Features
The Metabolic Diseases of Pregnant Ewes
by Dr Neville Suttle
The main metabolic diseases are all caused by short term failure to meet increased demand for nutrients in late pregnancy and/or lactation. Predisposing factors are: multiple pregnancies; cold, wet and windy conditions which increase demand and restrict delivery of or access to food; husbandry practices which cause stress and disrupt feeding ( e.g. transportation, vaccination, drenching) as well as poor body condition whereby nutrient reserves contribute less to supplies. Since each metabolic disorder reduces appetite and nutrient intake, one can precipitate another, however losses and morbidity may be reduced by combining treatments.
Hypocalcaemia
Cause and effect The disease differs from its more widely studied bovine counterpart, milk fever, in that peak demand for Calcium (Ca) - and hence risk of disease - occurs before and not after parturition in the case of multiple births. Inability to meet demand by absorption of Ca from the diet and mobilisation from skeletal reserves causes subnormal plasma Ca concentrations (<1.5mmol/l). Eventually, Ca levels at neuromuscular junctions become too low for normal transmission of impulses and the ewe becomes comatose, then prostrate, dying within 48 hours unless treated.
Treatment Inject subcutaneously a Ca-complex, borogluconate, developed by Moredun biochemists in the 1940's, 100ml of a 20% or 50ml of a 40% solution being required. Response is normally rapid and confirms diagnosis; lack of response suggests that Pregnancy Toxaemia was or has become the primary problem. Oral administration of Ca propionate controls milk fever and may have a role to play in ewes when Pregnancy Toxaemia is also present.
Prevention Optimise Ca supplies from both the diet and the skeleton. The whole ration in late pregnancy should contain 3.2-3.9gCa/kgDM, the higher the quality of the diet the more Ca it should contain. Cereals and cereal by-products are notoriously low in Ca (often < 1gCa/kgDM) but mixing with sugar beet pulp (>5gCa/kgDM) redresses the imbalance. Vitamin D status normally falls to its lowest in winter and supplementation will ensure maximal absorption of the Ca provided. Feeding grass silage rather than hay will shift acid:base status of the ewe in the acid direction and optimise Ca mobilisation from the skeleton: overfeeding calcined magnesite (MgO) to prevent Grass Tetany will have the opposite effect. Avoid undernutrition of the outwintered ewe which depletes her skeletal reserves of Ca prior to lambing. Planned Ca undernutrition in late pregnancy protects dairy cows from milk fever but is NOT recommended for ewes.
Grass or lactation tetany
Cause and effect Peak demand for Magnesium (Mg) occurs after lambing because the needs of even twin foetuses are small relative to those for milk production. Supply of Mg comes principally from the diet and is adequate while lactating ewes are housed because Mg is well absorbed (>30%) from rations containing plenty of concentrates. Risk of disorder rises dramatically as increased reliance is placed on pasture in spring because the efficiency of Mg absorption plummets to <15%, due largely to an antagonism from potassium which is often abundant in new growth (>3%K in DM). Plasma Mg concentrations rapidly decline to marginal levels (0.6-0.8mmol/l); further reductions cause hyperexcitability, ear and facial muscle twitching, followed by collapse, retraction of the head and paddling movements of the legs; these reflect the accelerated transmission of nerve impulses. Lowered food intake and ongoing milk secretion probably contribute to the hypocalcaemia which often accompanies hypomagnesaemia and dulls the nervous symptoms.
Treatment Inject subcutaneously 50ml of a 2.5%Mg hypophosphite solution in 25% Ca borogluconate, the clinical response should be immediate.
Prevention This has traditionally relied on the excessive provision of MgO at around 7g/head/d but provision of half this amount in Mg-supplemented concentrates should suffice. Salts of Mg such as the sulphate and chloride cause less disturbance of acid:base balance than MgO and they can be provided via the drinking water. Foliar applications of Mg(OH)2 in suspension to provide 3kgMg/hectare also works. Reductions or delays in the use of K fertilisers and the provision of pure salt (NaCl) licks may enhance Mg absorption sufficiently during the critical early spring period to reduce risk.
Pregnancy toxaemia or twin lamb disease
Cause and effectsThe unborn lamb has a unique requirement for glucose and in the last 6 weeks of a twin pregnancy the ewe has problems synthesising enough glucose to meet foetal demand. Synthesis of glucose occurs principally in the liver, using propionate absorbed from the rumen as substrate. Inadequate intakes of fermentable carbohydrate starve the liver of propionate and maternal blood or plasma glucose concentrations fall below those necessary for the brain to function (c.1.5mmol/l). The ewe gradually develops a hypoglycaemic coma; initially, she may be found separate from the flock, sometimes 'star-gazing' and showing bilateral blindness. When metabolisable energy (ME) intake is inadequate, fat reserves are transported to the liver as free fatty acids (FFA) and oxidised to meet the energy deficit; however, that process also requires propionate and impaired FFA metabolism in the liver leads to increases in conversion products or ketone bodies such as ß-hydroxybutyrate (BOHB). The twin bearing ewe can find herself on a downward spiral, her liver increasingly incapacitated by engorgement with fat and less able to synthesise the glucose needed by her lambs. The presence of a white or pale yellow liver post mortem and unborn lambs is strongly suggestive of pregnancy toxaemia although fatty livers are found in ewes which lamb normally. Serum BOHB values >3mmol/l and high 'liver enyme' (glutamate dehydrogenase & gamma glutamyl transferase) activities confirm diagnosis.
Treatment Immediate administration of 50-100ml physiological glucose solution by subcutaneous or intravenous routes, followed several hours later by the oral administration of glucose precursors such as propylene glycol or glycerol (50 ml) sometimes effects a recovery. Simultaneous provision of Ca by injection covers the possibility of precipitating or concomitant hypocalcaemia. The success of Ca propionate in treatment of milk fever suggests a possible role in treating pregnancy toxaemia.
Prevention Prevention begins in autumn with the analysis of conserved forages for ME, recording of tupping date and establishment of uniformly good body condition scores (BCS) of '3 - 3.5'; it continues through mid-pregnancy with scanning and further scoring (target range now '2.5-3'). Energy nutrition for late pregnancy can then be planned for groups with contrasting needs (twin bearers, 'thinnies', late lambers), saving the best feeds for late pregnancy and the most needy ewes ( a good silage has >10.5MJME/kgDM) and allowing plenty of rack and trough space. The ewe must approach lambing with (a) a healthy, 'metabolically focused' liver (fluke infestations long past ,copper overload and cobalt deficiency avoided, Pasteurella vaccination completed and (b) her BCS now stable within the range '2-2.75'. Avoid unfamiliar feeds and make any changes of ration gradual. Screening cohorts of a first clinical case for serum (BOHB) will indicate the extent of energy malnutrition in a group, individual values of 1.5-3.3mmol/l indicating potential disease. Increases in energy supply can be calculated from the average BOHB value, using a higher 'target value' in grouped than in single flocks (1.0 v. 0.8mmol/l ) because of lower variability and thus saving on feed costs.
Footnote: this article first appeared in the Sheep Farmer magazine and is reproduced with their permission