Histologic and bacteriologic findings in valvular endocarditis of slaughter-age pigs

Endocarditis lesions from 117 slaughter pigs were examined pathologically and etiologically in addition to 90 control hearts with cardiac valves. Lesions were located on the valves; however, the lesions had extended to the walls in 21 cases (18%). Lesions predominated on the mitral valve (59%). A total of 28 cases, from which no growth was obtained or a contamination flora was grown, were screened by fluorescence in situ hybridization (FISH) for bacteria (general bacterial probe) and probes specific for Streptococcus suis and Erysipelothrix rhusiopathiae, respectively. Using FISH, an additional 10 cases of endocarditis due to S. suis and E. rhusiopathiae were disclosed. Within lesions, streptococci predominated (53%) followed by E. rhusiopathiae (30%). Distinct features of both the lesions and the shape and localization of bacterial colonies were related to streptococci and E. rhusiopathiae. The propensity for streptococci to be localized on more than 1 valve in single hearts may be because S. suis–infected pigs tend to have been infected for a longer period compared with E. rhusiopathiae. Mineralization of endocarditis lesions was significantly associated with infection by streptococci, and was seen in 71% of the cases, whereas it was present in only 28% of lesions caused by E. rhusiopathiae. In addition, areas with mineralization were significantly correlated to the presence of a granulomatous reaction. Granulomatous endocarditis is likely a result of a foreign body reaction due to dystrophic mineralization. Local proliferation of valvular endothelial cells, found in 9 hearts in the current study, may increase the risk of developing thrombosing endocarditis in pigs. </jats:p

Phenotypic and genetic characterization of a novel phenotype in pigs characterized by juvenile hairlessness and age dependent emphysema

<p>Abstract</p> <p>Background</p> <p>A pig phenotype characterized by juvenile hairlessness, thin skin and age dependent lung emphysema has been discovered in a Danish pig herd. The trait shows autosomal co-dominant inheritance with all three genotypes distinguishable. Since the phenotype shows resemblance to the integrin β₆-/- knockout phenotype seen in mice, the two genes encoding the two subunits of integrin α_vβ₆, i.e. <it>ITGB6 </it>and <it>ITGAV</it>, were considered candidate genes for this trait.</p> <p>Results</p> <p>The mutated pig phenotype is characterized by hairlessness until puberty, thin skin with few hair follicles and absence of <it>musculi arrectores pili</it>, and at puberty or later localized areas of emphysema are seen in the lungs. Comparative mapping predicted that the porcine <it>ITGB6 </it>and<it>ITGAV </it>orthologs map to SSC15. In an experimental family (n = 113), showing segregation of the trait, the candidate region was confirmed by linkage analysis with four microsatellite markers. Mapping of the porcine <it>ITGB6 </it>and <it>ITGAV </it>in the IMpRH radiation hybrid panel confirmed the comparative mapping information. Sequencing of the <it>ITGB6 </it>and <it>ITGAV </it>coding sequences from affected and normal pigs revealed no evidence of a causative mutation, but alternative splicing of the <it>ITGB6 </it>pre-mRNA was detected. For both <it>ITGB6 </it>and <it>ITGAV </it>quantitative PCR revealed no significant difference in the expression levels in normal and affected animals. In a western blot, ITGB6 was detected in lung protein samples of all three genotypes. This result was supported by flow cytometric analyses which showed comparable reactions of kidney cells from affected and normal pigs with an integrin α_vβ₆monoclonal antibody. Also, immunohistochemical staining of lung tissue with an integrin β₆antibody showed immunoreaction in both normal and affected pigs.</p> <p>Conclusion</p> <p>A phenotype resembling the integrin β₆-/- knockout phenotype seen in mice has been characterized in the pig. The candidate region on SSC15 has been confirmed by linkage analysis but molecular and functional analyses have excluded that the mutated phenotype is caused by structural mutations in or ablation of any of the two candidate genes.</p

Refinement of a hematogenous localized osteomyelitis model in pigs

We have previously developed a model of localized osteomyelitis by injecting Staphylococcus aureus (S. aureus) unilaterally into the femoral artery of juvenile domestic pigs (Johansen et al., 2012; Nielsen et al., 2015). We used this model for the evaluation of bone-infection tracers applicable for positron emission tomography (PET) and single-photon emission computed tomography (SPECT) (Nielsen et al., 2015). However, several of the 40 kg pigs were euthanized prior to PET and SPECT scanning due to lameness, shallow respiration, fever and anorexia; the last three clinical signs indicating dissemination of S. aureus to the lungs and other internal organs. We therefore decided to refine our model in order to improve the success rate. We speculated that younger pigs might respond differently to inoculations. A total of ten female domestic pigs were included in our study, three with a body weight of 40 kg