Vitamin E, selenium and polyunsaturated fatty acids in clinically normal grower (9-16 weeks old) pigs and their feed: their relationship to the vitamin E/selenium deficiency ("VESD") syndrome

Vitamin E, selenium and polyunsaturated fatty acids (PUFAs) were determined in feed used at three piggeries over.a four week period and compared with corresponding concentrations in clinically normal grower pigs at slaughter. Mean values were vitamin E: 59 IU/kg (feed), 6 micromol/kg (liver), 1.7 micromol/l (serum); and selenium: 310 microg/kg (feed), 5200 nmol/kg (liver), 1700 nmol/l (blood). Alpha-tocopherol accounted for 80% of the mean vitamin E activity in the feed and over 95% that in the liver and serum. The mean ratio of PUFA to total fatty acid (FA) in the feed (38%) was similar to that in the serum (36%) and liver (39%), but the ratio of peroxidisable PUFA (PPUFA) to FA increased from 1.7% in the feed to 4.2% in the serum and 10.8% in the liver. The ratio of alpha-tocopherol (mmol) to PPUFA (mol) in the liver varied from 0.16 to 0.48. The relationship of these data to the VESD syndrome is discussed in the light of other published data.     

A blind test of the serological response of dogs to infection with Taenia ovis

Fifty six dogs of mixed age and sex were acquired from farms in the Otago/Southland region, and maintained at the Hydatid Research Unit, Taieri, where 43 were each fed two Tueniu ovis cysts. All were bled fortnightly for six or 12 weeks. Coded sera were sent to Wallaceville Animal Research Centre for testing using ELISA, with antigen from T. ovis scoleces. Dog treatments were identified after all tests were complete. A discriminant level was derived from the mean absorbance value plus three standard deviations of 56 sera taken at time zero and 78 sera from serially bled uninfected dogs. None of these 134 sera registered as a false positive using this discriminant level. The data showed no significant deviation from normality, and the expected frequency of the occurrence of false positives is therefore less than 0.14%. Four weeks after infection 63% of dogs proved to be infected were serologically positive, rising to 78% after 6 weeks. When worms were removed by anthelmintic treatment, ELISA absorbance levels decreased. Four weeks after removal 70% of previously infected dogs remained positive, decreasing to 30% after 6 weeks. Six weeks after infection the sensitivity of the test was 78%, and the specificity 63%. However, if dogs with positive ELISA absorbance levels, but which did not purge worms, were regarded as having had worms, the respective figures would be 82% and 100%. The latter figures are similar to our previously published laboratory results. The test is of comparable efficiency to arecoline purgation for surveillance, and has the additional advantage of detecting infection in the majority of those dogs that have been infected for three weeks or more but fail to pass worms on purgation, and a substantial proportion of those infected dogs that were treated by their owners prior to presenting them for purgation in order to avoid detection of infection.     

Incarceration of the small intestine by the epiploic foramen in fifteen horses

In 15 horses with acute abdominal disease, a diagnosis of incarceration of small intestine through the epiploic foramen was made, either at the time of exploratory celiotomy or at necropsy.     

Acquired hydrocephalus and hydromyelia in a cat with feline infectious peritonitis: A case report and brief review

A one-year-old domestic long-haired cat was referred to the New York State College of Veterinary Medicine because of acute onset of paraparesis and hyperesthesia associated with trauma. Myelography and cerebrospinal fluid analysis revealed severe hydromyelia and myelitis, respectively. The definitive diagnosis of feline infectious peritonitis was made by histological examination at necropsy. Lesions were confined exclusively to the brain and spinal cord. Partial occlusion of the third and fourth ventricles with pyogranulomatous debris caused hydrocephalus and subsequent hydromyelia. The hydromyelia may have been the primary means of compensation for the hydrocephalus, thus masking subclinical disease.