The influence of dietary crude protein intake on bone and mineral metabolism in sheep

Increased dietary protein consumption is thought to cause calciuresis, a negative calcium balance and increased bone loss that may result in skeletal deformities and fracture. To explore this hypothesis, 40 approximately 100-day-old meat-type Merino ram lambs were fed, for 6 months, diets with an increasing crude protein (CP) content (114, 142, 171 and 190 g/kg DM) but approximately on an iso-nutrient basis with regard to metabolisable energy, calcium and phosphorus. Increased protein consumption modestly (NS) enhanced calciuresis and resulted in significant (P < or = 0.01) limb skewness. This could not, however, be ascribed to osteopaenic bones, and compared with animals consuming lower protein rations, the bone mineral density (BMD) and vertebral trabecular bone volume of animals fed high protein diets were significantly increased: the BMD of thoracic vertebrae was positively related to the CP intake (r = 0.62; P < or = 0.001). In animals consuming higher protein diets, skeletal radiology and quantitative bone histology revealed no evidence of increased bone turnover as would be expected in animals that are in negative calcium balance. No relationship existed between limb skewness and the growth rate of lambs. However, the ratio of Ca:P in the forelimb (r = -0.98), vertebrae (r = -0.72) and rib (r = -0.42) was found to be inversely correlated with increased protein intake and resulted from an increase in the phosphorus content of bone, while the amount of bone calcium was unaffected. We conclude that qualitative micro-architectural abnormalities, and not mere bone loss, may underlie the skeletal deformities induced by increased protein consumption in sheep.     

Acute cortisol responses of lambs to ring castration and docking after the injection of lignocaine into the scrotal neck or testes at the time of ring application

OBJECTIVE: To test whether injecting lignocaine into the scrotal neck 5 to 10 s before or into both testes immediately after ring castration and docking wound significantly reduce the plasma cortisol response to castration and docking. DESIGN: A physiological study with controls. PROCEDURE: Lambs were given one of six treatments: control handling, injection of lignocaine into scrotal neck, injection of lignocaine into both testes, ring castration and docking, ring castration and docking after lignocaine was injected into the scrotal neck, and ring castration and docking before lignocaine was injected into both testes. Blood samples were taken before and regularly after treatment and analysed for plasma cortisol concentrations. RESULTS: The plasma cortisol concentrations of lambs castrated and docked after lignocaine had been injected into the scrotal neck were significantly lower between 20 and 60 min after treatment than in lambs castrated and docked without local anaesthesia. Injecting lignocaine into the testes after ring application did not significantly reduce the cortisol response to ring castration and docking. CONCLUSIONS: Lignocaine injected into the scrotal neck 5 to 10 s before ring castration will reduce the cortisol response and by inference the pain associated with ring castration.     

Effect of sodium bicarbonate and sodium bentonite on digestion, solid and liquid flow, and ruminal fermentation characteristics of forage sorghum silage-based diets fed to steers

Six ruminally cannulated steers, five Holsteins and one Hereford (250 to 295 kg), were fed 84% forage sorghum silage plus 16% supplement or 50% forage sorghum silage plus concentrate and supplement diets containing either no addition (controls), 1% sodium bicarbonate (NaHCO3) or 2% sodium bentonite in a 2 X 3 factorial arrangement of treatments in a 6 X 6 Latin-square experiment with 3-wk periods. Sodium bicarbonate increased dry matter (DM) intake when concentrate was included, but neither compound affected intake of the 84% silage diet. Bentonite lowered DM, neutral detergent fiber (NDF), and acid detergent fiber (ADF) digestibilities, but NDF disappearance from nylon bags was unchanged. Ruminal pH, osmolality and L(+) and D(-) lactate were not affected by treatment. Both NaHCO3 and bentonite tended to lower ruminal NH3-N concentrations. Bentonite lowered the molar proportion of isobutyrate in ruminal fluid relative to controls, but proportions of other volatile fatty acids (VFA) and total VFA concentrations were unchanged. Neither NaHCO3 nor bentonite affected ruminal liquid or solid volumes, dilution rate constants or ruminal outflow rates. Markers overestimated volumes, but correction with measured volumes did not change interpretation of treatment effects. It was concluded that control diets had sufficiently high baseline values of pH, dilution rate and acetate proportion to preclude changes induced by either compound, especially at 1 or 2% of DM intake. An effect on palatibility through neutralization of silage acids may have been responsible for the intake response to NaHCO3.     

Necropsy of sheep and goats

In this article, diseases will be discussed by system. Common differential diagnoses that may be associated with gross lesions are pointed out, and practical laboratory tests are presented that may help establish a specific diagnosis.     

Pulmonary edema in a dog with acute pancreatitis and cardiac disease

Acute pancreatitis and cardiac disease were diagnosed in a dog with pulmonary edema. The early clinical course and initial thoracic radiographs suggested that the pulmonary edema was noncardiogenic. The late clinical course was complicated by heart failure. The dog died, and a necropsy was performed. Histologically, an acute, severe capillary-alveolar membrane lesion was found in the lungs. Review of the human medical literature indicated that respiratory complications, including pulmonary edema, are commonly recognized in people with acute pancreatitis. Furthermore, in acute pancreatitis of human beings, the existence of specific mechanisms of pulmonary injury is suspected. Retrospective consideration of this case suggested that the initial pulmonary edema was induced by acute pancreatitis.