Assessment of the pathogenesis of Streptococcus suis type 2 infection in piglets for understanding streptococcal toxic shock-like syndrome, meningitis, and sequelae

- Piglets were used as animal model for the human Streptococcus suis type 2 virulent 05ZYH33 strain.
- Different clinical symptoms with septic-like shock or prostration syndrome, and the action impairment appeared in the infected animals.
- The infected piglets progress into septic-like shock or prostration are closely related to the degrees of bacteremia and cytokine secretion.
- TLR1 and TLR2 polymorphisms are found in the animals with different syndromes.

Streptococcus suis type 2 (SS2) is an zoonotic pathogen that had caused outbreaks in 1998 and 2005 in China. It is still not very clear how the disease progresses into the streptococcal toxic shock-like syndrome (STSLS) or meningitis, as well as the sequelae from the survivals. The present study used piglets as infection model to systematically investigate the pathogenesis of the infection caused by the SS2 strain 05ZYH33. The infected piglets showed joint swelling, lameness, and crouch at beginning, then developed into septic-like shock syndrome (SLSS) or prostration syndrome, at last the survivals showed physical activity impairment. The morbidity and mortality were 100% (71% for SLSS, 29% for prostration syndrome) and 29%, respectively. The pigs exhibiting SLSS had deep invasive infections in tissues and organs, and displayed more severe bacteremia and cytokine secretion in the bloodstream and organs than pigs with prostration syndrome. Moreover, the polymorphisms in the toll-like receptor 1 (TLR1) and TLR2 genes varied between the pigs affected with SLSS and prostration syndrome. Several lines of evidence indicated that SS2 infection progression into SLSS or relatively lighter prostration syndrome in pigs is closely related to the degrees of bacteremia and cytokine storm, which may be inherently determined by the diversity of innate immunity-associated genes. Furthermore, brain lesions, such as venous thrombosis, may directly contribute to the sequelae in human cases, were identified in the pigs. These results might help us to further understand the pathogenesis of SS2 in humans.