Towards control of Streptococcus iniae

Abstract

Streptococcus iniae is an emerging zoonotic pathogen; such infections generally occur through injuries associated with preparing whole fresh fish for cooking. Those infected to date have been of Asian descent, are usually elderly (average age 68 years), and have had >/=1 underlying conditions that may predispose them to infection. Studies of the foundations of growth characteristics of S. iniae and its interactions with piscine host cells have recently been complemented by molecular studies. Advances in molecular biology have allowed research groups to identify numerous virulence factors and to explore their roles in the progression of S. iniae infection. Many of these virulence factors are homologous to those found in the major human pathogen S. pyogenes. An increased understanding of the properties of these factors and their effect on the success of infection is leading to novel approaches to control S. iniae infection; in particular, vaccination programs at fish farms have reduced the reservoir of infection for additional clinical cases.

Figure

Virulence factors of Streptococcus iniae. A diagrammatic representation of a cell of S. iniae showing the regulatory genes involved in virulence factor expression (inside cell) and the virulence factors on the outside of the cell. In a clockwise direction, SiM protein (simA) expression is likely to be regulated by mgx. SiM protein binds immunoglobulin (Ig) and fibrinogen. C5a peptidase and interleukin-8 (IL-8) protease degrade their respective chemokines to impair phagocyte signaling. Production of the cytolysin streptolysin S (sag; SLS) is regulated by the sivS/R system. SLS lyses lymphocytes (L), erythrocytes (E), and neutrophils (N). The CAMP factor gene, cfi, is also regulated by sivS/R and is known to bind immunoglobulin by the Fc region. Capsular polysaccharide (cpsA; CPS) synthesis is controlled by sivS/R and is represented by a haze around the cell. Exopolysaccharide (EPS) is produced in excess and contributes to highly viscous growth. α–enolase degrades fibrin clots and promotes dissemination.