SPI-2 of Salmonella Typhimurium is not necessary for long term colonization of pigs

Date
2007-01-01
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Haesebrouck, Freddy
Boyen, F.
Volf, J.
Botteldoorn, N.
Adriaensen, C.
Hernalsteens, J.-P.
Ducatelle, R.
van Immerseel, F.
Heyndrickx, M.
Pasmans, F.
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Abstract

Unravelling the role of Salmonella virulence factors in the porcine host could greatly contribute to the development of control measures such as vaccination. The virulence genes located on the Salmonella Pathogenicity Island 2 (SPI-2) are indispensable for the induction of systemic disease and persistence in BALB/c mice. The role of this pathogenicity island in the pathogenesis of Salmonella Typhimurium infections in pigs is not documented. Therefore, in the present study, the interactions of a porcine field strain of Salmonella Typhimurium and a non-polar isogenic SPI-2 (D-ssrA) deletion mutant were compared in both in vitro and in vivo models. The ssrA mutant strain displayed decreased SPI-2 expression levels in vitro and was attenuated in a mouse model after oral inoculation. No difference was seen in the expression of SPI-1 related virulence genes. Through flowcytometric analysis, the ssrA mutant strain was found to be moderately attenuated in intracellular replication in porcine macrophages in vitro. In an infection experiment, 2 groups of 10 piglets were orally inoculated with the wild type or the ssrA mutant strain. The infection of the animals inoculated with the ssrA mutant strain followed a similar course as the animals infected with the wild type strain. At days 5 and 28 post inoculation, the animals of both groups were infected to the same extent in the gut and gut-associated lymphoid tissue, as well as in the mternal organs. These results suggest that SPI-2 of Salmonella Typhimurium may not contribute to the colonization of pigs to the same extent as it contributes to the colonization of BALB/c mice.

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