Showing papers on "White Muscle Disease published in 1997"

White Muscle Disease of Foals

Abstract: White muscle disease (nutritional myodegeneration) of foals is a peracute to subacute myodegenerative disease affecting skeletal and cardiac muscle. It is caused by a dietary deficiency of selenium and vitamin E, usually in association with predisposing factors such as a high intake of dietary unsaturated fats or unaccustomed exercise. White muscle disease has been observed in foals from birth to 1 year of age, particularly those foals born to dams fed selenium-deficient diets during gestation. The disease in foals may present as an acute, fulminant syndrome, which is rapidly fatal, or a subacute syndrome characterized by profound muscular weakness. Failure of passive transfer, aspiration pneumonia, and stunting are frequent complications. Markedly increased muscle enzyme and low glutathione peroxidase activities are common findings in affected foals. Foals with the subacute form of the disease may survive if they are supplemented early with selenium; however, mortality rates ranging from 30% to 45% have been reported, even for this form of the disease.

Electromyographic evaluation of a calf with white muscle disease

Abstract: centrate a day, had a condition score of 2 and was small, weighing only 135 kg. Mucous membranes were moist and pink and the capillary refill time was normal at 2 to 3 seconds. Peripheral pulse was strong and regular with a rate of 70 bpm. The jugular pulse and filling time were also unremarkable. Haematological and biochemical parameters were within the normal ranges. Auscultation of the heart revealed a grade 4/6 holosystolic crescendo-decrescendo coarse murmur with a point of maximal intensity (PMI) cranially on the left side of the thorax, which was also audible as a grade 3/6 murmur with the same characteristics on the right side. There was a wide radiation of the murmur but no precordial thrill. In addition, a grade 3/6 early diastolic decrescendo murmur, with a PMI cranially on the left, was auscultated and audible on the right as a grade 2/6 murmur. An echocardiographic examination was performed. A left parasternal long axis view (Long and others 1992), using a 2-75 MHz mechanical sector ultrasound (Interspec unit), imaged a patent vascular structure originating at the base of the pulmonary artery (Fig 1). Intermittent blood flow within the vessel was confirmed using colour flow Doppler (Fig 2). Examination of the cardiac septum revealed no evidence of a defect at either the ventricular or atrial level and there was no evidence of flow between the ventricles and the atria. On the basis of the characteristics of the cardiac murmurs and the echocardiographic findings, a diagnosis of PDA was made. The heifer was euthanased and a postmortem examination performed. Significant findings consisted of 200 ml of clear fluid within the abdominal cavity, 100 ml of clear fluid within the pericardium, unremarkable cardiac atria and ventricles, and a PDA linking the pulmonary artery and the aorta. The vasculature around the aortic entrance of the PDA had an area of focal roughening approximately

Investigation of Glutathione and Lipid Peroxidation Levels with Respect to Haemoglobin Types in Lambs with White Muscle Disease

Abstract: In this study, haemoglobin types were researched in lambs with White Muscle Disease. Effect of disease to plasma lipid peroxidation and glutathione levels was investigated. The GSH levels by Seutler Methods and Lipid peroxidation were analysed by using calarimetric technique, Haemoglobin types were aLsa determinated by electrophoresis technique. In lambs with White Muscle Disease, MDA (Malondialdehid) levels were 2 .245 ± 0.1 nmal/dl, GSH levels viere 20.08 ± 3.6 mg/di : in healthy lambs, these values were 2.25 ± 0.18 nmol/dl , 42.95 ± 4.4 mg/di respectively. There was statistically significant difference between GSH (p