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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two fatal cases of Japanese pieris poisoning in goats are reported. The clinical symptoms of the two animals consisted in vomiting, salivation, excitation and depression. Despite rumenotomy and symptomatic treatment, the goats died within four days after the onset of the symptoms. Pulmonary oedema accompanied by lobular aspiration pneumonia was found to be present in one goat at autopsy. Hyperaemia, pulmonary oedema and acute tubular nephrosis were observed in the other animal.
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PMID:[Pieris japonica pieris poisoning in 2 goats]. 337 72

The gross and histopathological lesions of 10 cases in a natural outbreak of aflatoxicosis amongst dogs in the Republic of South Africa are reported. The 10 cases were classified as acute (1 case), subacute (7 cases) and chronic (2 cases) on the basis of the nature, degree and extent of the following histopathological fractures: hepatocellular fatty degeneration, necrosis or regeneration; proliferation of bile ductules; accumulation of bile within the canaliculi; fibroplasia; and, mucoid degeneration, necrosis or segmental atrophy of the larger intrahepatic bile ducts. Fatty degeneration was noted grossly in the livers of all 10 cases and bile stasis in 4. Varying degrees of fibrosis were present depending on the stage of the disease. In the 2 chronic cases in which nodular regeneration was also observed fibrosis was pronounced. Other macroscopic findings included icterus, anaemia, ascites, hydrothorax, hydropericardium, anasarca, pulmonary oedema, gastro-enterorrhagia and nephrosis.
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PMID:Pathological findings in a natural outbreak of aflatoxicosis in dogs. 344 19

The effect of decreases in plasma colloid osmotic pressure (COP) on the development of lung edema was studied in nephrotic rats. Five control animals were compared with five animals with nephrotic syndrome induced by administration of anti-rat glomerular basement membrane antibody. The COP and the left ventricular diastolic pressure (LVDP) were significantly decreased in nephrotic rats. However, no significant differences were seen in the COP - LVDP gradient, weight-to-dry lung weight ratio, or arterial oxygenation between the nephrotic and control animals. These data suggest that decreases in COP during nephrosis are not associated with accumulation of extravascular lung water.
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PMID:Absence of lung edema in nephrotic rats. 376 Jun 75

An isolate of Fusarium verticillioides (MRC826) that induced experimental leukoencephalomalacia, also caused acute toxicity when fed to pigs and administered per rumen fistula to sheep. Pigs developed severe pulmonary oedema while sheep manifested severe nephrosis and hepatosis. A less toxic isolate (F. verticillioides MRC602), fed to baboons, resulted in acute congestive heart failure or hepatic cirrhosis, depending on the dose. Both isolates were toxic to rats and caused similar lesions, namely, hepatic cirrhosis and intraventricular cardiac thrombosis.
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PMID:A comparative study of the toxicity of Fusarium verticillioides (= F. moniliforme) to horses, primates, pigs, sheep and rats. 731 7

Fumonisins are a class of mycotoxins produced by Fusarium moniliforme and other Fusarium spp. These compounds are widely distributed in corn. Equine leukoencephalomalacia, pulmonary oedema in swine, and nephrotoxicity, hepatotoxicity and liver cancer in male rats, all of which are caused by toxic F. moniliforme, have been experimentally reproduced using fumisin B1 (FB1) (ca 90-94% purity). To investigate the effect of purified (> or = 99% purity) FB1, to compare the effects of FB1 in males and females, and to obtain dose-response information for FB1, three rats per sex were fed diets containing 0, 15, 50 or 150 FB1 for 4 weeks. Serum chemical, organ weight and histopathological evidence showed that 150 mg/kg FB1 was hepatotoxic in both sexes. Nephrosis was found in males fed > or = 15 mg/kg and females fed > or = 50 mg/kg FB1. Altered sphingolipid profiles, specifically increased free sphinganine concentrations and increased sphinganine:sphinogosine ratios, were found in the liver, kidney, serum and urine of FB1-fed rats. These findings support the hypothesis that in vivo toxicity caused by fumonisins may result from altered sphingolipid metabolism.
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PMID:Subchronic toxicity of fumonisin B1 to male and female rats. 766 45

Aflatoxin (AF)-contaminated and fumonisin B1 (FB1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of AF and 0 mg of FB1/kg of feed (control); 2.5 mg of AF/kg of feed; 100 mg of FB1/kg of feed; or 2.5 mg of AF plus 100 mg of FB1/kg of feed for 35 days. The effects on production performance, serum biochemical, hematologic, immunologic, and pathologic measurements were evaluated. Body weight, gain, and feed consumption were significantly (P < 0.05) decreased by AF and AF plus FB1 diets. The FB1 diet decreased feed consumption, and although body weight was numerically decreased, it was not statistically significant. Aflatoxin increased serum gamma-glutamyltransferase (GGT) activity and total iron concentration and decreased urea nitrogen concentration and unsaturated iron-binding capacity. The FB1-alone diet increased serum GGT activity, whereas the AF plus FB1 diet increased serum aspartate transaminase, cholinesterase, alkaline phosphatase, and GGT activities, increased RBC count, triglycerides, and total iron concentrations, and decreased unsaturated iron-binding capacity and urea nitrogen concentration. For the most part, the effects of the AF plus FB1 diet on body weight and hematologic measurements could be considered additive. However, the effect of the AF plus FB1 diet on cholinesterase and alkaline phosphatase activities was greater than additive and was a synergistic response. One pig in the FB1-diet group and 2 pigs in the combination-diet group died. Postmortem lesions in pigs of the FB1-diet group consisted of ascites and increased liver weight. Observations at necropsy for pigs of the AF plus FB1-diet group consisted of hydrothorax, ascites, pulmonary edema, gastric erosions and ulceration, and increased liver and spleen weights. The AF diet increased relative liver weight and resulted in liver that was pale, rubbery, and resistant to cutting. Histologic lesions consisted of hepatic necrosis or degeneration, or both, with variable degrees of bile duct proliferation in barrows of the AF-diet groups. Renal tubular nephrosis was observed in barrows of the FB1-diet group, but this was not consistent in the AF plus FB1-diet group. Cell-mediated immunity, as measured by mitogen-induced lymphoblastogenic stimulation index, was decreased in barrows of the AF and FB1-diet groups, and values in barrows given the combination diet were significantly decreased from those in barrows given the single toxin diets. It was concluded that AF and FB1 (from culture material), singly or in combination, can adversely affect clinical performance, serum biochemical, hematologic, and immunologic values and induce lesions in growing barrows. For most of the variables we evaluated under our study conditions and dosages of toxins, measurements were affected more by the combination diet than by either single toxin diet, and the toxic responses could be described as additive or more than additive, particularly for induction of liver disease.
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PMID:Influence of aflatoxin and fumonisin B1-containing culture material on growing barrows. 859 31

Unusual clinical and pathological observations in the field in goats and sheep suffering from Strongyloides papillosus infection prompted experimental work on this parasite. Goats were infected percutaneously with either single or multiple, low or high levels of S. papillosus. Young goats up to 12 months of age were found to be the most susceptible. Some animals, however, showed substantial resistance to infective doses. Clinical signs included transient diarrhoea, misshapen, elongated faecal pellets terminally, dehydration, anorexia, cachexia, gnashing of teeth, foaming at the mouth, anaemia and nervous signs such as ataxia, a wide-based stance, stupor and nystagmus. A 'pushing syndrome' was seen in 22% of the animals. The pathological changes are described and included enteritis, status spongiosus in the brain, hepatosis leading to rupture of the liver, nephrosis, pulmonary oedema, interstitial pneumonia and pneumonia. About 6% of the goats died acutely from fatal hepatic rupture. The development of an acquired immunity was determined. The immunity elicited an allergic skin reaction at the application site of larvae or injection sites of larval metabolites. This immunity, however, could be breached by large doses of larvae. The most profound clinicopathological changes induced by the parasites were an anaemia (most pronounced in the young goats) and hypophosphataemia. Trace element analyses provided evidence of Cu, Mn and possibly Se deficiencies in some goats.
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PMID:Experimental studies with Stronglyloides papillosus in goats. 1063 9

A flock of goats received a diet with 1% urea for at least 1 y. A new batch of concentrate was offered increasing the level of urea to 4.2%. Eighteen of 54 goats showed acute signs of ammonia toxicosis. Ten goats died within 60 min; 4 goats and a buck with convulsions recovered when treated by administration of vinegar and infusion of saline solution, diuretics, and atropine. Three goats with mild signs recovered within 1 h without treatment. The mean ammonia concentration and rumen pH content were 820 mg/L and 7.7, respectively. Generalized congestion, intense pulmonary edema, and slight tubular nephrosis were found in 3 goats on necropsy. The outbreak was self-limiting and no more cases occurred when the diet was removed.
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PMID:Ammonia toxicity from urea in a Brazilian dairy goat flock. 1075 Jan 72

The pathological findings in sheep with peracute experimental Clostridium perfringens type D enterotoxemia are described. Of 16 animals inoculated intraduodenally with a whole culture of this microorganism and a starch solution in the abomasum, 12 developed clinical signs including increased respiratory efforts, recumbency, paddling, bleating, convulsions, blindness, and opisthotonus. Diarrhea was not observed in any of the animals. The time lapse between the beginning of intraduodenal infusion and onset of clinical signs varied between 30 minutes and 26 hours, and the clinical course varied between 1 and 9 hours. Gross postmortem changes were observed in these 12 animals and included pulmonary edema; excess pericardial, peritoneal, or pleural fluid with or without strands of fibrin; liquid small intestinal contents; leptomeningeal edema; cerebellar coning; and subcapsular petechiae on kidneys. Histological changes consisted of severe edema of pleura and interlobular septa and around blood vessels and airways and acidophilic, homogeneous, proteinaceous perivascular edema in the brain. Five of 12 animals (42%) with clinical signs consistent with enterotoxemia lacked specific histological lesions in the brain. None of the intoxicated or control animals developed nephrosis. Glucose was detected in the urine of 3 of 6 animals that were tested for this analyte. These results stress the importance of the use of histological examination of the brain, coupled with epsilon toxin detection, for a definitive diagnosis of C. perfringens type D enterotoxemia in sheep.
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PMID:The pathology of peracute experimental Clostridium perfringens type D enterotoxemia in sheep. 1546 Mar 22

Discussed in the paper are thanatologically significant morphological signs in intoxication with some of psychic drugs. It was demonstrated that, in intoxication with azaleptin, phenazepam and aminazin, death comes mostly from affection of the brain including its edema and irreversible severe changes of neurons. In intoxication with tizercin, benzodiazepines and barbiturates, cardiac thanatogenesis as fibrillation of heart chambers combined with foci of myocytolysis. Sodium oxybutyrate brings about vascular collapse with subsequent development of fibrillation of heart chambers and of pulmonary edema. Intoxication with amitriptyline causes naturally necrotic nephrosis entailing uremic pneumonia and edema of the brain and heart.
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PMID:[Thanatogenesis in poisoning with psychopharmaceuticals]. 1588 Nov 37


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