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Query: UMLS:C0013911 (emaciation)
 1,059 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of pigs by the whipworm (Trichuris suis) resulted in profuse diarrhea on postinfection days 17 to 21. Anorexia, retardation of growth, dehydration, and emaciation were observed in infected pigs. Scanning electron micrography showed nematodes embedded in the mucosa of the cecum and colon, with resultant disruption of the mucosa. Infected pigs had decreased values of albumin, amylase, calcium and creatine phosphokinase, but increased values of alpha-, beta-, and gamma- globulins, total iron-binding capacity, copper, potassium, uric acid, and aspartate aminotransferase.
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PMID:Pathophysiology of swine trichuriasis. 88 15

Twenty-three ospreys (Pandion haliaetus) found dead or moribund in the eastern United States during 1975-1982 were necropsied and selected tissues were analyzed for organochlorines and metals. Major causes or factors contributing to death were trauma, impact injuries, and emaciation. DDE was detected in 96% of the osprey carcases, DDD in 65%, DDT and heptachlor epoxide in 13%, dieldrin, oxychlordane, and cis-nonachlor in 35%, cis-chlordane in 52%, trans-nonachlor in 45%, and PCB's in 83%. Carcasses of immature ospreys from the Chesapeake Bay had significantly lower concentrations of DDE, DDD + DDT, cis-chlordane, and PCB's than carcasses of adults from the same area. Concentrations of some organochlorines in ospreys from the Chesapeake Bay declined significantly from 1971-1973 to 1975-1982. Significant differences in concentrations of certain metals in the ospreys' livers were noted between time periods, and sex and age groups for birds from the Chesapeake Bay. During 1975-1982, adults had significantly lower concentrations of chromium, copper, and arsenic than immatures and nestlings, and adult males had higher mercury concentrations than adult females. Adult females had lower zinc concentrations in 1975-1982 than in 1971-1973. Immatures and nestlings had higher concentrations of chromium and lead in 1975-1982 than in 1971-1973. A slightly elevated concentration of chromium (1.7 ppm) or arsenic (3.2 ppm) was found in the livers of individual ospreys. Several ospreys had elevated concentrations of mercury in their livers; two ospreys had more than 20 ppm which may have contributed to their deaths.
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PMID:Environmental pollutant and necropsy data for ospreys from the eastern United States, 1975-1982. 358 6

Brindled mottled is a neurological mutant mouse. Hemizygous males have many clinical and biochemical features in common with kinky hair syndrome (KHS) in humans, and usually die around postnatal day 15, after severe emaciation. Neuronal mitochondrial abnormalities and neuronal degeneration in the cerebrum and cerebellum were constant neuropathological findings in this mutant. A single intraperitoneal injection of cupric chloride, 10 micrograms/g body weight, resulted in an improvement of clinical symptoms and prevention of neuronal degeneration. The degree of improvement was dependent on the date of injection, and day 7 to 10 postnatal appeared to the most effective date. The male hemizygotes which received cupric chloride injections at day 7 or 10 overcame the lethality, and no neuronal degeneration was detected in these mice, although neuronal mitochondrial changes were still persistent. However, following two injections at days 7 and 10, no abnormalities were detected in the cerebral cortical neurons. Even at the ultrastructural level, abnormal mitochondria were very scarce. In the cerebellum, however, mitochondrial changes in the Purkinje cells, particularly in the rostral portion, and generation of white matter were noted in these mice, which were clinically perfectly healthy, judging from the growth rate and behavior. However, cerebellar changes were far less in those which received additional injections later on. These observations indicate that, at least in brindled mutant mice, supplementation of copper is quite beneficial for clinical improvement and the prevention of neuropathological lesions, but the date of administration appears to have crucial importance.
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PMID:The effect of copper supplementation on the brindled mouse: a clinico-pathological study. 719 26

Five Karan Swiss crossbred (Sahiwal x Brown Swiss) calves were abruptly switched over from a diet of concentrate and maize fodder to ad libitum air dried Leucaena leucocephala leaves plus twigs. After 17 days on the L. leucocephala diet, 3 of the calves were supplemented with copper sulphate (10 mg/kg DM L. leucocephala) for 12 days. Thereafter all the calves were taken off the L. leucocephala diet and returned to the pre-experimental concentrate and maize fodder diet. While on the L. leucocephala diet, the average DM intake/d of L. leucocephala declined to 497 g within 3 weeks and all calves lost weight. This weight loss was reversed in the 3 calves that received copper sulphate, and all calves gained weight when they resumed the concentrate and maize fodder diet. The toxic effects of L. leucocephala feeding for 24 days were characterised by poor growth, emaciation, alopecia, loss of hair from the tail switch, ear and eye lesions, ulceration of the mouth region, drooling viscid saliva and vomiting of thick green saliva in one of the calves. Mean levels of 3,4 dihydroxypyridone (DHP) (mg/100 ml) were 30.35 +/- 13.52 and 55.57 +/- 13.77 on days 2 and 4 respectively in rumen liquor and up to 136.01 +/- 80.18 in urine. The mean ratios of mimosine: DHP of 3.14, 0.12 and 0.04 in feed, faeces and urine respectively revealed extensive degradation of mimosine to DHP in the calves fed the L. leucocephala diet and it was concluded the calves were unable to tolerate a diet consisting solely of L. leucocephala.
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PMID:Mimosine degradation in calves fed a sole diet of Leucaena leucocephala in India. 790 Feb 14

The moose (Alces alces L.) in an acid rain affected region in south-west Sweden has developed a complex disease with numerous clinical signs, most of which are consistent with those of secondary copper (Cu) deficiency and/or molybdenosis in cattle and sheep. The clinical signs of the moose disease reported to date include diarrhoea, anorexia, emaciation, achromotrichia, alopecia, sudden heart failure and osteoporosis. Findings at necropsy included mucosal oedema, atrophied lymphoid tissues of the mucous membranes of the alimentary tract, neuropathy, neuronal degeneration and uni- or bilateral corneal opacity. In a study of clinically healthy animals from the affected region in Sweden over a 12-year period (1982-1994), the hepatic Cu concentration decreased by 50% and the liver and kidney cadmium (Cd) concentration decreased by 25-35%, while the molybdenum (Mo) concentration increased by 20-40%. These changes are probably related to an increase in the pH of the soil and water in the moose environment and a consequent change in the uptake of these elements by the plants consumed by the moose. It is noteworthy that the occurrence of the disease in the mid 1980s coincided with increased liming undertaken to counteract the noxious effects of acid rain in this region. Clinical signs and lesions of the moose disease resemble those reported for Cu deficiency and/or molybdenosis in cattle and sheep. To elucidate the complex, multi-faceted clinical signs of the moose disease, the clinical signs and necropsy findings are discussed in relation to the biochemical functions of certain well-known Cu-dependent enzymes, e.g. depigmentation of hair due to depressed tyrosinase activity, osteoporosis by depressed lysyl oxidase activity, sudden heart failure due to decreased activity of lysyl oxidase, cytochrome c oxidase and Cu/Zn-superoxide dismutase; in addition, mucosal lesions and ulcerations due to loss of activity of diamine oxidase as well as of lysyl oxidase and cytochrome c oxidase. It is concluded from the present findings that the moose disease is most probably a Cu deficiency and/or a molybdenosis-type syndrome.
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PMID:'Mysterious' moose disease in Sweden. Similarities to copper deficiency and/or molybdenosis in cattle and sheep. Biochemical background of clinical signs and organ lesions. 949 61

This study involved 14 ostriches of both sexes between 3 and 24 mo of age. Some hematologic and biochemical parameters were studied in animals with stomach impaction. Clinical examination of the birds revealed anorexia, emaciation, decreased defecation, listlessness, separation from the flock, and recumbence. The total number of leukocytes (10.4 x 10(3) mm3), the concentrations of serum glucose (166 mg/dl), and total protein (2.4 g/dl) decreased; serum creatine phosphokinase (1240 U/L) and alkaline phosphatase (598 U/L) increased; whereas no changes were found in the concentrations of calcium, phosphorus, magnesium, zinc, and copper. Medical treatment was initiated in 13 animals; six of them recovered and seven birds died. Necropsy revealed edema, erosions, and hemorrhagic ulcers in the stomach of the dead birds. Foreign bodies such as sand; stone; pieces of wood, glass, and plastic; and metallic objects were encountered in the stomach at the necropsy. In one bird, metallic foreign body was diagnosed and the bird was referred to surgery. Under stress factors, ostriches tend to eat foreign material; therefore, adequate housing, nutrition, and care are crucial in prevention of stomach impaction.
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PMID:Stomach impaction in ostriches (Struthio camelus): blood chemistry, hematology, and treatment. 1224 48

Over 23 months, zinc toxicosis was diagnosed in 35 baboons aged 5-12 months in one galvanized metal and concrete cage complex with conditions that led to excessive exposure to environmental zinc. Clinical signs included reduced pigmentation of hair, skin, and mucous membranes (whiteness), alopecia, dehydration, emaciation, cachexia, dermatitis, diarrhea and, in six cases, severe gangrenous dermatitis of extremities. The syndrome was characterized by pancytopenia, elevated zinc and low copper serum concentrations, low vitamin D and bone-specific alkaline phosphatase levels, and atypical myelomonocytic proliferation of bone marrow. This syndrome emphasizes the importance of proper husbandry and cage design and indicates the potential of infant baboons as a model to study the effects of excessive zinc on development. This is the first report describing the epidemiologic and clinical presentation of zinc toxicosis in infant baboons in captivity.
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PMID:White monkey syndrome in infant baboons (Papio species). 1527 Oct 69

Schistosome infections in mammals cause chronic proliferative vascular lesions associated with the presence of adult parasites in the lumen of mesenteric and portal veins. In birds, however, this has never been reported. In this study, we found obliterative endophlebitis associated with the presence of adult schistosomes (Trichobilharzia sp., probably Trichobilharzia filiformis) as the main pathologic finding in five of eight mute swans (Cygnus olor). On histologic examination, the intestinal and portal veins of these swans showed moderate to severe, diffuse, hyperplastic endophlebitis, characterized by myointimal hyperplasia, often with obliteration of the vascular lumen. In addition, moderate to severe lymphocytic and granulocytic enteritis occurred in all eight swans associated with the presence of schistosome eggs in the intestinal mucosa. Other findings included hepatic and splenic hemosiderosis and high hepatic copper levels. The vascular lesions associated with Trichobilharzia sp. infection may have contributed to the emaciation and death of those mute swans by obstruction of venous return in the intestinal and portal veins.
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PMID:Obliterative endophlebitis in mute swans (Cygnus olor) caused by Trichobilharzia sp. (Digenea: Schistosomatidae) infection. 1555 74

The clinical signs of a disorder known locally as "shakeback disease" in yaks in the North of the Qing Hai-Tibetan Plateau of China were defined: they included emaciation, unsteady gait, a 'shivering' back and deprived appetites. Coat colour was not affected. The mineral composition of soil and forages, and samples of blood and hair from yaks in affected ranches in this region were compared with those of 20 samples from unaffected areas. The mean concentration of molybdenum (Mo) in soil and forage was 4.85+/-0.21 and 4.96+/-0.25 microg/g (dry matter), respectively; the mean copper (Cu) to Mo ratio in the forage was only 1.34+/-0.36 compared to 8.12+/-1.31 for unaffected areas. The mean concentrations of Cu in blood and hair from the affected yaks were 0.29+/-0.17 and 3.51+/-1.12 microg/g, respectively, compared with 0.85+/-0.24 and 6.42+/-1.21 microg/g, for controls. The highest value for Cu in the blood of affected yaks was 0.58 mug/g and the lowest 0.03 microg/g (the corresponding highest values for unaffected yaks were 1.03 mug/g, the lowest 0.56 microg/g). There was a hypochromic microcytic anaemia and a low level of ceruloplasmin in the blood. The Cu deficiency in yaks was most severe during pregnancy and lactation, but oral administration of copper sulphate prevented and cured the disease. We conclude that "shakeback disease" of yaks in this region is probably caused by a secondary Cu deficiency, mainly due to the high Mo content in soils and forage.
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PMID:Studies of a naturally occurring molybdenum-induced copper deficiency in the yak. 1649 Jul 20

A 48-year-old man was referred to our hospital in December, 2005 because of general fatigue, gait disturbance and bradycardia. He had a history of polysurgery due to recurrent ileus and had been treated with home total parenteral nutrition for the short-bowel syndrome since 2003. Clinical findings on admission included marked emaciation and severe weakness of the extremities. Pancytopenia was noted in the peripheral blood. The serum levels of copper and ceruloplasmin were 3 microg/dl and 3 mg/dl, respectively, while Vit. B12 and folate were within the normal range. The bone marrow demonstrated cytoplasmic vacuolation in the myeloid and megakaryocytic series, and sideroblastic changes. No evidence of hematologic malignancies was presented. The diagnosis was copper deficiency and the patient was treated with copper supplementation. Four weeks after copper therapy, the serum level of copper rose to 50 microg/dl and ceruloplasmin to 14 mg/dl. Significant improvements in the hematologic profile, ECG findings and weakness of extremities were noted. Although bicytopenia (anemia and neutropenia) is considered to be a feature of hematologic disorders caused by copper deficiency, the present case showed pancytopenia. The exact mechanism of the unusual association of thrombocytopenia and other abnormalities with copper deficiency remains to be elucidated.
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PMID:[Copper deficiency with pancytopenia, bradycardia and neurologic symptoms]. 1744 78


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