Chronic copper poisoning was diagnosed in feedlot lambs in September 2017 on a property near Forbes, central New South Wales following an investigation into sporadic sudden deaths. While an initial investigation on a single dead animal proved to be a red herring, a subsequent visit to examine further dead animals yielded post mortem findings classically found with copper poisoning.
Approximately six hundred first cross weaned lambs of mixed sex were purchased in May for the purpose of growing out in a feedlot. They were administered a multivalent clostridial vaccine (vaccine not specified), and given a broad spectrum drench (drench not specified) on induction, and fed commercial pellets, barley and hay, with the hay phased out of the ration early on.
After 6 weeks, ‘water belly’, or urolithiasis, became an issue in a number of wether lambs, and lime and salt was added to the ration. The group was separated into ewe and wether pens for monitoring purposes.
After 4 months in the feedlot the producer recorded sporadic sudden deaths in the wether lambs not associated with any of the signs they understood as being attributed to ‘water belly’. They had also noticed that as a group, all of the lambs in the feedlot seemed quiet and slightly ‘off’.
On the initial visit one dead wether lamb was presented for examination. With post mortem findings of glucosuria and a large amount of straw coloured fluid clotting on exposure to air in the abdomen and thorax, a preliminary diagnosis of enterotoxaemia was made. Samples were collected and submitted for confirmation, and in the meantime a recommendation was given to administer a booster vaccination for clostridial disease. In the days following vaccination the odd lamb continued to die, and when it was reported that 3 animals had died suddenly 5 days following vaccination, a second visit was made to the property.
At the subsequent visit, all three deceased animals had mild yellowing of the sclera and grey-yellow oral mucosa. Post mortem revealed generalised jaundice, bronze-coloured friable livers, dark red, swollen kidneys and dark red urine in each carcase.
Copper poisoning was strongly suspected on the basis of the findings of these post mortems and samples were collected and submitted to confirm this. Pending these results possible sources of copper in the diet were evaluated. With no obvious environmental source on inspection of the pens and a good, clean water supply it was thought most likely that the copper was in the pellets and these were removed from the feeders in the wether pens. Treatment with molybdate and sulphate as a drench or loose lick was considered, however the 8 week slaughter withholding and export slaughter interval period was prohibitive.
Following removal of the pellets two wethers died two days later, and then the deaths stopped. Within a week the owner reported that the sheep had improved in demeanour.
Histopathological examination found marked hepatic necrosis and degeneration, with variable pale, golden pigment accumulation suggestive of copper. Acute, severe tubular necrosis was present in the kidney with marked haemoglobin deposition and protein loss, consistent with haemoglobinuric nephrosis following haemolysis. The copper level was elevated in the kidney tissue submitted, 0.67 mmol/kg (reference range 0.00-0.20 mmol/kg). No histopathological changes were present in the liver to suggest the involvement of a primary phytogenous hepatopathy.
Enterotoxaemia was not confirmed in the first animal examined. The cause of death was determined on histological examination to be massive hepatic necrosis. The level of copper in the liver of this animal was normal, 2.86 mmol/kg wet wt (0.23-3.67 mmol/kg wet wt).
Feed analysis of the pellets determined the level of copper to be 33mg/kg.
Approximately 12 days after the pellets were removed from the wether pens, both ewe and wether lambs were yarded for crutching. One wether and one ewe lamb died in the following two days, jaundice being recorded by the owner.
Four weeks later the wethers were sold direct for slaughter and one animal was condemned at the abattoir for jaundice. The ewe portion was retained for the purposes of breeding.
Chronic copper poisoning in these lambs appears to have been induced by long term ingestion (>4 months) of a ration including commercially formulated feed pellets which contained copper at 33 mg/kg.
While there is a suggested a maximum tolerance level of only 25mg/kg sheep dietary copper1, overall ovine copper metabolism is complicated with multiple factors influencing the degree to which dietary copper is absorbed. These include breed, age and dietary factors. In general, British breed sheep and their crosses are found to be more susceptible than Merinos2, and young, growing animals are said to be more efficient than mature ewes at absorbing copper3. Also, within the diet, presence of certain minerals, trace elements and other feed additives can be significant. Molybdenum and sulfur act as antagonists to copper, binding together to prevent copper absorption and increasing its excretion4. Zinc and copper also have a competitive relationship, so that a high level of zinc in the diet reduces copper uptake1. Conversely a diet high in calcium is recognised to encourage the development of copper poisoning, probably by its interaction with zinc and creating a secondary zinc deficiency1. It is also reported that ionophores such as monensin or lasalocid can increase the efficiency of copper uptake in sheep4.
The prolonged time on feed was likely the biggest contributing factor to the development of chronic copper poisoning in these lambs. The producer also acknowledged that the lambs were particularly young and small on feedlot induction, and copper absorption may have been very efficient during the early growing stages. Greater growth rates may also explain why losses were predominantly in the wether group despite both wethers and lambs receiving exactly the same feed ration - approximately 20 dead wethers and only 2 ewe lambs were recorded overall.