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Infection and Immunity, February 2003, p. 629-640, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.629-640.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Molecular and Phenotypic Analysis of the CS54 Island of Salmonella enterica Serotype Typhimurium: Identification of Intestinal Colonization and Persistence Determinants

Robert A. Kingsley,1 Andrea D. Humphries,1 Eric H. Weening,1 Marcel R. de Zoete,1 Sebastian Winter,1 Anastasia Papaconstantinopoulou,2 Gordon Dougan,2 and Andreas J. Bäumler1*

Department of Medical Microbiology and Immunology, College of Medicine, Texas A&M University System Health Science Center, College Station, Texas 77843-1114,1 Centre for Molecular Microbiology and Infection, Imperial College of Science, Technology and Medicine, London SW7 2AZ, United Kingdom2

Received 12 July 2002/ Returned for modification 29 August 2002/ Accepted 25 October 2002

The shdA gene is carried on a 25-kb genetic island at centisome 54 (CS54 island) of the Salmonella enterica serotype Typhimurium chromosome. In addition to shdA, the CS54 island of Salmonella serotype Typhimurium strain LT2 contains four open reading frames designated ratA, ratB, sivI, and sivH. DNA hybridization analysis revealed that the CS54 island is comprised of two regions with distinct phylogenetic distribution within the genus Salmonella. Homologues of shdA and ratB were detected only in serotypes of Salmonella enterica subsp. I. In contrast, sequences hybridizing with ratA, sivI, and sivH were present in S. enterica subsp. II and S. bongori in addition to S. enterica subsp. I. Deletion of the ratA and sivI genes did not alter the ability of Salmonella serotype Typhimurium to colonize the organs of mice. Insertional inactivation of the sivH gene resulted in defective colonization of the Peyer's patches of the terminal ileum but normal colonization of the cecum, mesenteric lymph nodes, and spleen. Deletion of the shdA gene resulted in decreased colonization of the cecum and Peyer's patches of the terminal ileum and colonization to a lesser degree in the mesenteric lymph nodes and spleen 5 days post-oral inoculation of mice. A strain containing a deletion in the ratB gene exhibited a defect for the colonization of the cecum but not of the Peyer's patches, mesenteric lymph nodes, and spleen. The shdA and ratB deletion strains exhibited a shedding defect in mice, whereas the sivH deletion strain was shed at numbers similar to the wild type. These data suggest that colonization of the murine cecum is required for efficient fecal shedding in mice.


* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, College of Medicine, Texas A&M University System Health Science Center, Reynolds Medical Building, College Station, TX 77843-1114. Phone: (979) 862-7756. Fax: (979) 845-3479. E-mail: abaumler{at}tamu.edu.

Editor: A. D. O'Brien


Infection and Immunity, February 2003, p. 629-640, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.629-640.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




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