Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SWINE DISEASES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed2002

Correlations between lung proinflammatory cytokine levels, virus replication, and disease after swine influenza virus challenge of vaccination-immune pigs.

During experimental infection of pigs with swine influenza virus (SIV), there is a strong temporal correlation between peak virus titers in the lungs, levels of different proinflammatory cytokines in bronchoalveolar lavage (BAL) fluids, and disease. Vaccination against SIV can greatly reduce or prevent virus replication after challenge and the resulting disease. Here, we took advantage of pigs from vaccination-challenge experiments, with different degrees of virological and clinical protection, to further correlate SIV replication with cytokines and disease. Forty-nine pigs were vaccinated twice with a commercial inactivated SIV vaccine or with experimental vaccines, and 35 control pigs were not vaccinated. Between 2 and 4 weeks after the last vaccination, all pigs were challenged intratracheally with SIV. Twenty-four hours after the challenge, we determined body temperatures, respiratory scores, lung virus titers, and neutrophils and cytokines in BAL fluids. Interferon-alpha (IFN-alpha), tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), and -6 (IL-6) were determined by bioassay, and IL-8 by a commercial ELISA. The results were analyzed for three comparison groups. The unvaccinated control pigs (group 1, n = 35) were positive for all or most parameters examined. Vaccinated pigs with challenge virus replication in the lungs (group 2, n = 28) had slightly lower virus titers than the challenge control pigs, and clear reductions in disease severity and mean titers of all five cytokines, but neutrophil numbers were not affected. Vaccinated pigs without detectable virus replication (group 3, n = 21) were largely protected against clinical signs and neutrophil infiltration. Mean levels of IFN-alpha, TNF-alpha, and IL-6, but not IL-1 or IL-8, were lower than in both other groups. Virus titers in the lungs of individual pigs showed highly significant correlations with IFN-alpha and IL-6, and lower correlations with TNF-alpha and IL-8. Clinical signs were most closely associated with IFN-alpha, IL-6, and TNF-alpha. The relationship between disease and IL-8 or IL-1 was much weaker. Our data provide further evidence for a role of IFN-alpha, TNF-alpha, and IL-6 in the pathogenesis of SIV. The similarities with cytokine profiles during human influenza virus infection are discussed.

Animals↗
PubMed2002

Characterization of neutralization sites on the circulating variant of swine vesicular disease virus (SVDV): a new site is shared by SVDV and the related coxsackie B5 virus.

Using a panel of new monoclonal antibodies (mAbs), five neutralizing, conformation-dependent sites have been identified on the antigenic variant of swine vesicular disease virus (SVDV) circulating currently. In studies on the antigenic conservation of these sites, the four antigenic/genetic groups of SVDV described showed distinguishable patterns, confirming this classification. By sequencing mAb-resistant mutants, the five sites have been mapped precisely and localized on a three-dimensional model of the SVDV capsid. All were found to be orientated, to a different extent, towards the external surface of the capsid. Three of the five sites, located in VP1, VP2 and VP3, correspond to epitopes identified previously in historic isolates as sites 1, 2a and 3b, respectively. Another site, site IV, which maps to position 258 of VP1, corresponds to an epitope reported recently and is described in this study to be specific for isolates of the most recent antigenic group of SVDV. A fifth site is described for the first time and corresponds to the unique neutralizing site that is common to both SVDV and coxsackie B5 virus; it maps to positions 95 and 98 of VP1, but may also include positions nearby that belong to site 1 on the BC-loop of VP1, suggesting the classification of site Ia. These results may have useful diagnostic and epidemiological applications, since mAbs to the new conserved site Ia provide universal reagents for SVDV detection systems, while the specificity of mAbs to site IV make them unique markers for the most recent strains of SVDV.

Animals↗
PubMed2000

The coxsackie-adenovirus receptor (CAR) is used by reference strains and clinical isolates representing all six serotypes of coxsackievirus group B and by swine vesicular disease virus.

Group B coxsackieviruses are etiologically linked to many human diseases, and cell surface receptors are postulated to play an important role in mediating their pathogenesis. The coxsackievirus adenovirus receptor (CAR) has been shown to function as a receptor for selected strains of coxsackievirus group B (CVB) serotypes 3, 4, and 5 and is postulated to serve as a receptor for all six serotypes. In this study, we demonstrate that CAR can serve as a receptor for laboratory reference strains and clinical isolates of all six CVB serotypes. Infection of CHO cells expressing human CAR results in a 1000-fold increase in CVB progeny virus titer compared to mock transfected cells. CAR was shown to be a functional receptor for swine vesicular disease virus (SVDV), as CHO-CAR cells but not CHO mock transfected controls were susceptible to SVDV infection, produced progeny SVDV, and developed cytopathic effects. Moreover, SVDV infection could be specifically blocked by monoclonal antibody to CAR (RmcB). SVDV infection of HeLa cells was also inhibited by an anti-CD55 MAb, suggesting that this virus, like some CVB, may interact with CD55 (decay accelerating factor) in addition to CAR. Finally, pretreatment of CVB or SVDV with soluble CAR effectively blocks virus infection of HeLa cell monolayers.

Animals↗
PubMed1982

congenital heart diseases in swine.

One hundred twenty-two congenital cardiac anomalies were diagnosed in 83 pigs (4.35%) during necropsies of 1906 pigs from one day to four years of age during an 11-month period. The incidence of cardiac malformation was higher at 29 to 56 days of age. Of the 83 pigs with cardiac anomalies, 47 (56%) were male and 36 (44%) were female, and of these, 15 (18%) were purebred and 68 (82%) were crossbred pigs. Of the 15 purebred pigs with cardiac malformation, there were seven Landrace pigs, four Large White pigs, three Duroc Jersey pigs, and one Yorkshire pig; whereas 94% of the 68 crossbred pigs were crossbred among Landrace, Duroc Jersey, and Large White. The 122 cardiac anomalies found in the 83 pigs were: dysplasia of the tricuspid valve in 42 pigs, atrial septal defect in 31 pigs, subaortic stenosis in 22 pigs, ventricular septal defect in nine pigs, persistent common atrioventricular canal in eight pigs, malformation of the moderator band in seven pigs, persistent vena cava in one pig, persistent truncus arteriosus in one pig, and pulmonary stenosis in one pig. The pathological features of the anomalies in swine were similar to those described in small animals and in man. The findings indicate that spontaneous porcine cardiac anomalies might provide models for cardiovascular investigators to study the etiology and pathogenesis of congenital heart diseases in man and other animals.

Animals↗
PubMed1981

[Control of veterinary communicable diseases in swine and fattening cattle stocks by serological testing of slaughtered animal blood samples].

Economy of prophylactic haemoserological control of pig stocks in a district as well as of a sow breeding unit and of cattle stocks on two industrialised fattening farms has been enhanced by including blood samples from routine slaughtering. Preliminary organisational experience is reported in this paper. The samples collected samples collected from normally slaughtered selected sows may contribute to an improvement of veterinary production control.

Abattoirs↗
PubMed1975

[Pathomorphological changes in a disease in swine caused by feeding bacterial-contaminated 1-lysine].

Studied were the lesions in the parenchymal organs and the hormonal glands in 20 pigs spontaneously died as a result of feeding with 1-lysine that had been contaminated with bacteria. The gross changes consisted of the enlargement and dark red coloration of the liver, gastroenteritis, hyperemia and hemorrhages in the kidneys and heart, oedema of the lungs and the wall of the gall bladder. Histologically, in the acute cases the liver showed hyperemia, pericapillary oedema, and granular dystrophia; in the subacute cases there were toxic dystrophy with the activation of the reticulo-endothelial system and subserous oedema in the gall bladder. The kidneys presented hyperemia, hemorrhages, and decreased volume of the glomeruloses in the subacute course of the disease. In terms of their function the heart, lungs, and kidneys displayed hemodynamic disturbances, and in the thyroid there were histologically changes characteristic of a follicular collapse. It is believed that the morphologic changes in the viscera investigated were due not to the intake of lysine itself, but to the effect of toxins produced by the concomitant microflora and the toxic amins (metabolites of the amino acids).

Animal Feed↗
PubMed2000

Highly cited article published in the Veterinary Quarterly in 1991.

In early 1991, the Dutch pig industry was struck by the so-called mystery swine disease. Large-scale laboratory investigations were undertaken to search for the aetiological agent. We focused on isolating viruses and mycoplasmas, and we tested paired sera of affected sows for antibodies against ten known pig viruses. The mycoplasmas M. hysonoviae, M. hyopneumoniae, and Acheloplasma laidlawii, and the viruses encephalomyocarditis virus and porcine enterovirus types 2 and 7 were isolated from individual pigs. An unknown agent however, was isolated from 16 of 20 piglets and from 41 of 63 sows. This agent was characterized as a virus and designated Lelystad virus. No relationship between this virus and other viruses has yet been established. Of 165 sows reportedly affected by the disease, 123 (75 per cent) seroconverted to Lelystad virus, whereas less than 10 per cent seroconverted to any of the other virus isolates or to known viral pathogens. Antibodies directed against Lelystad virus were also found in pigs with mystery swine disease in England, Germany, and the United States. We conclude that infection with Lelystad virus is the likely cause of mystery swine disease.

Animals↗
PubMed1973

Mycoplasma hyorhinis swine arthritis. 3. Modified disease in Piney Woods swine.

Piney Woods miniature swine, when injected with Mycoplasma hyorhinis, develop an acute arthritis. The disease in these animals is limited clinically, microbiologically, and pathologically to a mild acute illness without the more chronic and destructive features noted in a previous study of the experimental disease in Yorkshire swine.

Acute Disease↗