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.     

Ulceration and stricture of the right dorsal colon after phenylbutazone administration in four horses

Four cases of ulceration and stricture of the right dorsal colon were encountered. Ulceration of the right dorsal colon is generally associated with nonsteroidal anti-inflammatory drug (NSAID) toxicosis but there are few reports of stricture following ulceration. All four horses had recent phenylbutazone use: three had been given doses well in excess of the recommended dose and in one the dose was marginally above those recommended but was combined with administration of other NSAIDs. All four horses presented with intermittent low-grade colic, weight loss and ventral oedema. Diarrhoea was also seen in three of them. All had hypoproteinaemia due to severe hypoalbuminaemia, and hyperfibrinogenaemia. Hypoalbuminaemia was less severe in one horse and this horse was successfully managed medically. Two cases were definitively diagnosed at exploratory celiotomy and two at necropsy. Exploratory celiotomy was performed in two horses: one was euthanased at surgery and one was managed successfully with medical treatment and remained normal 1 year after surgery. Medical management included feeding of a low-roughage pelleted ration, corn oil, psyllium mucilloid, and discontinuation of NSAID administration.