Deficiency In Pigs Research Articles

Platelet storage pool deficiency in pigs

We report a new bleeding disease--storage pool deficiency (SPD) of platelets--in pigs from the Mayo swine colony of homozygous von Willebrand's disease (vWD) and of heterozygous carriers of vWD. Levels of factor VIII, von Willebrand factor antigen (vWF:Ag), and ristocetin cofactor (RCof) were similar in the vWD carriers and SPD pigs. The latter pigs, however, had bleeding times of 15 minutes or more and were severe bleeders, in contrast to clinically normal vWD carriers. Platelet aggregation in response to collagen was reduced in most SPD pigs. Total platelet content of ADP, ATP, and serotonin was less than that of normal pigs. While the initial uptake of 14C-labeled serotonin into platelets was similar in SPD and normal pigs, retention of serotonin was reduced in platelets of SPD pigs. Transmission electron microscopy showed a large decrease of dense bodies in the platelets of SPD pigs. These findings support a diagnosis of SPD. Genetic analyses suggest an autosomal recessive mode of inheritance. A breeding program is under way to produce pigs affected only at the SPD gene, thus allowing further characterization of SPD and SPD-carrier pigs.

Platelet Storage Pool Deficiency in Pigs

We report a new bleeding disease--storage pool deficiency (SPD) of platelets--in pigs from the Mayo swine colony of homozygous von Willebrand's disease (vWD) and of heterozygous carriers of vWD. Levels of factor VIII, von Willebrand factor antigen (vWF:Ag), and ristocetin cofactor (RCof) were similar in the vWD carriers and SPD pigs. The latter pigs, however, had bleeding times of 15 minutes or more and were severe bleeders, in contrast to clinically normal vWD carriers. Platelet aggregation in response to collagen was reduced in most SPD pigs. Total platelet content of ADP, ATP, and serotonin was less than that of normal pigs. While the initial uptake of 14C-labeled serotonin into platelets was similar in SPD and normal pigs, retention of serotonin was reduced in platelets of SPD pigs. Transmission electron microscopy showed a large decrease of dense bodies in the platelets of SPD pigs. These findings support a diagnosis of SPD. Genetic analyses suggest an autosomal recessive mode of inheritance. A breeding program is under way to produce pigs affected only at the SPD gene, thus allowing further characterization of SPD and SPD-carrier pigs.

Sorbitol dehydrogenase deficiency in several pig tissues: potential implications for studies of experimental diabetes

Screening for red blood cell sorbitol dehydrogenase deficiency in 12 different mammalian species was performed. A wide inter-species variability in red cell sorbitol dehydrogenase with a virtually complete deficiency in pigs was observed. Aldose reductase and sorbitol dehydrogenase activities in 12 different pig tissues also were measured. Aldose reductase activity was present in all the tissues studied, whereas organ specificity for sorbitol dehydrogenase was observed. Sorbitol dehydrogenase activity was not detectable in lenses, among other tissues, making the pig a potential model for studies in experimental diabetes, particularly for the investigation of sorbitol dehydrogenase deficiency as a risk factor in the development of cataracts.

Congenital Ascorbic Acid Deficiency in Pigs

In a swine production herd, spontaneous scurvy was observed among piglets 2–3 weeks after weaning. All affected pigs had the same boar as both maternal and paternal grandfather. The affected pigs had only traces of ascorbic acid in blood and tissues as compared to litter mates and other normal pigs. The ratio between the total numbers of normal and affected pigs in the 4 litters concerned was in agreement with a 3:1 segregation, which is characteristic of simple autosomal recessive inheritance in matings between non-affected carriers. Two affected pigs were restored to normal when given ascorbic acid in the diet. Without vitamin C supplement affected pigs died or had to be euthanized. Liver microsomes from an affected pig were unable to synthesize ascorbic acid in vitro with 1-gulonolactone as a substrate, unlike microsomes from normal control pigs.

Tryptophan deficiency in pigs: changes in food intake and plasma levels of glucose, amino acids, insulin and growth hormone.

Pigs were fed alternately tryptophan deficient diet and the same diet supplemented with tryptophan. The deficient diet depressed food intake, caused changes in the pattern of plasma amino acids, increased plasma glucose levels and increased plasma urea levels per unit food intake. Plasma levels of insulin and growth hormone gave no indication that either hormone was involved in the suppression of food intake.

Selenium and Vitamin E Deficiency in Pigs

The effect of dietary selenium (Se) and vitamin E (Vit. E) in pigs on Se and Vit. E in plasma and on Se in tissue from liver, heart, m. long, dorsi and m. psoas major was studied; and furthermore was the influence on the enzymes ASAT and ALAT studied. Two levels of Se were used, 0.03 and 0.06 mg Se per kg feed. Within each Se level 2 levels of Vit. E were used, 15 and 45 i. u. per kg feed. This resulted in 4 groups: 1. low Se and low Vit. E; 2. low Se and high Vit. E; 3. high Se and low Vit. E; 4. high Se and high Vit. E. Ten% of all pigs fed low Se, and 4% of the pigs fed low Se and high Vit. E diet died with severe symptoms of Se deficiency. None of the pigs fed the high Se diet died with such symptoms. Plasma Se determinations have been shown to indicate the Se status in pigs almost as accurately as liver Se determination. ASAT and ALAT enzyme determinations were not of any diagnostic value. There was a good agreement between dietary Vit. E level and the corresponding levels in plasma. Oxidized herring oil seems to enhance the Vit. E need.

Selenium and Vitamin E Deficiency in Pigs

The effect of selenium (Se) and vitamin E (Vit. E) on reproductive performance, growth and health was studied in pigs. Two levels of Se were used, 0.03 and 0.06 nag per kg feed. The major component of the experimental diets was barley originating from soil which had formerly produced crops with a very low content of Se. Prior to seeding, the area was divided into 2 plots, 1 of which was treated with Se in the form of sodium selenite, 100 g Se per ha. The use of Se enriched fertilizer was an effective way of increasing the Se concentration of the grain. Thus the concentration of Se in the barley produced on the treated area was 5 times higher than in barley from the untreated one. Vit. E was added at a level of 30 i.u. per kg feed, and the concentrations were approx. 15 and 45 i.u. in the basal and experimental diets, respectively. The higher level of Se or Vit. E was not significantly associated with milk yield of the sow, litter size, birth weight or haemoglobin levels. However, there was a tendency to an increase in milk yield of the sows following additions of Se plus Vit. E, and litter size was slightly higher from sows which had received an addition of Vit. E. The concentration of Se and Vit. E was much higher in colostrum than in sow milk, and additions of dietary Se and Vit. E were associated with marked increases in the concentrations of these compounds in both colostrum and sow milk. There was a moderately improving effect of a high Se concentration in feed on growth rate and feed utilization. Low dietary levels of Se and Vit. E were followed by increased mortality rate in piglets; iron toxicity in connection with iron treatment was observed in piglets on low dietary Vit. E. Symptoms characteristic of PSE were not observed in the Se and Vit. E deficient pigs.

Acute nicotinamide deficiency in pigs

Acute nicotinamide deficiency in pigs

Serum and Tissue Enzyme Activity and Trace-Element Content in Response to Zinc Deficiency in the Pig

Zinc deficiency is associated with poor growth and development. It has been postulated that a deficiency of the various zinc metalloenzymes results from the lack of dietary zinc. From present study, an examination of some aspects of this postulate, we conclude the following about zinc deficiency in pigs: (1) Of the tissues studied, it results im diminished zinc content only in liver, kidney, and pancreas. (2) It is associated with tissue abnormalities of various trace elements other than zinc. (3) Histochemical enzyme assays are satisfactory for qualitative but not quantitative determination of zinc metalloenzymes. (4) Deficiency of various tissue zinc metalloenzymes is difficult to demonstrate, even in severe zinc deficiency. (5) It is associated with decreased activity of hepatic leucine aminopeptidase and ornithine transcarbamylase, and decreased serum cholesterol concentrations. Our findings are consistent with the postulate that alterations in a number of trace elements may occur in the entity called zinc deficiency.

Suspected thiamine deficiency in pigs.

Suspected thiamine deficiency in pigs.

Influence of dietary zinc, corn oil and cadmium on certain blood components, weight gain and parakeratosis in young pigs.

Forty virus-pneumonia-free Yorkshire growing pigs were used in each of two experiments to study the effects of supplemental Zn, corn oil and Cd on body weight gain, incidence of parakeratosis and levels of certain blood constituents. In experiment 1, when part of the corn in the diet of 3-week-old pigs was replaced by glucose so as to reduce the Zn concentration from approximately 33 ppm to 24 ppm, there was no reduction in weight gain but an 80% incidence of parakeratosis occurred. There was no parakeratosis among pigs fed diets containing no glucose or among those fed the low-Zn diet supplemented with corn oil. Blood glucose level was not significantly affected by diet, but serum cholesterol tended to be elevated after 4 weeks and 6 weeks in pigs fed added corn oil. Serum alkaline phosphatase was greatly reduced (P< .01)after 4 and 6 weeks in pigs fed the low-Zn diets, but there was no effect of added corn oil on this constituent despite the absence of parakeratosis. In experiment 2 no parakeratosis was observed, even when the Zn concentration was reduced to 22 ppm by replacement of corn with glucose. The failure to produce parakeratosis was probably associated with the older age (8 weeks) at the beginning of the experiment, which allowed body storage of Zn from the Zn-fortified postweaning diet. There was no significant effect of level of Zn or corn oil on weight gains, but the addition of 154 ppm Cd to the low-Zn diet resulted in reduced weight gains during the first 3 weeks and subsequent steady weight loss. The addition of 52 ppm Zn to the high-Cd diet resulted in less severe weight loss. Serum alkaline phosphatase was significantly (P<.01) reduced after 4 and 6 weeks in pigs fed low-Zn diets, regardless of the corn oil or Cd level. The failure of Cd to produce symptoms of Zn deficiency in pigs fed low-Zn diets despite severe weight loss indicates that its main action in the pig is not an antagonism of Zn.

Some clinical and experimental observations on naturally-occurring pantothenic-acid deficiency in pigs

Some clinical and experimental observations on naturally-occurring pantothenic-acid deficiency in pigs

The Teratogenic Effect of Vitamin a Deficiency in Pigs

In connection with experiments concerning the utilization of perorally and parenterally administered vitamin A in pigs and the transfer of this vitamin from the mother to the fetuses investigations were performed concerning the teratogenic effect of vitamin A deficiency in this animal. 9 sows and gilts which throughout the pregnancy or in the first third of this were depleted of vitamin A gave birth to 91 piglets all of which had malformations cf. Table 1. The most frequent anomaly was microphthalmia; of other characteristic malformations may be mentioned heart defects, diaphragmatic hernia, malformed and not ascended kidneys, underdevelopment of genital organs, internal hydrocephalus and herniations of the spinal cord. Of this syndrome of malformations only one, namely the herniations of the spinal cord, seems to be specific for vitamin A deficiency. This malformation may be due to retarded growth of the bone tissue in relation to the relative normal growth of the nerve tissue. I forbindelse med forsøg over udnyttelsen af parenteralt og peroralt appliceret A-vitamin til svin samt overførsel af dette vitamin fra so til fostre blev der foretaget undersøgelser over A-vitaminmanglens teratogene effekt. 9 gylte og søer, der under hele drægtigheden eller i den første trediedel af denne, var fuldstændig udtømt for A-vitamin, fik ialt 91 grise, der alle udviste misdannelser, jvfr. tabel 1. Den hyppigst forekommende anomali var mikrophthalmi. Af andre karakteristiske misdannelser kan nævnes hjertedefekter, diafragmabrok, manglende ascenxiering af misdannede nyrer, underudvikling af kønsorganer samt intern hydrocephali og rygmarvsprotrusioner. Efter den komparative litteratur at dømme synes kun en enkelt af dette syndrom af misdannelser, nemlig rygmarvsprotrusionerne, at være specifik for A-vitaminmanglen. Denne misdannelse skyldes sandsynligvis en forsinket vækst af knoglevævet i forhold til den relativt normale vækst af nervevævet.

Absence of Nerve Degeneration in Chronic Thiamine Deficiency in Pigs: One Figure

Absence of Nerve Degeneration in Chronic Thiamine Deficiency in Pigs: One Figure

Electrocardiographic changes associated with thiamine deficiency in pigs: Wintrobe, M. M., Alcayaga, R., Humphreys, S., and Follis, R. H., Jr.: Bull. Johns Hopkins Hosp. 72: 169, 1943

Electrocardiographic changes associated with thiamine deficiency in pigs: Wintrobe, M. M., Alcayaga, R., Humphreys, S., and Follis, R. H., Jr.: Bull. Johns Hopkins Hosp. 72: 169, 1943

Ascariasis and Vitamin A Deficiency in Pigs

In 1927 and 1928 Hiraishi published some observations which he had made on Ascariasis in swine in the absence of Vitamin A. He claimed that he had been successful in overcoming the resistance of the pigs to the human strain of Ascaris lumbricoides by lowering the vitamin A content of the diet and that he was able to produce much heavier infestations with Ascaris lumbricoides of swine origion in A-avitaminosed pigs. As all other factors were apparently controlled, he draws the conclusion that vitamin A has a direct bearing on the susceptibility of the pig to infestation with round worms. Unfortunately these publications are not readily available in England and only summaries of results have been available to the present writer. But from the data given and in comparison with the effect of the vitamins on Ascaridia (Ackert et alia, 1929 and 1931 a &amp; b) and on hookworm (Foster &amp; Cort, 1931 and 1932), these conclusions would seem to be justified.

Iron Deficiency in Pigs

Iron Deficiency in Pigs