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Infect Immun. 2009 Jul;77(7):2866-75. doi: 10.1128/IAI.00039-09. Epub 2009 Apr 13.

Salmonella enterica serovar enteritidis pathogenicity island 1 is not essential for but facilitates rapid systemic spread in chickens.

Author information

1
Vaccine and Infectious Disease Organization, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.

Abstract

Salmonella enterica subsp. enterica serovar Enteritidis is a leading cause of human food-borne illness that is mainly associated with the consumption of contaminated poultry meat and eggs. To cause infection, S. Enteritidis is known to use two type III secretion systems, which are encoded on two salmonella pathogenicity islands, SPI-1 and SPI-2, the first of which is thought to play a major role in invasion and bacterial uptake. In order to study the role of SPI-1 in the colonization of chicken, we constructed deletion mutants affecting the complete SPI-1 region (40 kb) and the invG gene. Both DeltaSPI-1 and DeltainvG mutant strains were impaired in the secretion of SipD, a SPI-1 effector protein. In vitro analysis using polarized human intestinal epithelial cells (Caco-2) revealed that both mutant strains were less invasive than the wild-type strain. A similar observation was made when chicken cecal and small intestinal explants were coinfected with the wild-type and DeltaSPI-1 mutant strains. Oral challenge of 1-week-old chicken with the wild-type or DeltaSPI-1 strains demonstrated that there was no difference in chicken cecal colonization. However, systemic infection of the liver and spleen was delayed in birds that were challenged with the DeltaSPI-1 strain. These data demonstrate that SPI-1 facilitates systemic infection but is not essential for invasion and systemic spread of the organism in chickens.

PMID:
19364835
PMCID:
PMC2708567
DOI:
10.1128/IAI.00039-09
[Indexed for MEDLINE]
Free PMC Article

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