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Infection and Immunity, January 2008, p. 403-416, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.01189-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Host Transmission of Salmonella enterica Serovar Typhimurium Is Controlled by Virulence Factors and Indigenous Intestinal Microbiota{triangledown}

Trevor D. Lawley,1,{dagger} Donna M. Bouley,2 Yana E. Hoy,1 Christine Gerke,1 David A. Relman,1,3,4 and Denise M. Monack1*

Department of Microbiology and Immunology,1 Department of Comparative Medicine,2 Department of Medicine, Stanford University, Stanford, California, 94305,3 Veterans Affairs Palo Alto Health Care System, Palo Alto, California 943044

Received 29 August 2007/ Returned for modification 9 October 2007/ Accepted 22 October 2007

Transmission is an essential stage of a pathogen's life cycle and remains poorly understood. We describe here a model in which persistently infected 129X1/SvJ mice provide a natural model of Salmonella enterica serovar Typhimurium transmission. In this model only a subset of the infected mice, termed supershedders, shed high levels (>108 CFU/g) of Salmonella serovar Typhimurium in their feces and, as a result, rapidly transmit infection. While most Salmonella serovar Typhimurium-infected mice show signs of intestinal inflammation, only supershedder mice develop colitis. Development of the supershedder phenotype depends on the virulence determinants Salmonella pathogenicity islands 1 and 2, and it is characterized by mucosal invasion and, importantly, high luminal abundance of Salmonella serovar Typhimurium within the colon. Immunosuppression of infected mice does not induce the supershedder phenotype, demonstrating that the immune response is not the main determinant of Salmonella serovar Typhimurium levels within the colon. In contrast, treatment of mice with antibiotics that alter the health-associated indigenous intestinal microbiota rapidly induces the supershedder phenotype in infected mice and predisposes uninfected mice to the supershedder phenotype for several days. These results demonstrate that the intestinal microbiota plays a critical role in controlling Salmonella serovar Typhimurium infection, disease, and transmissibility. This novel model should facilitate the study of host, pathogen, and intestinal microbiota factors that contribute to infectious disease transmission.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, 299 Campus Drive, Stanford University, Stanford, CA 94305. Phone: (650) 725-7282. Fax: (650) 725-1756. E-mail: dmonack{at}stanford.edu

{triangledown} Published ahead of print on 29 October 2007.

Editor: B. A. McCormick

{dagger} Present address: The Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, United Kingdom CB10 1SA.

Infection and Immunity, January 2008, p. 403-416, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.01189-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Sekirov, I., Tam, N. M., Jogova, M., Robertson, M. L., Li, Y., Lupp, C., Finlay, B. B. (2008). Antibiotic-Induced Perturbations of the Intestinal Microbiota Alter Host Susceptibility to Enteric Infection. Infect. Immun. 76: 4726-4736 [Abstract] [Full Text]  


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