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Secondary copper poisoning in ewes on subterranean clover

Bruce Watt, Central Tablelands Local Land Services, Bathurst NSW

This paper was presented at the Australian Sheep, Camelid and Goat Veterinarians Conference, Wagga Wagga NSW, 30 June to 2 July 2021
Posted Flock & Herd August 2021


'Toxaemic jaundice' due to secondary copper poisoning has been an important cause of ewe mortality in NSW flocks for almost a century. Secondary copper poisoning occurs despite normal dietary intakes of copper whereas primary copper poisoning occurs on diets high in copper or from treatment overdoses. Sheep, and particularly some British breed sheep, are the most susceptible domestic species. They readily absorb copper but have difficulty in excreting high levels, so it accumulates in the liver. When secondary copper poisoning occurs in sheep with concurrent liver disease, (which exacerbates this predisposition), it is referred to as hepatogenous chronic copper poisoning. Secondary copper poisoning, in the absence of liver disease, most notably on subterranean clover-based pastures that are molybdenum deficient, is referred to as phytogenous chronic copper poisoning.

While copper accumulation is usually chronic, deaths occur from an acute haemolytic crisis (Seaman 1990, Radostits et al. 2007). This paper describes an outbreak of copper poisoning in British breed cross ewes on clover dominant pastures, on five properties on the Central Tablelands of NSW, between late October 2020 and early February 2021, often without concurrent liver disease.

Case reports

All cases occurred in large commercial prime lamb operations. Four of five ran self-replacing composite ewe flocks while the deaths in the other flock were in first cross ewes purchased three years previously. In most cases ewes were found dead. If seen before death, affected ewes were usually dull, separated from the mob, sometimes with head pressing and trembling before collapsing and dying. Sick ewes had pale, brownish mucous membranes. On necropsy most ewes were in fat condition with pale yellow to orange body fat, brownish liver and lungs, swollen and black kidneys and red brown urine.

Laboratory findings supported the diagnosis of copper poisoning, toxaemia and a haemolytic crisis. Liver and kidney copper levels were elevated (Table 1), while liver enzymes were also elevated, consistent with hepatobiliary injury. There was azotaemia consistent with renal damage and anaemia as expected in a haemolytic crisis.

Histological findings from the liver all showed evidence of hepatocellular degeneration and necrosis, with hepatocytes and macrophages containing brown pigment indicative of copper accumulation. In some cases, there were minimal chronic changes indicative of exposure to hepatotoxic plants such as pyrrolizidine alkaloids. In other samples however, there were changes consistent with mild to moderate exposure to pyrrolizidine alkaloids (PA).

Kidney histology demonstrated acute, severe tubular injury and necrosis. A lung sample collected at property 5 showed multifocal oedema with no other significant findings.

Liver and kidney samples from both properties contained elevated copper levels (Table 1).

Kidney copper levels
(0.00 - 0.20 mmol/kg wet weight)
Liver copper levels
(0.23 - 3.67 mmol/kg wet weight)
Property 1 0.75 mmol/L 7.15 mmol/L
Property 2 0.49 mmol/L
1.01 mmol/L 9.76 mmol/L
Property 3 5.50 mmol/L∗
1.11 mmol/L∗ 1.04 mmol/L∗
Property 4 0.82 mmol/L 7.87 mmol/L
Property 5 1.09 mmol/L 6.59 mmol/L
Table 1. Tissue liver and kidney copper levels. ∗ Samples from property 3 were markedly autolysed. The laboratory comment that under these circumstances significant loss of copper from the tissue fraction expected.


On the first three properties affected ewe mobs were drenched with a mix of sodium sulphate and sodium molybdate consistent with an Australian Pesticides and Veterinary Medicines Authority (APVMA) permit as described by Edmonstone (2019). On properties four and five, as losses appeared to be waning, ewes were not treated.


'Toxaemic jaundice' has been a major cause of ewe mortality in NSW flocks since the late 1920s. In some areas it appeared following the widespread establishment of subterranean clover in the late 1930s, and in others following the proliferation of common heliotrope and Paterson's curse. Such was the problem that in 1936 a multijurisdictional committee was initiated to investigate, with its final report published in 1956 (Anon 1956). The committee member noted that chronic copper poisoning seen on an irrigated property in Victoria following the 'over-liberal' application of copper sulphate for fluke control, 'appeared to be indistinguishable from the disease called toxaemic jaundice.' It was realised that toxaemic jaundice occurred on pastures (usually subterranean clover dominated) with normal amounts of copper. In some cases, there was evidence of severe liver damage consistent with pyrrolizidine alkaloidosis but in some cases the liver only showed histological evidence of acute injury.

The Committee concluded that there were three diseases within the toxaemic jaundice complex. The first was a 'special form of chronic copper poisoning' (phytogenous chronic copper poisoning), the second was heliotrope poisoning and the third was heliotrope-chronic copper poisoning (hepatogenous chronic copper poisoning). Seawright (1982) considered that elucidating the mechanism behind the toxaemic jaundice complex 'stands as one of the great achievements of Australian veterinary science.'

The Committee noted that phytogenous chronic copper poisoning is relatively rare in most of Australia. They however noted a case with 20% mortality in cross bred ewes grazing abundant clover pastures that followed exceptional autumn and winter rains in 1946. Keast (1954) reported that in endemic areas, such as the Southern Tablelands, a few cases of copper poisoning occurred on subterranean clover pastures each year but few properties running crossbred sheep on improved pastures escaped losses in years of luxuriant clover growth.

In the experience of the author, hepatogenous chronic copper toxicity is far more common than phytogenous chronic copper poisoning on the central western plains of NSW, a view shared by Salmon in the Riverina (Salmon D, pers. comm.). The then Wagga Wagga Regional Veterinary Laboratory noted that of 5577 submissions from sheep for which histopathological findings were recorded between 1977 and 1996, 165 had copper poisoning diagnosed and, of these 22 were recorded as hepatogenous and 4 as phytogenous. Of the phytogenous cases, there were 2 in 1992 and one each in 1993 and 1995.However, phytogenous chronic copper poisoning is more common in good springs in the area bounded by Young, Gundagai and Cootamundra (Glastonbury J, pers. comm.).

While chronic copper poisoning of any type is uncommon on the Central Tablelands, with the benefit of hindsight, outbreaks were predictable in 2020, an exceptional year for clover growth. In all cases reported here, the ewes were grazing improved phalaris and cocksfoot pastures that in 2020 were dominated by subterranean clover. In all cases there was minimal to no pasture contamination with weeds containing pyrrolizidine alkaloids (most notably Paterson's curse, common heliotrope and blue heliotrope). Ewes on four of five flocks were homebred while the first cross ewes in case three were purchased from central Western NSW three years previously.

While there was some evidence of chronic liver damage caused by PAs, none of the ewes had a history of exposure in at least the previous three years. This appears to be an outbreak of phytogenous copper presumably caused by relatively high pasture copper and relatively low pasture molybdenum and sulphur levels.

In sheep, the rate of copper accumulation is controlled by dietary copper, molybdenum and sulphur. Rumen microorganisms convert sulphates to sulphides which then bind with molybdenum to form thiomolybdates. These then combine with copper to form insoluble copper-thiomolybdates, limiting the uptake of dietary copper. Poisoning has occurred on pastures with a relatively low copper content (15-20 ppm) when pasture molybdenum levels are very low. Ideally the diet of sheep should contain a copper to molybdenum ratio of 10:1. (Seaman 1990).

Monitoring of these levels is planned for the spring of 2021 although at this stage pastures have become grass dominant so the risk in 2021 is anticipated to be low.

Fortunately, measures recommended to prevent chronic copper poisoning are also consistent with good pasture management. The occasional used of fertiliser containing molybdenum is recommended to improve nodulation and rhyzobial bacterial function as well as restoring plant molybdenum levels. Liming of soils to reduce acidification improves pasture growth as well as making molybdenum more available. As grasses are higher in molybdenum and lower in copper than clover, restoring perennial grass pastures with a component of clover has numerous benefits including improving the balance of copper and molybdenum. If producers had the option, they should avoid grazing British breed or crosses on clover dominant pastures and, if they have no choice, to consider supplementing with loose mixes molybdenum and sulphur as described in the APVMA permit (Edmonstone 2019).


  1. Seaman JT, Pyrrolizidine alkaloidosis. In Sheep Medicine, Proceedings 141, Post Graduate Committee in Veterinary science, University of Sydney, 16-20 July 1990, pp 311-313
  2. Radostits OM, Gay CC, Hinchcliff KW and Constable PD. (2007). Veterinary Medicine, 10th Edition, pp 1820-1824
  3. Edmonstone B. Treatment of Chronic Copper Toxicity in Sheep. www.flockandherd.net.au February 2019
  4. Anon (1956). Toxaemic Jaundice of Sheep: Phytogenous Chronic Copper Poisoning, Heliotrope poisoning and Hepatogenous Chronic Copper poisoning. Australian Veterinary Journal, 32:229-236
  5. Seawright AA (1982). Chemical and Plant Poisons, in Animal Health in Australia, Volume 2, p 158
  6. Keast JC (1954). Chronic copper poisoning and Heliotrope Poisoning of Sheep, Institute of Stock Inspectors of NSW, Year Book www.flockandherd.net.au


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