Streptococcus suis serotype 2 mutants deficient in capsular expression

Abstract

Streptococcus suis serotype 2 is responsible for a wide variety of porcine infections. In addition, it is considered a zoonotic agent. Knowledge about the virulence factors for this bacterium is limited but its polysaccharide capsule is thought to be one of the most important. Transposon mutagenesis with the self-conjugative transposon Tn916 was used to obtain acapsular mutants from the virulent 5. suis type 2 reference strain 5735. Clones were screened by colony-dot ELISA with a monoclonal antibody specific for a type 2 capsular epitope and clones that failed to react with the antibody were characterized. Two mutants, 2A and 79, having one and two Tn916 insertions respectively, were chosen for further characterization. Absence of capsule was confirmed by coagglutination, capillary precipitation and capsular reaction tests and by transmission electron microscopy. Absence of capsular polysaccharides correlated with increased hydrophobicity and phagocytosis by both murine macrophages and porcine monocytes compared to the wild-type strain. Furthermore, both mutants were shown to be avirulent in murine and pig models of infection. Finally, mutant 2A was readily eliminated from circulation in mice compared to the wild-type strain, which persisted more than 48 h in blood. Thus, isogenic mutants defective in capsule production demonstrate the importance of capsular polysaccharides as a virulence factor for 5. suis type 2.

Loss of capsule among Streptococcus suis isolates from porcine endocarditis and its biological significance

“…Compared with the parent strains, the isogenic unencapsulated mutants of S. suis serotype 2 were more susceptible to phagocytosis by both macrophages and neutrophils (Benga et al, 2008;Chabot-Roy et al, 2006;Charland et al, 1998;Smith et al, 1999a). Moreover, capsule loss reduced the virulence of S. suis in both mouse and swine models of infection (Charland et al, 1998;Smith et al, 1999a).…”

“…Compared with the parent strains, the isogenic unencapsulated mutants of S. suis serotype 2 were more susceptible to phagocytosis by both macrophages and neutrophils (Benga et al, 2008;Chabot-Roy et al, 2006;Charland et al, 1998;Smith et al, 1999a). Moreover, capsule loss reduced the virulence of S. suis in both mouse and swine models of infection (Charland et al, 1998;Smith et al, 1999a). In contrast, Salasia et al (1995) and Benga et al (2004Benga et al ( , 2005 reported that isogenic unencapsulated mutants showed increased adherence to various types of cells, including porcine endothelial cells and human epithelial cells, when compared with the parent serotype 2 strains.…”

“…However, more than 50 % of the S. suis isolates from porcine endocarditis were shown to be untypable by agglutination tests (Katsumi et al, 1997), although a high percentage of isolates from meningitis and pneumonia were serotypable (Kataoka et al, 1993). Although the polysaccharide capsule is believed to be essential for the virulence of S. suis (Benga et al, 2008;Chabot-Roy et al, 2006;Charland et al, 1998;Smith et al, 1999a), these observations imply that many endocarditis isolates, especially those of serotypes 2 and 1/2, frequently lose their ability to synthesize capsules.To confirm this speculation, we investigated the capsule production of cps2J-positive isolates from porcine endocarditis and meningitis. Furthermore, the genetic backgrounds of several unencapsulated isolates and the biological significance of unencapsulation were examined.…”

Isolation and characterization of α-enolase, a novel fibronectin-binding protein from Streptococcus suis

“…Once in the bloodstream, S. suis resists phagocytosis and killing by neutrophils and monocytes (Chabot-Roy et al, 2006;Charland et al, 1998;Segura et al, 1998;Smith et al, 1999). In the event that S. suis fails to cause acute fatal septicaemia, bacteria are able to reach the CNS via different mechanisms that are only partially elucidated, such as adhesion to, with or without toxicity, and invasion of brain microvascular endothelial cells (BMEC) (Benga et al, 2005;Charland et al, 2000;Vanier et al, 2004) and/or choroid plexus epithelial cells (Tenenbaum et al, 2005(Tenenbaum et al, , 2006.…”

Production of Muraminidase-Released Protein (MRP), Extracellular Factor (EF) and Suilysin by field isolates of Streptococcus suis capsular types 2, 1/2, 9, 7 and 3 isolated from swine in France

“…The production of this S. suis haemolysin was evidenced in strains collected from diseased pigs, but its role has not been determined [19,27]. Moreover, other surface components may be implicated in the virulence of S. suis [4,11,20].…”