Chao Wu, Zhewen Zhang, Chao Kang, Qiang Zhang, Weifeng Zhu, Yadong Zhang, Hao Zhang, Jingfa Xiao, Meilin Jin
is a causative agent of erysipelas in animals and erysipeloid in humans. However, current information regarding pathogenesis remains limited. Previously, we identified two strains, SE38 and G4T10, which were virulent and avirulent in pigs, respectively. Here, to further study the pathogenic mechanism of , we sequenced and assembled the genomes of strains SE38 and G4T10, and performed a comparative genomic analysis to identify differences or mutations in virulence-associated genes. Next, we comparatively analyzed 25 virulence-associated genes in SE38 and G4T10. Compared with that of SE38, the gene of the G4T10 strain lacked 120 bp, encoding repeat units at the C-terminal of SpaA. To examine whether these deletions or splits influence virulence, these 120 bp were successfully deleted from the gene in strain SE38 by homologous recombination. The mutant strain displayed attenuated virulence in mice and decreased adhesion to porcine iliac artery endothelial cells, which was also observed using the corresponding mutant protein SpaA'. Our results demonstrate that SpaA-mediated adhesion between and host cells is dependent on its C-terminal repeat units.
