Wahkiakum County elk are in poor health, and citizens want something done about it.
Residents and county commissioners discussed the situation Tuesday, and commissioners said they would invite officials from the Washington Department of Fish and Wildlife (WDFW) to visit and discuss the hoof rot syndrome seen in local elk.
Commissioner Dan Cothren, who travels the region in his logging industry employment and who is also a long-time hunter, said he has seen sick, dying and dead elk in most of the county's valleys.
"It's pretty severe," Cothren said. "It can devastate a herd."
He recently observed a herd of 21 elk on KM Mountain, he said; of them, five cows and three spikes showed signs of hoof rot.
The hoof rot syndrome has been observed for several years in areas along the I-5 corridor, he added.
Elochoman Valley resident John Rua said he has had three sick animals on his property, and when he called WDFW for assistance, he was told he could just chase them away.
"We as a county need to do something for these animals," he said.
He added that he wasn't sure the illness would affect domestic animals, but that was a concern.
Following are two articles from the WDFW website that talk about the hoof rot syndrome.
How widespread is the elk hoof rot and/or elk hoof deformation problem in Washington?
--5/24/2011 http://wdfw.wa.gov/help/questions/159
Elk with hoof disease have been observed in Southwest Washington since the mid-1990s. This problem is most apparent in the lower Cowlitz River Valley in game management units (GMUs) 504, 530, 520, and 550, although it has also been observed in GMUs 506 and 556.
Research on elk in SW Washington has shown the presence of the bacterium Dichelobacter nodosus. This bacterium is a common cause of hoof rot in domestic cattle and sheep. However, interviews with several large animal veterinarians who practice in the areas where affected elk have been observed have not revealed an increase in the incidence of hoof rot in domestic species.
As a standard precaution, WDFW recommends that hunters avoid harvesting wild animals that are obviously sick.
Hoof rot is generally limited to the feet of the elk, and the rest of the carcass is usually unaffected. As always, use your best judgment and nose to help you decide what to trim away and discard.
If the animal appears to be diseased throughout the entire body and none of the meat is suitable for consumption, contact your local WDFW Regional Office for advice and possibly a replacement tag.
See WDFW's "Severe Hoof Deformities in Free-Ranging Elk in Western Washington State" and the Merck Veterinary Manual for more information on hoof rot.
Severe Hoof Deformaties in Free Ranging Elk in Western Washington State
--2010 http://wdfw.wa.gov/publications/pub.php?id=01124
Summary
Severe overgrowth and deformity of the hooves in the Cowlitz river basin Roosevelt elk population has been sporadically noted in individual animals for the last decade. However, recently the incidence of affected elk and the severity of cases has seemingly increased to involve most herds surveyed within this study area, affecting up to as many as 90% of elk in some herds. Cases of overgrown and deformed hooves similar to this have been occasionally recorded throughout the US in populations of wild deer, moose, and bighorn sheep. The cause of hoof deformity in these other herds and species has never been definitively elucidated, though several predisposing factors have been suggested. These factors include severe copper deficiency, selenium toxicosis, chronic ingestion of high carbohydrate diets, chronic ingestion of a predominantly alfalfa diet (with or without recurrent laminitis), exposure to infectious viruses such as epizootic hemorrhagic disease (EHD) or blue tongue virus (BTV), and change of behavior and habitat that include limited ambulation or ambulation on soft soils which may prevent normal hoof wear . . .
Possibly our most important finding in this study is marked copper and selenium deficiency in this population of elk. Though certainly this area has been historically deprived of copper and selenium, perhaps changes in habitat, encroachment of farmed fields and livestock, emergence of new plant populations, significant dietary changes, or behavioral changes, may have favored the recent development of severe hoof lesions. Copper in particular is known to be vitally important for proper bone and keratin development. A. Flynn described in1977, populations of Alaskan moose with similar severely overgrowth of hooves. The cause of this lesion, described as “slipper foot”, was not definitively determined; however, affected moose were found to be significantly deficient in copper. Copper deficiency in domestic cattle is known to be associated with an increased incidence of foot rot, heel cracks, and sole abscesses. Whether copper deficiency alone can induce or predispose hoof deformity in the Cowlitz basin elk, or if copper deficiency is one contributor to a multi-factorial problem, remains yet to be determined.
A more extensive understanding of the habitat and the principal diet of these herds, as well as the movement within the home range, is necessary to completely understand the dynamics of nutritional deficiencies, toxicities, systemic infections, potential exposures to toxic fungi, and to determine what influence movement, soil substrate, or behavioral changes might play in the pathogenesis of these hoof lesions.
In our study population we found that hoof deformity affected either the fore or rear pair of limbs and did not appear to be restricted to particular age or sex classes, indicating that even severe lesions could develop rapidly enough to affect animals under one year of age. Lesions in the study animals varied markedly from extensive overgrowth and deformity of an otherwise intact hoof, to complete sloughing or breakage of abnormal hooves and hoof walls. Additionally, some hooves had extensive necrotizing and cavitating lesions of the sole or hoof wall. Focal hoof necrosis could be indicative of local infection, or weakness or abnormality in the keratin or underlying lamina that would focally devitalize the hoof or predispose more fragile foci to trauma and infection. In the majority of cases, the keratin of the hoof wall and sole was thick, well organized, and very hard, similar to hoof keratin in unaffected hooves of the same animal, or the hooves of normal elk collected from the study site. Histologically, keratin of the hoof wall and sole and the germinal epithelium of the coronet was well organized and no significant primary lesions were detected, making the likelihood of a developmental or free living moose and roe deer genetic keratin disorder less likely.
In all cases soft tissue lesions, which would be most indicative of a primary infectious foot rot, were lacking or minimal. Bacterial culture of affected hooves was positive for Dichelobacter nodosus, a known cause of infectious foot rot in domestic livestock; however this environmental pathogen can be readily isolated from soil and would be an anticipated opportunistic pathogen in any foot condition. Therefore, a primary foot rot should be interpreted with some degree of caution.
Most animals had some degree of soft tissue and lamellar perivasculitis that was predominantly lymphocytic-plasmacytic. Though this lesion may be due to distal limb inflammation and chronic trauma, causes of vasculopathy are considered. Of particular interest are causes of vasculopathy that may compromise normal peripheral blood flow, induce aberrant neovascularization in the hoof or lamellae, or result in random thrombosis of these structures and consequently alter normal hoof growth and integrity. Causes of vasculopathy considered are recurrent laminitis, EHD, BTV, and ergot or fescue toxicity. Serology and PCR to determine viral exposure or current viremia in the study elk are currently pending.
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