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)

The toxicity of sodium selenite was studied in 28 Nubian goats, 20 of which died or were killed in extremis 2 h to 21 d after dosing. Single or repeated daily oral doses of 160, 80, 40, 20 and 5 mg sodium selenite/kg were toxic to goats while daily doses of selenite ranging from 0.25 to 1 mg/kg/d for 225 d were not toxic to this species of animals. The main signs of poisoning were uneasiness, inappetence, dyspnea, salivation, diarhea, paresis of the hind limbs, arching of the back, and recumbency. The main lesions were hemorrhages in the rumen, reticulum, osmasum and abomasum, hemorrhagic or catarrhal abomasitis and enteritis, fatty change and necrosis of the centrilobular hepatocytes and of the cells of the renal convoluted tubules, splenic hemosiderosis, pulmonary congestion, haemorrhage, edema and emphysema, accumulation of lymphocytes in the vital organs, and straw-colored fluid in the serous cavities.
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PMID:Experimental selenium poisoning in Nubian goats. 235 37

The clinical, biochemical and pathological effects of the fresh shoots of Chrozophora plicata on Nubian goats and Desert sheep were investigated. The animals were given single or repeated daily doses of 10, 5, 1 and 0.5 g/kg of chrozophora shoots by stomach tube and died at various times post dosing. The main signs of Chrozophora poisoning in both species of ruminants were salivation, dyspnea, bloat, inappetence, dullness, diarrhea, paresis of the hind limbs, recumbency and lateral deviation of the head and neck. The main lesions were hemorrhage in the lungs, heart and kidneys, pulmonary cyanosis and edema, hepatic fatty change and depletion of glycogen, catarrhal enteritis, ascites, hydropericardium and serous atrophy of the cardiac fat and renal pelvis. An increase in the concentration of urea, ammonia and bilirubin and in the activity of GOT and a decrease in total protein were detected in the serum. Hematological changes indicated the development of anemia.
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PMID:Experimental Chrozophora plicata poisoning in goats and sheep. 318 65

Twelve of fifteen 6-9-mo-old clinically healthy Desert sheep were given single or repeated daily doses of 25 to 4000 mg cotoran/kg by drench. Cotoran poisoning was characterized by grinding of the teeth, ruminal tympany, mydriasis, dyspnea, staggering, paresis of the hind and forelimbs, and recumbency. Lesions were widespread congestion and hemorrhage, hepatic fatty change, catarrhal enteritis and degeneration of the epithelial cells of the renal proximal convoluted tubules. These were accompanied by significant increases in the activities of GOT, LDH and GGT and decreases in serum total protein and calcium.
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PMID:Toxicity of cotoran (fluometuron) in Desert sheep. 757 46

The acute toxicity of dried Nerium oleander leaves to Najdi sheep is described in 12 sheep assigned as untreated controls, N. oleander-treated once at 1 and 0.25 g/kg body weight and N. oleander-treated daily at 0.06 g/kg body weight by drench. Single oral doses of 1 or 0.25 g of dried N. oleander leaves/kg body weight caused restlessness, chewing movements of the jaws, dyspnea, ruminal bloat, incoordination of movements, limb paresis, recumbency and death 4-24 hr after dosing. Lesions were widespread congestion or hemorrhage, pulmonary cyanosis and emphysema, hepatorenal fatty change and catarrhal abomasitis and enteritis. The daily oral doses of 0.06 g dried N. oleander leaves/kg body weight caused less severe signs and death occurred between days 3 and 14. In these animals, the main lesions were hepatonephropathy and gelatinization of the renal pelvis and mesentry and were accompanied by significant increases in serum AST and LDH activities, in bilirubin, cholesterol and urea concentrations and significant decreases in total protein and albumin levels, anemia and leucopenia.
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PMID:Acute toxicity of various oral doses of dried Nerium oleander leaves in sheep. 1178 96

An 18-yr-old Bengal tiger (Panthera tigris) presented with acute onset hind limb paresis. Radiographic and ultrasonographic imaging revealed a caudal abdominal aortic thrombus and a cranial mediastinal mass. Necropsy confirmed aortic thrombosis. Necrotizing enteritis and multifocal renal thrombosis were also noted. The cranial mediastinum contained a bilobed mass that histologically and ultrastructurally was consistent with a carcinoid.
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PMID:A thymic carcinoid in a Bengal tiger (Panthera tigris). 1731 79

Non-enterotoxin (CPE)-producing Clostridium perfringens type A has been associated with enteritis in calves. Recent evidence has suggested that a novel toxin, named beta2 (CPB2), is implicated in the pathogenesis of this disease, although there is little evidence supporting this. In the current study, the role of C. perfringens type A in an outbreak of enteritis in calves was studied. Two 20-day-old dairy calves exhibiting apathy and reluctance to eat, with paresis of the anterior limbs, were euthanized for postmortem examination. Gross and histological changes compatible with acute enteritis, rumenitis, meningitis, and pneumonia were seen in both calves. Clostridium perfringens type A non-CPE, non-CPB2 was isolated from the abomasum and the small intestine. Escherichia coli ONTH8 (with cdtBIII and f17 virulence genes detected by polymerase chain reaction) was also isolated from the brain, abomasum, and intestine from both calves. All the samples were negative for Salmonella spp. When the C. perfringens strain was inoculated into bovine ligated small and large intestinal loops, cell detachment, erosion, and hemorrhage of the lamina propria were observed, predominantly in the small intestine. The results suggest that non-CPE, non-CPB2 C. perfringens type A is able to induce pathologic changes in the intestine of calves, probably enhanced by other pathogens, such as some pathogenic E. coli strains.
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PMID:Necrotic enteritis in young calves. 2139 44