This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Desin, T. S.
Right arrow Articles by Köster, W.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Desin, T. S.
Right arrow Articles by Köster, W.

 Previous Article  |  Next Article 

Infection and Immunity, July 2009, p. 2866-2875, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00039-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Salmonella enterica Serovar Enteritidis Pathogenicity Island 1 Is Not Essential for but Facilitates Rapid Systemic Spread in Chickens{triangledown}

Taseen S. Desin, Po-King S. Lam, Birgit Koch,{dagger} Claudia Mickael, Emil Berberov, Amanda L. S. Wisner, Hugh G. G. Townsend, Andrew A. Potter, and Wolfgang Köster*

Vaccine and Infectious Disease Organization, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5E3, Canada

Received 12 January 2009/ Returned for modification 10 February 2009/ Accepted 3 April 2009

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 {Delta}SPI-1 and {Delta}invG 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 {Delta}SPI-1 mutant strains. Oral challenge of 1-week-old chicken with the wild-type or {Delta}SPI-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 {Delta}SPI-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.

* Corresponding author. Mailing address: Vaccine and Infectious Disease Organization, University of Saskatchewan, 120 Veterinary Road, Saskatoon, Saskatchewan S7N 5E3, Canada. Phone: (306) 966-7479. Fax: (306) 966-7478. E-mail: wolfgang.koester{at}usask.ca

{triangledown} Published ahead of print on 13 April 2009.

Editor: A. J. Bäumler

{dagger} Present address: Department of Science, Systems and Models, Roskilde University, Building 27, Universitetsvej 1, DK-4000 Roskilde, Denmark.

Infection and Immunity, July 2009, p. 2866-2875, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00039-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»