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)

Toxicosis caused by Anabaena spiroides was diagnosed in 7 of 26 finishing hogs in a farrow-to-finish operation in Kentucky. Several sick pigs in the herd had the following clinical signs: vomiting, dull appearance, lethargy, anorexia, muscle tremors, frothing at the mouth, coughing, sneezing, dyspnea, and bloody diarrhea. Of the 7 dead pigs, 2 were necropsied. Tissue speciments and stomach contents were obtained for microscopic, microbiologic, and toxicologic evaluations. In addition, vomitus from sick pigs and pond water samples were collected for laboratory analysis. Direct microscopic examination of pond water, vomitus, and stomach contents revealed nearly pure A spiroides, a toxic blue-green algae. The possible involvement of bacterial toxins in these pigs was not established; however, the laboratory and field data suggested that the clinical signs and death losses were attributable to the consumption of pond water mixed with the bloom of the alga, A spiroides.
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PMID:Blue-green algae (Anabaena spiroides) toxicosis in pigs. 250 12

Two hundred ten dogs that had primary lung tumors diagnosed between 1975 and 1985 were evaluated. The majority of the tumors were classified as adenocarcinoma (74.8%) and alveolar carcinoma (20%). The most common clinical signs of disease were cough (52%), dyspnea (23.8%), lethargy (18.1%), weight loss (12.4%), and tachypnea (4.8%). The clinical methods that were most successful in directly or indirectly leading to a diagnosis of primary lung tumor were thoracic radiography (77.1%) and cytologic examination of fine-needle aspirate specimens (24.8%).
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PMID:Classification of primary lung tumors in dogs: 210 cases (1975-1985). 254 42

Three groups of turkeys were inoculated with strains of C. psittaci (B577, VS1, TT3) from different restriction endonuclease groups. Turkeys were necropsied at 15 times through post-inoculation day 70. Birds infected with the TT3 strain were lethargic and had decreased body weight. After forced exercise, dyspnea was seen in VS1-infected turkeys. Pericarditis was the most severe lesion in TT3-infected birds. Airsacculitis and bronchopneumonia were the most severe lesions in VS1-infected turkeys. Lateral nasal adenitis was in both VS1- and TT3-infected birds. Only mild peribronchial pneumonia was in B577-infected turkeys. Chlamydial antigen, identified by light microscopy using an immunoperoxidase technique, was seen from post-inoculation days 9 through 50 in the lateral nasal gland and at earlier times in other tissue from VS1- and TT3-infected turkeys. No chlamydial antigen was detected in tissue from B577-infected birds. These studies showed that chlamydial strains from different restriction endonuclease groups are associated with distinct disease syndromes in turkeys.
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PMID:Respiratory and pericardial lesions in turkeys infected with avian or mammalian strains of Chlamydia psittaci. 268 47

Male and female 16 to 18 month old C3Hf/Bd mice in a dermal carcinogenicity study were moribund or died at earlier time points than the expected 24 to 30 months. Clinical signs observed in both treated and control animals included dyspnea, lethargy, and death. Lesions seen in treated as well as control mice were cardiomegaly with myocardial degeneration and necrosis, hydrothorax and pulmonary edema, and ascites and chronic passive congestion of the liver. Mice were negative for serologic, bacteriologic and microscopic evidence of viruses, bacteria and protozoa which can induce heart lesions. Possible causes of the cardiomyopathy include metabolic, degenerative, genetic or undetermined infectious disease.
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PMID:Idiopathic cardiomyopathy in C3Hf/Bd mice. 270 3

A large hypertensive population of patients in general practice was used to assess the tolerability of nifedipine in previously untreated patients and was compared with other antihypertensive drugs in previously treated patients. A total of 3972 patients with a sitting diastolic blood pressure between 95 and 115 mmHg were treated with 20 mg nifedipine twice daily for 1 month. In non-responders the dose was increased to 40 mg twice daily for a second month; responders continued to take 20 mg twice daily. A total of 2772 patients had been previously untreated for hypertension, whereas 857 had previously been treated with beta-blockers alone or in combination and 346 had received diuretics alone or in combination. Adverse events were recorded for 28 days prior to treatment being initiated with or changed to nifedipine and for two 28-day nifedipine treatment periods. Flushing and headache, which diminished with time, occurred during nifedipine treatment. Ankle oedema did not diminish with time. Reductions were seen in occurrences of dyspnoea, impotence, lethargy and cold extremities.
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PMID:General practice data derived tolerability assessment of antihypertensive drugs. 280 16

Hyperadrenocorticism was diagnosed in 7 cats with concurrent diabetes mellitus. Four cats had pituitary adenoma with bilateral adrenocortical hyperplasia, 1 cat had pituitary carcinoma with bilateral adrenocortical hyperplasia, 1 cat had adrenocortical carcinoma, and 1 cat had adrenocortical adenoma of the left adrenal gland. One year later, adrenocortical adenoma involving the right adrenal gland also was diagnosed in this cat. Clinical signs included polyuria and polydipsia (n = 7), development of pot-bellied appearance (n = 5), dermatologic alterations (n = 5), lethargy (n = 3), weight loss (n = 3), dyspnea/panting (n = 2), and recurrent bacterial infections (n = 2). In 6 cats, the diagnosis of hyperadrenocorticism was established before death on the basis of results of the ACTH stimulation test (n = 3) and the dexamethasone screening test (n = 5). Pituitary-dependent hyperadrenocorticism was differentiated from adrenocortical neoplasia on the basis of results of the dexamethasone suppression test (n = 4), endogenous ACTH concentration (n = 3), results of abdominal radiography and ultrasonography (n = 3), and exploratory celiotomy (n = 1). Four cats died or were euthanatized without treatment attempts. Treatment with mitotane followed by 60Co teletherapy was ineffective in one cat with pituitary adenoma. One cat with pituitary carcinoma died one week after bilateral adrenalectomy. Bilateral adrenocortical adenomas were removed surgically in the affected cat.
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PMID:Hyperadrenocorticism in cats: seven cases (1978-1987). 284 Dec 69

Prizidilol (SK&F 92657-A2), an anti-hypertensive agent, has undergone a range of prescribed toxicity studies required for the investigation of possible adverse drug effects. During the second year of the 2-year rat oral study, a variety of symptoms were exhibited by males receiving 1600 mg of the compound day-1kg-1 by gavage. These animals became lethargic, slouched and developed dyspnoea which became progressively more severe during the course of the study. Necropsy of the affected rats revealed severely haemorrhagic lungs, cardiac hypertrophy and lordosis of the spine into the thoracic cavity. At the 2-year terminal kill, a proportion of the male rats receiving 100 and 400 mg of prizidilol day-1kg-1 were identified with similar but less severe spinal deformation. No female was found with spinal changes but all the rats receiving prizidilol showed haemorrhagic lungs and enlarged hearts. The lordosis of the affected males was always confined to the thoracic spine and this, along with the cardiac hypertrophy, presumably led to marked reduction in the volume of the thoracic cavity, inducing the dyspnoea. Thoracic vertebral body damage, possibly a precursor to the spinal deformities, was found in male rats from both drug-treated and control groups. The nature of the spinal lesion is at present under investigation.
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PMID:Dyspnoea and thoracic spinal deformation in rats after oral prizidilol (SK&F 92657-A2). 287 53

To evaluate the health effects of occupational phosphine exposure, 22 workers engaged in fumigation of stored grains were subjected to a clinical and environmental study. These workers were used to placing aluminum phosphide tablets on the stacks of grains and covering it with a gas-proof plastic cover. The mean age of the workers was 48 years (range 24-60) and mean duration of exposure 11.1 years (range 0.5-29). After fumigation they reported minor symptoms, which included cough (18.2%), dyspnoea (31.8%), tightness around the chest (27.3%), headache (31.8%), giddiness, numbness and lethargy (13.6% each), anorexia and epigastric pain (18.2% each). The abnormal physical signs included bilateral diffuse rhonchi and absent ankle reflex each occurring in one worker. Motor nerve conduction velocity of median and peroneal nerves, and sensory conduction velocity of median and sural nerves were normal. Phosphine concentration in the work environment ranged from 0.17 to 2.11 ppm. Occupational phosphine exposure in the workers was associated with mild to moderate symptoms, which were transient. However, to assess the chronic effects, long-term follow-up is recommended.
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PMID:Occupational phosphine exposure in Indian workers. 317 55

Sarcoidosis is a multisystem disease of unknown etiology that is rarely diagnosed in children. When mass screening is performed, the incidence of the disease in children approaches that of adults with similar demographics. Most childhood cases occur around ages 9 to 15 years, with small clusters of cases occurring in children under age 4 years. The disease in these two age groups has very different clinical features. Children under age 4 have a clinical triad of rash, arthritis, and uveitis. The classic syndrome in older children involves primarily lungs, lymph nodes, and eyes. In older children, constitutional symptoms (fatigue, lethargy, malaise) and pulmonary symptoms (cough, dyspnea) predominate. Mortality in childhood sarcoidosis is about 5%, with long-term sequelae in 10% to 20%. Early recognition may prevent complications such as blindness, pulmonary insufficiency, and renal impairment.
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PMID:Sarcoidosis in children. 332 85

A 7-year-old adult male ferret had progressive hair loss that was bilaterally symmetric. Also clinically evident were severe dehydration, polydipsia, muffled heart sounds, weak femoral pulses, hepatomegaly, lethargy, weakness, temporal muscular atrophy, dyspnea, and weakness. The blood profile of the ferret indicated profound leukopenia, eosinopenia, and high phosphorus, BUN, creatinine, and potassium concentrations, as well as high aspartate transaminase activity; the albumin concentration was low. The serum cortisol concentration was 8.1 micrograms/dl. Necropsy and histologic findings confirmed a diagnosis of hyperadrenocorticism, complicated by dilatative cardiomyopathy, chronic active hepatitis, and renal disease.
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PMID:Hyperadrenocorticism in a ferret. 365 2


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