Owners of a small flock of 60 sheep grazing amongst grape vines became alarmed when seven died over the course of a few days in May 2019. The sheep had previously appeared healthy, were in good body condition, and had not been observed unwell.
The final diagnosis was copper toxicity, presumably from the long-term use of copper-containing compounds in the vineyard.
Sheep are commonly used for grazing amongst vines when they are dormant as a means of weed and grass management so this case may have lessons for others using small groups of sheep for this purpose.
In mid-May, a vineyard owner near Waikerie in the SA Riverland area reported deaths of some young dorper ewes to his local veterinarian and Primary Industries and Regions South Australia (PIRSA). The sheep had not been observed unwell, or recumbent, no obvious poisonous plants were seen in the area, and no treatments had been applied recently that could be considered toxic to sheep. In fact, the sheep were in very good (prime) condition, most were early pregnant and the onset appeared acute.
Seven sheep died over a period of 2-3 days and two dead sheep was taken to the local veterinary clinic for post-mortem (PM). Costs of the examination and lab fees were subsidised by the PIRSA Disease Surveillance Program.
No obvious lesions or abnormalities were seen in dead sheep and a range of samples including fixed tissues and ocular fluid were tested for ammonia, urea, D Lactate, and Ca/P levels to rule out some common causes of sudden death. Rumen pH was normal and no internal parasites were seen, faecal egg count (FEC) was 0.
The significant histopathological findings were acute, massive hepatic necrosis. There was marked lobular necrosis and haemorrhage involving the periacinar and midzonal regions with only portal hepatocytes not affected. Changes in lung and intestines were also noted, but not considered to be the cause of sudden death.
The pathologist’s comments were: "Consider mushroom toxicity—with wet weather may have mushrooms amongst grasses and other vegetation between the vines. Other causes of such lesions include:— algal toxicity including Microcystis (blue green algae), but there are indications that other as yet unreported or unidentified algae may be toxic — Cycads — Xanthium species (2 leaf stage) — burrs (may be a weed between vines) — certain Solanum species, in particular Cestrum (not found naturally in SA) — several plant species of the Asteraceae family (but there have not been reports in Australia of toxicity with these). The lung lesions are consistent with verminous pneumonia, most likely due to Dictyocaulus filaria."
The kidney samples were autolysed and therefore not suitable for histopathology.
Aqueous humor ammonia levels were very high in one sheep (2636 µmol/L, normal range 0 – 200 µmol/L) but Nitrate/ nitrite levels were normal, suggesting the elevated ammonia was likely a post-mortem artifact. Copper levels in kidney and liver were measured with all levels high.
|Kidney copper levels||Liver copper|
|(0.00- 0.20mmol/kg)||(0.23 – 3.67 mmol/kg)|
Both acute and chronic copper toxicity are described in texts.1,2 Acute copper toxicity is usually described as producing severe gastroenteritis, abdominal pain, diarrhoea, and central nervous system signs and death in prolonged cases. On PM ascites, hydropericardium, haemoglobinuria and liver lesions may be seen. Animals with chronic copper poisoning may present with jaundice, haemoglobinuria and death.
Clinical signs of chronic copper toxicity: "Sheep rarely show clinical signs until the animal is stressed, resulting in a massive liver necrosis and copper release. The released copper then causes intravascular hemolysis of red blood cells, resulting in hemoglobinuria, icterus, anoxia, and death. Urine is dark red (port wine) as a result of the presence of hemoglobin in the urine. Usually only one or two animals in the group die at any one time, while the remainder of the flock appears clinically normal. However, once a stressor affects the flock again, several more animals may die".3
Sheep are more sensitive to copper accumulation in the liver than other ruminants2 as accumulation of copper in liver exceeds the ability to excrete it in bile. During the period of copper accumulation in the liver, associated with subclinical changes to liver tissue, sheep are considered to be in the pre-haemolytic phase of copper poisoning. Following the sudden increase in blood copper concentrations and consequent haemolytic episode, sheep are considered to be in the post-haemolytic phase. In most field cases in which a haemolytic crisis occurs, death occurs within one to three days of the event. The sudden elevation of blood copper concentration and the acute fatal haemolytic syndrome is the best recognised clinical expression of the chronic intoxication, but cases have also been reported in which copper concentrations in the blood are elevated for several weeks before the acute haemolytic episode. In some cases, milder forms occur from which animals recover.
Diagnostic Testing: "Serum copper levels can be difficult to interpret. Even though excessive copper is being accumulated in the liver, the serum copper levels often remain normal until hepatocellular necrosis occurs. This elevation may be transient and quickly returns to normal values as a result of renal and hepatic reabsorption if the damage is mild. However, once hepatic reabsorption is lost, the copper is released from the liver into the bloodstream and a toxic amount of copper is detectable in the serum. At necropsy it is best to test both the liver and kidney for copper. In many cases the liver releases enough stored copper so that a non-toxic level of copper remains in the hepatic tissues. However, in these cases the released copper will have accumulated in the kidneys, resulting in markedly elevated levels of copper in the kidneys".3
Chronic forms of poisoning have been associated with contamination of plants sprayed with fungicides, water due to snail or algae treament, pasture grazing after some topdressings and other sources.1
Copper-based sprays are commonly used in viticulture and on this property for fungal treatments or protection and it is reasonable to suggest that as a result grasses around the drip zone of grape vines may contain high copper levels. No plant samples were collected in this case, but the ingestion of concentrated copper from spray runoff is a plausible hypothesis in this case.
Copper toxicity can be managed and treated in sheep both on an individual basis for valuable animals using ammonium tetrathiomolybdate (ATTM), or sulphur and molybdate for larger groups.2
"Groups of ewes with chronic copper poisoning have been successfully treated with ammonium molybdate (40 g) and sodium sulphate (1200 g) mixed in water (10 L) and sprayed on hay such that the sheep each received 40 to 50 mg ammonium molybdate per head each day. Treatment was continued for three weeks but deaths in the flock ceased three days after treatment began. There are limited, if any, products for treatment of copper poisoning registered in Australia. Provision of a home-made loose lick consisting of salt, finely ground gypsum (calcium sulphate) and sodium molybdate in the ratio by weight of 187:140:1 has been recommended and reported to be successful when used in Australia. The salt (75 kg) and gypsum (56 kg) are mixed together on a flat surface and then the sodium molybdate in solution (400 g in 20 L) is sprayed onto the mixture and thoroughly mixed. The product should then be placed in open containers and offered to the sheep in the field, ensuring that all sheep have uninhibited access." (The Practice of Sheep Veterinary medicine, pg 560).2
Owners of vineyards that have small groups of sheep grazing the land in dormant periods should be aware of the possibility of copper toxicity in these sheep when using copper-containing products to control diseases on the vines.