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Logan, Utah, United States

Kelly E.J.,Central Utah Veterinary Diagnostic Laboratory | Rood K.A.,Utah State University | Skirpstunas R.,Central Utah Veterinary Diagnostic Laboratory | Skirpstunas R.,Utah Veterinary Diagnostic Laboratory
Journal of Wildlife Diseases | Year: 2012

We isolated Corynebacterium pseudotuberculosis from an abscess of the head of a captive elk submitted for necropsy and from a similar abscess of a living herd mate. To our knowledge, this is the first documented case in elk and should be considered a potential cause of subcutaneous abscesses in wild elk. © Wildlife Disease Association 2012. Source

Davis T.Z.,Logan Research | Stegelmeier B.L.,Logan Research | Lee S.T.,Logan Research | Green B.T.,Logan Research | Hall J.O.,Utah Veterinary Diagnostic Laboratory
Toxicon | Year: 2013

Rayless goldenrod (Isocoma pluriflora) sporadically poisons horses and other livestock in the southwestern United States. Similar to livestock poisoning by white snakeroot (Ageratina altissima) in the midwestern United States, previous research suggests that benzofuran ketones (BFK: tremetone, dehydrotremetone, 6-hydroxytremetone, and 3-oxyangeloyl-tremetone) are responsible for the toxicity of rayless goldenrod. However, experimental reproduction of rayless goldenrod-induced disease and detailed descriptions of poisoning in horses with known concentrations of tremetone and other BFK has not been documented. In this study four horses were fed increasing amounts of rayless goldenrod to obtain doses of approximately 0, 10, 30, and 60mg BFK/kg BW for 14 days. After seven days of dosing the horse dosed with 60mg BFK/kg BW horse developed depression, reluctance to eat, dehydration, trembling, and muscle fatigue. Biochemical alterations including increases in the serum enzyme activities of CK, AST, ALT, and LDH, and increased cardiac troponin I concentration, were also identified. Physiologically the clinically poisoned horse had decreased endurance seen as reluctance to perform on the treadmill with increased resting heart rate and a prolonged recovery of heart rate following treadmill exercise. The condition of the horse continued to decline and it was euthanized and necropsied on day 10. At necropsy the myocardium was pale and soft and many of the appendicular and large apical muscles were pale and moist. Histologically, the myocardium had extensive myocardial degeneration and necrosis with extensive fibrosis and multifocal mineralization. Several of the large appendicular muscles in this horse also had small foci of skeletal muscle degeneration and necrosis. Less severe myocardial changes were also identified in the horse dosed with 30mg BFK/kg BW after 14 days of dosing. No clinical, biochemical or histologic changes were identified in the control horse and the horse dosed with 10mg BFK/kg BW. These results suggest that doses of 60mg BFK/kg BW for seven days produceextensive myocardial lesions in horses. The horse dosed with 30mg BFK/kg BW developed less severe, but similar myocardial lesions over a longer duration, this suggests that poisoning may be cumulative and lower doses of longer duration are also toxic. Horses seem to be uniquely sensitive to rayless goldenrod-induced myocardial disease, therefore cardiac troponin I may be a useful marker of rayless goldenrod poisoning in horses. More work is needed to determine which BFK produce myocardial toxicity and better determine the effects of dose and duration on poisoning in horses. •The first report of the benzofuran concentrations in a toxic dose of rayless goldenrod fed to horses.•A complete report of the serum biochemical changes associated with rayless goldenrod poisoning in horses.•Cardiac troponin I is identified as a sensitive marker of rayless goldenrod poisoning in horses.•A complete description of the histopathological changes associated with rayless goldenrod poisoning in horses. © 2013. Source

Scharton D.,Utah State University | Van Wettere A.J.,Utah State University | Van Wettere A.J.,Utah Veterinary Diagnostic Laboratory | Bailey K.W.,Utah State University | And 4 more authors.
PLoS ONE | Year: 2015

Rift Valley fever virus (RVFV) is a formidable pathogen that causes severe disease and abortion in a variety of livestock species and a range of disease in humans that includes hemorrhagic fever, fulminant hepatitis, encephalitis and blindness. The natural transmission cycle involves mosquito vectors, but exposure can also occur through contact with infected fluids and tissues. The lack of approved antiviral therapies and vaccines for human use underlies the importance of small animal models for proof-of-concept efficacy studies. Several mouse and rat models of RVFV infection have been well characterized and provide useful systems for the study of certain aspects of pathogenesis, as well as antiviral drug and vaccine development. However, certain host-directed therapeutics may not act on mouse or rat pathways. Here, we describe the natural history of disease in golden Syrian hamsters challenged subcutaneously with the pathogenic ZH501 strain of RVFV. Peracute disease resulted in rapid lethality within 2 to 3 days of RVFV challenge. High titer viremia and substantial viral loads were observed in most tissues examined; however, histopathology and immunostaining for RVFV antigen were largely restricted to the liver. Acute hepatocellular necrosis associated with a strong presence of viral antigen in the hepatocytes indicates that fulminant hepatitis is the likely cause of mortality. Further studies to assess the susceptibility and disease progression following respiratory route exposure are warranted. The use of the hamsters to model RVFV infection is suitable for early stage antiviral drug and vaccine development studies. © 2015 Scharton et al. Source

Davis T.Z.,U.S. Department of Agriculture | Stegelmeier B.L.,U.S. Department of Agriculture | Hall J.O.,Utah Veterinary Diagnostic Laboratory
Journal of Agricultural and Food Chemistry | Year: 2014

Horses are very susceptible to chronic selenosis if grazed on seleniferous forages for a prolonged period. In this study, mane and tail samples from horses that exhibited classical hoof lesions of chronic selenosis were analyzed by inductively coupled plasma mass spectrometry for selenium (Se) content. The horses had grazed for 6 months, from approximately May 15 until November 15, each year for three grazing seasons in a pasture containing seleniferous forages and water sources with elevated Se concentrations. The segmented hair samples showed a cyclic pattern in Se concentrations in the mane and tail, which corresponded to entering and exiting the contaminated pasture. The Se concentration in the tail of one horse could be traced for three grazing seasons. These results demonstrate that in some cases hair samples can be used to determine Se exposure in horses for up to 3 years postexposure. © 2014 American Chemical Society. Source

Davis T.Z.,U.S. Department of Agriculture | Stegelmeier B.L.,U.S. Department of Agriculture | Welch K.D.,U.S. Department of Agriculture | Pfister J.A.,U.S. Department of Agriculture | And 2 more authors.
Journal of Animal Science | Year: 2013

Consumption of Se accumulator plants by livestock can result in Se intoxication. Recent research indicates that the Se forms most common in Se accumulator plants are selenate and Se-methylselenocysteine (MeSeCys). In this study the absorption, distribution, and elimination kinetics of Se in serum and whole blood of lambs dosed with a single oral dose of (1, 2, 3, or 4 mg Se/kg BW) of sodium selenate or MeSeCys were determined. The Se concentrations in serum and whole blood for both chemical forms of Se followed simple dose-dependent relationships. Se-methylselenocysteine was absorbed more quickly and to a greater extent in whole blood than sodium selenate, as observed by a greater peak Se concentration (Cmax; P < 0.0001), and faster time to peak concentration (Tmax; P < 0.0001) and rate of absorption (P < 0.0001). The rate of absorption and Tmax were also faster (P < 0.0001) in serum of lambs dosed with MeSeCys compared with those dosed sodium selenate at equimolar doses; however, Cmax in serum was greater (P < 0.0001) in lambs dosed with sodium selenate compared with those dosed MeSeCys at equimolar doses. The MeSeCys was absorbed 4 to 5 times faster into serum and 9 to 14 times faster into whole blood at equimolar Se doses. There were dose-dependent increases in the area under the curve (AUC) for Se in serum and whole blood of lambs dosed with both sodium selenate and MeSeCys. In whole blood the MeSeCys was approximately twice as bioavailable as sodium selenate at equimolar doses as observed by the AUC, whereas in serum there were no differences (P > 0.05) in AUC at the same doses. At 168 h postdosing the Se concentration in whole blood remained much greater (P < 0.0001) in lambs dosed with MeSeCys as compared with lambs dosed with sodium selenate; however, the serum Se concentrations were not different between treatments at the same time point. The results presented in this study demonstrate that there are differences between the kinetics of different selenocompounds when orally dosed to sheep. Therefore, in cases of acute selenosis, it is important to understand the chemical form to which an intoxicated animal was exposed when determining the importance and meaning of Se concentration in serum or whole blood obtained at various times postexposure. © 2013 American Society of Animal Science. All rights reserved. Source

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