Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013911 (emaciation)
 1,059 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred fifty lactating mink on one ranch in southern Ontario were monitored over the lactation period in 1989 for evidence of clinical disease, and serial blood samples were collected for biochemical analysis. Antemortem blood samples were collected and necropsies performed on the 17 females that developed nursing disease and on 17 controls matched to the same stage of lactation and on ten nonlactating controls. Twenty-two additional nursing disease cases were selected from seven ranches in the following year and processed similarly. The clinical signs typically observed in affected females were sudden onset lethargy and anorexia followed by dehydration, ataxia, and a reluctance to move. The major clinical-pathologic findings were a marked increase in serum osmolality and total protein, urea nitrogen, creatinine, phosphorus, glucose, and potassium concentrations and a decrease in sodium and chloride concentration. In addition, the animals were acidotic, there was a reduction in the urine specific gravity, and the hemogram was consistent with a stress response. Emaciation and dehydration were the only pathologic changes consistently present in cases of nursing disease and not in controls. In almost all cases, bacteria were not cultured from the liver, spleen, and mammary gland, but Campylobacter jejuni was cultured from the intestinal contents of 15/17 affected mink and 2/5 controls. Aleutian disease virus antibody was not present in any of the affected mink. Lipid vacuoles in hepatocytes and renal tubular epithelium, hypertrophy of cells in the adrenal cortex, and pulmonary congestion and atelectasis were present in both diseased females and controls, as were various sporadic inflammatory lesions. Nursing disease may result from energy depletion due to lactation. All lactating females are affected by this process; clinical disease reflects the terminal physiologic decompensation of the most susceptible individuals.
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PMID:Nursing disease in mink: clinical and postmortem findings. 811 44

Five Holstein Friesian calves varying in age from 7 to 9 weeks old, were suspected of suffering from an inherited granulocytopathy known as bovine leucocyte adhesion deficiency (BLAD). Four of them were examined clinically and at necropsy. The most significant clinical findings were fever, depression, weakness, emaciation, diarrhoea, pseudomembranous gingivitis, loose teeth, respiratory infection and occult blood in the faeces. Significant clinicopathological findings were marked leucocytosis, mainly due to a neutrophilia, hypoalbuminemia, hypogammaglobulinemia, increased alpha- and beta-globulins, elevated alkaline phosphatase enzyme activity, hypoglycaemia, and decreased blood urea concentrations. The necropsy revealed emaciated carcasses, granulomatous to necrotising gingivitis, pseudomembranous to necrotising enteritis with perforations, bronchopneumonia, splenic atrophy, and hypoplasia of the thymus. Histopathological examination supported the macroscopic findings.
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PMID:[Suspected inherited granulocytopathy in four Holstein Friesian calves]. 817 99

The subchronic (14-18 wk) toxicity of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), a mutagenic by-product in chlorinated drinking water, was evaluated in Wistar rats. In a range-finding study, MX was administered daily for 14 days by gavage in deionized water to male rats (five animals per group) at doses of 12.5, 25, 50, 100 or 200 mg/kg body weight. The doses above 50 mg/kg were lethal and three out of five animals also died during treatment at 50 mg/kg. The range-finding study was repeated with doses of 5, 10 and 20 mg MX/kg, given on 5 days a week, to both males and females (10 animals per group). These doses were not overtly toxic but caused several changes in plasma clinical chemistry at 10 and 20 mg MX/kg in comparison with the controls. These included increased urea, creatinine and bilirubin and decreased inorganic phosphate and potassium in females and increased cholesterol in males. In the subchronic toxicity study, rats (15 per group, were given MX by gavage, on 5 days a week, at doses of 0 (controls) or 30 md/kg (low dose) for 18 wk, or, in the high-dose group, at doses increasing from 45 to 75 mg/kg over 14 wk. The high dose was finally lethal (two males and one female died) and caused hypersalivation, wheezing respiration, emaciation and tangled fur in animals. The body weights of the high-dose males decreased by 15%, and food consumption was decreased by 15 to 20%, but the water consumption increased by 15% to 60%. Plasma cholesterol and triglycerides were elevated and urine excretion was increased. Urine specific gravity was decreased and the relative weights of the liver and kidneys were increased in both sexes at both doses in comparison with the controls. At both doses, duodenal hyperplasia occurred in males and females, and slight focal epithelial hyperplasia in the forestomach was observed in males. Splenic atrophy and haemosiderosis were seen in two high-dose females, and epithelial cell atypia in the urinary bladder of one high-dose male and female. The frequency of bone marrow polychromatic erythrocytes with micronuclei was slightly increased in low-dose males. The results indicate that repeated administration of MX disturbs the fluid-electrolyte balance and induces diuresis, causes mucosal hyperplasia in the gastro-intestinal tract as a local effect, and affects lipid metabolism.
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PMID:Subchronic toxicity of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) in Wistar rats. 884 98

The acute and subacute toxicity of five biogenic amines-tyramine, spermidine, spermine, putrescine and cadaverine-were examined in Wistar rats. Tyramine and cadaverine had a low acute oral toxicity of more than 2000 mg/kg body weight. Putrescine had an acute oral toxicity of 2000 mg/kg body weight and spermidine and spermine each of 600 mg/kg body weight. All amines investigated caused a dose-related decrease in blood pressure after intravenous administration, except for tyramine, where an increase was found. In 6-wk studies the biogenic amines were administered in the diet to groups of 10 male and 10 female rats. Tyramine and cadaverine were given at levels of 0, 200, 2000 or 10,000 ppm, spermine and putrescine at levels of 0, 200, 2000 or 5000 ppm and spermidine at levels of 0, 20, 200 or 500/1000 ppm in the first study and at levels of 0 or 10,000 ppm in a second study. Spermine was the most toxic. The high dose level showed a great number of changes, such as emaciation, aggressiveness, convulsions and paralysis of the hind legs. Growth, food intake and water intake were considerably decreased. Slight anaemia (males) and changes in plasma clinical chemistry occurred. The relative weights of the thyroid, adrenals, spleen and heart were increased and that of the liver decreased. Impaired kidney function, together with renal histopathological changes and changes in plasma electrolytes and urea, occurred with spermine. Histopathological examinations also revealed decreased glycogen content in the liver, reduction of spermatogenesis, severe depletion of splenic white pulp, acute involution of the thymus and moderate myocardial degeneration in the heart. Myocardial degeneration was also seen in one mid-dose male. Adverse effects were also observed in the top dose groups of all other amines. Decreased body weights associated with diminished food intake were generally seen. Slight increases in packed cell volume, haemoglobin concentration and thrombocytes occurred with cadaverine. With spermidine, decreased plasma creatinine, calcium and inorganic phosphate were observed and decreased potassium levels with cadaverine. The no-observed-adverse-effect level was 2000 ppm (180 mg/kg body weight/day) for tyramine, cadaverine and putrescine, 1000 ppm (83 mg/kg body weight/day) for spermidine and 200 ppm (19 mg/kg body weight/day) for spermine.
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PMID:Acute and subacute toxicity of tyramine, spermidine, spermine, putrescine and cadaverine in rats. 920 96

From 1984 through 1992, staff at The Marine Mammal Center (TMMC, Sausalito, California, USA) examined 207 northern elephant seals (Mirounga angustirostris) with a condition of unknown etiology called northern elephant seal skin disease (NESSD). The skin lesions were characterized by patchy to extensive alopecia and hyperpigmentation, punctate or coalescing epidermal ulceration, and occasionally, massive skin necrosis. Microscopic lesions included ulcerative dermatitis with hyperkeratosis, squamous metaplasia and atrophy of sebaceous glands. All diseased seals were less than 2 years of age and suffered from emaciation, depression, and dehydration. Mortality from septicemia increased significantly with severity of skin ulceration. Compared to 14 apparently unaffected seals, diseased seals had depressed levels of circulating thyroxine, triiodothyronine, retinol, serum iron, albumin, calcium, and cholesterol. Levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transpeptidase, blood urea nitrogen, and uric acid were elevated. Morphometrically, diseased animals were approximately 15% smaller than normal seals of the same sage. Serum and blubber concentrations of 36 polychlorinated biphenyl congeners (sigma PCB) and dichloro-diphenyl-dichloroethylene (p,p'-DDE) were negatively correlated with body mass. Mean concentrations of sigma PCB and p,p'-DDE in serum in diseased seals were elevated as compared to apparently normal seals. Etiology of this syndrome remains unknown, but the possibility of PCB toxicosis cannot be ruled out.
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PMID:Clinical and pathological characterization of northern elephant seal skin disease. 924 88

The feeding of lactating goats on usual green fodder, contaminated with Euphorbia helioscopia or E. nubica, results in poisoning of the dams as well as their suckling kids. General signs of toxicity were emaciation, depression, shedding of body hair, arching of back, and possible death. Post-mortem changes of dams and dead suckling kids included congestion and hemorrhage in cardiac muscle, lung, liver, and kidneys. Blood analyses of goats exposed to these contaminants showed an increased level of serum alanine amino transferase compared to control samples, indicating cellular destruction in the liver. The latter was confirmed by histopathological changes in the organ which include severe congestion, necrosis, and degenerative changes. The goats also suffered from deterioration of renal function as indicated by increased blood urea nitrogen and creatinine levels. In histopathologic inspections of kidney, severe congestion, hemorrhage in the cortex and medulla, as well as necrosis of epithelial cells of kidney tubules were noticed. Considerable degenerative changes were also observed in heart and lung. The pathophysiological appearances indicate that by feeding on the Euphorbia species mentioned above, the goats are poisoned in a way similar to the case of E. peplus reported previously. Such intoxication most likely is due to irritant and hyperplasiogenic diterpene ester (DTE) toxins, usually present in the aerial parts of Euphorbia species and well known as tumor promoters in mouse skin. After ingestion of the toxic plant parts by the goats, the DTE toxins might be metabolized and thereby partially detoxified. Yet, at least in part, they may show up in the milk of the goats, as indicated by severe poisoning of their suckling kids. As discussed previously in lactating goats fed on fodder contaminated with E. peplus, tumor promoters of the DTE type may enter the human food chain via this source of milk. Such milk may be considered a valuable etiologic model for the investigation of economic, ecologic, and public health problems raised by human diet polluted with tumor promoters, i.e., conditional (non-genotoxic) cancerogens.
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PMID:Dietary cancer risk from conditional cancerogens (tumor promoters) in produce of livestock fed on species of spurge (Euphorbiaceae). IV. Toxicologic and pathophysiologic observations in lactating goats and their suckling kids fed on the irritant herbs Euphorbia nubica and Euphorbia helioscopia: an etiologic model for investigations on the putative risk of cancer by consumption of food p. 1120 69

Wet belly, when the reindeer becomes wet over the lower parts of the thorax and abdomen, sometimes occurs in reindeer during feeding. In a feeding experiment, 11 out of 69 reindeer were affected by wet belly. The problem was first observed in 7 animals during a period of restricted feed intake. When the animals were then fed standard rations, 3 additional animals fed only silage, and 1 fed pellets and silage, became wet. Four animals died and 1 had to be euthanized. To investigate why reindeer developed wet belly, we compared data from healthy reindeer and reindeer affected by wet belly. Urea, plasma protein, glucose, insulin and cortisol were affected by restricted feed intake or by diet but did not generally differ between healthy reindeer and those with wet belly. The wet animals had low body temperature and the deaths occurred during a period of especially cold weather. Animals that died were emaciated and showed different signs of infections and stress. In a second experiment, with 20 reindeer, the feeding procedure of the most affected group in the first experiment was repeated, but none of the reindeer showed any signs of wet belly. The study shows that wet belly is not induced by any specific diet and may affect also lichen-fed reindeer. The fluid making the fur wet was proven to be of internal origin. Mortality was caused by emaciation, probably secondary to reduced energy intake caused by diseases and/or unsuitable feed.
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PMID:Wet belly in reindeer (Rangifer tarandus tarandus) in relation to body condition, body temperature and blood constituents. 1217 6

The health status of 83 loggerhead sea turtles (Caretta caretta; 39 foraging, 31 nesting, and 13 stranded turtles) was analyzed using physical examinations, hematology, plasma biochemistry, plasma protein electrophoresis, and toxicologic parameters. Significant differences were noted in a number of health parameters between turtles exhibiting each of these behaviors. On physical examinations, stranded turtles had the highest prevalence of heavy carapace epibiont loads, miscellaneous abnormalities, emaciation, and weakness. Differences in hematologic values included a lower packed cell volume, higher number of lymphocytes, and lower number of monocytes in stranded turtles; lower white blood cell counts in foraging turtles; and significant differences in total solid values among turtles exhibiting all behaviors with the lowest values in stranded turtles and the highest values in nesting turtles. Differences in plasma biochemistry values included the highest uric acid, creatine kinase, and CO(2) values in stranded turtles; the highest glucose and potassium values in foraging turtles; and the highest cholesterol and triglyceride values, and lowest alanine aminotransferase, in nesting turtles. Differences in total protein, albumin, and globulin were found using plasma biochemistry values, with lowest values in stranded turtles and highest values in nesting females, whereas differences in blood urea nitrogen between turtles included the lowest values in nesting turtles and the highest in foraging turtles. Plasma organochlorine and polychlorinated biphenyl levels were below their limits of quantification in the 39 foraging, 11 nesting, and three stranded turtles tested. A statistically significant difference was noted in the level of whole blood mercury between the 23 foraging and 12 nesting turtles tested. There was no difference in arsenic or lead levels between turtles exhibiting any of the three behaviors. Although a few limitations exist with the present study and include unknown ambient temperatures, turtle handling times that varied from 15 min to 53 min per turtle, and the use of a different laboratory for processing complete blood counts and plasma biochemistries in stranded versus foraging and nesting turtles, we provide baseline blood values for two cohorts (foraging and nesting) of loggerhead sea turtles on the coast of Georgia. Additionally, we demonstrate significant differences in clinical findings and blood parameters between foraging, nesting, and stranded loggerhead turtles in the region.
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PMID:Comparison of blood values in foraging, nesting, and stranded loggerhead turtles (Caretta caretta) along the coast of Georgia, USA. 1920 34

A study was conducted to examine the clinical signs, hematological, biochemical and histopathological changes in vitamin D(3) toxicity at a dose rate 2 mg/kg b.wt. of vitamin D(3) and to assess the protective effect of Aloe vera in vitamin D(3) toxicity. The clinical signs observed were anorexia, progressive weight loss, difficulty in movement and respiration, diarrhea, epistaxis, subnormal body temperature and nervous signs before death. Mortality was observed in treated rats between day 10 and day 19 of treatment. The gross postmortem changes observed were severe emaciation, white chalky deposits on epicardial surface of heart, pin point white deposits on cortical surface of kidneys with pale yellow discoloration and diffused white deposits on serosal surface of stomach and intestine with bloody ingesta in lumen. The hematological changes included non-significant increase in hemoglobin and total leukocyte count and significant increase in relative neutrophil count. The biochemical changes observed were significant increase in plasma concentration of calcium, phosphorus and blood urea nitrogen, whereas a significant decrease in the concentration of albumin and total plasma protein was observed. The histopathological lesions included calcification of various organs, viz., tongue, stomach, intestines, kidney, heart, aorta, larynx, trachea, lungs, spleen, choroid plexus arteries of brain and vas deferens. The Aloe vera juice (2.5% in drinking water) has no protective effect on vitamin D(3) toxicity (2 mg/kg b.wt.).
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PMID:Clinicopathological Studies on Vitamin D(3) Toxicity and Therapeutic Evaluation of Aloe vera in Rats. 2143 Sep 19

Trypanosomiasis caused by Trypanosoma evansi commonly produces wasting disease with signs of emaciation and cachexia mainly at the end stage. The present study was conducted to explore the possible hyperlipaemia or hyperlipidaemia and its association with cachexia-anorexia in equine trypanosomiasis. Out of the fifteen confirmed animals, none of the plasma sample was opaque. There was a significant increase in plasma triglyceride, total cholesterol and blood urea nitrogen and a highly significant increase in low-density lipoprotein (LDL) levels. A mild increase in high-density lipoprotein (HDL) and very low-density lipoprotein levels were observed, while the relative percentage of HDL and LDL was altered with high significance. A moderate increase in triglyceride and highly significant increase in LDL might be the reasons for retention of appetite and lipolysis. Possible protein breakdown and presence of lipolysis might be the reasons for cachexia in equine trypanosomiasis.
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PMID:Hyperlipidaemia in trypanosomiasis of naturally infected horses: possible cachexia-anorexia syndrome? 2283 85


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