Mitogen Stimulation of Lymphocytes in Pigs with Hereditary Vitamin C Deficiency

Recently an inherited vitamin G deficiency in the pigs presumably based on an autosomal recessive gene was decribed* Homozygotes are in contrast to heterozygotes and normal pigs unable to synthesize ascorbic acid. In an experiment comprising 3 littermate pigs, 2 homozygous and 1 heterozygous for the vitamin C deficiency gene, the influence of ascorbic acid depletion, and repletion on mitogen stimulation of peripheral blood lymphocytes was studied. Ascorbic acid depletion of the vitamin C dependent pigs resulted in a rapid decline in plasma ascorbic acid. Response of lymphocytes to stimular tion with Concanavalin A (Con A) and phytohemagglutinin M (PHA) decreased more slowly reaching a minimum, which coincidedi with the occurrence of the first clinical symptoms of scurvy. Following resupplementation with vitamin C the plasma content of ascorbic acid rapidly returned to normal, while the lymphocyte response to Con A and PHA stimulation only gradually approached the initial values. The repletion with ascorbic acid caused a transitory increase in the response to pokeweed mitogen (PWM) stimulation. The significance of these findings in relation to the cellular immune system in normal pigs is discussed.     

The Zinc-Myoglobin Relationships in Porcine Muscles

Zinc and myoglobin content in muscles from pigs were studied under various conditions. Zinc concentration was considerably higher in red than in white muscles. In muscles, where the metabolic pattern changes from glycolytic to oxidative during the period from birth to weaning, a simultaneous increase in zinc content was seen. A significant positive correlation exists between myoglobin and zinc content under normal conditions. However, while myoglobin concentration decreases due to iron deficiency anaemia no changes occur in zinc content. It is concluded that no functional link seems to exist between zinc metabolism and myoglobin synthesis in porcine muscles.     

Tryptophan Metabolism in Pigs

Contrary to blood serotonin the level of free and total tryptophan is distinctly influenced by feed intensity and composition. Piglets show a considerably higher plasma free tryptophan and blood serotonin content than adult pigs, just as boars possess a significantly higher blood level of tryptophan and serotonin than sows. A pronounced individual variation of blood serotonin and a much less variable content among littermate pigs provide evidence that blood serotonin is genetically controlled. Tryptophan is readily absorbed and distributed in a characteristic manner among investigated organs and tissues. A genetical control of blood serotonin and its possible relation with type of reaction exhibited by ergometer exercised pigs support the influence of tryptophan and serotonin on the ability of pigs to withstand controlled environmental conditions such as physical exercise.     

PLasma Cholesterol in Swine Genetic Variations and Relation to Alkaline Phosphatase

A variety of environmental factors such as feeding and climate may influence the plasma cholesterol concentration. Earlier experiments have, however, indicated that genetic differences also exist (Heidenreich et al. 1964). The present study was undertaken to elucidate this possibility in pigs of Danish Land-race reared under strictly standardized environmental conditions. Besides, the plasma cholesterol concentration was compared with other genetically variable blood parameters to examine if any correlations existed. Only the relation to alkaline phosphatase (AP) will be dealt with here.     

Experimental Maedi Infection in Sheep

Eight sheep were inoculated with Icelandic maedi strain M 88; 2 sheep served as control sheep and were in close contact with the inoculated ones. Four of the sheep were inoculated via the respiratory tract with 7×106 TGID50 of strain M88 and the other 4 intracerebrally with 5×105 TGID50 of the same strain. Maedi M88 strain was isolated from peripheral blood leukocytes of all inoculated sheep. There was a striking difference between the 2 groups in the appearance of demonstrable viremia after inoculation. Viremia could be demonstrated in the intrapulmonarily inoculated sheep within 2–6 months but not until 8–11 months after inoculation in the intracerebrally inoculated ones. This finding is thought most probably to reflect a weak neurotropism of the strain used. After the first demonstration of viremia, maedi virus has been recovered quite reqularly in peripheral leukocytes of all intrapulmonarily inoculated sheep, but less regularly in the intracerebrally inoculated ones. Maedi virus was isolated from 1 of the uninoculated control sheep 15 months after inoculation. The first clinical case with a clinical appearance suggesting combined involvement of maedi and visna was found among the intrapulmonarily inoculated sheep, 8% months after inoculation. Histopathological examination and virus isolation confirmed maedi. The cause of paraplegia could not be confirmed. No histopathological changes were found and no virus isolation was made from the central nervous system of this animal. One of the intracerebrally inoculated sheep died suddenly without any observed clinical signs 11 months after inoculation. Histopathological examination revealed pulmonary lesions of maedi, but no visna lesions in the central nervous system, although maedi virus was isolated from various parts of brain. None of the other experimental sheep displayed clinical signs of maedi or visna during the observation period of 18 months.