Abstract

Streptococcus suis is an important porcine bacterial pathogen and a zoonotic agent responsible for sudden death, septic shock and meningitis, of which serotype 2 is the most widespread, with serotype 14 also causing infections in humans in South-East Asia. Knowledge of its pathogenesis and virulence are almost exclusively based on these two serotypes. Though serotype 9 is responsible for the greatest number of porcine cases in Spain, the Netherlands and Germany, very little information is currently available regarding this serotype. Of the different virulence factors, the capsular polysaccharide (CPS) is required for S. suis virulence as it promotes resistance to phagocytosis and killing and masks surface components responsible for host cell activation. However, these roles have been described for serotypes 2 and 14, whose CPSs are structurally and compositionally similar, both containing sialic acid. Consequently, we evaluated herein the interactions of serotype 9 with host cells and the role of its CPS, which greatly differs from those of serotypes 2 and 14. Results demonstrated that serotype 9 adhesion to but not invasion of respiratory epithelial cells was greater than that of serotypes 2 and 14. Furthermore serotype 9 was more internalized by macrophages but equally resistant to whole blood killing. Though recognition of serotypes 2, 9 and 14 by DCs required MyD88-dependent signaling, in vitro pro-inflammatory mediator production induced by serotype 9 was much lower. In vivo, however, serotype 9 causes an exacerbated inflammatory response, which combined with persistent bacterial presence, is probably responsible for host death during the systemic infection. Though presence of the serotype 9 CPS masks surface components less efficiently than those of serotypes 2 and 14, the serotype 9 CPS remains critical for virulence as it is required for survival in blood and development of clinical disease, and this regardless of its unique composition and structure.

Highlights

  • Streptococcus suis is an important encapsulated bacterial pathogen of young piglets and a zoonotic agent causing a variety of pathologies including sudden death, septic shock and meningitis [1]

  • Previous studies have demonstrated that deletion of various capsular polysaccharide (CPS) biosynthesis genes from serotypes 2 and 14 results in a non-encapsulated phenotype [3, 17, 18, 21, 22, 49]

  • The serotype 9 wild-type strain possessed a layer of CPS at its surface, indicative of being well-encapsulated (Fig 2A), that is similar to that of the serotype 2 wild-type P1/7 strain and serotype 14 wild-type DAN13730 strain used [3, 21, 35]

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Summary

Introduction

Streptococcus suis is an important encapsulated bacterial pathogen of young piglets and a zoonotic agent causing a variety of pathologies including sudden death (pigs), septic shock (humans) and meningitis (both species) [1]. Of the thirty-five described serotypes, serotype 2 is the most widespread and virulent, being responsible for the majority of porcine and human cases of infection [2]. Serotype 14 is an emerging threat to human health in South-East Asia [2]. Other than a few reports on serotype 14 [3, 4], serotype 2 remains by far the most studied serotype, with current understanding of the S. suis pathogenesis and virulence almost exclusively based on it [5, 6]. Together with serotypes 2 and 14, serotype 9 has emerged in Europe in recent years and is presently responsible for the greatest number of porcine cases of S. suis infection in Spain, the Netherlands and Germany [2]. Very few studies have addressed the interactions of this serotype with host cells [10,11,12]

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