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

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

An 18-month-old alpaca developed nervous signs, including swaying of the head and neck, a wide-based stance and hind-limb ataxia. No certain diagnosis was made but the animal recovered after successive treatment with amoxycillin, vitamin B1, ivermectin and copper oxide, followed by vitamin E and selenium. The differential diagnosis rationale of treatment is described.
 ...
PMID:Ataxia and head tremor in an alpaca (Lama pacos) 832 51

A clinical, viral, hematologic , and genetic study was conducted over a 4-year period on a family of Appaloosas with high incidence of clinical ataxia and pathologic features of equine degenerative myeloencephalopathy. Marginal to deficient serum vitamin E (alpha-tocopherol) and blood selenium values were the only other consistent antemortem abnormalities in the affected horses. Members of this family were all descendants of a clinically normal mare and were raised in 3 separate environments with variable quality of feed. All horses had access to pasture grasses. Normal chromosomal karyotypes were found in 11 affected and/or related horses examined. Equine herpesvirus type 2 was isolated from 4 of the horses, but evidence for a role of this virus in the pathogenesis of the disease was not found. The role of antioxidant deficiency in the pathogenesis of neurologic dysfunction in this equine family and in others reported to be affected with equine degenerative myeloencephalopathy remains speculative.
 ...
PMID:Clinical, viral, and genetic evaluation of equine degenerative myeloencephalopathy in a family of Appaloosas. 203 2

Neuroaxonal dystrophy and minimal diffuse degenerative myelopathy was diagnosed in two female full sibling, 1- and 2-year-old, Haflinger horses. Both animals developed slowly progressive ataxia from the age of 4 months. Clinical signs, which were more prominent in the hind legs, included hypermetria and dysmetria. Histological examination revealed neuroaxonal dystrophy characterized by spheroid formation, vacuolation, astrogliosis and lipofuscin pigment deposition in macrophages and neuronal perikarya. These changes were restricted to the gracilis and cuneate nuclei, nucleus of the solitary tract, nucleus intermediomedialis in the sacral and the seventh segment of the cervical spinal cord and Stilling-Clarke's column in both horses and the medial vestibular nucleus in the older horse. Both diseased Haflingers had significantly reduced serum alpha- and gamma-tocopherol values. No significant alteration in serum total lipid concentrations and serum selenium values were observed. It is likely that the condition has a familial hereditary basis. It is unclear whether there is a link between the observed neuroaxonal dystrophy and vitamin E deficiency and further investigations are warranted.
 ...
PMID:Neuroaxonal dystrophy associated with vitamin E deficiency in two Haflinger horses. 239 44

Selenium poisoning occurs worldwide in nearly all domestic animals. Acute selenium poisoning is associated with feeding high levels or injecting excessive amounts of selenium and is usually fatal. The acute poisoning may cause gastrointestinal disturbance, muscle weakness, depression of the central nervous system, prostration and death (1-2). Chronic selenium poisoning in cattle, sheep and horses may result from the consumption of seleniferous plants over an extended period of time. Chronic selenium results in ataxia, incoordination, partial blindness, paralysis, loss of hair or wool, abnormal hoof growth and possibly abnormal changes in behavior (1). There is little information regarding the clinical signs and pathology of selenium toxicosis in marine mammals. Likewise, there is little information regarding normal tissue levels or toxicologically significant levels of selenium in these species. The results of these investigations in sea lions, based on clinical signs, pathologic findings and tissue levels of selenium, suggest subacute or chronic selenium poisoning was most likely from dietary fish high in selenium.
 ...
PMID:Selenium toxicosis in three California sea lions (Zalophus californianus). 261 40

Three groups of 5 pigs each were fed a high selenium (Se) diet by mixing either Astragalus praelongus (31.6 ppm Se in feed), A bisulcatus (31.7 ppm Se in feed), or sodium selenate (26.6 ppm Se in feed) with commercial hog feed. Ten control pigs were fed only commercial hog chow containing trace selenium (0.44 ppm Se). Pigs were fed for 9 weeks and necropsied when they had ataxia or paralysis. Blood was collected for hematologic and serum biochemical determinations, and samples of various tissues were collected and fixed in neutral-buffered 10% formalin for histologic evaluation or frozen for determination of selenium concentration. All forms of selenium induced clinical signs of weight and hair loss, with cracked hooves and inflamed coronary bands developing in all Na2SeO4-fed pigs and 1 A praelongus-fed pig, but not in A bisulcatus-fed pigs. Serum calcium, phosphorus, and albumin concentrations were unchanged or significantly decreased from prefeeding values in groups fed selenium. Serum aspartate transaminase (AST) activities in Astragalus species-fed groups, and amylase activities and PCV in all groups of pigs fed selenium, were increased. Serum alkaline phosphatase and creatine kinase activities were significantly increased in the A praelongus-fed pigs and significantly decreased in Na2SeO4-fed pigs. Terminal tissue and body fluid selenium concentrations were determined in all groups of pigs fed selenium and compared with values in control pigs. Urine and bile concentrations were increased by the greatest factor (40 to 100x), with tissue concentrations of selenium increased by a lesser factor (6 to 17x).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Toxicosis in pigs fed selenium-accumulating Astragalus plant species or sodium selenate. 278 23

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.
 ...
PMID:Aflatoxin B1 toxicosis in dairy calves pretreated with selenium-vitamin E. 308 Sep 29

Two-to-5-week-old turkey poults from three large Minnesota flocks exhibited ataxia, flaccid paralysis, and up to 5% mortality as unexpected death. The major post-mortem finding was cerebellar hemorrhage and softening detected in 22 of 89 clinically affected poults. Histologic findings were severe focal or multifocal poliomyelomalacia in the lumbosacral intumescentia of the spinal cord, cerebellar malacia, and single-cell or multifocal coagulative necrosis of pancreatic acinar cells. Thirty of 32 clinically affected poults examined had microscopic spinal cord lesions, 12 of 48 had cerebellar lesions, and 26 of 47 had pancreatic lesions. Gross and microscopic cerebellar lesions resembled those of vitamin E deficiency in chicks. Hepatic selenium levels were approximately twice normal expected levels for poults.
 ...
PMID:Poliomyelomalacia, pancreatic necrosis, and cerebellar malacia in turkey poults. 319 75

Stated are the values of the basic microelements in fallow deer in the region of Northeast Bulgaria as established through biogeochemical analysis. In unfavourable years metabolism is disturbed resulting in lowering the defense mechanism of the body. A number of bacterial species, and, more specifically, Escherichia coli increase their virulence and cause gastrointestinal disorders and diseases. Copper, selenium, and arsenic deficiency lead to endemic ataxia with characteristic clinical symptoms--the so-called spring diarrhea and endemic paresis. The Microsal Nesse polymicroelement preparation has been tested to prevent diseases as applied to the drinking water and to the forest and fruit silage. It contributes to strengthening the resistance of fallow deer, lowering the chronic diseases of the lungs, stomach, and intestines as well as to improving the shooting trophies.
 ...
PMID:[Diseases of the fallow deer in northeastern Bulgaria and their prevention]. 354 70

Modulation of acute monensin toxicosis in swine was evaluated in 2 studies. In study 1, 56 weanling male pigs were allotted to 14 groups of 4 each. Pigs in 7 groups were given tiamulin in the drinking water (to supply 7.7 mg/kg of body weight/day) for 3 days before and for 2 days after monensin administration. Monensin was given as a single oral dose (at 0, 7.5, 15, 25, 50, 75, or 100 mg/kg) to pigs in groups with or without tiamulin exposure. Prominent acute clinical signs of monensin toxicosis (hypermetria, hind limb ataxia, paresis, knuckling of hind limbs, and recumbency) developed by 2 to 6 hours after dosing in pigs given 15 or 25 mg of monensin/kg with tiamulin exposure, but not in pigs given the 15 or 25 mg of monensin/kg without tiamulin exposure. Also, the extent of monensin-induced skeletal muscle damage at 4 days after monensin dosing was enhanced in pigs given 7.5, 15, or 25 mg of monensin/kg and exposed to tiamulin. In study 2, 48 weanling male pigs were allotted to 8 groups of 6 each. Four groups of pigs were given 20 mg of monensin/kg orally, and 4 groups were given 100 mg of monensin/kg orally. For each monensin dose, a group was treated 24 hours before monensin administration with (i) selenium (Se)-vitamin E preparation, 0.25 mg of Se and 68 IU of d-alpha-tocopheryl acetate (vitamin E)/kg, IM; (ii) vitamin E only, 68 IU of d-alpha-tocopheryl acetate/kg; (iii) Se only, 0.25 mg of Se/kg; or (iv) vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and/or vitamin E. 367 64


1 2 3 Next >>