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

Feeding of 260 ppm of leptophos to mallard ducklings caused delayed neurotoxicity similar to that reported for hens. Thus leptophos caused ataxia, with subsequent paralysis, loss of appetite, and slow-down in the growth rate of the treated birds. Spinal lesions were identical in morphology and distribution to those seen in hens following leptophos administration. The severity of histologic changes correlated both with the clinical condition and the duration of intoxication.
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PMID:Delayed neurotoxicity induced by organophosphorus compounds in the wild mallard duckling: effect of leptophos. 8 97

A large number of reports have been devoted to the physiologic and toxic effects of methyl chloride, many of which are based on case histories involving occupational exposure. The detrimental actions of methyl chloride on the central and peripheral nervous systems are well established effects. It is a moderately severe narcotic and potentially severe nerve poison. Chronic intoxication is associated with damage to the central nervous system (CNS), kidneys, liver, bone marrow, cardiovascular system, respiratory system, and intestinal tract. The signs and symptoms range from the more severe medical dysfunctions such as cardiac irregularities, respiratory paralysis, nerve degeneration, and severe convulsions to the more subtle clinical observations such as CNS depression, nervousness and emotional instability, insomnia and anorexia, ataxia, blurred vision, light-headedness, nausea, dizziness, narcosis, and disorientation. The behavioral correlates of these and other neurotoxic effects of methyl chloride suggest that a gradual behavioral degradation occurs. Pharmacodynamic studies have shown the compound to be rapidly absorbed by the blood with most authors attributing the toxicity to an enzyme-catalyzed methylation reaction in the body. Despite the fact that several investigators have attempted to correlate such biological responses of methyl chloride with its toxicity, the present knowledge of the problem still lacks a detailed mechanism of action. Until such mechanisms are verified, adequate methods to assess subclinical neurological and behavioral changes must be effectively developed.
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PMID:Behavioral, neurological, and toxic effects of methyl chloride: a review of the literature. 38 67

In the course of multiple episodes of thiamine deficiency in the rhesus monkey, the triad of anorexia, apathy, and hind limb weakness is the earliest clinical manifestation. In later episodes, nystagmus, abducens paresis, midline ataxia, dysmetria, and congestive heart failure are also seen. With the exception of dysmetria, the neurologic signs promptly respond to thiamine administration. Pair-fed controls showed no clinical signs. Neither peripheral neuropathy nor edema was observed. Thiamine-deficiency in the experimental animals was confirmed by blood transketolase assays.
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PMID:Clinical manifestations of chronic thiamine deficiency in rhesus monkey. 40 80

Vitamin B-6 deficiency in the laying hen causes an immediate anorexia, loss of body weight, greatly reduced body fat stores and severe effects upon primary and secondary sex characteristics resulting in severely reduced hatchability culminating in complete cessation of egg production. While inanition may have been largely responsible for involution of the ovaries and oviducts in the vitamin B-6 deficient hens, regression of combs and wattles appears to be a more specific sign of vitamin B-6 deficiency. Serum cholesterol levels of vitamin B-6-deficient hens were lower than those of hens receiving an adequate diet. Egg cholesterol values remained relatively constant regardless of dietary B-6 levels or of alterations in serum cholesterol. No ataxia or mortality was observed in vitamin B-6-deficient hens or roosters. The effects of vitamin B-6 deficiency were almost completely reversed upon repletion of the hens with adequate dietary vitamin B-6.
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PMID:Influence of vitamin B-6 upon reproduction and upon plasma and egg cholesterol in chickens. 44 40

Twenty-seven dogs with lead poisoning were admitted to the University of Pennsylvania Veterinary Hospital from July, 1963, to April, 1975. The major source of the lead was paint. A common history was ingestion of plaster or paint scrapings during room renovation. Most of the dogs were less than 1 year old and had clinical signs referable to the gastrointestinal or the nervous system, or both. The gastrointestinal signs, in order of frequency, were vomiting, anorexia, tender abdomen, diarrhea, and constipation. The neurologic signs, in order of frequency, were hysteria, convulsions, ataxia, blindness, and mydriasis. The finding of many nucleated erythrocytes without severe anemia was nearly pathognomonic for lead poisoning. Of 14 affected dogs subjected to abdominal radiography, 9 had evidence of ingested radiopaque material. A mean blood lead concentration of 18.8 mug/100 ml, with a range of 0 to 50 mug/100 ml, was found for 26 dogs that were hospitalized for problems unrelated to lead poisoning. Of the 27 dogs with lead poisoning, 22 had their blood analyzed for lead. This group had blood lead values ranging from 40 to 530 mug/100 ml. Seven of the affected dogs were monitored throughout their period of treatment with calcium ethylenediaminetetraacetate. The concentration of lead in the blood decreased quickly after the initiation of treatment but leveled off after 2 or 3 days. The initial rapid phase probably corresponded to the removal of weakly bound or extracellular lead, whereas the slow phase probably corresponded to strongly bound or intracellular lead.
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PMID:Lead poisoning in dogs at the University of Pennsylvania Veterinary Hospital. 81 31

The nomenclature, life cycles, and pathogenicity of Sarcocystis of domestic animals are reviewed. Sarcocystis had a 2-host life cycle, with carnivores as definitive hosts and herbivores as intermediate hosts. The following species are found in domestic animals (with the definitive hosts given in parentheses): 3 species in the ox: S cruzi (dog, wolf, coyote, raccoon, fox), S hirsuta (cat), S hominis (man, monkey); 2 species in the sheep: S ovicanis (dog), S tenella (cat); 3 species in the pig: S miescheriana (dog), S porcifelis n sp (cat), S porcihominis n sp (man); and 1 species in the horse: S bertrami (dog). Sarcocystis cruzi, S ovicanis, and S porcifelis are highly pathogenic to the ox, the sheep, and the pig, respectively. Clinical signs of acute bovine sarcocystosis are: anorexia, pyrexia (42 C, or more), anemia, cachexia, enlarged palpable lymph nodes, excessive salivation, and loss of hair at the tip of the tail. Anemia, anorexia, ataxia, and abortions are the chief clinical signs of acute ovine sarcocystosis. These signs are evident at the time of vascular endothelium is parasitized by schizonts. The schizonts disappear in about 1 month, and cysts are formed in the muscles. The cystic phase of sarcocystosis is virtually nonpathogenic. Carnivores shed sporocysts in their feces after ingesting the intramuscular cysts from the herbivores. Sarcocystis is nonpathogenic to the definitive host. Feline and canine coccidia are also reviewed. The following 11 species are found in cats: Toxoplasma gondii, Hammondia hammondi, Isospora felis, Isosporarivolta, Besnoitia besnoiti, Besnoitia sp, and 5 types of Sarcocystis (S hirsuta from the ox, S tenella from the sheep, S muris from the mouse, S porcifelis from the pig, and Sarcocystis sp from Grant's gazelle). The following 10 species are found in canine feces (Isospora canis, Isospora ohioensis, Isospora wallacei n sp; and 7 types of Sarcocystis (S cruzi from the ox, S ovicanis from the sheep, S bertrami and Sarcocystis sp from the horse, S miescheriana from the pig, S hemionilatrantis from mule deer, and Sarcocystis sp from Grant's gazelle). The history of Isospora begemina in dogs is reviewed; life cycles of feline and canine coccidia are given; oocysts of common feline and canine coccidia are compared and illustrated; and public health significance of Toxoplasma gondii oocysts is discussed, especially in relation to cats in the household of pregnant women.
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PMID:A review of Sarcocystis of domestic animals and of other coccidia of cats and dogs. 82 60

Clinical signs of toxicosis, neurologic lesions, and increased tissue residues of methylmercury (MM)were produced in 9 cats by oral administration of 1.29 and 0.86 mg of Hg/kg of body weight/day as methylmercuric hydroxide. Clinical signs, which began after 15 days of exposure, included anorexia, ataxia, hypermetria, proprioceptive impairment, blindness, vertical nystagmus, and grand mal convulsions. Significant lesions occurred in cerebrum, brainstem, and cerebellum and correlated well with clinical signs. Microscopic central nervous system lesions consisted of neuronal degeneration, necrosis and loss of neurons, swollen axons, demyelination, loss of nerve cell processes, vacuolation of neuropil, gliosis, neuronophagia, perivascular cuffs, endothelial hypertrophy and hyperplasia, leptomeningitis, and infrequent vascular necrosis. Overall distribution of central nervous system lesions was unrelated to daily dose, but more advanced lesions were produced by the smaller daily dose. Mean tissue residues of MM were generally directly related to daily dose, and the average distribution among tissues was constant, with highest concentrations in liver, followed by kidney, spleen, muscle, and brain. In utero exposure of kittens to MM, revealed transplacental accumulation.
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PMID:Pathology of subacute methylmercurialism in cats. 83 68

Gelded horses of mixed breeding, ranging in weight between 360 and 455 kg, were fed pellets that contained monensin at concentrations of 279, 124, 31, and 0 ppm. Of 2 horses fed 279 ppm (253 g/T), both died. Of 3 horses fed 125 ppm (113 g/T), 1 died; feed intake was reduced in the 2 survivors. Of 3 horses fed 31 ppm (28 g/T), 1 had a transitory reduction in feed intake and the other 2 remained clinically normal. The 2 horses fed 0 ppm remained clinically normal. Monensin was also given to horses by gavage, at dosages of 1, 2, 3, 4, or 20 mg/kg of body weight. The LD50 was estimated to be between 2 and 3 mg/kg of body weight. The signs of toxicosis were partial to complete anorexia, ataxia, and intermittent profuse sweating.
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PMID:Evaluation of monensin toxicity in the horse. 97 40

Five-week-old broilers were submitted to the diagnostic laboratory showing sudden onset of incoordination, ataxia, anorexia, dehydration and coma. Groups of birds were being fed the New England Conference (NECC) broiler diets in which scallop viscera was added. Moribund birds receiving thiamine hydrochloride recovered without complications.
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PMID:Observations of possible thiaminase activity in scallop viscera fed in broiler diets. Case report. 116 88

Acute and subacute toxicities to cats of T-2 toxin, 12-13 epoxytrichothec mycotoxin from fungi Fusarium species and others, were investigated. Major symptoms of toxicity in cats as the result of T-2 toxin were emesis, vomiting, diarrhea, anorexia, ataxia of the hind legs, discharge from the eyes and ejection of hemorrhagic fluid. Consecutive administration of the crude and pure sample of T-2 toxin in a sublethal dose caused a marked decrease in the number of circulating white blood cells. In the early stage of intoxication, a temporal leukocytosis was observed after each administration. Autopsy revealed extensive cellular damages in the bone marrow, intestine, spleen and lymph nodes. Greatly evident were meningeal hemorrhage of the brain, bleeding in the lungs and vacuolic degeneration of the renal tubles. Mycotoxicological significance of T-2 toxin and related trichothecenes is discussed in relation to the food-borne diseases in humans and farm animals.
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PMID:Toxicological approaches to the toxic metabolites of Fusaria. VIII. Acute and subacute toxicities of T-2 toxin in cats. 118


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