral concentration, bacteriology of select tissues, virus isolation of key viscera, and parasitology of feces was performed. Necropsy, radiology, histopathology, and parasitology were in all cases unremarkable and failed to indentify an underlying cause of hoof deformity. Hepatic selenium and copper levels interestingly, were severely deficient based on domestic livestock normal values. A variety of aerobic and anaerobic organisms were cultured from the hoof lesion, including Dichelobacter nodosus, an environmental organism, but also a known cause of infectious foot rot in domestic sheep and cattle.
The severe overgrowth and marked deformity of hooves from this cohort of free-ranging Roosevelt elk is unique. As it is not associated with underlying systemic disease, an etiology of toxicity, nutritional deficiency, or potentially infectious etiologies are all considered. Potential etiologies include recurrent laminitis, ergot toxicity, fescue toxicity, secondary conditions associated with severe copper and potentially severe selenium deficiency, or other infectious and toxic causes that may induce regional vasculopathy in the distal limbs. Distantly, a genetic etiology is considered.