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Infection and Immunity, December 1999, p. 6385-6393, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Identification of a Putative Salmonella enterica Serotype Typhimurium Host Range Factor with Homology to IpaH and YopM by Signature-Tagged Mutagenesis

Renée M. Tsolis,1 Stacy M. Townsend,2 Edward A. Miao,3 Samuel I. Miller,3 Thomas A. Ficht,1 L. Garry Adams,1 and Andreas J. Bäumler2,*

Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station, Texas 77843-44671; Department of Medical Microbiology and Immunology, College of Medicine, Texas A&M University Health Science Center, College Station, Texas 77843-11142; and Departments of Medicine and Microbiology, University of Washington, Seattle, Washington 981953

Received 24 May 1999/Returned for modification 30 July 1999/Accepted 30 September 1999

The genetic basis for the host adaptation of Salmonella serotypes is currently unknown. We have explored a new strategy to identify Salmonella enterica serotype Typhimurium (S. typhimurium) genes involved in host adaptation, by comparing the virulence of 260 randomly generated signature-tagged mutants during the oral infection of mice and calves. This screen identified four mutants, which were defective for colonization of only one of the two host species tested. One mutant, which only displayed a colonization defect during the infection of mice, was further characterized. During competitive infection experiments performed with the S. typhimurium wild type, the mutant was defective for colonization of murine Peyer's patches but colonized bovine Peyer's patches at the wild-type level. No difference in virulence between wild type and mutant was observed when calves were infected orally with 1010 CFU/animal. In contrast, the mutant possessed a sixfold increase in 50% lethal morbidity dose when mice were infected orally. The transposon in this mutant was inserted in a 2.9-kb pathogenicity islet, which is located between uvrB and yphK on the S. typhimurium chromosome. This pathogenicity islet contained a single gene, termed slrP, with homology to ipaH of Shigella flexneri and yopM of Yersinia pestis. These data show that comparative screening of signature-tagged mutants in two animal species can be used for scanning the S. typhimurium genome for genes involved in host adaptation.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, College of Medicine, Texas A&M University Health Science Center, 407 Reynolds Med. Bldg., College Station, TX 77843-1114. Phone: (409) 862-7756. Fax: (409) 845-3479. E-mail: abaumler{at}tamu.edu.

Infection and Immunity, December 1999, p. 6385-6393, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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