Acorn poisoning in sheep

Abstract

Extract

No record appears to have been made of oak poisoning in New Zealand, Connor (1951 Connor, H. E. 1951. “N.Z. Dept. of Scientific and Industrial Research”. In Bulletin No. 99  [Google Scholar]) considering that only extremely isolated cases are likely to occur.     

Tunicamycin and corynetoxin poisoning in sheep

Quantitative toxicity studies were carried out in sheep using corynetoxin, tunicamycin and toxic annual ryegrass (Lolium rigidum). Sheep were very sensitive to these toxins. The lethal dose was about 35 micrograms/kg bodyweight for pure tunicamycin given by subcutaneous injection and 3 to 5 mg/kg for corynetoxin administered orally as slurries of bacterial galls of known corynetoxin content. The total lethal dose was of the same order, whether given as a single dose or as repeated smaller doses, the maximum interval tested being 9 weeks between doses. This finding indicates that a second exposure of animals to toxic rye grass in the one season would present a greater risk than would a first exposure to the same field. It also demonstrates the advisability of the monitoring of pasture levels of gall contamination, as levels below those that produce clinical signs of the disease may still contribute to an accumulating burden of toxicity.     

绵羊马铃薯中毒的诊治

近年来,家畜因误食有毒马铃薯发生中毒时有发生,笔者通过采取综合治疗措施,取得了满意效果.现将1例治疗病例介绍如下.     

Lantana poisoning of cattle and sheep in New Zealand

The investigation of a field case of Lantana camara poisoning in cattle is reported. Toxicity was confirmed by the experimental dosing of two sheep with dried leaf powder at 6 and 12 mg/kg body weight. Marked cholestatic hepatophy and renal tubular disease resulted. This is the first reported case of toxicity due to grazing a Lantana camara variety grown in New Zealand.     

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.     

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.     

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.     

Superphosphate poisoning of sheep: the role of fluoride

Earlier work confirmed that the fundamental lesion of superphosphate poisoning is an acute toxic tubular nephritis in which both phosphate and fluoride may play a part but their respective roles could not be determined. In this study, sheep poisoned by sodium fluoride (NaF) were compared with sheep poisoned by superphosphate containing approximately 1.5% fluoride. The LD50 of NaF was in the range 100 to 300 mg/kg (45 to 135 mg F/kg). This range is of the same order as the amount of fluoride in a toxic dose of superphosphate (70 to 90 mg F/kg). A lethal dose of NaF caused severe depression, salivation, hyperpnoea, blindness, ataxia and incoordination. Death ensued three to 52 hours after dosing. Acute necrotizing rumino-reticulitis and abomasitis and necrosis of epithelial cells in the proximal convoluted tubules of the kidney were the characteristic lesions of NaF toxicity. Superphosphate poisoning took a more protracted course with depression and diarrhoea as the predominant clinical signs until the terminal coma. As with NaF, the notable lesions were in the gastrointestinal tract and kidneys, but were less severe. Although there were differences in the clinical and pathological manifestations of the two forms of poisoning, the comparable toxic dose of NaF and of the fluoride in a toxic dose of superphosphate, and the similar target organs involved, support the view that fluoride plays a dominant role in the pathogenesis of superphosphate poisoning. It is probable that phosphate plays a contributory role but the nature of the interaction of fluoride and phosphate remains to be established.     

Superphosphate poisoning of sheep: the role of fluoride

Earlier work confirmed that the fundamental lesion of superphosphate poisoning is an acute toxic tubular nephritis in which both phosphate and fluoride may play a part but their respective roles could not be determined. In this study, sheep poisoned by sodium fluoride (NaF) were compared with sheep poisoned by superphosphate containing approximately 1.5% fluoride. The LD₅₀ of NaF was in the range 100 to 300 mg/kg (45 to 135 mg F/kg). This range is of the same order as the amount of fluoride in a toxic dose of superphosphate (70 to 90mg F/kg).

A lethal dose of NaF caused severe depression, salivation, hyperpnoea, blindness, ataxia and incoordination. Death ensued three to 52 hours after dosing. Acute necrotizing rumino-reticulitis and abomasitis and necrosis of epithelial cells in the proximal convoluted tubules of the kidney were the characteristic lesions of NaF toxicity.

Superphosphate poisoning took a more protracted course with depression and diarrhoea as the predominant clinical signs until the terminal coma. As with NaF, the notable lesions were in the gastrointestinal tract and kidneys, but were less severe.

Although there were differences in the clinical and pathological manifestations of the two forms of poisoning, the comparable toxic dose of NaF and of the fluoride in a toxic dose of superphosphate, and the similar target organs involved, support the view that fluoride plays a dominant role in the pathogenesis of superphosphate poisoning. It is probable that phosphate plays a contributory role but the nature of the interaction of fluoride and phosphate remains to be established.