Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When 2 horses were dosed with cultures of a Fusarium moniliforme isolate that had previously caused only hepatosis, 1 developed brain oedema and hepatosis, and the other only leukoencephalomalacia. A 3rd horse developed both leukoencephalomalacia and hepatosis after being dosed with another isolate obtained from maize which was associated with a natural outbreak of the nervous form of the disease. Since leukoencephalomalacia and hepatosis could be induced by the same culture material, it was concluded that both syndromes were manifestations of the same toxicosis. There was also some evidence that leukoencephalomalacia might be specifically induced by the administration of smaller doses of the culture material to horses over a longer period. The clinical signs of nervous disorder included ataxia, paresis, apathy, hypersensitivity, frenzy, and other locomotory and psychic disturbances. Autopsy showed that the brains were oedematous, and focal areas of liquefactive necrosis were present in the cerebral white matter. In 1 case the malacic areas were not confined to the subcortical white matter but were microscopically visible in the cerebral cortex as well. An histopathological examination of the areas bordering on the malacic areas revealed rarefication of the white matter, perivascular haemorrhages, oedema and cellular infiltration composed mainly of plasma cells and eosinophiles. Many of the macrophages in these areas contained lipfuscin-like granules, but these granules also occurred extracellularly in the neuropil. In the layers of the cortex nearest the malacic areas, satellitosis and neurophagia were commonly seen.
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PMID:Leukoencephalomalacia: a mycotoxicosis of Equidae caused by Fusarium moniliforme Sheldon. 101 50

Each of two horses was dosed by stomach tube with culture material on maize of Fusarium moniliforme MRC 826. One horse developed severe hepatosis and mild oedema of the brain after 6 doses of 2.5 g of culture material/kg body mass/day in 7 days. The second horse, in a similar experiment but at a dosage rate of 1.25 g/kg/day, developed mild hepatosis and moderate oedema of the brain. In both animals the brain oedema was particularly noticeable in the medulla oblongata. The mycotoxin fumonisin B1 was extracted and purified from the culture material of F. moniliforme MRC, 826 which contained approximately 1 g/kg of this compound. A horse was injected intravenously 7 times from Day 0-Day 9 with 0.125 mg of fumonisin B1/kg body mass/day. Clinical signs of neurotoxicosis, which appeared on Day 8, included nervousness followed by apathy, a wide-based stance, trembling, ataxia, reluctance to move, paresis of the lower lip and tongue, and an inability to eat or drink. Euthanasia was performed on the horse on Day 10 while the animal was in a tetanic convulsion. The principal lesions were severe oedema of the brain and early, bilaterally symmetrical, focal necrosis in the medulla oblongata. This report provides experimental evidence that fumonisin B1, produced by F. moniliforme, causes equine leukoencephalomalacia.
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PMID:Leukoencephalomalacia in a horse induced by fumonisin B1 isolated from Fusarium moniliforme. 321 91

Perioperative complications and deaths occurred while developing a novel surgical model of pediatric kyphosis in 10 to 12 kg male farm-raised Yorkshire piglets. All piglets appeared clinically normal preoperatively. Intraoperative complications included tachycardia, respiratory acidosis, and death. Postoperatively, clinical signs included posterior paresis, head pressing, prolonged anesthetic recovery, difficulty rising, and sudden death. Necropsies were performed on all piglets. Some morbidity and mortality were accurately attributed to the spinal surgery. However, the index piglet for this report died suddenly approximately 16 to 18 h after surgery. Necropsy of this animal revealed clear, serosanguineous pleural and pericardial effusions along with myocardial hemorrhage and hepatic lesions, consistent with mulberry heart disease and hepatosis dietetica, respectively. Serum vitamin E and selenium levels from this animal were below age-specific lab reference ranges. Clinical signs of vitamin E and selenium deficiency are most common in fast-growing weaner piglets. The added stress of major surgery may exacerbate the condition in young piglets. Resolution of morbidity and mortality in both juvenile and adult pigs occurred upon the use of an alternate vendor able to provide feed analyses meeting industry standards, although serum levels of vitamin E and selenium in similar ages and breed of swine were still occasionally slightly below reference ranges.
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PMID:Mulberry Heart Disease and Hepatosis Dietetica in Farm Pigs (Sus scrofa domesticus) in a Research Setting. 3267 51