Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifteen coyotes (Canis latrans) shed sporulated sporocysts in their feces after eating freshly ground skeletal muscles from a mule deer (Odocoileus hemionus hemionus) infected with microscopic-sized cysts of Sarcocystis. Sporocysts were shed intermittently from 12 to 36 days after ingestion of the infected meat. Sporocyst size averaged 14.4 X 9.3 mum. Eleven mule deer fawns orally inoculated with these sporocysts became infected and 9 of 11 died between post-inoculation days (PID) 27 and 63. Clinical signs of anorexia, weight loss, pyrexia and weakness were evident prior to death. A calf (Bos taurus) and two lambs (Ovis aries) orally inoculated with these sporocysts did not become infected and remained healthy throughout the experiments. Similarly, uninoculated control animals consisting of three mule deer fawns, two lambs and one calf remained healthy during the experiment. Preliminary histologic examinations conducted on selected tissues from all animals revealed microscopic-sized schizogonous stages in macrophages, between muscle fibers and near blood vessels in the esophagus, heart, biceps femoris, semi-membranosus, diaphragm and tongue from seven of eight fawns which died between PID 27 and 39. Developing or mature muscle cysts were not found in fawn tissue until PID 60. Sarcocysts were found in the three infected fawns examined after this time. Muscle cysts or earlier schizont stages were not found in tissues from the inoculated or uninoculated calves and lambs. A single muscle cyst was found in one control fawn; the other two control fawns were negative for both muscle cysts and other schizogonous stages. These results established that the life cycle of this species of Sarcocystis can be completed with coyotes as the definitive host and mule deer as the intermediate host. Based on the demonstrated host specificity and earlier findings, the name Sarcocystis hemionilatrantis is proposed for this parasite of mule deer and coyotes.
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PMID:Sarcocystis hemionilatrantis (Sp. N.) life cycle in mule deer and coyotes. 40 85

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

Adult cotton top marmosets made niacin deficient by long-term dietary deprivation, developed a syndrome characterized by anorexia, weight loss, weakness, diarrhea, dermatitis, enterocolitis and stomatitis. The stomatitis was highlighted by a necrotizing gingivitis and periodontitis and by an ulcerative and atrophic glossitis.
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PMID:Studies on the biology of the periodontium of marmosets. XIII. Histopathology of niacin deficiency stomatitis in the marmoset. 40 31

Seven Florida sandhill cranes (Grus canadensis pratensis) and 6 greater sandhill cranes (Grus canadensis tabida) were exposed to lead-base paint containing 27% lead. One bird of each subspecies died enroute to the hospital, with a clinical history of anorexia, weakness, and open-mouth breathing of 36 hours' duration. There were no gross lesions, and microscopic lesions were limited to focal hepatic necrosis and hemosiderosis. Two of each subspecies of cranes developed clinical signs of lead poisoning, which included anorexia, weakness, green diarrhea, regurgitation, and open-mouth breathing. Diagnosis of lead poisoning was confirmed on the basis of blood lead concentrations ranging from 146 microgram/100 ml to 378 microgram/100 ml. These 4 cranes were treated successfully with calcium disodium edetate intramuscularly. Seven of the birds remained clinically normal despite high blood lead levels, especially in the greater sandhill cranes.
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PMID:Lead poisoning in sandhill cranes. 41 73

Intestinal bypass surgery, performed for weight reduction in the morbidly obese patient, is frequently complicated by the development and hepatic complications. In 44 morbidly obese individuals, 55 inches of proximal jejunum were anastomosed, end to side, to 5 inches of distal ileum. All the patients were followed with body composition measurements, performed by multiple isotope dilution, prior to and at regular time intervals following bypass surgery. In 33 patients a decrease in body fat accounted for the entire postbypass weight loss, while the lean body mass remained normal in both size and composition. In these patients, at 1 year, body weights had decreased by 24.4 +/- 2.1%, while the body cell masses had decreased by 2.1 +/- 7.1%. In the remaining 11 patients, the postbypass weight loss resulted from a loss of both body fat and body cell mass. Their body weights at 1 year had decreased by 27.0 +/- 3.0%, while the body fat and body cell mass. Their body weights at 1 year had decreased by 27.0 +/- 3.0%, while the body cell masses decreased by 22.0 +/- 6.1%. Furthermore, their body compositions were characteristic of protein malnutrition with a contracted body cell mass and an expanded extracellular mass. Six of these 11 patients have required admission to hospital on 10 occasions because of malaise, anorexia, debilitating weakness, hypokalemia, and abnormal liver function. They were treated for 14.5 +/- 1.9 days with an intravenous infusion of amino acids without additional nonprotein calories. The body composition, initially characteristic of malnutrition, became normal. Their symptoms disappeared and hepatic function returned to normal. Subsequently a high-protein diet was required to prevent a recurrence of symptoms and to maintain a normal body composition. The data indicate that protein malnutrition developed in 11 of 44 patients undergoing jejunoileal bypass for weight reduction.
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PMID:Protein malnutrition following intestinal bypass for morbid obesity. 45 87

A case report of lead poisoning in Canada geese at Cheyenne Bottom Wildlife Management Area in Kansas is presented. Seventy-nine dead geese and 10 geese too weak too fly were found by management personnel. Clinical signs in the live geese were weakness, lethargy, anorexia, emaciation and bile stained diarrhea. Seventeen geese were necropsied. Lesions were impacted roots and fibrous stalks in the esophagus and proventriculus and numerous lead shot in the gizzard. One to 44 lead shot (mean 13) were found in the 17 gizzards examined. The concentration of lead in liver and kidney was 9.21 to 102.56 ug/g (wet weight). The presence of lead shot in the gizzard, characteristic clinical signs, and the concentration of lead in the liver and kidney confirmed the diagnosis of lead poisoning.
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PMID:Lead poisoning in Canada geese: a case report. 49 80

Hyponatremia with simultaneous renal sodium loss was associated with the inappropriate secretion of antidiuretic hormone in a dog with heartworm disease. Antidiuresis caused expansion of extracellular fluid volume, which induced renal salt wasting and a negative sodium balance. The combination of water retention, salt wasting, and inactivation of intracellular solute contributes to the decrease in serum sodium concentration. Water intoxication due to hypotonicity of body gluids induced anorexia, depression, weakness, and incoordination.
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PMID:Inappropriate secretion of antidiuretic hormone in a dog. 50 Apr 39

Mice and dogs, were treated iv with the cytostatic proteins abrin and ricin and observed for clinical, biochemical, and morphological aberrations. In both mice and dogs death occurred within a narrow dose range. Dogs given toxic doses of ricin and abrin showed weakness, anorexia, apathy, and moderate fever. No signs attributable to the central nervous system were observed. Dogs dying from intoxication expired after 15-40 h. After nonlethal doses the animals recovered, apparently completely, in 1-3 wk. No delayed changed were observed in dogs after 4 mo. Abrin and ricin, in contrast to most other cytostatic agents, did not inhibit myelopolesis. However, after sublethal dpses a rapid but translent decrease of peripheral thrombocytes was observed. No evidence for specific liver damage or impairment of kidney function was obtained. Few abnormalities were observed at autopsy or on microscopic and electron microscopic examination of the tissues, in contrast to the findings of some earlier investigators. The results indicate that in mice and dogs given sublethal doses of highly purified toxins the symptoms are reversible. There was no finding militating against a phase 1 clinical trial.
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PMID:Toxicity of abrin and ricin in mice and dogs. 52 41

This is a report on the experimental infection of cattle with Leptospira interrogans serotype szwajizak. The principal clinical features in three 4-week-old Holstein-Friesian heifers intravenously inoculated were fever, listlessness, anorexia, weakness, and diarrhea. Szwajizak was isolated from the blood for the first 5 to 8 days after inoculation. Leptospires were recovered from kidneys, but not from liver, spleen, brain, or urine. Two of the 3 calves produced homologous agglutinins, with maximum serum titers of 1:80 and 1:160. The sera of the 2 calves that developed szwajizak agglutinins showed cross reactivity with wolffi and hardjo antigens. There were not significant differences of plasma and urine constituents between the inoculated calves and the control calf. Endocardial hemorrhages and large soft black-red spleen were present in the 2 calves given the greatest numbers of leptospires. Histopathologically, kidney of all infected calves had multiple small foci of lymphoid cells, chiefly pasmacytes, which were present in periglomerular and interstitial areas.
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PMID:Experimental infection of calves with Leptospira interrogans serotype szwajizak. 63

Two groups of weanling pigs, injected with 45Ca, were fed diets containing optimal calcium and phosphorus, and vitamin D3 at 1320 IU/kg feed in the control group, and 825,000 IU/kg feed in the test group. The groups were further subdivided with 2 pigs in each subgroup, with survival times of 1, 2, 3, 4, 7, and 14 days. Pigs fed the high level of vitamin D3 lost weight and anorexia, weakness, rough hair coat and labored breathing were observed. Hypercalcemia began at 12 hours and progressed rapidly after 2 days. Radioisotope sutdies interpreted in the light of histopathologic findings indicated that bone was the primary source of increased plasma calcium. Calcium was released at a rapid rate into blood from prelabeled bone which was undergoing necrosis; it was also removed from blood and deposited into bone at a slower rate due to decreased apposition. Histopathologic examination of bones from test pigs showed regressive changes in the osteocytes, chondrocytes and osteoblasts which bean within 1 day of treatment and resulted in evidence osteopenia within 7 days. Arrested osteocytic osteolysis led to the appearance of cementing lines and to chondroid core retention. Further regressive changes in the osteocytes resulted in osteocytic death and osteonecrosis with subsequent osteoclasia and osteopenia. Retardation and arrest of cartilage maturation as well as osteoblastic deficiency contributed to the osteopenia. The osteopenia was further evidenced by decreased specific gravity and ash content per unit volume of humerus. The initial negative effect on the osteocytes, chondrocytes and osteoblasts is attributed to a direct toxic effect of excessive dietary vitamin D3 since hypoparathyroidism and hypercalcitoninism, which occur secondarily to hypercalcemia, could not account for the rapid appearance of this effect, nor are they known to induce osteocytic death. The release of bone calcium and the resulting hypercalcemia in vitamin D3 toxicosis is therefore due to a direct toxic effect of the vitamin, or its metabolites, on the osteocyte resulting in osteonecrosis. It is not due to increased resorption as has been reported previously from both in vivo and in vitro investigations. Degeneration, with subsequent inflammation, but without calcification, was observed in the kidneys and in the lungs. Epithelial cells, basement membranes, and smooth muscle were affected. This conclusively demonstrates that degeneration is the primary soft tissue lesion in vitamin D3 toxicosis, and that the subsequent calcification is therefore dystrophic. Degenerative changes occurred in the parathyroid glands within 1 day of treatment resulting in necrosis, inflammation and atrophy within 4 days. Relative fibrosis was seen as the parenchyma receded. The parathyroid gland changes were considered a direct effect of vitamin D3 toxicity since they occurred with only mild hypercalcemia and since necrosis of parathyroid cells has not been demonstrated with hypercalcemia either in vivo or in vitro.
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PMID:Vitamin D toxicity. Initial site and mode of action. 66 94


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