Effect of selenium on performance, serum selenium concentration and glutathione peroxidase activity in pigs

Pigs from sows fed a diet deficient in Se and low in vitamin E were fed a Torula yeast diet supplemented with 100 IU dl-alpha-tocopheryl acetate/kg of diet. Dietary treatments were levels of supplemental Se of 0, .025, .050, .075 or .100 ppm. Some death loss occurred in pigs receiving no supplemental Se at approximately 5 wk of age. Autopsy revealed liver and heart lesions typical of vitamin E-Se deficiency. Selenium supplement had no significant effect on average daily gain, feed intake or gain to feed ratio for the 4-wk experiment. Selenium status of pigs was determined by serum Se concentration and serum glutathione peroxidase (GSH-Px) activity. Serum Se increased linearly (P less than .01) with increasing supplemental Se. Serum GSH-Px activity increased linearly (P less than .01) and quadratically (P less than .05) with increasing supplemental Se. With time, the level of serum Se and GSH-Px activity decreased in unsupplemental pigs, but increased in pigs fed diets supplemented with Se and resulted in significant interactions (P less than .01) between dietary Se level and time on experiment. The correlation between serum Se concentration and GSH-Px activity was .81 (P less than .01).     

Selenium and vitamin E deficiency in pigs. I. Influence on growth and reproduction.

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.     

Selenium toxicosis in feeder pigs.

Selenium toxicosis was diagnosed in feeder pigs on a central Michigan farm. Use of a commercial supplement, found to contain approximately 20 times the intended Se concentration, resulted in a Se concentration of 8.1 mg/kg of the complete feed. This was fed for 34 days during which daily feed consumption decreased approximately 35%, several pigs developed weakness and forelimb paresis, and 1 pig died. The highest serum Se concentration measured was 1,550 ng/ml (normal range, 140 to 190 ng/ml). Normal feed consumption returned when an alternative feed was provided. Mean serum Se concentrations of representative pigs, monitored over the subsequent 26 days, decreased from 905 to 258 ng/ml. Histologic examination of a recovering pig revealed skeletal and cardiac myopathy and bilaterally symmetric malacia of the gray matter of the ventral horns of the spinal cord. During the developing toxicosis, the pigs consumed an estimated 11.4 mg of Se/pig/d.     

Selenium and vitamin E deficiency in pigs. II. Influence on plasma selenium, vitamin E, ASAT and ALAT and on tissue selenium.

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.     

Cryptosporidiosis in guinea pigs: a retrospective study

Cryptosporidiosis was diagnosed in 81 guinea pigs (Cavia porcellus) from 1979 through 1985 at a research animal diagnostic laboratory. Most of the guinea pigs were juveniles of Hartley stock and originated from 6 commercial laboratory animal suppliers or from one pet store supplier. Common clinical signs reported were failure to gain weight, weight loss, diarrhea, and death. At necropsy, macroscopic findings included emaciation, hyperemia of the small intestine, serosal edema of the cecal wall, and increased fluidity of ingesta throughout the intestines. Oval to round cryptosporidia (1 to 4 microns) were seen microscopically within or on the brush border of mucosal epithelial cells from the duodenum through the cecum. Acute histologic lesions consisted of necrosis and sloughing of enterocytes at the villus tips, inflammation, hyperemia and edema of the lamina propria, and hyperplasia of crypt epithelium. More chronic lesions consisted of marked villus bridging or villus fusion and blunting, metaplasia of the mucosal epithelium, and lymphocytic infiltration of the lamina propria.     

Role of haemophilus pleuropneumoniae lipopolysaccharide endotoxin in the pathogenesis of porcine Haemophilus pleuropneumonia

Intact Haemophilus pleuropneumoniae cells (strain Shope 1, serotype 1), highly purified lipopolysaccharide (LPS) obtained from this strain of H pleuropneumoniae, as well as from Escherichia coli O111:B4, filter-sterilized H pleuropneumoniae cell-free culture supernatant fluid, and heat-inactivated supernatant fluid were given intranasally to CF1 mice and intratracheally to pigs. Pulmonary lesions induced by H pleuropneumoniae in mice were similar to those induced by H pleuropneumoniae in pigs. Histologically, lungs of mice and pigs killed 1 or 2 days after inoculation with 200 micrograms of highly purified H pleuropneumoniae LPS had lesions similar to one another and were similar to those in mice and pigs given intact H pleuropneumoniae, except that little or no necrosis or hemorrhage was observed. In mice killed 1 or 2 days after inoculation of 200 micrograms of E coli O111:B4 LPS, pulmonary lesions were similar to those in mice given H pleuropneumoniae LPS. Pulmonary lesions in mice given cell-free culture supernatant fluid obtained from a midlog-phase growth culture of H pleuropneumoniae cultivated in a chemically defined medium were severe and consisted of neutrophil infiltration and extensive necrosis. In mice, the heat-inactivated supernatant fluid produced mild lesions that consisted of foci of neutrophil aggregation and no necrosis. Extensive necrosis observed in lesions caused by cell-free culture supernatant fluid could be attributed to the action of a heat-labile component, perhaps by the extracellular heat-labile hemolysin produced by H pleuropneumoniae cultivated in chemically defined medium. A LPS endotoxin and a heat-labile factor may be involved in the pulmonary lesion development in the acute phase of porcine Haemophilus pleuropneumonia.     

Cellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.

The effects of dietary restriction of vitamin E (Vit E) and selenium (Se) on lymphocyte proliferation, natural killer (NK) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), and on burst respiratory response of stimulated granulocytes as measured by chemiluminescence (CL) were studied in pigs. Six male weanling pigs were maintained for 25 d on a torula yeast-based diet containing no measurable amount of alpha-tocopherol and less than .02 mg of Se per kilogram of feed. Six others received the same basal diet supplemented with 33 IU of DL-alpha-tocopheryl acetate and .2 mg of Se per kilogram of feed. All pigs were inoculated with Salmonella typhisuis on d 21 of the feeding period and killed on d 25. Tests to measure cellular immune functions were performed on cells isolated from blood samples taken on d 21 and 25. After 21 d of feeding, lymphocyte blastogenesis responses to phytohemagglutinin, concanavalin A, and pokeweed mitogen in pigs fed the Vit E- and Se-deficient diet were normal compared with the response in pigs fed the supplemented diet. Moreover, the cytotoxic activity of NK cells, the ADCC response, and the CL response of granulocytes were not affected. After 25 d, a marked suppression of lymphocyte response to mitogens occurred in pigs fed the Vit E- and Se-deficient diet when the cells were cultured in the presence of autologous serum. When fetal bovine serum replaced autologous serum in the cultures, no suppression was observed. No effect on NK activity and ADCC was observed, whereas the CL peak response of granulocytes tended to be higher in pigs fed the deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Excessive dietary selenium to primiparous sows and their offspring. I. Influence on reproduction and growth

The effect of high dietary selenium (Se) on the reproductive performance, growth and health in pigs was examined. Addition of 0 to 16 mg Se per kg feed to sows and their piglets up to nine weeks of age did not cause any manifest toxic effect. None of the sows died due to the Se treatment. The piglets were all fullborn and showed no macroscopic abnormalities. The treatment did not influence neither the number of liveborn and stillborn piglets in the litter, nor the survival of the piglets until 9 weeks of age. The weight of the whole litter at birth was unaffected by the Se supplementation, while there was a significant difference in body weight of the piglets at 9 weeks of age. The weaned pigs receiving 8 or 16 mg Se per kg feed had a reduced feed intake. As the feed utilization was unaffected by treatment, these pigs had a significantly lower weight at 9 weeks of age.     

Toxicosis in pigs fed selenium-accumulating Astragalus plant species or sodium selenate

Three groups of 5 pigs each were fed a high selenium (Se) diet by mixing either Astragalus praelongus (31.6 ppm Se in feed), A bisulcatus (31.7 ppm Se in feed), or sodium selenate (26.6 ppm Se in feed) with commercial hog feed. Ten control pigs were fed only commercial hog chow containing trace selenium (0.44 ppm Se). Pigs were fed for 9 weeks and necropsied when they had ataxia or paralysis. Blood was collected for hematologic and serum biochemical determinations, and samples of various tissues were collected and fixed in neutral-buffered 10% formalin for histologic evaluation or frozen for determination of selenium concentration. All forms of selenium induced clinical signs of weight and hair loss, with cracked hooves and inflamed coronary bands developing in all Na2SeO4-fed pigs and 1 A praelongus-fed pig, but not in A bisulcatus-fed pigs. Serum calcium, phosphorus, and albumin concentrations were unchanged or significantly decreased from prefeeding values in groups fed selenium. Serum aspartate transaminase (AST) activities in Astragalus species-fed groups, and amylase activities and PCV in all groups of pigs fed selenium, were increased. Serum alkaline phosphatase and creatine kinase activities were significantly increased in the A praelongus-fed pigs and significantly decreased in Na2SeO4-fed pigs. Terminal tissue and body fluid selenium concentrations were determined in all groups of pigs fed selenium and compared with values in control pigs. Urine and bile concentrations were increased by the greatest factor (40 to 100x), with tissue concentrations of selenium increased by a lesser factor (6 to 17x).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of selenium and vitamin E supplementation on selenium distribution and meat quality of pigs

Abstract

The study was conducted on 60 pigs kept in individual pens. The animals were allocated to four groups. The growing-finishing pigs from the control group were fed with basic feed containing 0.3 mg selenium (Se) derived from Na₂SeO₃ kg^?1 and 60 mg of dl-α-tocopheryl acetate kg^?1. The remaining three groups were differentiated by adding 0.2 mg kg^?1 Se-enriched yeast (Saccharomyces cerevisiae) and/or 60 mg vitamin E to feed (grower and finisher). Our results show that the addition of organic Se to inorganic Se commonly used in pig feed caused a significant increase in hepatic Se and muscle. This indicates the possibility of using these products as functional foods to improve Se status in humans residing within regions which are deficient in this trace element. We found no beneficial effect of supplementation with vitamin E and Se on the quality of the meat.     

Increasing daily feeding occasions in restricted feeding strategies does not improve performance or well being of fattening pigs

Background

The natural feeding behaviour of the pig is searching for feed by rooting activities throughout the day; self-feeding pigs randomly space their eating and drinking periods throughout the day consuming ten to twelve meals per day. Pigs in conventional fattening pig production are normally fed 2–3 times daily with the feed consumed within 15 minutes. The aim of this study was to determine if more frequent feedings could improve the performance of conventionally kept fattening pigs.

Methods

The experiment was carried out on 360 fattening pigs (27–112 kg live weight), weighed and assigned to pens stratified by weight and sex. Each treatment group consisted of 180 pigs, allocated to 20 pens with nine pigs in each pen. To evaluate how more feeding occasions affects performance and well-being the pigs were divided into two groups and fed three (control group) or nine (treatment group) times daily. The same total amount of liquid feed was fed to each group and the feed ration was correlated to the live weight of the pigs. All weight and slaughter recordings were made individually and recordings of feed consumption were made pen-wise. At slaughter the stomach of each pig was examined for lesions in the pars oesophagea and scored on a scale from 1–6.

Results

Frequent feeding occasions influenced both performance and status of gastric lesions of the pigs adversely. Pigs in the treatment group grew slower compared to pigs in the control group; 697 g/day (± 6.76) versus 804 g/day (± 6.78) (P < 0.001) with no difference in within-pen variation. There was also a lower prevalence of gastric lesions within pigs in the control group (2.4 (± 0.12) compared to 3.0 (± 0.12) (P < 0.01)). There was a positive correlation between gastric lesions in the treatment group and daily weight gain (r = 0.19; P < 0.01).

Conclusion

Increased daily feeding occasions among group housed pigs resulted in a poorer daily weight gain and increased mean gastric lesion score as compared with pigs fed three times daily. This may be a consequence of more frequently occurring competition for feed in the treatment group. The present study does not support increased daily feeding occasions in fattening pigs.     

Effect of inorganic selenium supplementation on selenosis in postweaning swine

A total of 72 pigs weaned at 4 wk of age were allotted by litter and weight to nine treatment groups and fed 20% protein cornsoybean meal diets supplemented with various levels of inorganic Se during a 37-d postweaning period. Eight groups were fed diets with 0, 2.5, 5.0, 7.5, 10, 15, 20 or 40 ppm Se provided as sodium selenite, while a ninth was offered the 0- and 40-ppm Se diets in separate feeders. Gains and feed intakes were similar during the trial for the 0- and 2.5-ppm Se diets. Both gain and feed intake declined as dietary Se levels above 5.0 ppm increased. At a dietary Se concentration of 40 ppm, feed consumption ceased within a few days of feeding and subsequent gains were negative. Pigs offered both the 0- and 40-ppm Se diets preferentially selected the basal as compared with the 40-ppm Se diet. When the feeders were switched at 28 d they refused the 40-ppm Se diet within a few hours. After a 17-d period, pigs fed the 20- or 40-ppm Se diet were not able to coordinate their walk, with many exhibiting an inability to stand. Alopecia was demonstrated in pigs fed 15 ppm Se or higher at 17 d, but was evident in the 5.0-ppm group at 37 d. At the termination of the trial, abnormal hoof formation at the coronary band was evident in pigs fed diets containing Se greater than or equal to 5 ppm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Feed associated haemorrhagic disorder in pigs accompanied by pancreatic lesions

The introduction of a new batch of feed to 400 pigs aged five to eight weeks resulted in 38 deaths and further morbidity associated with multiple haemorrhages. Signs abated within two days of withdrawal of the feed. Widespread haemorrhages were present in many tissues including the pancreas. Additional pancreatic lesions comprised focal necrosis, atrophy and fibrosis of exocrine tissue. The condition was reproduced experimentally in pigs and vitamin K protected mice against the injurious effects of the feed. The cause was not determined but it is speculated that more than one toxic factor and an imbalance of nutritional factors may have been present in the diet.     

Selenium toxicity and porcine focal symmetrical poliomyelomalacia: description of a field outbreak and experimental reproduction.

An acute afebrile paretic condition was diagnosed in 18 of 225 feeder pigs between eight to ten weeks of age. Nine pigs died acutely, seven pigs were euthanatized and two appeared to recover. Macroscopic lesions in the ventral horns of the cervical and lumbar/sacral spinal cord enlargements consisted of focal, bilateral, depressed areas. Histopathologically, the lesion consisted of endothelial proliferation, glial cell reaction and microcavitation. Similar lesions were observed in some brain stem motor nuclei. High selenium levels were detected in the pig feed and in pig tissues and blood. Two of five experimental pigs fed a commercial grower ration and supplemented with 52 ppm selenium as sodium selenite developed paresis and paralysis after a 29 day feeding trial. Histopathological lesions of focal symmetrical poliomyelomalacia confined to the cervical and lumbar/sacral spinal cord enlargements, and identical to those in the field cases, were produced. Select brain stem motor nuclei were also affected.     

Prolonged feeding of high dietary levels of organic and inorganic selenium to gilts from 25 kg body weight through one parity

An experiment evaluated the selenosis effects from feeding high dietary Se levels of organic or inorganic Se sources to growing gilts with the dietary treatments continued through a reproductive cycle. A total of 88 gilts were allotted at 25 kg BW to two replicates in a 2 x 4 factorial arrangement in a randomized complete block design. Inorganic Se (sodium selenite) or organic (Se-enriched yeast) Se were added to diets at 0.3, 3, 7, or 10 ppm Se. At 105 kg BW, four gilts per treatment were killed and livers collected for Se analysis. At 8 mo of age, three gilts from each treatment group were bred and fed their treatment diet, with subsequent reproductive performance and selenosis effects evaluated. Serum collected at various intervals in gilts, sows, and progeny measured glutathione peroxidase activity and Se concentrations. Sow colostrum and milk was analyzed for their Se concentrations. Three pigs per treatment were killed before colostrum consumption and at weaning (14 d) and tissue collected for Se analysis. Gilt gains (P < 0.01) and feed intakes (P < 0.05) declined during the grower period as dietary Se level increased for both Se sources. Serum and liver Se concentrations increased as dietary Se level increased and was higher when organic Se was fed (P < 0.01). Sows fed dietary Se levels at > 7 ppm had lower gestation weights (P < 0.05) and lower lactation feed intakes (P < 0.05). As Se level increased, sows fed organic Se had a lower number of live pigs born (P < 0.05) and weaned fewer pigs (P < 0.05) with lower litter gains (P < 0.05) than did sows fed inorganic Se. Colostrum and milk Se concentrations increased as dietary Se levels increased particularly when organic Se was fed (P < 0.01). Neonatal and weanling pig tissue Se and serum Se concentrations increased as dietary Se level increased and when organic Se was fed, resulting in interaction responses (P < 0.01). Pigs nursing sows fed > 7 ppm inorganic Se had hoof separation and alopecia, with the severity being greater when sows were fed the inorganic Se source. These results suggest that both the organic and inorganic Se sources were toxic when fed at 7 to 10 ppm for a prolonged period, but organic Se seemed to express the selenotic effects more on reproductive performance, whereas inorganic Se was more detrimental during lactation.     

Effect of feed withdrawal prior to slaughter on prevalence of gastric ulcers in pigs

OBJECTIVE: To determine whether withdrawing feed from pigs prior to slaughter had any effects on prevalence or severity of gastric ulcers. DESIGN: Split-plot design. ANIMALS: 873 pigs. PROCEDURES: At the finishing barn, pigs were assigned to 30 pens. Feed withdrawal times (0, 12, or 24 hours) were assigned to pens at random, and pigs in each pen were marketed in 3 groups over a period of 4 weeks. The first marketing group consisted of the 10 heaviest pigs in each pen, the second consisted of the next 10 heaviest, and the third consisted of all remaining pigs. Feed was withheld from all pigs in each pen prior to removal of each marketing group. Thus, feed was withheld once, twice, or 3 times for pigs in the first, second, and third marketing groups, respectively. RESULTS: Feed withdrawal time was not significantly associated with ulcer score at the time of slaughter. Ulcer scores and prevalence of chronic damage were higher in the third marketing group, regardless of feed withdrawal time. Prevalence of severe damage, prevalence of chronic damage, and prevalence of esophageal constriction increased as carcass weight decreased. No pigs died of gastric ulceration. CONCLUSION AND CLINICAL RELEVANCE: Results suggest that withdrawal of feed from pigs prior to slaughter does not increase damage to the stomach and that repeated feed withdrawal does not result in fatal gastric ulceration.     

Vascular ultrastructure and DNA fragmentation in swine infected with Shiga toxin-producing Escherichia coli

Shiga toxins (Stx) produced by Escherichia coli cause systemic vascular damage that manifests as edema disease in swine and hemolytic uremic syndrome in humans. In vitro, Stx inhibit protein synthesis and, depending on circumstances, induce necrosis, apoptosis, or both. The mechanism of in vivo Stx-mediated vascular damage is not known. The ability of Stx to cause apoptosis of vasculature in vivo was studied in pigs with edema disease that was produced by oral inoculation with Stx-producing E. coli. Arterioles of ileum and brain were evaluated by terminal dUTP nick-end labeling (TUNEL) assay for DNA fragmentation in myocytes (10 infected pigs, 5 control pigs) and by transmission electron microscopy for ultrastructural changes characteristic of apoptosis (17 infected pigs, 8 control pigs). In comparison with controls, increased numbers of TUNEL-positive arterioles were detected in 6/10 (60%) subclinically affected pigs 14-15 days after inoculation. Ultrastructurally, lesions in myocytes consisted of lysis (necrosis), with cytoplasmic debris and nuclear fragments contained between intact basement membranes. Endothelial cell changes ranged from acute swelling to necrosis and detachment from basement membrane. Subclinically affected pigs (n = 14) tended to have changes predominantly in myocytes, whereas pigs with clinical illness (n = 3) more commonly had changes in endothelial cells. The arteriolar lesions and clinical signs of edema disease are attributed to the effects of Stx on vasculature. Therefore, our findings suggest that the Stx-induced arteriolar lesions seen in this study were primarily necrotic, not apoptotic. We suspect that necrosis was the principal cause of the DNA fragmentation detected.     

Effects of dietary Selenomethionine supplementation on growth performance,antioxidant status,plasma selenium concentration,and immune function in weaning pigs

Background:This study was designed to evaluate the efficacy of DL-selenomethionine(DL-SeMet) supplementation on growth performance,antioxidant status,plasma selenium(Se) concentration,and immune function of weaning pigs.216 weaning pigs were randomly allocated to 6 treatments with 6 replicates each according to a complete randomized block design.Each replicate had six pigs.Diet of group one was corn-soybean basal diet without any additional Se supplement.Group 2 was supplemented with 0.3 mg/kg of Se from sodium selenite.Groups 3-6 were supplemented with 0.1,0.3,0.5,and 0.7 mg/kg of Se from DL-SeMet,respectively.The trial lasted for 42 days.Results:Pigs supplemented with 0.3 and 0.7 mg/kg DL-SeMet obtained better feed gain ratio(P 0.05).The best antioxidant ability(serum,liver,and muscle) was shown in 0.1-0.3 mg/kg DL-SeMet groups(P 0.05).The plasma Se concentration increased as the dietary DL-SeMet level elevated.The immunity among groups was not affected.Conclusions:DL-SeMet supplementation in the diet significantly improved the growth performance,antioxidant ability and plasma Se content of weaning pigs.DL-SeMet can replace sodium selenite in the diet of weaning pigs.     

Vascular lesions in nine Göttingen minipigs with thrombocytopenic purpura syndrome

Tissues from 9 G?ttingen minipigs, aged 7 weeks to 1 year, with clinically diagnosed thrombocytopenic purpura syndrome were examined microscopically. All pigs had a history of spontaneous cutaneous purpura that was generally accompanied by disseminated visceral hemorrhages. Hematologic abnormalities included anemia (8 out of 9 pigs) and thrombocytopenia (7 out of 9 pigs), with platelet counts consistently below 20,000/microl. Microscopically, degenerative vascular lesions with morphologic features of arteriosclerosis were present in all 9 pigs. Vascular lesions affected small- to medium-sized muscular arteries and arterioles in various organs and extraparenchymal tissues; vessels of the renal pelvis and coronary arteries were consistently involved. Microscopic lesions in small- to medium-sized muscular arteries consisted of neointimal proliferation, medial thickening, luminal stenosis, thrombosis, disruption and fragmentation of the internal elastic lamina, necrosis of the tunica media, and medial deposits of myxoid matrix material. Microscopic lesions in arterioles included concentric laminar thickening of vessel walls (onion-skin pattern), endothelial cell hypertrophy, smooth muscle cell vacuolation, necrosis of the tunica media, thrombosis, and partial to complete luminal stenosis. Arteritis and/or periarteritis were also noted in 4 out of 9 pigs. Additional microscopic lesions included membranoproliferative glomerulonephritis (3 out of 9), myocardial microinfarcts (4 out of 7), renal interstitial fibrosis (2 out of 9), extramedullary hematopoiesis (6 out of 9), and intracapillary hyaline thrombi (2 out of 9). Degenerative vascular lesions have not been previously described in G?ttingen minipigs with thrombocytopenic purpura syndrome. The etiopathogenesis of both the vascular lesions and thrombocytopenic purpura syndrome is currently unknown.     

An experimental model for subclinical edema disease (Escherichia coli enterotoxemia) manifest as vascular necrosis in pigs.

An experimental model for subclinical edema disease was developed in weanling pigs. In multiple experiments, 3-week-old pigs were weaned, then inoculated intragastrically with 10(10) colony-forming units of an SLT-IIv-positive strain of Escherichia coli originally isolated from a pig with edema disease (principals). Control pigs were inoculated with a nonpathogenic E coli strain. Of 39 principals, 8 developed clinical edema disease within 14 days after inoculation. However, 20 of 21 principals that did not develop clinical signs of edema disease, but were submitted for necropsy examination at 14 days after inoculation, had characteristic vascular lesions of edema disease. Vascular lesions, found principally in ileum and brain, consisted of segmental necrosis of myocytes in the tunica media of small arteries and arterioles. None of the pigs inoculated with a nonpathogenic strain of E coli developed edema disease or vascular lesions. None of the principals necropsied at 2 days after inoculation had vascular lesions. Development of vascular lesions by 14 days after inoculation was used as the end point for detecting subclinical edema disease in the model.