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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of a single IM injection of selenium-vitamin E (Se-E; 5 mg of Se + 68 IU of alpha-tocopherol/60 kg of body weight) as a pretreatment 14 days before an oral dose of aflatoxin B1 (1.0 mg/kg) were studied in 24 dairy calves. Treatment groups were designated as follows: group 1 = no Se-E or aflatoxin B1 (control); group 2 = Se-E supplementation only; group 3 = aflatoxin B1 dose only; and group 4 = Se-E supplementation before aflatoxin B1 dose. Clinical signs of toxicosis in aflatoxin B1-treated calves included anorexia, ataxia, rough haircoats, increased respiration rates, dyspnea, dehydration, and nasal discharge. Packed-cell volume, RBC, WBC, and hemoglobin were increased in aflatoxin-treated calves. Significant increases in serum aspartate aminotransferase (P less than 0.05) and gamma-glutamyl-transferase (P less than 0.001) activities and prothrombin times (P less than 0.001) were observed in aflatoxin-treated calves, indicating that there was hepatic involvement. Although aflatoxin exposure caused a significant decrease in body weight (P less than 0.01) and feed intake (P less than 0.001) in treatment groups 3 and 4, Se was demonstrated to interact significantly (P less than 0.001) with aflatoxin B1 for feed intake, causing an improved feed intake in treatment group 4 calves.
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PMID:Aflatoxin B1 toxicosis in dairy calves pretreated with selenium-vitamin E. 308 Sep 29

Toxicity to butyrate was observed in 100-250 kg male Holstein calves following intravenous injection of 0.7-3.6 mmole/kg body weight, intravenous infusion with 0.12-0.53 mmole/min/kg body weight and intraruminal dosage with 19.4 mmole/kg body weight butyrate. Lower doses produced ataxia and serous nasal discharge. Higher doses produced sudden flaccid paralysis and death from asphyxia. No postmortem lesions, gross or histological, were observed. Plasma K+ was reduced to 2.2-2.5 mEq/L. When infusions were stopped, rapid recovery preceded clearance of butyrate and low K+ remained. Nerve depolarization in the central nervous system may be the cause of the toxic effects. Butyrate acidosis is suggested as a factor in unexplained sudden deaths in ruminants.
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PMID:Excess rumen product anions in cattle. II. Toxic and lethal effects with butyrate. 688 90

An outbreak of equine herpesvirus-1 (EHV-1) occurred on a large stud farm with 133 mares, 54 foals and four stallions, and at least 85 mares, 22 foals and three stallions were infected. Clinical disease was observed in 16 mares, two stallions and 13 foals and the predominant clinical signs were scrotal oedema, ataxia and loss of libido in the stallions, ataxia and recumbency in the mares and uveitis and nasal discharge in the foals, although pneumonia and colic with intussusception were also recorded at autopsy. Neurological disease was more common in the mares nursing foals (12 of 38 infected) than in barren mares (one of 46 infected). Three mares died during the outbreak and no mares that had been recumbent bred again. Control procedures were based on virological and serological testing and stringent management practices to limit the spread of infection between groups of mares and foals and away from the stud farm. There were marked antibody responses in the adult horses, but they were generally poor in the foals; three of the nine viraemic foals did not develop significant increases in the levels of circulating antibody. Recommendations are made for the management of future outbreaks.
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PMID:Clinical, serological and virological characteristics of an outbreak of paresis and neonatal foal disease due to equine herpesvirus-1 on a stud farm. 790 Feb 64

Clinical and pathologic findings of avian paramyxovirus type 1 (PMV-1) in 19 houbara bustards (Chlamydotis undulata macqueenii) imported from Pakistan into the United Arab Emirates and one captive-bred bird are reported. Clinical signs included circling, walking backward, ataxia, opisthotonos, torticollis, recumbency, head tilt, head shaking, head tremor, tucking of head under keel, nasal discharge, conjunctivitis, and diarrhea. The length of time imported birds exhibited clinical signs varied from 4 days to 18 mo after importation. Hemagglutinating antibodies against PMV-1 were detected in the sera of all 17 birds from which blood samples were collected, and PMV-1 was isolated from pooled brain, spleen, and lung tissues from two birds with acute clinical signs. There were no distinctive gross lesions at necropsy, and histologic findings were consistent with but not pathognomonic for PMV-1. All houbara bustards managed in a captive breeding and restoration program established by the National Avian Research Center have been vaccinated against PMV-1 since October 1992, and no case of PMV-1 has been reported in this collection since that time.
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PMID:Avian paramyxovirus type 1 infection in houbara bustards (Chlamydotis undulata macqueenii): clinical and pathologic findings. 936 47

A 5-year-old cow was evaluated because of a 2-week history of ataxia and other vague neurologic signs. Previous treatments included intravenous and orally administered calcium, but improvement was not seen. Bilateral mucoserous nasal discharge and a pair of firm, smooth masses caudodorsal to the eyes were found on the frontal bones on physical examination. The cow's condition deteriorated rapidly within 48 hours; head pressing and inability to rise were observed. The frontal sinuses were radiographically normal. Trephination of the frontal sinuses revealed a space-occupying mass that was interpreted on histologic examination to be lymphosarcoma. Other evidence of neoplasia was not discovered on gross necropsy or histologic examination. Primary lymphosarcoma has not been described at this location in cows. Clinically it resembles chronic frontal sinusitis, and trephination may be necessary to differentiate the 2 diseases.
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PMID:Lymphosarcoma of the frontal sinus and nasal passage in a cow. 982 47

Five of 24 cows pastured in a 40-acre field in east Tennessee died after they consumed leaves from a privet (Ligustrum amurease) hedge. Clinical findings included ataxia, recumbency with an inability to stand, depression, greenish nasal discharge, cessation of rumination, normal body temperature, and increased heart and respiratory rates. Differential diagnoses included grass tetany, nitrate toxicosis, and plant toxicosis. Privet toxicosis was confirmed by finding privet in ruminal contents, by the presence of a large quantity of privet in the field, by observing places where this privet had been eaten by the cows, by the immediate cessation of the problem when the cows were removed from the field, and by observing no recurrent problems after the privet was destroyed with a herbicide and the cows were returned to the field.
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PMID:Fatal privet (Ligustrum amurease) toxicosis in Tennessee cows. 1092 96

Oxazepam and related benzodiazepine drugs are used in the treatment of anxiety. All benzodiazepines currently in use share a number of effects, including sedation, hypnosis, decreased anxiety, muscle relaxation, amnesia, and anticonvulsant activity. Oxazepam and four other benzodiazepines (chlordiazepoxide, chlorazepate, diazepam, and flurazepam) were nominated for study by the Food and Drug Administration (FDA) and by the NIEHS based on their widespread use, use by pregnant women, and the lack of adequate rodent carcinogenicity studies. Oxazepam was evaluated in 14-week and 2-year studies by the NTP, and Technical Report No. 443 contains the results of the studies performed with the Swiss-Webster and B6C3F1 strains of mice. Studies with rats were not initiated at the same time as the mouse studies because adequate carcinogenicity studies of oxazepam with the Sprague-Dawley rat strain had been submitted to the FDA. Subsequently, because of the marked neoplastic responses found in the two mouse strains, the NTP initiated 2-year studies of oxazepam with the F344/N rat. Groups of male and female F344/N rats were exposed to oxazepam (greater than 99% pure) in feed for 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium and cultured Chinese hamster ovary cells, and mouse peripheral blood samples were analyzed for the frequency of micronucleated normochromatic erythrocytes. 2-YEAR STUDY: Groups of 50 male and 50 female F344/N rats were fed diets containing 0, 625, 2,500, or 5,000 ppm oxazepam for up to 105 weeks. A stop-exposure group of 50 males and 50 females received 10,000 ppm oxazepam in feed for 26 weeks, after which animals received undosed feed for the remainder of the 2-year study. The continuous-exposure concentrations resulted in average daily doses of 25, 100, or 250 mg oxazepam/kg body weight to males and 25, 110, or 220 mg/kg to females. Stop- exposure males and females received an average daily dose of 630 mg/kg during the exposure period. Survival, Body Weights, and Clinical Findings: All 5,000 ppm continuous-exposure and 10,000 ppm stop-exposure males died before the end of the study. Survival of 2,500 ppm continuous-exposure males and females was significantly less than that of the controls. The mean body weight gains of 2,500 and 5,000 ppm males and females were less than those of the controls throughout the study. The mean body weights of 10,000 ppm stop-exposure males were generally less than those of the controls throughout the study; those of 10,000 ppm stop-exposure females were less than those of the controls during the exposure portion of the study but increased steadily after the cessation of dosing at week 27. Feed consumption by exposed groups was similar to that by the controls after week 1 of the study. Treatment-related eye/nasal discharge, hyperactivity when handled, and/or ataxia were observed in exposed male and female rats on or about day 2 of exposure but were no longer apparent after day 7. Plasma Oxazepam Determinations: Plasma oxazepam concentrations were measured at the end of the study. The concentrations ranged from approximately 0.5 (625 ppm males) to 2.8 &mgr;g/mL (5,000 ppm females). Pathology Findings: In the standard histopathologic evaluation, the incidence of renal tubule adenoma was slightly increased in male rats exposed to 2,500 ppm and was at the upper limit of the historical control range for this neoplasm in 2-year NTP feed studies. In an extended evaluation (step section) of the kidneys of male rats, the incidences of renal tubule adenoma occurred with a positive trend in exposed groups. In standard and step sections (combined), male rats exposed to 2,500 or 5,000 ppm showed a significant increase in the incidences of renal tubule adenoma and hyperplasia. In addition, the incidences of renal tubule adenoma and hyperplasia were significantly increased in the 10,000 ppm stop-exposure group. The incidences of nephropathy in continuously exposed female rats were significantly greater than in the controls, and the severity of nephropathy increased wised with increasing exposure concentration in males. The incidences of epithelial hyperplasia and chronic inflammation of the forestomach in males exposed to 2,500 and 5,000 ppm and of ulcers in 2,500 ppm males were significantly greater than in the controls. Incidences of mineralization of the glandular stomach in 5,000 ppm and 10,000 ppm (stop-exposure) males and of erosion of the duodenum in 5,000 ppm males were significantly greater than in the controls. Female rats exposed to 2,500 ppm had greater incidences of epithelial hyperplasia, chronic inflammation, and ulcers of the forestomach and of erosion in the glandular stomach. Centrilobular hepatocyte hypertrophy occurred more frequently in 2,500 and 5,000 ppm males and females than in the controls. GENETIC TOXICOLOGY: Oxazepam was not mutagenic in any of several strains of S. typhimurium, nor did it induce sister chromatid exchanges or chromosomal aberrations in cultured Chinese hamster ovary cells. These in vitro tests were performed with and without S9 metabolic activation. Results from an in vivo mouse peripheral blood micronucleus test performed on B6C3F1 mice used in a 14-week study were also negative. CONCLUSIONS: In summary, under the conditions of these 2-year dosed-feed studies, there was equivocal evidence of carcinogenic activity in male F344/N rats, based on small increases in the incidences of renal tubule adenomas in exposed groups also exhibiting significantly enhanced nephropathy. There was no evidence of carcinogenic activity of oxazepam in female F344/N rats exposed to feed containing 625, 2,500, or 5,000 ppm for 2 years or 10,000 ppm for 6 months. Administration of oxazepam to rats resulted in nonneoplastic lesions in the forestomach, glandular stomach, and small intestine as well as centrilobular hypertrophy of hepatocytes in the liver. In addition, nephropathy was increased in incidence in female rats and was markedly increased in severity in male rats, resulting in early mortality at the higher exposure concentrations. Synonym: 7-Chloro-1,3-dihydro-3-hydroxy-5-phenyl-2H-1,4-benzodiazepin-2-one Trade Names: Tazepam, Wy-3498, Serax
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PMID:NTP Toxicology and Carcinogenesis Studies of Oxazepam (CAS No. 604-75-1) in F344/N Rats (Feed Studies). 1257 5

Monochloroacetic acid, a colorless crystalline material, is used as a postemergence contact herbicide and as an intermediate in the synthesis of other organic compounds. Toxicology and carcinogenicity studies were conducted by administering monochloroacetic acid (99% pure) in deionized water by gavage to groups of F344/N rats and B6C3F1 mice of each sex once daily, 5 days per week for 16 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, mouse lymphoma L5178Y cells, Chinese hamster ovary cells, and Drosophila melanogaster. 16-Day Studies: Groups of five rats of each sex received 0, 7.5, 15, 30, 60, or 120 mg monochloroacetic acid/kg body weight. Doses administered to mice were 0, 15, 30, 60, 120, or 240 mg/kg to groups of five males and 0, 30, 60, 120, 240, or 480 mg/kg to groups of five females. One of five male rats given 120 mg/kg died during the studies. Clear nasal discharge, lacrimation, or both, were observed in all groups of male and female rats receiving monochloroacetic acid. No compound-related gross lesions were observed in rats. All male mice given 240 mg/kg and all females given 240 or 480 mg/kg died during the studies. Hypoactivity, piloerection, ataxia, and lacrimation were observed in mice given 240 or 480 mg/kg. No compound-related gross lesions were observed in mice at necropsy. 13-Week Studies: Groups of 20 rats of each sex received 0, 30, 60, 90, 120, or 150 mg/kg monochloroacetic acid, and groups of 20 mice of each sex received doses of 0, 25, 50, 100, 150, or 200 mg/kg. Three to five animals in each dose group were killed at weeks 4 and 8 for the evaluation of hematology parameters. Compound-related deaths occurred in rats in the three highest dose groups (all males given 120 or 150 mg/kg, 9/10 males given 90 mg/kg, and all females given 90 to 150 mg/kg) and in mice given 200 mg/kg (all males and 2/10 females). Final mean body weights of surviving rats and mice receiving monochloroacetic acid were similar to those of controls. In rats, dose-related increases in blood urea nitrogen, alanine aminotransferase, and aspartate aminotransferase levels were observed, and relative liver and kidney weights were elevated. There were no compound-related changes in the various hematologic or clinical pathology parameters in mice. A dose-related increase in the incidence and severity of cardiomyopathy was observed in male and female rats receiving monochloroacetic acid, and hepatocellular cytoplasmic vacuolization was observed in the high-dose mice that died during the studies. 2-Year Studies: Based on the mortality and compound-related histopathologic lesions observed in the 13-week studies, doses selected for the 2-year studies of monochloroacetic acid were 0, 15, or 30 mg/kg, administered to groups of 70 rats of each sex, and 0, 50, or 100 mg/kg, administered to groups of 60 mice of each sex. Interim evaluations were conducted on 10 rats per dose group after 6 months of treatment with monochloroacetic acid and on seven rats per dose group after 15 months of treatment. Body Weight and Survival in the 2-Year Studies: Mean body weights of low- and high-dose female and low-dose male rats receiving monochloroacetic acid were within 10% of those of controls throughout the studies; however, after week 30, the mean body weights of high-dose male rats were 4% to 8% less than those of controls. In mice, the mean body weights of dosed males were similar to controls, but those of low- and high-dose females were 6% to 10% less than control values after week 52. Survival of high-dose male and dosed female rats and high-dose male mice was significantly lower than that of controls (male rats: control, 27/53; low-dose, 21/53; high-dose, 16/53; female rats: 37/53; 19/53; 26/53; male mice: 46/60; 39/60; 21/60; female mice: 42/60; 40/60; 44/60). Neoplasms and Nonneoplastic Lesions in the 2-Year Studies: There was no compound-related increase in the incidence of neoplasms or nonneoplastic lesions in rats given monochloroacetic acid for 2 years. The incidence of uterine stromal polypss. The incidence of uterine stromal polyps in low- and high-dose female rats was slightly higher than that in controls (2/60; 7/57; 10/60). However, the incidence in the controls was unusually low, and those in the dosed groups were well within the range for NTP historical controls (mean: 21%, range: 10%-38%). Further, because the only malignant stromal neoplasm occurred in a control animal, the polyps were not considered to be related to the administration of monochloroacetic acid. Similarly, there was no monochloroacetic acid-related increase in the incidence of neoplasms in male or female mice, and malignant lymphoma occurred with a significant negative trend in dosed female mice. Increases in the incidence of inflammation of the mucosa of the nasal passages, respiratory epithelial metaplasia of the olfactory epithelium of the nose, and focal squamous cell hyperplasia of the forestomach occurred in dosed male and female mice. Genetic Toxicology: Monochloroacetic acid was not mutagenic in Salmonella typhimurium strains TA100, TA1535, TA1537, or TA98, with or without exogenous metabolic activation (S9). It induced trifluorothymidine resistance in L5178Y cells in the absence of S9 and induced sister chromatid exchanges without S9 in Chinese hamster ovary cells. Monochloroacetic acid did not induce a significant increase in chromosomal aberrations in Chinese hamster ovary cells, with or without S9. Monochloroacetic acid administered in feed was negative for the induction of sex-linked recessive lethal mutations in germ cells of male Drosophila melanogaster; however, when it was administered by injection, the results were equivocal. Conclusions: Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity for monochloroacetic acid in male or female F344/N rats given 15 or 30 mg/kg. There was no evidence of carcinogenic activity for monochloroacetic acid in male or female B6C3F1 mice given 50 or 100 mg/kg. Monochloroacetic acid administration was associated with inflammatory lesions of the nasal mucosa, metaplasia of the olfactory epithelium, and squamous cell hyperplasia of the forestomach in male and female mice. Synonyms: Chloroacetic acid, a-chloroacetic acid, chloroethanoic acid
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PMID:NTP Toxicology and Carcinogenesis Studies of Monochloroacetic Acid (CAS No. 79-11-8) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1263 63

Blastomycosis was diagnosed in six nondomestic felids from eastern Tennessee, including two Asian lions (Panthera leo persicus), one African lion (Panthera leo), one Siberian tiger (Panthera tigris), one cheetah (Acinonyx jubatus), and one snow leopard (Panthera uncia). Clinical signs included lethargy, anorexia, weight loss, dyspnea, sneezing. ataxia, and paresis. Variable nonspecific changes included leukocytosis, monocytosis, moderate left shift of neutrophils, moderate hypercalcemia, hyperproteinemia, and hyperglobulinemia. Thoracic radiographs revealed interstitial and alveolar changes, consolidation or collapse of a lung lobe, bullae formation, and a pulmonary mass. Agar gel immunodiffusion (AGID) serology for Blastomyces dermatitidis was performed in five felids and was positive in three. The tiger had cerebral blastomycosis and was positive for AGID serologic tests of both cerebrospinal fluid and serum. One percutaneous lung aspirate in the snow leopard and one bronchial aspirate in an Asian lion demonstrated B. dermatitidis organisms. whereas tracheal wash samples and a nasal discharge were nondiagnostic in others. Treatment with itraconazole was attempted in four cats. The tiger improved before euthanasia, whereas the others did not survive beyond initial treatments. In four felids, B. dermatitidis was found in the lungs and tracheobronchial lymph nodes associated with a florid pyogranulomatous reaction; the tiger had a pyogranulomatous encephalomyelitis, and the cheetah had a single pulmonary granuloma. Thoracic radiography, cytologic examination of lung lesion aspirates, and B. dermatitidis AGID serology should be performed on clinically ill zoo felids in endemic areas to rule out blastomycosis.
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PMID:Blastomycosis in nondomestic felids. 1458 83

We report a case of atraumatic pneumocephalus associated with prolonged use of nasal continuous positive airway pressure. Initial symptoms included headache, ataxia, vertigo, and a "gurgling" sensation in the head; and a CT image showed small air bubbles along the falx of cerebrum and adjacent to the temporal epidural spaces bilaterally. Although no evidence of cerebrospinal fluid (CSF) leak was either reported by the patient or found at initial clinical examination, subsequent nasal discharge tested positive for beta2-transferrin, a finding consistent with CSF leak in the paranasal sinus region or through the cribriform plate. To try to prevent infection from an open communication between the paranasal sinuses and intracranial structures, an attempt should be made to localize the anatomic defect.
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PMID:Atypical headache after prolonged treatment with nasal continuous positive airway pressure. 1595 84


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