Increased production of suilysin contributes to invasive infection of the Streptococcus suis strain 05ZYH33

Abstract

Streptococcus suis serotype 2 (SS2) is widely recognized in the veterinary world as the cause of rapidly progressive and fatal sepsis in infant pigs, manifested with meningitis, polyarthritis and pneumonia. It has evolved into a highly infectious strain, and caused two large-scale outbreaks of human epidemic in China, characterized bytypical toxic-shock syndrome and invasive infection. However, the molecular basis of virulence of this emerging zoonotic pathogen is still largely unknown. The present study shows that the sequence type (ST)7 epidemic strain S. suis 05ZYH33 causes higher mortality, higher necrosis of polymorphonuclear neutrophils and a significantly higher damage to human umbilical vein endothelial cells compared to the non-epidemic strain S. suis 1940. These differences appear to associate with the enhanced secretion of suilysin (sly) by S. suis 05ZYH33 compared to the non-epidemic strain 1940. Inclusion of additional strains confirmed that the epidemic ST7 strains produce more sly protein (mean, 1.49 g/ml; range, 0.76–1.91 g/ml) than non-epidemic strains (mean, 0.33 g/ml; range, 0.07–0.94 g/ml), and this difference is significant (P<0.001). The nonpolar mutant strain S. suis Δsly, constructed from the epidemic ST7 strain S. suis 05ZYH33 confirmed the role of sly on the enhanced virulence of S. suis ST7 strains. These findings suggest that increased sly production in S. suis 05ZYH33 facilitates penetration to the epithelium and its survival in the bloodstream, thereby contributing to the invasive infection.

Suilysin-induced Platelet-Neutrophil Complexes Formation is Triggered by Pore Formation-dependent Calcium Influx

“…Moreover, ST-7 strains were more toxic to human peripheral blood mononuclear cells (PBMCs) than ST-1 strains (mainly referring to the European virulent strains)26. In particular, we have previously shown that the ST-7 strains produced more SLY than the non-epidemic strains, contributing to invasive infection27. Therefore, SLY may be a potential therapeutic target for preventing S. suis -mediated platelet activation, thrombocytopenia, liver failure and purpura gangrenosa.…”

“…The isogenic sly mutant Δsly was constructed in our previous study27. The Canadian avirulent strain 1330, which does not express SLY, was donated by Prof Marcelo Gottschalk (Université de Montréal).…”

Amentoflavone Ameliorates Streptococcus suis-Induced Infection In Vitro and In Vivo

“…SLY was shown to contribute to the development of bacterial meningitis and the increased mortality in mouse infection models (9). S. suis with an increased SLY production caused higher mortality in intraperitoneally infected mice than a nonvirulent strain, indicating that an increase in SLY production was associated with an enhanced S. suis virulence (10). Although the role of SLY in its contribution to human SS2 infections is not fully understood, SLY-positive strains have been reported to result in more severe symptoms than SLY-negative strains (11,12).…”

Initial steps of the pathogenesis of the infection caused byStreptococcus suis: fighting against nonspecific defenses

“…However, the fact that many virulent serotype 2 strains (mainly from North America) as well as virulent strains belonging to other serotypes are not able to produce the suilysin, seems to indicate that this toxin does not play a critical role in virulence . Although it has been recently reported that increased suilysin production in virulent S. suis facilitates survival in mouse bloodstream after intraperitoneal infection , a previous work has shown that mutants lacking the suilysin are as virulent as the wild‐type strain after an aerosol infection in pigs . Confusing observations about the role of the suilysin as a virulence factor in both the early infection and meningitis caused by S. suis are due to the use of different animals models.…”