Copper poisoning in a flock of sheep. Copper excretion patterns after treatment with molybdenum and sulfur or penicillamine

During an outbreak of chronic copper poisoning, fecal and urinary copper excretion were measured following treatment with molybdenum and sulfur supplementation of the feed (0.1 g ammonium molybdate plus 1 g sodium sulfate/sheep/day) or oral penicillamine (50 mg/kg bodyweight/day) using rams in metabolism cages. Serum glutamic-oxaloacetic transaminase activities and liver levels of molybdenum and copper in sheep that died were also monitored. Within four days of starting molybdenum and sulfur supplementation a highly significant increase in fecal copper excretion was evident and the increase persisted throughout the monitoring period (five weeks — general treatment of the flock continued for another three weeks). There was no effect of the molybdenum and sulfur supplementation on urinary excretion of copper. The molybdenum and sulfur supplementation was very effective, resulting in a rapid marked decrease in mortality. Oral penicillamine treatment induced cupruresis but did not affect fecal copper excretion. The results indicated that, while the cost of penicillamine may be a limiting factor for general treatment of a flock, it may be the drug of choice for the therapy of valuable breeding animals because cupruresis may be accurately and individually controlled. Serum glutamicoxaloacetic transaminase activities were a valuable aid in diagnosing chronic copper toxicosis as well as for monitoring recovery. High initial liver copper levels were gradually reduced following molybdenum and sulfur treatment. However, at the end of the study the liver copper levels of dead sheep varied within wide limits and there were still some sheep with high liver copper levels.     

Alsike clover poisoning: A review

Trifolium hybridum (alsike clover) has been implicated as the cause of two diseases of the horse. One of these is photosensitivity, of which alsike clover is only one of a number of presumed causal agents. The other is a fatal syndrome which is known as “alsike clover poisoning” and which is manifest by progressive loss of condition, signs of hepatic failure, and varying degrees of neurological impairment. The underlying lesion of alsike clover poisoning is fibrosis and proliferation of the biliary tree. The experimental evidence implicating alsike clover as the cause of this syndrome comes entirely from a series of feeding trials performed by Dr. Frank Schofield between 1928 and 1933.

This review surveys the literature on the association of alsike clover with both photosensitivity and biliary fibrosis in horses, and summarizes the clinical and pathological features of “alsike clover poisoning”. The experimental evidence that has been used to implicate Trifolium hybridum as the cause of alsike clover poisoning is critically examined. It is concluded that the existing experimental evidence is insufficient to prove that Trifolium hybridum is the cause of alsike clover poisoning.

     

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.     

Acorn poisoning in sheep

Abstract

Extract

Robins and Shapcott (1954 Robins, J. H. and Shapcott, R. 1954. N.Z. vet. J., 2: 55–55. [Taylor &; Francis Online] , [Google Scholar]) recorded cases of presumed acorn poisoning in sheep.