Sheep Poisoned Research Articles

Superphosphate poisoning of sheep: a study of natural outbreaks

Superphosphate poisoning is typically a disease of pregnant and lactating ewes under nutritional stress. Poisoning has been observed only in the late winter and spring. Most episodes occurred when hungry sheep were forced to graze short pastures top-dressed within one week prior to the onset of clinical signs. Fine weather which is favourable for the application of fertiliser also favours the occurrence of poisoning. Clinical signs include anorexia, thirst, diarrhoea, weakness and incoordination. Death usually occurs within 48 hours of the onset of clinical signs. In some outbreaks the presenting signs are those of hypocalcaemia but response to calcium therapy is transient. Poisoning results in a toxic tubular nephritis and uraemia. No satisfactory treatment can be suggested but poisoning can be prevented by avoiding exposure of sheep to top-dressed pastures.

Intravenous administration of thiomolybdate for the prevention and treatment of chronic copper poisoning in sheep.

1. Twenty-six sheep were used in experiments designed to test the effectiveness of ammonium tetrathiomolybdate in the prevention and treatment of chronic copper poisoning. 2. Intravenous injections of 100 mg ammonium tetrathiomolybdate twice weekly (a) prevented the occurrence of haemolytic crisis in sheep repeatedly dosed with copper sulphate and (b) minimized tissue damage and prevented further haemolytic crisis when given to sheep already in haemolysis. 3. Thiomolybdate prevented excessive deposition of Cu in the liver of sheep receiving orally large amounts of Cu and decreased liver Cu levels in sheep that were not given additional Cu. In the latter sheep, 50 mg ammonium tetrathiomolybdate given twice weekly did not produce histologically-detectable tissue damage even though liver and kidneys contained high levels of molybdenum, and kidneys contained elevated levels of Cu. 4. It is concluded that chronic Cu poisoning can be successfully prevented or treated by intravenous injection of appropriate doses of ammonium tetrathiomolybdate.

Chronic copper poisoning of sheep in Nigeria.

An outbreak of chronic copper poisoning in sheep is described. At least 145 out of 687 sheep (21.1%) on a government farm died during a period of 2 months. The clinical and post-mortem picture was one of sudden, profound intravascular haemolysis and subsequent jaundice. Mortality approached 100%. Plasma copper levels ranged from 22 to 76 mumol/litre. There was no obvious source of exogenous copper. Possible causes of the elevated copper levels are discussed.

Creatine kinase release and muscle changes in chronic copper poisoning in sheep

Chronic copper poisoning was induced in sheep by repeated dosing with an aqueous solution of copper sulphate. A sudden rise in the level of plasma creatine kinase (CK) occurred at haemolysis but the level returned to normal once the 'crisis' was over. The level of CK in the cerebrospinal fluid remained normal throughout the experiments. An isoenzyme study showed that the CK was liberated from muscle. Light microscopic studies failed to reveal consistent changes in muscle structure but ultrastructural changes in mitochondria, similar to those described as the earlies changes in muscle fibres in vitamin E deficiency, were seen in sheep killed during and after haemolysis. The elevations of CK levels and the mitochondrial changes were most marked in sheep that did not receive selenium and vitamin E supplements. It is suggested that the CK release at haemolysis may occur because of a transient increase in the permeability of muscle membranes which may be brought about by a number of factors such as: (a) hypoxia, (b) hypercupraemia, (c) decrease in vitamin E and/or selenium content in blood and tissues.

Autophagy and apoptosis in liver during the prehaemolytic phase of chronic copper poisoning in sheep

Fine structural changes in the liver during the prehaemolytic phase of chronic Cu poisoning in sheep were investigated in biopsy and post-mortem samples obtained from 24 Finn-Dorset × Suffolk ewe lambs. From the beginning of the prehaemolytic phase excessive accumulation of Cu was accompanied by sublethal injury to liver parenchymal cells, reflected by changes in the endoplasmic reticulum and an increase in the numbers of autophagic vacuoles. Towards the later stages of the prehaemolytic phase there was a high incidence of cell death and apoptosis.

Evaluation of tests for the diagnosis of lead exposure in sheep.

Several laboratory tests that are currently used for the diagnosis of lead poisoning in man were evaluated for the detection of lead poisoning in sheep given 3 or 10 mg Pb/kg body weight/day for 7 weeks. Urinary porphyrins and basophilic stippling of erythrocytes were not sensitive indicators of lead poisoning in sheep, while urinary lead and urinary delta-aminolevulinic acid concentrations were too variable to have diagnostic value. However, erythrocyte delta-aminolevulinic acid dehydratase was strongly inhibited by exposure to relatively low doses of lead, while blood lead concentrations gave an indication of the level of exposure to lead poisoning.

Reducing the potential copper toxicity of concentrates to sheep by the use of molybdenum and sulphur supplements

A high copper (Cu) diet (45.3 μg Cu/g DM) was given to three groups of animals, ♂ or ♀ Scottish Blackface and ♂ Finnish Landrace lambs, without added molybdenum (Mo), or with 2, 4, 8 or 16 mg Mo/kg DM added in a 3 × 5 factorial experiment lasting 18–27 weeks. Sodium sulphate, providing 2 g S/kg, was added with each Mo supplement. Six of the nine lambs not given supplementary Mo + S died of Cu poisoning but those given Mo + S survived. Histological evidence of subclinical hepato-toxicity was found in Mo + S supplemented lambs but it decreased in severity as the level of added Mo increased. Plasma aspartate amino-transferase (PAAT) concentrations were elevated in unsupplemented lambs from week 9 and in lambs given 2 mg Mo/kg from week 12 but they remained normal in lambs given 4–16 mg Mo/kg DM. Successive increments in dietary Mo reduced the increase in liver Cu after 18–20 weeks from 1450 to 735, 483, 445 and 131 μg/g DM. The proportion of ingested Cu (y%) retained in the liver was related to dietary Mo ( x, mg/kg DM) by the equation y = 2.6 − 1.66 log x ± 0.21 ( r = 0.98; 2 d.f.). Finnish Landrace lambs retained 50% less Cu in their livers, had lower PAAT levels and showed less histological evidence of liver damage than ♂ Scottish Blackface lambs. The latter had higher PAAT levels and a higher mortality from Cu poisoning than ♀ Scottish Blackface lambs although the two sexes retained similar proportions of ingested Cu in their livers. The results are discussed in relation to the practical use of Mo + S to prevent Cu poisoning in sheep.

The protective effect of zinc sulphate in experimental sporidesmin poisoning of sheep

Summary Aqueous solutions of zinc sulphate were administered orally to sheep over 5 days (0.125, 0.5 and 2.0 g Zn++/sheep/day) to bracket a 3-day period during which sporidesmin also was dosed. The zinc sulphate treatment gave protection from the effects of sporidesmin when compared with control groups dosed sporidesmin alone. Body weight changes were improved and liverdamage scores, numbers of animals showing photosensitisation, serum levels of glutamic oxaloacetic acid transaminase and total bilirubin were lower. The protective effects of zinc sulphate were obtained at levels well abovethose required for growth and maintenance. Protection increased but at a diminishing rate with increasing dose rate of zinc. Because of the small safety margin which exists between the dose rate of zinc sulphate which will provide adequate protection and that which will cause toxicity the use of zinc for the control of facial eczema is not recommended.

Chronic Copper Poisoning in Sheep. I. The Relationship of Methaemoglobinemia to Heinz Body Formation and Haemolysis during the Terminal Crisis

The values of haematocrit, total haemoglobin in plasma, methaemoglobin percentages in erythrocytes and plasma, the osmotic fragility of the erythrocytes, and the occurrence of Heinz bodies were investigated during the terminal crisis in 4 cases of experimental chronic copper poisoning in sheep. At the beginning of the crisis, which lasted for well over one day, 10-20 per cent methaemoglobin was detected in the erythrocytes, before any haemolysis occurred. Later on severe haemolysis developed, and maximum levels of haemoglobin in the plasma were close to 2.5 g/100 ml. During the haemolytic stage both methaemoglobin and haemoglobin were detected in the plasma at approximately the same proportions as in the erythrocytes. No changes were observed in the osmotic fragility of the red cells until the onset of the haemolysis. It is concluded that the methaemoglobin formation is mainly an intra-corpuscular process and that most of the methaemoglobin detected in plasma in chronic copper poisoning in sheep, comes from the erythrocytes.

Chronic Copper Poisoning in Sheep

Four cases of experimental copper poisoning in sheep were examined. Light microscopical and ultrastructural alterations of erythrocytes were observed a few hours before a significant haemolysis was evident. Heinz body formation in otherwise unchanged red cells was the first morphological alteration observed. The Heinz bodies were predominantly membrane-attached. During the haemolytic crisis severe erythrocytic distortion, structural membrane alteration and Heinz body-containing ghost cells were observed. Erythrophagocytosis was mainly located to the RE cells of the spleen. Intrafollicular necroses were found in all histological sections from the spleen. Pathological changes in liver and kidney were comparable to those of earlier reports, comprising hepatocellular and renal tubular necrosis.

Deaths in cattle suggestive of subacute fluorine poisoning following ingestion of superphosphate.

Abstract Extract Poisoning of cattle and sheep with superphosphate where the fertilizer was stored within reach of the animals has been reported by Romanenko (1954). In New Zealand losses of pregnant and lactating ewes grazing pastures topdressed with phosphatic fertilizers have been recognixed for several years, and records kept since 1965 show that 39 outbreaks have been reported to Ruakura Animal Health Laboratory (P. J. O'Hara, pers. comm.). Swan and McIntosh (1952) have described the toxicity to dairy cows of grazing pasture topdressed with North African phosphate and superphosphate. The toxic factor was later identified as fluorine (Animal Research Division of the New Zealand Department of Agriculture Reports 1952–3, p. 28; 1953–4, p. 34; 1954–5, p. 35). Phosphatic fertilizers are known to contain 1 to 4% fluorine (Caro, 1964), and the danger of poisoning stock with fluorine in untreated phosphates used as feed supplements has been described by many authors (Emmerling, 1902; Dammann and Manegold, 19...

Role of pentose-phosphate pathway in haemolytic crisis of chronic copper toxicity of sheep

Although the rise in blood copper is associated with onset of the acute haemolytic crisis of chronic copper poisoning in sheep, the sudden fall in erythrocyte glutathione is apparently not due to a direct action of the copper. Moreover the reduced glutathione of the red cells is converted to some form that is not capable of regeneration by the pentose-phosphate mechanism. Only negligible inhibition of the pentose-phosphate enzymes occurs. As the haemolysis proceeds, there is a rapid recovery of erythrocyte glutathione levels, and a marked increase in pentose-phosphate enzyme activity, consistent with influx of young red cells. It seems that the release of copper into blood from liver at the haemolytic crisis is associated with an increase of the oxidative state of the blood, possibly by simultaneous release of other components from the liver.

Nitrate poisoning in cattle grazing crops.

Abstract Extract Although nitrate/nitrite poisoning of cattle, sheep and pigs has been recognized in New Zealand for many years, it has become more widely publicized in the past 2 years owing to the greater prevalence of poisoning and the involvement of hitherto unsuspected crops, notably ‘Grasslands Tama’ ryegrass. In this review, experiences with recent outbreaks of nitrate poisoning are compared with published observations. Throughout this paper the disease will be referred to as nitrate poisoning.

Letter: Methemoglobinemia in acute copper sulfate poisoning.

Letters1 February 1975Methemoglobinemia in Acute Copper Sulfate PoisoningK. S. CHUGH, M.D., P. C. SINGHAL, M.D., B. K. SHARMA, M.D.K. S. CHUGH, M.D.Search for more papers by this author, P. C. SINGHAL, M.D.Search for more papers by this author, B. K. SHARMA, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-82-2-226_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAlthough Todd and Thompson had recorded methemoglobinemia in chronic copper poisoning in sheep in 1961 (1), the occurrence of methemoglobinemia in man has been reported only recently in two patients who, it was suspected, had had lethal acute copper intoxication during hemodialysis (2). The evidence of copper intoxication in these patients was circumstantial and retrospective; blood copper levels were not measured in either of them. We wish to report a case of methemoglobinemia in acute copper sulfate poisoning in a patient who came under our observation recently, with direct evidence of copper poisoning.A young man, aged 27 years, was...

An outbreak of metaldehyde poisoning in sheep.

An outbreak of metaldehyde poisoning in sheep.

Muscle Damage in Chronic Copper Poisoning of Sheep

A sudden mid dramatic rise in the level of serum CPK occurs at the haemolytic crisis period of chronic copper poisoning. This suggests that changes occur in the muscle cell membrane, as well as in the liver, erythrocyte, kidney and brain, which have been previously recorded. There is no evidence for muscle lesions during the passive accumulating phase of copper toxicity, and once over the crisis, the serum CPK rapidly returns to normal levels.

Effects of Ipomoea carnea on the liver and on serum enzymes in young ruminants

The sequential changes in the livers of 10 goats, 3 sheep and 2 calves given daily oral doses of 5 g./kg. body weight of fresh leaves of Ipomoea carnea were studied by serial biopsy. Seven goats and 2 sheep died during the 5 to 107 day period and 3 other goats and 1 sheep were killed in a moribund state, 121 days after the commencement of dosing. Neither of the 2 calves died during the experiment. Inappetence, dullness, dyspnoea and paresis of the hind limbs were prominent clinical signs of Ipomoea poisoning in both goats and sheep. Gradual deterioration of the general condition and debility were seen in one of the calves. Both calves were killed on the 121st day. Reduction in cytoplasmic basophilia of the liver cells, fatty change, loss of glycogen, focal hepatocellular necrosis, accumulation of mononuclear cells and polymorphs, new bile ductule formation and portal fibrosis developed between the 21 and 121 days in goats and sheep. None of the calves showed hepatic portal fibroplasia. Regression of the parenchymal-cell changes was seen in one of the calves. All animals showed an increase in the concentrations of glutamate-oxaloacetate transaminase and arginase in the serum. Glutamate pyruvate transaminase activity did not change. Post-mortem examination of goats, sheep and one of the calves revealed excess fluid in the serous cavities, oedema of the lungs, congestion of the kidneys, subendocardial haemorrhage and necrosis of the liver and hepatic fibrosis.

Effect of copper on red cell glutathione and enzyme levels in high and low glutathione sheep.

SummaryEffects of copper on red cell glutathione and enzyme levels were investigated in sheep of high- and low-glutathione types. No significant differences were observed in copper induced inhibition of glutathione regeneration or erythrocyte enzyme activities in the two groups of sheep. These results, together with those showing the effect of copper on GSH oxidation suggest that low-glutathione sheep should not be more sensitive to small doses of copper, commonly encountered in chronic copper poisoning in sheep than are high-glutathione sheep.

Halogeton poisoning of sheep: effect of high level oxalate intake.

Halogeton poisoning of sheep: effect of high level oxalate intake.

Letter: Kikuyu poisoning in sheep.

Letter: Kikuyu poisoning in sheep.