Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fischer 344 rats and B6C3F1 mice were fed diets that contained 0.03, 0.06, 0.1 and 0.2% 4,4'-oxydianiline for 13 weeks. The 0.1 to 0.2% diet caused 40 to 70% mortality in female rats. Although mice ate about 3.5 times more chemical than rats, no mice died. Alopecia, dyspnea and cyanosis in rats, and lethargy in both species occurred in the 0.1 to 0.2% groups. Goiter was found in rats that died as early as the 4th to 5th week of study in the groups given the 0.06 to 0.1% diet. At the end of the study, diffuse parenchymatous goiter was seen in all rats given the 0.06% and higher concentration diets and in most mice given the 0.2% diet. In rats, the thyroids also were heavily encapsulated and had interstitial fibrosis and vascular degeneration. There was concomitant hyperplasia of pituitary basophils in both species, but an increase of cells that secrete thyrotropin was seen in rats only.
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PMID:The goitrogenic effect of 4,4'-oxydianiline in rats and mice. 71 59

An acute respiratory distress syndrome in 10 adult dogs was usually preceded by vomiting, anorexia and lethargy followed, after a short interval, by dyspnoea. The dyspnoea became increasingly severe, despite oxygen therapy, and cyanotic respiratory failure ensued. All 10 dogs died or were killed after illnesses lasting between one and eight days. Necropsies revealed pulmonary congestion, oedema, collapse and haemorrhage with loss of alveolar epithelial cells. Early alveolar fibrosis was also found. Paraquat was identified in post mortem samples from four of the 10 dogs.
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PMID:Acute respiratory distress in the dog associated with paraquat poisoning. 86 Mar 82

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)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

A novel canine retrovirus was isolated from mononuclear cells of the peripheral blood of a leukaemic dog. The main clinical and pathological findings in this dog were lethargy, anorexia, weakness, dyspnoea, severe anaemia, thrombocytopenia and a high white blood cell count, practically all of which were lymphoblasts. The virus was isolated from mononuclear cells obtained from the blood, cocultivated with indicator cells. The virus particles encode a reverse transcriptase with Mg++ preference, have a density in sucrose gradients of 1.16 g ml-1, and induce syncytia in permissive cell cultures such as Himalayan tahr ovary and canine fetal thymus lines. This agent replicates to high titres. The virus exhibits a morphogenesis and morphology typical of lentiviruses. Immunoblotting and competitive radioimmunoassays failed to detect immunological crossreactivity with other representative lentiviruses and oncoviruses of the retrovirus family.
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PMID:Isolation and preliminary characterisation of a novel retrovirus isolated from a leukaemic dog. 137 29

An overdose of up to 850 levothyroxine sodium tablets (0.2 mg) in a healthy 6-year-old 16.8-kg dog induced an episode of vomiting and hippus within 9 hours of ingestion. The dog was treated with activated charcoal and saline (magnesium sulfate) cathartic. Initially the serum concentration of thyroxine (T4) 4,900.9 nmol/L. On the second day, serum concentration of triiodothyronine (T3) was 5.3 nmol/L. Serum T4 concentration decreased slowly and was not determined to be normal until day 36. Serum T3 concentration was found to be normal on day 6. Serum alanine transaminase activity peaked on day 6 at 345 U/L. Significant abnormalities were not found during the following 36 days. Clinical signs of thyroid hormone toxicosis in dogs and cats include hyperactivity, lethargy, tachycardia, tachypnea, dyspnea, abnormal pupillary light reflexes, vomiting, and diarrhea. High overdoses of levothyroxine sodium in dogs should be managed by initial decontamination and administration of activated charcoal with a cathartic followed by supportive care.
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PMID:Acute overdose of levothyroxine in a dog. 161 89

Nitrates are frequently found in vegetables and ground water. Nitrate levels in ground water have increased over the past two decades because of the heightened use of nitrogenous fertilizers. Following ingestion, nitrates are converted to nitrites by fecal organisms. Nitrites are absorbed and form methemoglobin, which interferes with the oxygen-carrying capacity of hemoglobin. Infants are particularly susceptible to nitrate poisoning because fetal hemoglobin is more readily oxidized to methemoglobin. In infants, the most common source of nitrate exposure is well water, which is mixed with infant formula. Affected infants may present with asymptomatic cyanosis, which can progress to dyspnea and lethargy or coma. Blood methemoglobin concentrations are elevated. Treatment consists of the administration of oxygen and intravenous and oral methylene blue.
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PMID:Methemoglobinemia: nitrate toxicity in rural America. 162 30

Four years after successful implantation of a pleuroperitoneal shunt in a dog with persistent pleural effusion, signs of lethargy and dyspnea reappeared. Although the shunt was still functional, compartmentalization of the right pleural space eventually isolated a pocket of fluid, causing dyspnea. Symptomatic relief was achieved for at least 11 months by contralateral implantation of a second shunt.
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PMID:Pleural compartmentalization in a dog with a pleuroperitoneal shunt. 162 95

The literature contains about 500 cases of equine leucosis, though the reports are deposited in a great number of journals and vary considerably concerning particular topics. During the last years there has been a remarkable increase of publications about this syndrome in the equine. The clinical leucosis key recommended by us has been confirmed in principle considering the latest literature. In about 70 individual symptoms which can be clinically observed in equine with leucosis 11 can be considered as main symptoms because of their frequency; they are again classified in primary (lymph node tumours including splenomegaly--loss of condition, weakness--cachexia, weight loss, periphery oedema), secondary (anorexia, inappetence--fever--paleness of mucous membrane--anaemia--tachycardia) and accessory (incoordination--tachypnoea, dyspnoea--apathy, lethargy) main symptoms. Furthermore in future it will be necessary to take into more consideration the symptoms "recurrent colic" and "hydrothorax" within differential diagnosis. The main symptom "incoordination" (ataxia, asynergy, paresis, paralysis) is used by us more precisely only in case of impairment of nervous system by neoplastic infiltrations and does not signify as possible symptoms of general physical weakness, for example faltering, staggering, tumbling or lameness. The morphological classification follows further on our previous recommendation. There exist generalized forms with tumour infiltrations in abdominal and in thoracic cavity as well as especially in peripheral lymph nodes. On the other hand there are characteristic manifestations in certain regions of the body, which establish distinctly the clinical symptomatology. They are marked as regional multicentric forms with the main localizations "mediastinal", "splenic", "mesenteric" or "intestinal".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical diagnostic keys and special manifestations in equine leukosis]. 195 30

Thirty-five patients with advanced malignant disease have been treated as outpatients with increasing doses (0.1-100 mcg) of interleukin 2 (IL2) by once daily self-administered subcutaneous (s.c.) injection, 5 days weekly for 8 weeks followed by a 4 week observation period. Systemic side effects were not experienced by patients at the 3 lower doses. Three patients required dose reduction from 100 mcg daily because of intolerance (fever, rash, lethargy, nausea and vomiting) and one patient was discontinued because of dyspnoea. We observed immunological effects at the 100 mcg dose (but not at the lower doses). These consisted of (a) a modest sustained lymphocytosis, (b) eosinophilia in six (out of nine) patients and (c) a significant rise in IL2-stimulated peripheral blood lymphocyte activated killer (LAK) cell activity in six (out of nine) patients to a mean of 2.0 times pretreatment levels (P less than 0.01). Two (out of nine) patients with renal cell carcinoma treated with 100 mcg daily had partial responses of duration 4 and 9 months respectively and a further three had disease stabilisation for at least 3 months. Low dose long-term s.c. IL2 is clinically and immunologically active, and in comparison to other IL2 regimens it has minor toxicity and is easy to administer. These characteristics make low dose s.c. IL2 suitable for study in the adjuvant setting.
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PMID:The clinical effects of prolonged treatment of patients with advanced cancer with low-dose subcutaneous interleukin-2 [corrected]. 199 6

Specimens from 10 cases of second-generation anticoagulant rodenticide poisoning in dogs and cats were submitted to the Texas Veterinary Medical Diagnostic Laboratory during 1986 and 1987. The clinical signs most frequently observed were lethargy, dyspnea, and ventral hematomas; common necropsy findings included hemoperitoneum, hemothorax, and pulmonary hemorrhage. In the instances when histopathological examination of the tissue was done, it supported a diagnosis of coagulopathy. The presence of anticoagulants in serum or liver was confirmed by high pressure liquid chromatography, gas chromatography/mass spectrometry, or a combination of the two. Five cases of brodifacoum poisoning, 2 of bromadiolone, and 3 of diphacinone toxicity were verified. Concentrations of these rodenticides ranged from approximately 0.001 to 12 ppm.
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PMID:Case studies on second-generation anticoagulant rodenticide toxicities in nontarget species. 248 51


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