Showing papers on "White Muscle Disease published in 2005"
TL;DR: Evaluating all examined horses, insufficient whole blood selenium and serum vitamin E concentrations were found in 42% and 96% of horses, respectively, which are important factors in the aetiology of WMD in horses in the Czech Republic.
Abstract: Ludvikova E., P. Jahn, L. Pavlata, M. Vyskoail: Selenium and Vitamin E Status Correlated with Myopathies of Horses Reared in Farms in the Czech Republic. Acta Vet. Brno 2005, 74: 377-384. The objective of the study was to compare selenium and vitamin E status in equine farms with and without occurrence of myopathies in order to evaluate the role of lack of these substances in the aetiology of myopathies in horses in the Czech Republic. Concentrations of selenium (in 136 horses) and vitamin E (in 131 horses) and glutathione peroxidase (GSH-Px) activities (in 136 horses) were measured in horses from farms with the occurrence of myopathies (group M including 46 horses from 10 farms) and in horses from farms without occurrence of myopathies (group H including 90 horses from 22 farms). Significantly lower concentrations of selenium (43.09 ±36.84 µg·l -1 ; p < 0.001), vitamin E (9.55 ± 9.29 µmol·l -1 ; p < 0.01) and GSH-Px activities (153.38 ± 177.28 µkat·l-1; p < 0.001) were found in horses from the farms with the occurrence of myopathies when compared to those without the occurrence of myopathies (Se 117.35 ± 52.10 µg·l-1; vitamin E 10.75 ± 4.34 µmol·l-1; GSH-Px 397.41 ± 242.15 µkat·l-1). The diagnosis of nutritional myodegeneration (white muscle disease, WMD) was established in six horses with myopathy. The aetiology of myopathy in the other four affected horses was probably different. Evaluating all examined horses, insufficient whole blood selenium and serum vitamin E concentrations were found in 42% and 96% of horses, respectively. Poor saturation with selenium and vitamin Eare important factors in the aetiology of WMD in horses in the Czech Republic. Apart from WMD, horses in the Czech Republic may be affected by some other myopathies. Glutathione peroxidase, nutritional myodegeneration, white muscle disease, tocopherol, creatine kinase, aspartate aminotransferase
15 citations
01 Jan 2005
TL;DR: In this article, an outbreak of white muscle disease was reported in a flock of 56 Red Friesian calves, where 18 calves of 4 to 5 months of age died in a period of 45 days.
Abstract: An outbreak of White Muscle Disease, WMD, or Nutritional Muscular Dystrophy is reported in a flock of 56 Red Friesian calves, where 18 calves of 4 to 5 months of age died in a period of 45 days. The signs observed were tachypnea, difficulty to walk, tachycardia, dilated jugular veins, temperature 3839°C. Signs of alterations of the nervous or digestive systems were not observed. Muscles of the hind legs, dorsal and gluteal region were moderate swollen, painful and temperature was increased. In the flock sudden deaths of calves were observed within a few hours after appears the first signs. The blood activity of the selenium (Se) dependent enzyme Glutation peroxidase (GSH-Px) was decreased, indicating a Se deficiency. The serum activity of the enzymes associated to muscle damage, Aspartate Amino Transferase (AST) and Creatin Kinase (CK) were increased. The necropsy findings were cardiac enlargement with hypertrophy of the right ventricle. In the myocardium white fine lines of degeneration and also multiple irregular areas with the same colour were observed. Similar lesions were observed on the skeletal muscles. Histologically the myocardium lesions were eosinophilic and irregular muscular cells, with lost of the striation, segmental destruction, as well as great and pleomorfic nuclei; in addition, the Purkinje fibres presented intense eosinophilia and hyaline degeneration corresponding to degeneration of Zenker. The skeletal muscles also presented hyaline degeneration of Zenker. It is concludes that it is White Muscle Disease associated to deficiency of Selenium or vitamin E. Surviving calves were treated with an intramuscular solution of Se and vitamin E, in dose equivalent to 8 mg of Se and 340 U.I. of vitamin E. The treatment was repeated after 7 days and new cases did not appear.
2 citations