Protective effects of antioxidants on bitterweed (Hymenoxys odorata DC) toxicity in sheep

Antidotal effects of the 2 antioxidants butylated hydroxyanisole (BHA) and ethoxyquin (EQ) were evaluated in bitterweed (Hymenoxys odorata DC) toxicosis in sheep. Bitteerweed contains a toxic sesquiterpene lactone, hymenoxon, the toxicity of which is reduced by cysteine. Both BHA and EQ are known to induce hepatic glutathione production in rodents. Treatment of sheep with EQ (2.5 g/sheep/day for 9 days before poisoning) gave significant protection from toxic doses of bitterweed, but the protective effect of BHA was insignificant. Of 6 sheep given EQ in the feed, 5 survived 7 doses of bitterweed (4 g/kg/day or higher for 7 days), whereas 5 of 7 controls and 4 of 7 sheep given feed with added BHA died. The added EQ in the feed decreased the serum alkaline phosphatase activity and total protein, albumin, and calcium concentrations. Seemingly, EQ is the first protective agent with field application potential for bitterweed toxicity.     

Phosphatic fertiliser poisoning of sheep: Experimental studies

The toxicity of serpentine phosphate and superphosphate for non-pregnant dry ewes, pregnant ewes and lactating ewes was investigated by oral dosing. An attempt was made to reproduce a natural episode of poisoning by exposing pregnant and lactating ewes to topdressed pasture.

A total dose in the range of 1200 to 1800 g of serpentine phosphate was required to kill two ewes and it was concluded that natural episodes of poisoning with this material are unlikely. The toxic process was similar to that caused by superphosphate.

The LD₅₀ of superphosphate was estimated to be in the range of 5 to 6 g/kg and a dose in the range of 200 to 300 g was sufficient to kill most sheep. The apparently greater susceptibility of pregnant and lactating sheep to poisoning suggested by the study of natural outbreaks was not demonstrated in these experiments, but the numbers of experimental animals may have been too small to detect diiering susceptibility.

The clinical disease resembled that seen in natural episodes; anorexia, diarrhoea, progressive depression and death in a period of 5 to 8 days after the start of dosing. Sublethal doses produced a transient diarrhoea and, in two sheep, a severe wool-break.

The principal biochemical changes were hyperphosphataemia and evidence of renal failure (oliguria, uraemia, azotaemia). Gross lesions were not consistently present but included abomasal ulceration and renal cortical swelling and pallor. The histopathological evidence of renal tubular obstruction by flocculant eosinophilic casts was characteristic.     

Lythrum hyssopifolia (lesser loosestrife) poisoning of sheep in Victoria

Objective To document an ovine disease attributed to the consumption of Lythrum hyssopifolia (lesser loosestrife). Procedures Historical and histological review of field and experimental cases. Results 1–20% mortality occurred in sheep flocks grazing paddocks where L. hyssopifolia was the predominant green vegetation. Well‐documented disease outbreaks occurred in summer on nine farms across Victoria between 1974 and 2002. Liver damage occurred in all nine outbreaks, with kidney damage in at least eight. Hepatocyte necrosis was usually zonal to midzonal (zone 2) in the liver samples from four farms and periacinar (zone 3) in those from three farms, but some livers showed only single‐cell necrosis. Multinucleate hepatocytes near necrotic areas were a feature in six cases. Proximal tubular epithelium appeared to be the primary renal target and brown granules were often present in renal tubules. Biochemical and histological evidence of liver and kidney damage was obtained from two sheep experimentally pen‐fed harvested L. hyssopifolia. Conclusion Chemicals in L. hyssopifolia are toxic to ovine hepatocytes and renal tubular epithelial cells.     

Patho-morphologic and histoenzymologic findings after VX (organophosphate) poisoning in sheep]

Sixty-one sheep were administered experimentally a VX chemical (organophosphate) at different rates. In the process of dissection, samples were taken for a histopathological examination. These were samples of brain, liver, kidneys, rumen wall, small intestine, muscles, myocardium, lungs and spleen. For another histochemical examination, samples of tongue, m. longissimus dorsi, jejunum, rumen, liver, kidneys and m. interconstalis were also taken. The activities of alkaline and acid phosphatase, nonspecific esterase, acetylcholinesterase and dehydrogenase of lactic acid were investigated. The most significant changes were found out in the lungs - in form of oedemas and acute catarrhal bronchopneumonias in those animals which died within three days after chemical administration. Sporadic haemorrhages or haemorrhages in form of vast spots were found out under the epicardium. Their range did not relate to the amount of the chemical administered. Rather dilated vessels were observed in the brain and also in the meninges. The histochemical examination showed different activities of enzymes in particular organs of sheep.     

Bur buttercup poisoning of sheep

Bur buttercup (Ceratocephalus testiculatus) has not been considered to be poisonous, but the sudden death loss of 150 ewes while grazing it prompted study of the plant. It was found that bur buttercup can be highly toxic to sheep, with a lethal dose being as little as 500 g of green plant for a 45-kg sheep. Clinical signs of bur buttercup poisoning are weakness, depression, diarrhea, labored breathing, anorexia, and occasional fever. Postmortem findings include inflammation and edema of the rumen; hemorrhage in the left ventricle of the heart; congestion of the lungs, liver, and kidneys; and excessive fluid in the thoracic and abdominal cavities.     

Kleingrass (Panicum coloratum L.) poisoning in sheep

Twenty-four lambs grazing pastures of Panicum coloratum developed photosensitization secondary to hepatic dysfunction. Lesions were necrosis of scattered hepatocytes, obstruction of small bile ducts and bile canaliculi by small aggregates of birefringent crystals, and accumulation of birefringent crystals in phagocytes within sinusoids. The number of crystals in livers of affected sheep varied, depending on the amount of time of exposure to toxic plants and severity of hepatic abnormalities. Crystals in the liver were soluble in acidified ethyl alcohol, acetic acid, pyridine, chloral hydrate, and methanol, but not in xylene, petroleum ether, diethyl ether, acetone, water, or cold ethyl alcohol. Crystals were not stained by oil red O. There was necrosis of epithelial cells in renal distal convoluted tubules, papillary muscles of the heart, and the adrenal cortex. Lesions of Panicum coloratum-associated disease are similar to those associated with photosensitization induced by Tribulus terrestris, Agave lecheguilla, and Nolina texana.     

Experimental acute yellow-wood (Terminalia oblongata) intoxication in sheep

SUMMARY An aqueous suspension of air-dried, hammer-milled leaf of Terminalla oblongata (yellow-wood) was administered to sheep by gavage, as a single dose of 5 to 20 g (dry weight)/kg body weight. Doses of 15 g/kg, or more, caused depression, Inappetence, abdominal pain and reduced ruminal movements within 24 to 48 h and some sheep also showed dyspnoea, oplsthotonus and champing of the Jaws. Haematology and blood gas and acid-base measurements were unaffected. In sheep given a dose of 12.5 g/kg, or more, plasma osmolality, aspartate aminotransferase activity and potassium and bilirubin concentrations Increased while plasma total protein markedly decreased and plasma sodium concentration and alkaline phosphatase activity remained normal. Most sheep were necropsled 48 h after dosing. The liver showed zonal hepatocellular necrosis, the pattern of which varied with the dose given. No renal lesions were observed, although one sheep given a very high dose became azotaemic and hyperkalaemic. Hydrothorax, hydroperlcardlum and ascltes developed In sheep given doses of 15 or 20 g/kg.     

Acute oxalate poisoning attributable to ingestion of curly dock (Rumex crispus) in sheep

Ten of 100 mature ewes were afflicted with acute oxalate toxicosis within 40 hours after being temporarily penned in a lot that contained considerable growing Rumex crispus (curly dock). Clinical signs of toxicosis included excess salivation, tremors, ataxia, and recumbency. Affected ewes were markedly hypocalcemic and azotemic. Oxalate crystals were not observed in urine. Gross postmortem lesions were minimal and nondiagnostic in 2 ewes that died peracutely, but perirenal edema and renal tubular degeneration were clearly observable in ewes euthanatized on the third day of toxicosis. Diagnosis of oxalate toxicosis was confirmed by histopathologic findings. Samples of Rumex spp contained 6.6 to 11.1% oxalic acid on a dry-weight basis, a concentration comparable with that in other oxalate-containing plants that have caused acute oxalate toxicosis.     

Experimentally-induced Cestrum laevigatum (Schlechtd.) poisoning in sheep.

Dried, milled Cestrum laevigatum plant material was drenched to 6 ewes at doses ranging from 2,5 to 10 g/kg/day for 1 to 47 days. The most noticeable clinical signs were depression, anorexia and ruminal stasis. These signs were accompanied by clinical pathological changes indicative of liver involvement such as increases in the serum activities of aspartate transaminase, lactate dehydrogenase and gamma-glutamyltransferase. Hepatosis characterized by accentuated lobulation, and centrilobular to midzonal coagulative necrosis, haemorrhage and congestion occurred in 2 of the 3 ewes given high doses of plant material. Liver lesions in the other animals included disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas. Spongy changes in the cerebral white matter were evident in the ewes of the high-dose group. Ultrastructural changes in the liver comprised degeneration and necrosis of hepatocytes and occasionally endothelial cells, and disruption of sinusoidal walls.