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)

Ibaraki disease, an epizootic disease of cattle in Japan resembling bluetongue, is characterized by fever and lesions affecting the mucous membranes, the skin, the musculature and vascular system. Degeneration of striated muscular tissue is observed in the oesophagus, larynx, pharynx, tongue and the skeletal muscles. Oedema and haemorrhage are marked in the mouth, lips, abomasum, around the coronets, etc., and are occasionally followed by degeneration of the epithelium leading to erosions or ulcerations. Severe lesions affecting the oesophageal and laryngopharyngeal musculature cause difficulty in swallowing which in turn produces dehydration and emaciation, and occasionally the aspiration pneumonia, which constitute the major causes of death of affected animals. These clinical and pathological findings indicate the similarity of the disease to bluetongue in sheep and cattle. Ibaraki disease was first recognised in Japan in 1959 and 1960. Seasonally its occurrence is limited to late summer and autumn, and geographically to the central and western parts of Japan, roughly south of 37 degrees north latitude. It is absent from the higher altitudes. The seasonal and geographical incidence suggests the possibility of an arthropod vector; but direct evidence for such a vector is still lacking. Serological data suggest the presence of Ibaraki virus on Bali Island in Indonesia and in Taiwan. The disease can be transmitted serially in calves by the intravenous inoculation of blood obtained at the height of a febrile reaction. Ibaraki virus can be isolated in bovine cell cultures from both natural and experimentally produced cases of the disease. The virus multiplies and induces cytopathic effects in primary cultures of bovine, sheep and hamster lung origin, and L cells; but it does not grow in primary cultures of horse and swine kidney nor in HeLa cell cultures. The virus is readily passaged serially in 4 to 5-day-old eggs by yolk-sac inoculation and incubation at 33.5 degrees C. It multiplies in the brains of mice of any age after incracerebral inoculation but younger mice give a better viral growth and develop encephalitis. No evidence has been obtained that rabbits and guinea pigs are susceptible to Ibaraki virus...
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PMID:Ibaraki disease and its relationship to bluetongue. 16 88

Toxicosis was induced in pregnant Holstein-Friesian heifers by giving polybrominated biphenyls a in gelatin capsules at the rate of 25 g/day. Initially, this dosage was approximately 67 mg/kg of body weight. Clinical signs were anorexia, excessive lacrimation and salivation, diarrhea, emaciation, dehydration, depression, and abortion. Fever was not evident during the experiment. Values for serum glutamic-oxalacetic transaminase, lactic dehydrogenase, blood urea nitrogen, and bilirubin were increased. Changes in packed cell volume, hemoglobin content, total erythrocyte and leukocyte counts, and differential leukocyte counts were minimal and reflected dehydration and secondary infection. The principal urine changes were decreased specific gravity and moderate proteinuria. Gross necropsy findings included dehydration; subcutaneous emphysema and hemorrhage; atrophy of the thymus; fetal death with concomitant necrosis of cotyledons; kidneys that were enlarged, pale tan to gray; thickened wall of the gallbladder; inspissated bile; edema of abomasal folds; mucoid enteritis; linear hemorrhage and edema of the rectal mucosa; and secondary pneumonia. Microscopic changes were most marked in the kidneys, gallbladder, and eyelid. In the kidney, the principal changes were extreme dilatation of collecting ducts and convoluted tubules, with epithelial degenerative changes of cloudy swelling, hydropic degeneration, and separation from the basement membrane. Common changes in the gallbladder were moderate to marked hyperplasia and cystic dilatation of the mucous glands in the lamina propria. The changes in the eyelids were characterized by hyperkeratosis, with accumulations of keratin in hair follicles of the epidermis and squamous metaplasia with keratin cysts in the tarsal glands. Clinical signs and lesions of toxicosis did not develop in heifers given the polybrominated biphenyls at the rate of 0.25 mg and 250 mg/day for 60 days. Initially these rates were approximately 0.00065 mg/kg and 0.65 mg/kg of body weight, respectively.
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PMID:Pathology of experimentally induced polybrominated biphenyl toxicosis in pregnant heifers. 18 92

The toxicity of a commercial blend of polybrominated biphenyls was determined in 24 pregnant Holstein heifers that were allotted randomly to one of four experimental groups given 0, .25, 250, or 25,000 mg/day of fire-Master BP-6. The polybrominated biphenyls were mixed with finely ground corn and given by bolus for 60 days or until the animal became moribund. Average body weight of heifers at onset of experiment was 381 kg. No clinical signs of toxicosis were evident in heifers fed 0, .25 or 250 mg/day. Toxicosis was induced in heifers fed 25,000 mg/day resulting in reduced dry matter intake, body weight, heart rate, and respiration rate. Clinical signs were anorexia, emaciation, dehydration, excessive lacrimation and salivation, diarrhea, depression, and abortion or fetal death. All heifers fed 25,000 mg/day became moribund within 33 to 66 days.
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PMID:Effects of polybrominated biphenyls on health and performance of pregnant Holstein heifers. 19 46

Toxicosis was induced in pregnant heifers by feeding 25,000 mg/head/day of FireMaster BP-6, a commercial blend of polybrominated biphenyls (PBB). The PBB feeding decreased dry matter intake approximately 50% by 4 days exposure. Emaciated animals became anorexic a few days prior to death at 33 to 66 days. Weight losses of heifers average 80 kg. Other clinical signs observed were dehydration, diarrhea, excessive salivation and lacrimation, fetal death, abortion, and general depression as evidenced by depressed heart and respiratory rates. Clinical signs were apparent after 10 days exposure and progressively intensified along with loss of condition until death. Clinicopathologic changes included significantly increased serum glutamic-oxaloacetic transaminase and decreased serum calcium by 30 days exposure. Lactate dehydrogenase, urea nitrogen, and bilirubin were elevated, and serum albumin decreased by 36 to 40 days. Principal urine changes were decreased specific gravity and moderate proteinuria. Pregnant heifers fed 0.25 or 250 mg/head/day for 60 days and nonpregnant heifers fed 250 mg/head/day for 180 days displayed neither clinical signs nor clinicopathologic changes indicating adverse effects from PBB exposure. Post-exposure, all heifers exposed to PBB for 60 days calved normally with zero calf mortality and were successfully rebred. Milk production was not different from control animals. Birth weights of calves from dams exposed to 250 mg PBB/head/day were significantly greater than calves of dams exposed to 0 mg or 0.25 mg/head/day. PBB exposure of dams produced no detrimental effects on calves as indicated by clinical signs, clinicopathologic changes, or performance.
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PMID:Effects of PBBs on cattle. I. Clinical evaluations and clinical chemistry. 21 5

A rotavirus isolated from a field outbreak of diarrhoea in artificially reared piglets was purified, filtered and administered orally to gnotobiotic and conventional piglets. Four successive passages of the virus in gnotobiotic piglets produced severe diarrhoea within 20 to 24 hours of administration. The diarrhoea lasted several days causing dehydration, emaciation, loss of body weight and some deaths. Virus was demonstrated in the faeces of the infected piglets by electron microscopy. Conventionally reared piglets developed little or no diarrhoea when given virus, whereas artificially reared piglets developed moderate to severe diarrhoea which lasted from 3 to 8 days with some deaths. No clinical disease was obvious in surviving piglets following challenge with the virus 10 or 17 days after initial infections.
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PMID:Diarrhoea in piglets inoculated with rotavirus. 21 Jul 55

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

An outbreak of salmonellosis in a gerbil colony was investigated. The clinical, bacteriologic, and pathologic findings are reported. Clinical signs included an occasional sudden death, depression, emaciation, dehydration, rough hair coat, and testicular enlargement. Not every sign was observed in every infected gerbil. At necropsy, 11 animals had lesions consistent with salmonellosis. Histopathologic lesions consisted of interstitial pneumonia, hepatic and splenic necrosis, meningitis, and suppurative orchitis. Splenic and intestinal amyloidosis were also noted. Salmonella, group D, was recovered from gerbil feces, a container in which adult mosquitos were reared, filarial inoculum, and a cockroach. An epizootiologic investigation led to salmonella-infected cockroaches as the possible source of animal contamination via mosquitos and the subsequent filarial inoculum.
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PMID:Salmonellosis in gerbils induced by nonrelated experimental procedure. 131 48

In a retrospective survey, the epidemiological characteristics of nursing sickness in Standard Black and Pastel mink (Mustela vison) were examined in a Danish fur research farm. Based on the clinical diagnosis of the disease, the overall morbidity in a total of 1774 lactating females amounted to 14.4% and the case fatality rate to 7.8%. Apparently healthy females weaned an average of 5.0 kits per litter, while dams suffering from nursing sickness raised and weaned an average of 5.4 kits per litter (p less than 0.01). Based on logistic regression analysis, the increasing age of the lactating dam, followed by littersize and female weight loss, appeared to be major determinants for the development of nursing sickness. The impact of additional covariates such as litter weight gain and female color type were remarkably low. At weaning (day 43) the mean individual live weight of the kits of either sex did not differ between healthy and sick dams. In Standard Black, the total biomass of the offspring raised by sick dams was significantly larger than that of the healthy controls (p less than 0.01). During the final two weeks of lactation, apparently healthy dams lost on average 14% of their body mass, whereas those affected by nursing sickness had a mean weight loss of about 31% (p less than 0.001). Postmortem examination of 25 dams with severe nursing sickness verified the clinical findings of progressive dehydration and emaciation. The gastrointestinal tract was empty and gastric ulcers and melaena were frequently present. Other common findings included small livers,enlarged adrenals and pitted kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nursing sickness in lactating mink (Mustela vison). I. Epidemiological and pathological observations. 159 61

An investigation of the pathophysiological characteristics of nursing sickness in mink was carried out as a follow-up study of a previous epidemiological survey at a Danish fur research farm during the 1989 breeding season. In a total of 48 nursing females of the Standard Black and Pastel type, concentrations of several pertinent biochemical constituents of whole blood, plasma, urine and skeletal muscle were determined in order to identify nutritional and metabolic factors involved in the origin and development of the disease. Compared to the reference data obtained in 17 apparently normal lactating dams the findings in 31 females suffering from nursing sickness presented varying clinical and biochemical signs of progressive dehydration and emaciation: aldosteronism, hypovolemia, hyponatremia, hyperkalemia (in the face of muscle potassium depletion), hyperglycemia and azotemic acidemia. Neither ketosis nor severe lactacidemia was observed. The urine was almost devoid of sodium and chloride, and urinary potassium concentration diminished by approximately 50%. The concentrating ability of the kidneys was reduced to less than one third of the maximum value. The results were consistent with severe dehydration and emaciation due to heavy losses of energy, water and body mass along with increasing milk production. The progressive nature of the disease supported the hypothesis that nursing sickness is due to the combined effects of heavy milk production and excessive tissue catabolism along with reduced or ceased dietary intake, and maybe increasing environmental stress. In the advanced stage of the disease coma and death appear to be the inevitable outcome of the metabolic strains for continuing milk production.
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PMID:Nursing sickness in lactating mink (Mustela vison). II. Pathophysiology and changes in body fluid composition. 159 62

The pathogenesis of the UT-1 strain, a newly isolated rat virus (RV), in juvenile and newborn rats was examined. Intracerebrally (ic) inoculated newborns developed severe pantropic infections resulting in emaciation, stunted growth, diarrhea, dehydration and icterus, and died 13 to 15 days after the inoculation. Newborns inoculated intraperitoneally (ip) developed similar, but milder diseases. The virus replicated in all the organs tested, which was followed by severe viremia. Histopathologically, diffuse vacuolation and necrosis of the hepatocytes were observed in the liver. Juvenile rats inoculated with the virus showed neither clinical signs nor histopathologic lesions, although viral recovery and antibody production were observed. Thus, we conclude that the UT-1 strain of RV caused asymptomatic infections in juvenile rats, and fatal infections with hepatic lesions in newborn rats.
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PMID:Pathogenesis of a newly isolated rat virus in newborn and juvenile rats. 165 98


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