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

Abstract

Streptococcus suis (S. suis) is a family of pathogenic gram-positive bacterial strains that represents a primary health problem in the swine industry worldwide. S. suis is also an emerging zoonotic pathogen that causes severe human infections clinically featuring with varied diseases/syndromes (such as meningitis, septicemia, and arthritis). Over the past few decades, continued efforts have made significant progress toward better understanding this zoonotic infectious entity, contributing in part to the elucidation of the molecular mechanism underlying its high pathogenicity. This review is aimed at presenting an updated overview of this pathogen from the perspective of molecular epidemiology, clinical diagnosis and typing, virulence mechanism, and protective antigens contributing to its zoonosis.

Keywords: Streptococcus suis; pathogenesis; zoonosis.

Figure 1. Global epidemiology of human SS2 infections. Countries/regions with human cases of SS2 infections were labeled and highlighted in yellow. Adapted from references and with permission.

Figure 2. Circular diagram and pan-genome analyses of SS2 genome. (A) Circular diagram of representative SS2 genome. (B) Pan-genome analyses of S. suis 2 species.

Figure 3. Characterization of S. suis and its natural host piglets. (A) Colony phenotype of S. suis serotype 2 grown on THB plate with 5% sheep blood. (B) Gram staining analyses of S. suis serotype 2 grown in liquid THB media. It was adapted from reference with permission. (C) Scanning electronic microscopic analyses of S. suis serotype 2 collected from overnight culture in THB media. (D) Phenotypic characterization of the reservoir of S. suis serotype 2, piglets maintained in backyard.

Figure 4. Clinical syndromes, genetic basis and working model for streptococcal toxic shock-like syndrome (STSLS) caused by S. suis 2. (A) 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 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. The two genetic elements of the transposable 89K pathogenicity island^, have been functionally defined: one is SalK-SalR (renamed as SuiK-SuiR¹⁵¹) TCS with requirement for full virulence, and other is VirD4-VirB4 T4SS-like system associated with clinical manifestation of STSLS in mouse model. (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. CNS, central nervous system. Integrated and modified from references , , , , , and with permission.