The Salmonella pathogenicity island 1 and Salmonella pathogenicity island 2 type III secretion systems play a major role in pathogenesis of systemic disease and gastrointestinal tract colonisation of Salmonella enterica serovar Typhimurium in the chicken
Résumé
Salmonella enterica serovar Typhimurium infection of chickens is a major public and animal health problem. In young chicks S. Typhimurium infection results in severe systemic infection, in older chicks infection results in prolonged gastrointestinal tract colonisation. Here we determined the role of the Salmonella pathogenicity island 1 (SPI-1) and 2 (SPI-2) type III secretion systems (TTSS) in systemic infection and gastrointestinal tract colonisation of the chicken though experimental infection of chicks with a S. Typhimurium strain with mutations in the genes encoding the secretion system machinery of SPI-1 (spaS) and SPI-2 (ssaU) that prevent secretion of effector proteins. In one-day-old chicks mutation of SPI-2 lead to a decrease in both systemic bacterial numbers and pathology, though no difference in gastrointestinal numbers was observed. Mutation of SPI-1 had little effect in one-day old chicks. In one-week-old animals the SPI-2 mutants could not be detected systemically and colonised the gastrointestinal tract only in low numbers in comparison to the parent strain and was cleared in one week. The SPI-1 mutant showed greatly reduced levels of systemic infection, and colonised the gastrointestinal tract at a lower level than the parent strain. The findings show that the SPI-2 TTSS is required for systemic S. Typhimurium infection in both infection models, and that it plays a significant role in gastrointestinal colonisation. The SPI-1 system has is involved in both systemic infection and gastrointestinal colonisation, but does not appear absolutely essential for either infection process.
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