Metabolic diseases represent a significant welfare burden in sheep flocks, particularly in productive ewes during late pregnancy and early lactation. Unlike infectious diseases, metabolic conditions arise from failures in nutritional management — they are largely preventable with proper feeding and monitoring. Understanding the causes, clinical presentations, and welfare impacts of the key metabolic conditions enables producers to protect their flocks and minimise preventable suffering.
Pregnancy toxaemia results from hypoglycaemia and ketoacidosis in late pregnancy (last 6 weeks), typically in ewes carrying multiple foetuses. The rapidly growing lambs make increasing energy demands on the ewe that exceed her capacity to maintain blood glucose through normal feed intake — exacerbated by the compression of rumen volume by the uterus. Fat mobilisation produces ketone bodies as an alternative fuel, but excessive ketosis depresses appetite and creates a vicious cycle.
Untreated pregnancy toxaemia causes progressive neurological deterioration:
The suffering associated with untreated pregnancy toxaemia is significant and prolonged. Prompt recognition and intervention are welfare imperatives.
While less common than in dairy cattle, hypocalcaemia occurs in ewes, particularly around lambing. Presents with muscle weakness, recumbency, and inability to care for lambs. Treatment with subcutaneous or IV calcium supplementation is effective when given promptly. The welfare concern is that lambs may be abandoned or crushed by a hypocalcaemic ewe who cannot rise.
Magnesium deficiency causes acute neurological signs including tetany, convulsions, and sudden death. Common in ewes on lush spring pasture or following weather stress. Unlike calcium, magnesium cannot be mobilised from body reserves — requiring constant dietary supply. Treatment is emergency subcutaneous magnesium sulphate; prevention requires magnesium supplementation during risk periods.
Primarily a welfare problem in male sheep (rams and castrates). Struvite or silicate crystals form in the urethra, causing painful urinary blockage. Untreated cases develop bladder rupture and uraemia. Risk factors include high-concentrate diets with poor calcium:phosphorus ratio, restricted water access, and low dietary salt. Prevention: appropriate dietary Ca:P ratio (2:1), ad libitum water, adequate roughage.
While technically parasitic/nutritional rather than metabolic, these conditions interact closely with metabolic disease risk. Anaemia from Haemonchus contortus (barber's pole worm) exacerbates pregnancy toxaemia risk by reducing oxygen-carrying capacity. Regular FAMACHA scoring and targeted selective treatment reduces this interaction.