Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighteen mixed-breed beef cattle died as the result of consuming "tacky lithium grease" discarded from a rubber reclaiming plant. Four experimental groups of mature cattle were given oral doses of a lithium salt at levels of 0, 20, 500, and 700 mg/kg body weight. Although all animals in the 250 mg/kg group showed signs of intoxication, the signs were mild and transient. Doses of 500 and 700 mg/kg proved toxic and fatal. Signs, serum levels, and tissue-organ deposition were dose and time-related. Signs of intoxication were salivation, depression, anorexia, hypodipsia, anuria, and diarrhea. The high dose group also showed severe depression and ataxia. The highest mean lithium serum values were 19, 40, and 54 ppm for the 250, 500, and 700 mg/kg groups, respectively. Postmortem and histopathologic examinations revealed dose-related gastroenteritis, slight interstitial nephritis, and hepatic cirrhosis. Tissue residues of lithium were in striated muscle (86.8 ppm), heart (79.3 ppm), liver (68.7 ppm), kidney (67.1 ppm) , and brain (51.8 ppm), in the high dose group. Since serum levels of cattle consuming the "tacky lithium grease" were 0.49 ppm of lithium, we believe other contaminants in this discarded grease may have caused or enhanced the toxic effect of lithium.
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PMID:Lithium toxicity in cattle. 740 86

The acute and subchronic toxicity of monenzine (preparation Elancoban -- 100 of Elanco Co., USA) to male lambs for fattening aged 3-4 months and weighing 16-28.5 kg was studied. It was established that the single per oral dose of 5 mg/kg weight of the natrium monoenzine salt causes a temporary lack of appetitie but no changes in the behavior and the general state of the animals. The use of a 10 and 30 mg/kg weight dose of the preparation led to death of the lambs on the 72nd-120th hour. The toxicity was clinically manifested by anurexia, arumination, ataxia, paresis, and paralysis of the limbs, tachicardia, taxipnea, hypothermia and showed down and weakened rumen movements. Erosive rumitis and abomasis, catharrhalhemorrhagis duodenitis, hemorrhages on the epicardis, hyperremia and parenchymal organ oedema, 3-4 times increased gall-bladder with numerous nodes having a sunken center on its walls were observed pathologo-anatomically, while microscopically blood vessel disturbances (hyperremia, hemorrhages and oedema) of the lungs, heart, spleen, endocrinal glands (thyroid, adrenal and hypophysis), the brain, and the leptomeninges, liver distrophy, distrophic nephrosis and necrotic holecystitis were obvious. Following a long term (30 days) application to the fodder in 10 and 50 g/t doses, monenzine-natrium does not have a negative effect on the behaviour, general condition, clinical and biochemical blood composition and the structural build up of the inner organs, but in the first 5-10 days of the treatment it causes loss of appetite. Additional specific investigations are needed to elucidate the effect of the preparation on body gain.
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PMID:[Acute and subchronic monensin toxicity for lambs]. 741 27

A Holstein cow was intubated with 182 mg of 97% pure T-2 toxin (0.44 mg/kg of body weight) for 15 days. A dairy ration containing 50 mg/kg (50 ppm) of T-2 toxin was refused. A calf, born four days after onset of maternal treatment, was intubated with 26.2 mg of purified T-2 toxin (0.6 mg/kg of body weight) for seven consecutive days and then on alternate days for a total of 16 days. The calf was severely affected clinically by the T-2 toxin. The T-2 toxin failed to cause bovine hemorrhagic syndrome in either animal. Unspecific gastrointestinal lesions were noted in the cow but none were detected in the calf. In the calf, severe depression, hindquarter ataxia, knuckling of the rear feet, listlessness and anorexia were caused by the T-2 toxin.
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PMID:The failure of purified T-2 mycotoxin to produce hemorrhaging in dairy cattle. 742 50

An adult horse with a 2-month history of anorexia, ataxia, and oral blisters had developed these clinical signs just prior to the appearance and growth of a cervical mass. Bullous stomatitis was characterized histologically as subepidermal clefting. Clinical signs were unresponsive to treatment with antibiotics or corticosteroids; however, surgical removal of the mass coincided with remission of all signs. Histologic findings of the mass were consistent with hemangiosarcoma. Results of indirect immunofluorescence and immunoprecipitation on frozen serum from the horse were characteristic of paraneoplastic pemphigus in human beings, a newly recognized mucocutaneous autoimmune disease associated with neoplasia.
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PMID:Paraneoplastic bullous stomatitis in a horse. 762 36

We reported a case of opsoclonus-myoclonus syndrome. A 63-year-old man was admitted to Kenwakai Hospital with rapidly progressing symptoms, including lumbago, whole body pain, vertigo, nausea, and anorexia. He became bed-ridden because of severe vertigo and truncal ataxia. Five days after admission, he developed opsoclonus followed by myoclonus and mild disturbance of consciousness, but he showed no appendicular ataxia or pyramidal tract sign. He was treated with prednisolone, 40 mg/day, which was effective for disturbance of consciousness, but opsoclonus and myoclonus persisted. He died of liver dysfunction and ventricular fibrillation 3 weeks after onset. Blood examination revealed high LDH (1,106 IU/l), Al-P, and gamma-GTP titers. Tumor markers were normal except for increase NSE activity (129 ng/ml). The cerebrospinal fluid showed normal cell count, 63.9 mg/dl of protein, 7.3 mg/dl of IgG, and normal glucose. A cranial CT scan showed an old lacune only. Chest rentgenogram and CT scan revealed mediastinal and hilar lymph node enlargement. An abdominal CT scan showed multiple low density masses in the liver. Small cell lung cancer associated with opsoclonus-myoclonus syndrome was suspected. Western blot analysis revealed that his serum reacted with protein in the cerebellum, cerebrum, and dorsal root ganglion with a molecular weight of 77 kDa. This is the first time such an antibody was ever been detected in patients with opsoclonus-myoclonus syndrome. The molecular weights of the antigens previously found by the serum of patients with this syndrome, were 55 kDa and 80 kDa in patients with breast cancer, and 210 kDa in patients with neuroblastoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of opsoclonus-myoclonus syndrome associated with anti-central nervous system antibody]. 782 Sep 64

This article describes the metabolic investigations to be applied in any clinical situation consistent with a late acute form of inborn error of metabolism: unexplained coma with or without focal neurological manifestations, recurrent vomiting with lethargy, episodes of ataxia with or without behaviour disorder, fits of psychiatric troubles. In each of these situations, careful medical history is of major importance searching for previous clinical manifestations such as episodes of coma, ataxia or vomiting, anorexia, failure to thrive, developmental delay, all very suggestive of metabolic disorder. The association of neurological symptoms and abnormal hepatic tests is also of great value and must not lead to the diagnosis of Reye's syndrome without considering a metabolic defect of fatty acid oxidation, urea cycle, respiratory chain, or Wilson's disease. When looking for an etiological origin, it is mandatory to collect all the biological information at the same time, also knowing that metabolic abnormalities may be mild and transitory, and that many of them are non specific (metabolic acidosis, hyperlactacidemia, hyperammonemia, hepatic tests disturbances) being encountered in collapsus, shock and multiple organ failure syndrome.
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PMID:[Diagnosis of metabolic coma in children]. 784 29

An epizootic of encephalomyelitis attributable to western equine encephalitis virus was identified in emus (Dromaius novaehollandiae) from several flocks in western Texas in July 1992. Affected emus ranged from 3 months to 3 years old. Morbidity of emus in 8 flocks ranged from 15 to 50%, and 17 of 193 (8.8%) emus died. The diagnosis was confirmed by isolation and characterization of the causative virus and detection of antibody to the virus in emus that were currently ill and emus that had been ill but recovered. Clinical signs varied from mild to severe and included anorexia, lethargy with sternal recumbency, ataxia, muscle tremors, head tilt, unnatural positioning of the head on the back, acute onset of paralysis, and lateral recumbency with paddling. A few emus died without prior evidence of clinical disease. Post-mortem examination revealed 3 to 5 ml of clear pale-yellow pericardial fluid that contained a fibrin clot. Volume of the contents of the proventriculus and ventriculus were less than anticipated. Microscopic examination of numerous tissues revealed multifocal vasculitis with infiltration of plasmacytes, lymphocytes, and a few heterophilic leukocytes. The epizootic developed during a period of unseasonably heavy rainfall that resulted in higher numbers of mosquitoes than was typical for that season of year. A concurrent increase in the number of horses with encephalomyelitis attributable to western equine encephalities virus was not reported.
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PMID:An epizootic attributable to western equine encephalitis virus infection in emus in Texas. 796 Oct 99

The toxicology of narasin has been extensively investigated in several species of laboratory animals. Acute median lethal po doses varied considerably between species (> 10 to 40.8 mg/kg). Animals of various species given acutely toxic doses of narasin manifested similar clinical signs of toxicity, including anorexia, hypoactivity, leg weakness, ataxia, depression and diarrhea. Clinical effects were usually delayed 1 to several days, depending on the dose, and some were reversible even with continued narasin administration. In repeated dose toxicity studies, narasin dosages have been demonstrated at which animals could be exposed daily for long periods of time without producing harmful effects. The no-observed effect levels (NOELs) by the dietary route were 60 ppm in mice and 15 ppm in rats after 3 mo of dosing and 15 ppm in rats after 1 y. In dogs, NOELs were 1 mg/kg body weight after 3 mo and 0.5 mg/kg body weight after 1 y of dosing. In breeding animals, narasin did not affect reproductive performance through 4 generations and was not teratogenic. Two-y chronic bioassays in 2 rodent species showed that narasin did not produce cumulative toxicity or carcinogenicity. In genetic toxicity tests narasin was not mutagenic to bacterial or mammalian cells and did not induce DNA repair or sister chromatid exchange. Narasin neither caused dermal toxicity nor skin sensitization, but was a severe eye irritant in rabbits. In dogs, local irritation and systemic toxicity occurred following repeated inhalation exposure to narasin aerosol concentrations greater than 0.114 mg/M3 of air.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The comparative toxicology of narasin in laboratory animals. 797 39

Between 1983 and 1990 a total of 74 freestyle mountaineers and 88 mountaineers with skis attempted to climb Mount Agri (Ararat). From the freestyle group two mountaineers were affected by acclimatisation disorder at 3200 m and seven at 4200 m above sea level. Acute mountain sickness (AMS) affected four mountaineers at 4200 m, eight at 4700 m, two at 5000 m and two at 5165 m, while 49 reached the summit. Only one of the mountaineers with skis was affected by AMS (at 4200 m), while all the others reached the summit. The symptoms of acclimatisation disorder and AMS, according to their degree of frequency, were headache, weakness, dyspnoea and palpitation, anorexia, nausea, vomiting, giddiness, ataxia and insomnia. Pulse rates varied between 115 and 124/min, and breathing between 30 and 38/min.
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PMID:Cases of acute mountain sickness on Mount Agri. 803 91

One hundred fifty lactating mink on one ranch in southern Ontario were monitored over the lactation period in 1989 for evidence of clinical disease, and serial blood samples were collected for biochemical analysis. Antemortem blood samples were collected and necropsies performed on the 17 females that developed nursing disease and on 17 controls matched to the same stage of lactation and on ten nonlactating controls. Twenty-two additional nursing disease cases were selected from seven ranches in the following year and processed similarly. The clinical signs typically observed in affected females were sudden onset lethargy and anorexia followed by dehydration, ataxia, and a reluctance to move. The major clinical-pathologic findings were a marked increase in serum osmolality and total protein, urea nitrogen, creatinine, phosphorus, glucose, and potassium concentrations and a decrease in sodium and chloride concentration. In addition, the animals were acidotic, there was a reduction in the urine specific gravity, and the hemogram was consistent with a stress response. Emaciation and dehydration were the only pathologic changes consistently present in cases of nursing disease and not in controls. In almost all cases, bacteria were not cultured from the liver, spleen, and mammary gland, but Campylobacter jejuni was cultured from the intestinal contents of 15/17 affected mink and 2/5 controls. Aleutian disease virus antibody was not present in any of the affected mink. Lipid vacuoles in hepatocytes and renal tubular epithelium, hypertrophy of cells in the adrenal cortex, and pulmonary congestion and atelectasis were present in both diseased females and controls, as were various sporadic inflammatory lesions. Nursing disease may result from energy depletion due to lactation. All lactating females are affected by this process; clinical disease reflects the terminal physiologic decompensation of the most susceptible individuals.
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PMID:Nursing disease in mink: clinical and postmortem findings. 811 44


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