The role of SPI-1 and SPI-2 type three secretion systems in persistent Salmonella enterica serovar pullorum infections of chicken

Salmonella enterica serovar Pullorum causes a septicaemic, persistent, systemic disease of poultry known as Pullorum Disease (PD). PD causes high mortality in young birds with those that survive becoming carriers of the disease. Transmission between birds in the same generation is predominantly faecal-oral, with birds in subsequent generations becoming infected via vertical transmission. Groups of viralence genes on the Salmonella genome cluster in areas known as pathogenicity islands. A range of in vitro and in vivo techniques were used to assess the role of Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2) in the establishment and persistence of serovar Pulloram infection in the chicken. The results collectively suggest that serovar Pullorum does not promote the induction of a pro inflammatory immune response in the gut, but virulence factors encoded by SPI-1 lead to up regulation of IL-lbeta, IL-6, CXCLi1 and CXCLi2 to recruit phagocytes to the site of infection. Thereby, although not required for full- virulence, SPI-1 enables faster dissemination of serovar Pullorum to systemic sites. At systemic sites away from the gut, SPI-1 is responsible for down-regulation of the antimicrobial peptides avian beta-defensins 1, 3 and 5, and of CXCLi1. SPI-2 is responsible for maintaining sustainable intracellular numbers within macrophages, inhibiting nitric oxide synthesis and down-regulating IL-6 expression. SPI-1 and SPI-2 both contribute to the virulence of serovar Pullorum, enabling the establishment of a more rapid and stealthy infection in the chicken