Streptococcus suis infection: An emerging/reemerging challenge of bacterial infectious diseases?

Feng, Youjun; Zhang, Huimin; Wu, Zuowei; Wang, Shihua; Cao, Min; Hu, Dan; Wang, Changjun

Pathogens have evolved capacity to recruit/hijack host cell factors for their successful infections/invasions. So far, the majority Clinical visualization of a representative SS2-infected patient with streptococcal toxic shock-like syndrome. it clearly shows purpura and gangrenous changes on this patient's legs. Partially adapted from reference 9 with permission. (B) Genetic evidence that 89K pathogenicity island carries elements associated with bacterial virulence and the clinical consequence of streptococcal toxic shock-like syndrome. PFGe assay reveals Chinese epidemic strain 05ZYH33 is distinct from the international strain S10. 4 The two genetic elements of the transposable 89K pathogenicity island 23, 28 have been functionally defined: one is SalK-SalR (renamed as SuiK-SuiR 151 ) TCS with requirement for full virulence, 27 and other is virD4-virB4 T4SS-like system associated with clinical manifestation of STSLS in mouse model. 160 (C) The proposed model of the two-stage hypothesis for STSLS. SS2 gets into blood vessels in stage i and results in an early burst of proinflammatory factors and Th1 cytokine storms. Such kind of inflammatory super-responses lead to STSLS with death as early as 13 h after SS2 infection. in stage ii (i.e., several days post-infection), SS2 might use virulence factors like suilysin to cause disease, particularly meningitis. 94 CNS, central nervous system. integrated and modified from references 4, 23, 27, 28, 94, and 160 with permission.