SnaPshot based genotyping of the RYR1 mutation in Portuguese breeds of pigs

The porcine stress syndrome or malignant hyperthermia is an inherited autosomic recessive disease, which results in neuromuscular disorders leading to death in homozygous individuals and is associated with deterioration of meat quality. The defect in susceptible animals results from modifications in the calcium release channel or Ryanodine Receptor (RYR1), with a mutation leading to a C to T transition in nucleotide 1843 of the gene. The objective of this work was to develop a method based on analysis of SNPs to detect the mutation described in the RYR1 locus in pigs, and study polymorphisms of the gene in four exotic (Large White, Landrace, Duroc and Pietrain) and three native (Bísaro, Alentejano and Malhado de Alcobaça) breeds of pigs in Portugal. The method was successful in identifying the mutation by analysis of SNPs, and results indicate a high incidence of the mutant allele in Pietrain (0.75) and, to a lesser degree, in Malhado de Alcobaça (0.34) and Landrace (0.28); frequencies in Alentejano, Bísaro and Large White ranged between 0.04 and 0.09. These results suggest the need to establish breeding programs aimed at eliminating the susceptibility allele from those populations.

Weaning

There is no RIGHT time to wean your baby from the breast. Family, friends, health professionals and even strangers might try to give you many reasons to stop nursing your baby, but the decision should depend on what you and your baby need and want. Get thoughts from people who know about breastfeeding and decide what is best for YOU and YOUR baby.

Seroprevalence of hepatitis e virus in domestic pigs and wild boars in Switzerland.

Hepatitis E is considered an emerging human viral disease in industrialized countries. Studies from Switzerland report a human seroprevalence of hepatitis E virus (HEV) of 2.6-21%, a range lower than in adjacent European countries. The aim of this study was to determine whether HEV seroprevalence in domestic pigs and wild boars is also lower in Switzerland and whether it is increasing and thus indicating that this zoonotic viral infection is emerging. Serum samples collected from 2,001 pigs in 2006 and 2011 and from 303 wild boars from 2008 to 2012 were analysed by ELISA for the presence of HEV-specific antibodies. Overall HEV seroprevalence was 58.1% in domestic pigs and 12.5% in wild boars. Prevalence in domestic pigs was significantly higher in 2006 than in 2011. In conclusion, HEV seroprevalence in domestic pigs and wild boars in Switzerland is comparable with the seroprevalence in other countries and not increasing. Therefore, prevalence of HEV in humans must be related to other factors than prevalence in pigs or wild boars.

Boar Presence Reduces Fighting in Mixed Slaughter-Weight Pigs

The article studies the presence of boars in reducing fighting in the groups of pigs therefore reducing skin blemishes.

Effect of Naltrexone on Relaxation Induced by Flank Pressure in Pigs

The study injected ten pigs with Naltrexone and ten pigs a saline injection to study the effects on relaxation. In the end, the study discovered that "treatment had no effect on the final degree of relaxation", but "pressure on the sides of a pig's body in a comfortable padded apparatus will induce pigs to relax".

The Welfare of pigs during Transport and Slaughter

The article researches "electric stunning, carbon dioxide stunning, pig behaviour during handling, return to sensibility, facility design, truck loading, density and transport stress".

Détermination des effets de l'administration des probiotiques sur l'attachement d'Escherichia Coli Entérotoxinogène F4 et l'expression de cytokines chez le porcelet sevré

Les diarrhées post-sevrages causées par des infections à Escherichia coli entérotoxinogène positif pour le fimbriae F4 (ETEC F4), entraînent des pertes économiques importantes chez les producteurs de porc. Depuis quelques années, l’utilisation de probiotiques, comme additif alimentaire pour prévenir ce type d’infection entérique et réduire les traitements aux antimicrobiens, suscite un intérêt grandissant en production porcine. Le but du présent travail est de déterminer l’influence de l’administration des probiotiques Pediococcus acidilactici (PA) et Saccharomyces cerevisiae boulardii (SCB) sur la colonisation et l’attachement des ETEC F4, l’accumulation de fluide intestinal et l’expression de cytokines dans l’iléon de porcelets sevrés. Dès la naissance, différentes portées de porcelets ont été affectées aux traitements suivants : PA, SCB, PA + SCB, témoin et témoin avec antibiotiques (ATB). Une dose quotidienne de probiotiques (1 × 109 UFC) a été administrée aux porcelets des groupes probiotiques durant la lactation et après le sevrage. Sept jours après le sevrage, à 28 jours d’âge, des porcelets positifs pour le récepteur intestinal spécifique pour F4 ont été infectés oralement avec une souche ETEC F4. Les porcelets ont été euthanasiés 24 heures après l’infection (jour 29) et différents échantillons intestinaux ont été prélevés. Chez les porcelets recevant des probiotiques, l’attachement des ETEC F4 à la muqueuse iléale était significativement diminué chez les groupes PA ou SCB en comparaison avec le groupe ATB. Finalement, l’expression de cytokines intestinales était plus élevée chez les porcs du groupe PA + SCB en comparaison avec les porcelets témoins. En conclusion, les résultats de cette étude suggèrent que l’administration de probiotiques pourrait être une alternative pour limiter les infections à ETEC F4 chez le porc.

Étude d'un variant de la toxine STb produite par Escherichia coli

Les E. coli entérotoxinogènes (ETEC) sont souvent la cause de diarrhée post-sevrage chez le porc. Deux types d’entérotoxines sont retrouvées chez les ETEC, soit les thermolabiles, comme la toxine LT, et les thermostables, comme EAST-1, STa et STb. Cette dernière est composée de 48 acides aminés et est impliquée dans la pathologie causée par les ETEC. Pour la première fois un variant de la toxine STb fut découvert dans une étude. Nous avons alors émis l’hypothèse qu’il y a présence de variants dans la population de souches ETEC du Québec. Dans les 100 souches STb+ analysées, 23 possédaient le gène de la toxine avec une variation dans la séquence génétique : l’asparagine était présente en position 12 remplaçant ainsi l’histidine. Une corrélation entre la présence du variant et la présence de facteurs de virulence retrouvés dans ces 100 souches ETEC étudiées a été effectuée. Ce variant semble fortement associé à la toxine STa puisque toutes les souches variantes ont hybridé avec le gène codant pour cette dernière. Étant donné sa présence répandue dans la population de souches ETEC du Québec, nous avons de plus émis l’hypothèse que ce variant a des caractéristiques biologiques altérées par rapport à la toxine sauvage. L’analyse par dichroïsme circulaire a montré que le variant et la toxine sauvage ont une structure secondaire ainsi qu’une stabilité similaires. Par la suite, l’attachement au récepteur de la toxine, le sulfatide, a été étudié par résonnance plasmonique de surface (biacore). Le variant a une affinité au sulfatide légèrement réduite comparativement à la toxine sauvage. Puisque l’internalisation de la toxine fut observée dans une étude précédente et qu’elle semble liée à la toxicité, nous avons comparé l’internalisation du variant et de la toxine sauvage à l’intérieur des cellules IPEC-J2. L’internalisation du variant dans les cellules est légèrement supérieure à l’internalisation de la toxine sauvage. Ces résultats suggèrent que le variant est biochimiquement et structurellement comparable à la toxine sauvage.

Systemic and regional hemodynamics in pigs with acute liver failure and the effect of albumin dialysis.

OBJECTIVE: Acute liver failure (ALF) is haemodynamically characterized by a hyperdynamic circulation. The aims of this study were to investigate the systemic and regional haemodynamics in ALF, to measure changes in nitric oxide metabolites (NOx) and to evaluate whether these haemodynamic disturbances could be attenuated with albumin dialysis. MATERIAL AND METHODS: Norwegian Landrace pigs (23-30 kg) were randomly allocated to groups as controls (sham-operation, n = 8), ALF (hepatic devascularization, n = 8) and ALF + albumin dialysis (n = 8). Albumin dialysis was started 2 h after ALF induction and continued for 4 h. Systemic and regional haemodynamics were monitored. Creatinine clearance, nitrite/nitrate and catecholamines were measured. A repeated measures ANOVA was used to analyse the data. RESULTS: In the ALF group, the cardiac index increased (PGT < 0.0001), while mean arterial pressure (PG = 0.02) and systemic vascular resistance decreased (PGT < 0.0001). Renal resistance (PG = 0.04) and hind-leg resistance (PGT = 0.003) decreased in ALF. There was no difference in jejunal blood flow between the groups. ALF pigs developed renal dysfunction with increased serum creatinine (PGT = 0.002) and decreased creatinine clearance (P = 0.02). Catecholamines were significantly higher in ALF, but NOx levels were not different. Albumin dialysis did not attenuate these haemodynamic or renal disturbances. CONCLUSIONS: The haemodynamic disturbances during the early phase of ALF are characterized by progressive systemic vasodilatation with no associated changes in metabolites of NO. Renal vascular resistance decreased and renal dysfunction developed independently of changes in renal blood flow. After 4 h of albumin dialysis there was no attenuation of the haemodynamic or renal disturbances.

Contractile response of femoral arteries in pigs with acute liver failure.

BACKGROUND: Acute liver failure (ALF) is characterized haemodynamically by a progressive hyperdynamic circulation. The pathophysiological mechanism is unknown, but impaired contractility of vascular smooth muscle may play an important role. The aim of this study was to evaluate the vascular response to stimulation with norepinephrine and angiotensin II in endothelium-denuded femoral artery rings. METHODS: Norwegian Landrace pigs weighing 27.1 +/- 0.5 kg (mean +/- sx (standard error of the mean)) were used. ALF was induced by performing a portacaval shunt followed by ligation of the hepatic arteries (n = 6). Sham-operated animals served as controls (n = 5). Cumulative isometric concentration contraction curves were obtained after in vitro stimulation of the femoral artery rings with either angiotensin II (10(-13) - 10(-5) mol/L) or norepinephrine (10(-13) - 10(-3) mol/L). RESULTS: Pigs suffering from ALF developed a hyperdynamic circulation with an increased ca^rdiac index (P = 0.017) and decreased systemic vascular resistance index (P = 0.015). Studies of the hind leg revealed a decreased vascular resistance index and increased blood flow compared to sham-operated controls (P = 0.003 and P = 0.01, respectively). Angiotensin II caused a concentration-dependent contraction of the arterial segments, with no significant differences in vascular responses between the two groups. Maximum force generated did not differ (55 +/- 7 versus 56 +/- 7 mN, P = 0.95). Furthermore, there were no differences for norepinephrine in the cumulative concentration-response curves and the maximum contractile force was not significantly different (87 +/- 8 versus 93 +/- 16 mN, P = 0.55). CONCLUSIONS: This study documents for the first time that there are no signs of endothelium-independent peripheral vascular hyporesponsiveness to angiotensin II and norepinephrine in pigs with ALF.

Effect of albumin dialysis on intracranial pressure increase in pigs with acute liver failure: a randomized study.

BACKGROUND: Increased intracranial pressure (ICP) worsens the outcome of acute liver failure (ALF). This study investigates the underlying pathophysiological mechanisms and evaluates the therapeutic effect of albumin dialysis in ALF with use of the Molecular Adsorbents Recirculating System without hemofiltration/dialysis (modified, M-MARS). METHODS: Pigs were randomized into three groups: sham, ALF, and ALF + M-MARS. ALF was induced by hepatic devascularization (time = 0). M-MARS began at time = 2 and ended with the experiment at time = 6. ICP, arterial ammonia, brain water, cerebral blood flow (CBF), and plasma inflammatory markers were measured. RESULTS: ICP and arterial ammonia increased significantly over 6 hrs in the ALF group, in comparison with the sham group. M-MARS attenuated (did not normalize) the increased ICP in the ALF group, whereas arterial ammonia was unaltered by M-MARS. Brain water in the frontal cortex (grey matter) and in the subcortical white matter at 6 hrs was significantly higher in the ALF group than in the sham group. M-MARS prevented a rise in water content, but only in white matter. CBF and inflammatory mediators remained unchanged in all groups. CONCLUSION: The initial development of cerebral edema and increased ICP occurs independently of CBF changes in this noninflammatory model of ALF. Factor(s) other than or in addition to hyperammonemia are important, however, and may be more amenable to alteration by albumin dialysis.

Neuropathological changes in the brain of pigs with acute liver failure.

Abstract Objective. Cerebral edema is a serious complication of acute liver failure (ALF), which may lead to intracranial hypertension and death. An accepted tenet has been that the blood-brain barrier is intact and that brain edema is primarily caused by a cytotoxic etiology due to hyperammonemia. However, the neuropathological changes in ALF have been poorly studied. Using a well characterized porcine model we aimed to investigate ultrastructural changes in the brain from pigs suffering from ALF. Materials and methods. Sixteen female Norwegian Landrace pigs weighing 27-35 kg were randomised into two groups: ALF (n = 8) and sham operated controls (n = 8). ALF was induced with an end-to-side portacaval shunt followed by ligation of the hepatic arteries. Biopsies were harvested from three different areas of the brain (frontal lobe, cerebellum, and brain stem) following eight hours of ALF and analyzed using electron microscopy. Results. Profound perivascular and interstitial edema were found in all three areas. Disruption of pericytic and astrocytic processes were seen, reflecting breakdown/lesion of the blood-brain barrier in animals suffering from ALF. Furthermore, neurons and axons were edematous and surrounded by vesicles. Severe damage to Purkinje neuron (necrosis) and damaged myelin were seen in the cerebellum and brain stem, respectively. Biopsies from sham operated animals were normal. Conclusions. Our data support the concept that vasogenic brain edema plays an important role in the development of intracranial hypertension in pigs with ALF.

Association of reduced extracellular brain ammonia, lactate, and intracranial pressure in pigs with acute liver failure.

We previously demonstrated in pigs with acute liver failure (ALF) that albumin dialysis using the molecular adsorbents recirculating system (MARS) attenuated a rise in intracranial pressure (ICP). This was independent of changes in arterial ammonia, cerebral blood flow and inflammation, allowing alternative hypotheses to be tested. The aims of the present study were to determine whether changes in cerebral extracellular ammonia, lactate, glutamine, glutamate, and energy metabolites were associated with the beneficial effects of MARS on ICP. Three randomized groups [sham, ALF (induced by portacaval anastomosis and hepatic artery ligation), and ALF+MARS] were studied over a 6-hour period with a 4-hour MARS treatment given beginning 2 hours after devascularization. Using cerebral microdialysis, the ALF-induced increase in extracellular brain ammonia, lactate, and glutamate was significantly attenuated in the ALF+MARS group as well as the increases in extracellular lactate/pyruvate and lactate/glucose ratios. The percent change in extracellular brain ammonia correlated with the percent change in ICP (r(2) = 0.511). Increases in brain lactate dehydrogenase activity and mitochondrial complex activity for complex IV were found in ALF compared with those in the sham, which was unaffected by MARS treatment. Brain oxygen consumption did not differ among the study groups. Conclusion: The observation that brain oxygen consumption and mitochondrial complex enzyme activity changed in parallel in both ALF- and MARS-treated animals indicates that the attenuation of increased extracellular brain ammonia (and extracellular brain glutamate) in the MARS-treated animals reduces energy demand and increases supply, resulting in attenuation of increased extracellular brain lactate. The mechanism of how MARS reduces extracellular brain ammonia requires further investigation.

L-ornithine phenylacetate attenuates increased arterial and extracellular brain ammonia and prevents intracranial hypertension in pigs with acute liver failure.

Hyperammonemia is a feature of acute liver failure (ALF), which is associated with increased intracranial pressure (ICP) and brain herniation. We hypothesized that a combination of L-ornithine and phenylacetate (OP) would synergistically reduce toxic levels of ammonia by (1) L-ornithine increasing glutamine production (ammonia removal) through muscle glutamine synthetase and (2) phenylacetate conjugating with the ornithine-derived glutamine to form phenylacetylglutamine, which is excreted into the urine. The aims of this study were to determine the effect of OP on arterial and extracellular brain ammonia concentrations as well as ICP in pigs with ALF (induced by liver devascularization). ALF pigs were treated with OP (L-ornithine 0.07 g/kg/hour intravenously; phenylbutyrate, prodrug for phenylacetate; 0.05 g/kg/hour intraduodenally) for 8 hours following ALF induction. ICP was monitored throughout, and arterial and extracellular brain ammonia were measured along with phenylacetylglutamine in the urine. Compared with ALF + saline pigs, treatment with OP significantly attenuated concentrations of arterial ammonia (589.6 +/- 56.7 versus 365.2 +/- 60.4 mumol/L [mean +/- SEM], P= 0.002) and extracellular brain ammonia (P= 0.01). The ALF-induced increase in ICP was prevented in ALF + OP-treated pigs (18.3 +/- 1.3 mmHg in ALF + saline versus 10.3 +/- 1.1 mmHg in ALF + OP-treated pigs;P= 0.001). The value of ICP significantly correlated with the concentration of extracellular brain ammonia (r(2) = 0.36,P< 0.001). Urine phenylacetylglutamine levels increased to 4.9 +/- 0.6 micromol/L in ALF + OP-treated pigs versus 0.5 +/- 0.04 micromol/L in ALF + saline-treated pigs (P< 0.001).Conclusion:L-Ornithine and phenylacetate act synergistically to successfully attenuate increases in arterial ammonia, which is accompanied by a significant decrease in extracellular brain ammonia and prevention of intracranial hypertension in pigs with ALF.

Transcriptional approach to study porcine tracheal epithelial cells individually or dually infected with swine influenza virus and Streptococcus suis

Background: Swine influenza is a highly contagious viral infection in pigs affecting the respiratory tract that can have significant economic impacts. Streptococcus suis serotype 2 is one of the most important post-weaning bacterial pathogens in swine causing different infections, including pneumonia. Both pathogens are important contributors to the porcine respiratory disease complex. Outbreaks of swine influenza virus with a significant level of co-infections due to S. suis have lately been reported. In order to analyze, for the first time, the transcriptional host response of swine tracheal epithelial (NPTr) cells to H1N1 swine influenza virus (swH1N1) infection, S. suis serotype 2 infection and a dual infection, we carried out a comprehensive gene expression profiling using a microarray approach. Results: Gene clustering showed that the swH1N1 and swH1N1/S. suis infections modified the expression of genes in a similar manner. Additionally, infection of NPTr cells by S. suis alone resulted in fewer differentially expressed genes compared to mock-infected cells. However, some important genes coding for inflammatory mediators such as chemokines, interleukins, cell adhesion molecules, and eicosanoids were significantly upregulated in the presence of both pathogens compared to infection with each pathogen individually. This synergy may be the consequence, at least in part, of an increased bacterial adhesion/invasion of epithelial cells previously infected by swH1N1, as recently reported. Conclusion: Influenza virus would replicate in the respiratory epithelium and induce an inflammatory infiltrate comprised of mononuclear cells and neutrophils. In a co-infection situation, although these cells would be unable to phagocyte and kill S. suis, they are highly activated by this pathogen. S. suis is not considered a primary pulmonary pathogen, but an exacerbated production of proinflammatory mediators during a co-infection with influenza virus may be important in the pathogenesis and clinical outcome of S. suis-induced respiratory diseases.