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)

An outbreak of narasin poisoning in swine is described. Forty nine out of 108 lactating sows died over a period of one month after being fed a ration accidentally contaminated with narasin. Clinical signs included anorexia, respiratory distress, lethargy and posterior paresis, progressing to lateral recumbency and death. Necropsy examination in 3 pigs revealed extensive myocardial and skeletal muscle damage. Analysis of the feed confirmed the presence of high concentrations of narasin.
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PMID:An outbreak of narasin poisoning in swine. 849 96

Ponderosa pine needles cause abortion and a poorly described toxicosis when eaten by cattle. In previous trials, the abortifacient compound of pine needles was identified as isocupressic acid. At abortifacient doses, isocupressic acid caused no other toxicosis. However, other pine needle fractions, similar in composition to several commercially available rosin products, caused no abortion but were very toxic. The purpose of this study was to describe the toxicoses of ponderosa pine, compare its toxicity with other rosin and related pine products, and identify the toxin. Four groups of three pregnant beef cows each were treated with either ponderosa pine tips, rosin gum, dehydroabietic acid, or ground alfalfa. The cows treated with pine tips aborted, had retained placentas with endometritis, and developed both renal and neurologic lesions. The cattle treated with rosin gum or dehydroabietic acid did not abort but developed similar signs and lesions of intoxication. Clinical signs of intoxication included anorexia, mild rumen acidosis, dyspnea, paresis progressing to paralysis, and death. Clinical biochemical results, suggestive of renal, hepatic, and muscular disease, included azotemia, hypercreatinemia, hyperphosphatemia, proteinuria, and marked elevations of various serum enzymes. Histologically, all poisoned animals had nephrosis, vacuolation of basal ganglia neuropil with patchy perivascular and myelinic edema, and skeletal myonecrosis. The alfalfa-treated controls were normal. These findings suggest that ponderosa pine needles and tips are both abortifacient and toxic. Because the lesions caused by pine tips, rosin gum, and dehydroabietic acid are similar, toxicosis is most likely due to the diterpene abietane acids, common in all three.
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PMID:The toxic and abortifacient effects of ponderosa pine. 882 3

Twenty-seven cases of neosporosis in European dogs are described. The disease was confirmed by immunohistochemistry, electron microscopy, or a favourable response to treatment in the dogs with appropriate clinical signs, and by the presence of antibodies to Neospora caninum but not to Toxoplasma gondii. The affected dogs were two days to seven years old, and of 13 different breeds. Both sexes were affected and in most cases littermates remained normal. Twenty-one cases had an initial hindlimb paresis or ataxia, in which muscle atrophy was the most consistent clinical sign. Rigid hyperextension developed in approximately half of the cases. Anorexia and pyrexia were rare. Other clinical signs included forelimb ataxia, head tremors with tetraparesis and sudden collapse due to myocarditis. Titres of > or = 1:800 in the N caninum indirect fluorescent antibody test were detected in the 20 cases from which serum samples were taken. Such high titres are rare in healthy dogs and strongly suggest a diagnosis of neosporosis. Sixteen of the dogs received appropriate antiprotozoal treatment with clindamycin, potentiated sulphonamides and/or pyrimethamine; 10 made a full or functional recovery. Recovery was less likely in peracute cases with severe clinical signs, and when the treatment was delayed.
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PMID:Clinical aspects of 27 cases of neosporosis in dogs. 893 Dec 99

Two human ehrlichioses occur in the United States: human monocytic ehrlichiosis (HME), which is caused by Ehrlichia chaffeensis that infects mononuclear phagocytes in blood and tissue, and human granulocytic ehrlichiosis (HGE), an infection of granulocytes that is caused by a similar but phylogenetically distinct organism. The clinical features of both forms of human ehrlichiosis are identical and include nonspecific constitutional manifestations, such as fever, headache, malaise, nausea, vomiting, myalgia, and anorexia; however, rare patients develop neurologic symptoms and signs. Few cases of human ehrlichiosis have been described in detail, and focal neurologic deficits have only rarely been reported in such cases. We describe a patient with HME who developed a trochlear nerve paresis associated with evidence of lymphocytic meningitis during the course of her illness. We believe this to be the first well-documented case of a focal neurologic complication of human ehrlichiosis.
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PMID:Fourth nerve palsy caused by Ehrlichia chaffeensis. 909 62

A free-ranging male red wolf (Canis rufus) in North Carolina (USA), exhibiting paresis, anorexia and heavy tick infection was diagnosed with tick paralysis. The wolf recovered completely following the removal of all ticks. This is the first record of tick paralysis in the red wolf.
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PMID:Tick paralysis in a red wolf. 939 81

A number of symptoms cause physical or mental distress and suffering in the terminal and dying patient. In this prospective study of 117 patients (96% with a cancer diagnosis) in a Danish hospice all symptoms causing distress were assessed daily in three degrees of severity. The ten most frequently recorded symptoms were: fatigue, pain, weakness, dyspnoea, immobility/paresis, anorexia, general malaise, nausea/vomiting, oedema and amnesia. Fatigue was registered on 60.9% of the admission days, pain on 27.3%, dyspnoea on 19.2% and nausea/vomiting on 8.5%. The prevalence of pain, dyspnoea, nausea/vomiting, thirst and anxiety did not increase during the last seven days of life. Unconsciousness occurred in 23% of the patients during the last 24 hours and in 5% on the day before.
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PMID:[Distress symptoms in hospice patients]. 941 5

Two privately owned domestic rabbits (Oryctolagus cuniculus) in Maryland were found to be infected with the raccoon variant of the rabies virus in 1998. Both rabbits had an acute onset of anorexia and paralysis or paresis of the left forelimb; 1 also developed head tremors and a head tilt. One of the rabbits became ill 25 days after being attacked by a raccoon (Procyon lotor) and was euthanatized 3 days after onset of illness. The other rabbit, which was housed in an outdoor hutch, died 4 days after onset of clinical signs; the source of infection in that rabbit remains unknown. Currently, there is not a rabies vaccine approved for use in rabbits; thus, the only way to prevent the infection in rabbits is to prevent exposure. Veterinarians in rabies-enzootic areas should be familiar with the clinical signs of rabies in rabbits and should caution rabbit owners about the need to protect their pets from contact with wildlife.
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PMID:Rabies in two privately owned domestic rabbits. 1061 16

Between April 1998 and June 1999, 8 palm vipers (Bothriechis marchi) were diagnosed with a disease similar to inclusion body disease (IBD) of boids. Six palm vipers were captive bred, and 2 were wild caught. All of the vipers were adults at the time of death. Three palm vipers were found dead with no premonitory clinical signs, and 5 had anorexia plus possibly 1 of the following clinical signs: regurgitation, paresis, and dehydration. Histologically, all snakes had intracytoplasmic, round to oval, single to multiple eosinophilic inclusion bodies in hepatocytes and renal tubular epithelial cells. Inclusion bodies were distributed among other organs with varying frequency. Common concurrent histologic lesions were urate nephrosis, septic thrombi, and hepatocellular degeneration. Ultrastructurally, inclusions had features similar to inclusions in boid snakes with IBD.
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PMID:A disease resembling inclusion body disease of boid snakes in captive palm vipers (Bothriechis marchi). 1124 71

Severe hypomagnesemia (0.8 mg/dl; reference range, 1.6 to 2.3 mg/dl), hypocalcemia, and protein-losing enteropathy were identified in a 5-year-old castrated male 3-kg (6.6 lb) Shih Tzu examined because of anorexia, lethargy, paresis, and abdominal distention. Histologic examination of intestinal biopsy specimens revealed lymphangiectasia and lymphocytic, plasmacytic, neutrophilic infiltrates. Initial treatment included administration of magnesium (0.80 mEq/kg [0.36 mEq/lb]) of body weight in a balanced electrolyte solution. This treatment resulted in normalization of the serum magnesium concentration (1.7 mg/dl); resolution of the lethargy, paresis, and tachycardia; and an increase in the serum parathyroid hormone and ionized calcium concentrations. Findings were consistent with secondary hypoparathyroidism attributable to hypomagnesemia. Magnesium concentration should be monitored in all dogs with gastrointestinal tract disease, especially those with protein-losing enteropathy, anorexia, and weakness.
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PMID:Secondary hypoparathyroidism attributed to hypomagnesemia in a dog with protein-losing enteropathy. 1176 24

Presumptive copper deficiency was diagnosed in hand-reared captive pronghorn (Antilocapra americana) at the Los Angeles Zoo. Clinical signs, which were manifested in growing fawns, included anemia, anorexia, diarrhea, progressive paresis/recumbency, and aortic rupture. The range of serum copper concentrations in fawns born during the 1989 season (0.08-0.67 ppm) was below levels considered normal for domestic sheep and goats (0.7-2.0 ppm) and below concentrations measured in adult pronghorn (0.4-1.43 ppm). Copper sulfate supplementation of the hand-rearing formula, which was initiated in 1989, resulted in a significant increase in mean (+/- SD) serum copper levels from 0.45 +/- 0.18 ppm before supplementation to 0.68 +/- 0.05 ppm after supplementation (P < 0.05). Fawns born in subsequent seasons (April 1990-August 1993) continued to be supplemented with copper in the hand-rearing formula. Mean serum copper concentration from these fawns (0.68 +/- 0.22 ppm) was similar to the mean values from supplemented 1989 fawns and adult pronghorn in this herd (0.85 +/- 0.34 ppm; P > 0.05). No clinical signs of copper deficiency were detected in any fawns after supplementation was started. Analyses of the herd's diet revealed marginal dietary copper levels. Suspected dietary deficiency was confirmed by marginal tissue and serum copper concentrations in some of the herd's adult animals. Dietary copper levels were corrected to prevent future cases of clinical copper deficiency.
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PMID:Presumptive copper deficiency in hand-reared captive pronghorn (Antilocapra americana) fawns. 1278 88


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