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An investigation of stillbirth and early neonatal lamb mortality was conducted in sheep flocks in Norway. Knowledge of actual causes of death are important to aid the interpretation of results obtained during studies assessing the risk factors for lamb mortality, and when tailoring preventive measures at the flock, ewe and individual lamb level. This paper reports on the postmortem findings in 270 liveborn lambs that died during the first 5 days after birth. The lambs were from 17 flocks in six counties. A total of 27% died within 3 h after birth, 41% within 24 h and 80% within 2 days. Most lambs (62%) were from triplet or higher order litters. In 81% of twin and larger litters, only one lamb died. The most frequently identified cause of neonatal death was infectious disease (n=97, 36%); 48% (n=47) of these died from septicaemia, 25% (n=24) from pneumonia, 22% (n=21) from gastrointestinal infections and 5% (n=5) from other infections. Escherichia coli accounted for 65% of the septicaemic cases, and were the most common causal agent obtained from all cases of infection (41%). In total, 14% of neonatal deaths resulted from infection by this bacterium. Traumatic lesions were the primary cause of death in 20% (n=53) of the lambs. A total of 46% of these died within 3 h after birth and 66% within 24 h. Severe congenital malformations were found in 10% (n=27) of the lambs, whereas starvation with no concurrent lesions was the cause of death in 6% (n=17). In 16% (n=43) of the lambs, no specific cause of death was identified, lambs from triplet and higher order litters being overrepresented among these cases. In this study, the main causes of neonatal lamb mortality were infection and traumatic lesions. Most neonatal deaths occurred shortly after birth, suggesting that events related to lambing and the immediate post-lambing period are critical for lamb survival.

INTESTINAL adenocarcinomas are the most frequently reported type of tumours in sheep (Ross 1980) and have also been reported in other domestic animal species and in human beings (Johnstone and others 1983, Hamir 1985, McCoy and others 2009). In sheep, these tumours have a low incidence (Else 2007), although an incidence of up to 6 per cent in some populations has been documented (Simpson and Jolly 1974). In Norway, intestinal adenocarcinomas were described in 2.9 per cent of 1256 adult sheep submitted for postmortem examination over a period of eight-and-a-half years at a research institute (Ulvund 1983). The tumour presents as a stenotic, often annular, firm tissue 3 to 5 cm in length, typically situated in the jejunum or ileum (Georgsson and Vigfusson 1973, Tontis 2006, Munday and others 2006). The neoplastic tissue has a tendency to grow via the intestinal wall to the mesentery and along the serosal lymphatics to the regional lymph node (Munday and others 2006, Brown and others 2007). Metastatic implantations on the peritoneum are common, and the tumour may occasionally spread to the serosal surfaces in the thoracic cavity. In a few cases, haematogenous metastasis to the liver and/or the lungs have been demonstrated (Ross 1980, Ulvund 1983). Accumulation of fluid in the abdomen and thorax is frequent in amounts of up to 35 litres (Ulvund 1983). This short communication describes scirrhous jejunal adenocarcinomas in three closely related ewes in a sheep flock. The flock consisted of approximately 120 winter-fed sheep in eastern Norway. The animals were of the Norwegian White breed, demonstrated high quality and production, and were routinely treated for endoparasites and vaccinated against clostridial infections. During the six-month winter season, the sheep were kept indoors on a slatted wooden floor and fed hay silage and commercial …

Aims: Transmissible spongiform encephalopathies (TSEs) or prion diseases are fatal neurodegenerative diseases of man and animals characterized by vacuolation and gliosis of neuropil and the accumulation of abnormal isoforms of a host protein known as prion protein (PrP). It is widely assumed that the abnormal isoforms of PrP (PrPd, disease-specific form of PrP) are the proximate cause of neurodegeneration. Methods: To determine the nature of subcellular changes and their association with PrPd we perfusion-fixed brains of eight bovine spongiform encephalopathy (BSE)-affected cows and three control cattle for immunogold electron microscopy at two different neuroanatomical sites. Results: All affected cattle presented plasma membrane alterations of dendrites and astrocytes that were labelled for PrPd. PrPd on membranes of dendrites and occasionally of neuronal perikarya was associated with abnormal endocytotic events, including bizarre coated pits and invagination of the plasma membrane. BSE-affected cattle also presented excess and abnormal multivesicular bodies, sometimes associated to the plasma membrane perturbations. In contrast, two TSE-specific lesions, vacuolation and rare tubulovesicular bodies, were not labelled for PrPd as were a number of other nonspecific lesions, such as autophagy and dystrophic neurites. At least two different morphological pathways to vacuoles were recognized. Conclusions: When compared with other TSEs, these changes are common to those of sheep and rodent scrapie and shows that there are consistent membrane toxicity properties of PrPd. This toxicity involves an aberration of endocytosis. However, it is by no means clear that the lesions are of sufficient severity to result in clinical deficits.