A mob of approx 500 ewes was grazing saltbush, barley grass, clover and crowfoot in the Lake Cargelligo region of NSW. The earliest lambs were approx six weeks of age in early November when a visit was made to the property three days after viewing a video clip of a ewe and a lamb both with coordination difficulties. The lamb had complete loss of function in the hind limbs. The ewe was recumbent, alert and body condition score 4. She could not stand which caused her distress. Rams continued to run with the mob of lambing ewes.
On arrival at the property the ewe and lamb had both died. The lamb was necropsied and found to have a spinal abscess in the lumbar area (Figure 1). A sample of the lime-green coloured pus was taken. The pus failed to culture. The ewe was too autolysed for necropsy. On review of the video clip, it is probable that the ewe had suffered a physical injury/trauma.
Whilst on the property, another lamb was showing ataxia in the hind limbs. On being made to walk, it walked with a lateral swaying motion for a few seconds before knuckling of the legs and falling to the ground (Figure 2). The lamb was euthanased and necropsied. There were no significant macroscopic findings.
Blood copper level was 1.7umol/L (7.5-20 umol/L). Histologically, changes were marked in the spinal cord, particularly in the axons of the dorsolateral tracts, with less severe changes in the obex and midbrain. In the spinal cord, the changes were characterized by myelin degradation in the white matter with an influx of gitter cells (Wallerian degeneration). A few swollen axons were also present randomly in the white matter. The neuronal bodies in the grey matter lacked stainable Nissl's substances with the displacing of the nucleus peripherally (Chromatolysis). There were a few degenerate axons in the white matter of the cerebrum with rare infiltrated gitter cells (Wallerian degeneration, Figure 3).
There are two main causes of copper deficiency in stock viz primary copper deficiency due to low copper in plants/soil, and secondary copper deficiency caused by the ingestion of high levels of molybdenum and suphur which together with copper, forms a highly insoluble compound which is excreted (WA DPI, 2004).
Copper deficiency occurs naturally in many parts of world (Radostits et al., 2007). In Australia there are few published references to copper deficiency (Ellem, Plant, pers. com.). In 1983, copper deficient areas in Australia were identified which included two small defined areas in North East NSW (Caple, 1983). There have also been anecdotal reports of copper deficiency near Cobar in the nineties (Plant, pers. Com.).
Copper deficiency in sheep is more prevalent during periods of lush growth of green feed (Caple, 1983). The copper intake of grazing sheep increases as pastures dry off over the summer period and a marginal deficiency detected in mid spring is usually resolved by mid-summer. Unfortunately the demand for copper is high during periods of pregnancy and lactation and then during rapid growth of the lamb in the first three months of life (Radostits et al., 2007). This coincides with lush feed with relatively low copper status during spring.
Copper is essential for enzymes that are important for neural function. Copper deficiency can cause swayback in sheep, goat, and piglets. Lambs with copper deficiency may show clinical symptoms at birth in severe cases (WA DPI, 2004). More commonly lambs appear normal at birth, and between one and six months may develop signs of uncoordinated gait. Treatment in lambs clinically affected is not recommended (Plant, pers. com.).