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Infection and Immunity, November 2005, p. 7161-7169, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7161-7169.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Analysis of the Contribution of Salmonella Pathogenicity Islands 1 and 2 to Enteric Disease Progression Using a Novel Bovine Ileal Loop Model and a Murine Model of Infectious Enterocolitis

Brian K. Coombes,1,{dagger} Bryan A. Coburn,1,2,{dagger} Andrew A. Potter,3 Susantha Gomis,4 Kuldip Mirakhur,3 Yuling Li,1 and B. Brett Finlay1,2*

Michael Smith Laboratories,1 Department of Microbiology and Immunology,2 University of British Columbia, Vancouver, British Columbia V6T 1Z4, Vaccine and Infectious Disease Organization, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5B4,3 Department of Veterinary Pathology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada4

Received 1 April 2005/ Returned for modification 15 June 2005/ Accepted 8 July 2005

We have developed a novel ileal loop model for use in calves to analyze the contribution of Salmonella enterica serovar Typhimurium type III secretion systems to disease processes in vivo. Our model involves constructing ileal loops with end-to-end anastamoses to restore the patency of the small intestine, thereby allowing experimental animals to convalesce following surgery for the desired number of days. This model overcomes the time constraint imposed by ligated ileal loop models that have precluded investigation of Salmonella virulence factors during later stages of the infection process. Here, we have used this model to examine the enteric disease process at 24 h and 5 days following infection with wild-type Salmonella and mutants lacking the virulence-associated Salmonella pathogenicity island 1 (SPI-1) or SPI-2 type III secretion systems. We show that SPI-2 mutants are dramatically attenuated at 5 days following infection and report a new phenotype for SPI-1 mutants, which induce intestinal pathology in calves similar to wild-type Salmonella in the 5-day ileal loop model. Both of these temporal phenotypes for SPI-1 and SPI-2 mutants were corroborated in a second animal model of enteric disease using streptomycin-pretreated mice. These data delineate novel phenotypes for SPI-1 and SPI-2 mutants in the intestinal phase of bovine and murine salmonellosis and provide working models to further investigate the effector contribution to these pathologies.

* Corresponding author. Mailing address: Michael Smith Laboratories, 301-2185 East Mall, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada. Phone: (604) 822-2210. Fax: (604) 822-9830. E-mail: bfinlay{at}interchange.ubc.ca.

Editor: V. J. DiRita

{dagger} B.K.C. and B.A.C. contributed equally to this work.

Infection and Immunity, November 2005, p. 7161-7169, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7161-7169.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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