Copper Toxicity 'Geelsiekte'
By Dr Mackie Hobson BSc(Agric),BVSc

1. Poisoning
2. Nutrition

Copper (Cu) toxicity may occur in the Karoo particularly in iron ‘ysterklip’ dolomite veld as well as on planted pastures. Angora goats are much less prone to toxicity than sheep  so toxicity is rare.

Sheep are the most susceptible species to chronic copper toxicity, because their liver cells have a high affinity for copper and they excrete copper into the bile at a very low rate, leading to a build-up of liver copper concentration over time.

The chronic accumulative form of toxicity is seen which is seen over weeks or months - usually in older animals. If excess Cu in the diets being fed then toxicity may occur at any age.

What causes the Copper toxicity

Cu is extracted from the feed and is accumulates in the liver. When at critical levels any stressful episode can cause the release of the copper into the blood stream, resulting in significant hemolysis and anaemia. This massive release of haemoglobin can result in haemoglobinuric nephrosis and renal failure.  

Predisposing factors influencing copper toxicity:

• Overgrazing (karoo bush contains higher levels of copper)
• Ironstone rocky areas (mineral relationships of the soil)
• Spring and early summer if no rains
• Stress factor implicated (dose, dip, movement, shearing, camp changes etc)
• Pastures fertilized by pig or chicken manure
• Chicken mature used in feed when fed high copper levels.

The ratio of copper to molybdenum in the feed is an important factor determining the risk of copper poisoning. Chronic copper toxicity typically involves the ingestion of feeds that have a high copper : molybdenum ratio.

Feed is considered toxic if:

• copper levels > 25 ppm or
• copper : molybdenum ratio of >10:1

Clinical signs:

• Acute deaths
• Lag behind flock, weak, recumbent
• Mucous membranes appear dirty yellow
• Urine clour is dark red, brown to black.

Sheep/Goats surviving  with low levels of Cu poisoning living longer

• Reduced appetite
• Poor condition

Post Mortem:

• Dirty yellow colour of carcase, icterus
• Yellow liver
• Intestinal content hard, dry and sometimes bloody
• Kidneys swollen and dark to black ‘gun metal blue’
• Yellow brown urine

Diagnosis:

• Liver and kidney samples for mineral analysis and histopathology.

If a farmer wants to determine the Cu levels in a flock:

• When slaughtering an old ewe take a liver sample the size of a matchbox and freeze this. It can then be sent to a laboratory for analysis.

 Serum copper levels are unreliable in live animals due to the primary storage in liver. If serum copper levels are elevated (> 2.0 ppm), this is diagnostic. If the levels are below this level, copper toxicity cannot be excluded because the elevation in serum copper concentration is often transient. Liver copper levels should also be interpreted with caution, because the release of copper from the liver during the disease process can significantly reduce liver copper concentrations.

Treatment:

Treatment is seldom successful.

• Once these clinical signs are recognized, the current feed for the flock should be withdrawn pending testing for both copper and molybdenum.
• Methylene blue (4-10mg/kg) slow i/v to effect helps control the methemoglobinemia. Response is seen within 15 minutes
• Sodium thiosulfate (1000mg per animal) orally once daily for 3 weeks. Removes copper from the liver.
• Blood transfusion and fluids, renal protectants

Prof Bath through decades of experience has advocated.

• 100mg ammonium or ‘natrium molidaat’ per sheep daily for 6 weeks or more. To make it practical best be via drinking water or lick.
• Sulphate has positive effect on Copper toxicity (excess causes diarrhoea)
• ZnSO4 (Zinksulphate) is easier and cheaper. 250mg per sheep for 6 weeks

If added via water then no other water must be available

• As a guidline add 125g ‘witvitrioel’ per 1000l water (6 weeks)

References:

Kleinvee-siektes J. de Wet and G.Bath

Prof.Gareth Bath, Fakulteit Veeartsenykunde, Universiteit van Pretoria