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Infection and Immunity, June 1999, p. 2815-2821, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Evaluation of Salmonella typhimurium Mutants in a Model of Experimental Gastroenteritis

Paul Everest,1,* Julian Ketley,2 Simon Hardy,3 Gill Douce,1,dagger Shahid Khan,4 Jacqui Shea,5 David Holden,5 Duncan Maskell,4 and Gordon Dougan1

Department of Biochemistry, Imperial College of Science, Technology and Medicine,1 and Department of Infectious Diseases, Imperial College School of Medicine, Hammersmith Hospital,5 London; Department of Genetics, University of Leicester, Leicester2; Department of Pharmacy, University of Brighton, Brighton3; and Department of Clinical Veterinary Medicine, University of Cambridge Veterinary School, Cambridge,4 United Kingdom

Received 23 October 1998/Returned for modification 21 December 1998/Accepted 5 March 1999

Salmonella typhimurium strains harboring independent, defined mutations in aroA, invA, ssrA, or msbB were assessed for their ability to induce fluid accumulation, tissue damage, and local inflammation in rabbit ileal loops. Three wild-type strains of S. typhimurium, TML, HWSH, and SL1344, and two mutant strains, S. typhimurium SL1344 ssrA and S. typhimurium SL1344 msbB, consistently induced fluid accumulation in the lumen of loops and inflammation of loop-associated tissues. In contrast, three different S. typhimurium aroA strains and an invA mutant of SL1344 did not induce significant fluid accumulation in the rabbit ileal loops. However, the S. typhimurium aroA strains did induce an inflammatory infiltrate and some local villus-associated damage, but the invA mutant did not. Histologically, wild-type S. typhimurium, S. typhimurium SL1344 ssrA, and S. typhimurium SL1344 msbB demonstrated more severe effects on villus architecture than S. typhimurium aroA strains, whereas S. typhimurium invA-infected loops showed no detectable damage. This suggests that villus damage most likely contributes to fluid accumulation within the loop.

* Corresponding author. Mailing address: Department of Infectious Diseases, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom. Phone: 441813832067. Fax: 441813832074. E-mail: p.everest{at}ic.ac.uk.

dagger Present address: Vaccine Research Unit, Medeva Development, Imperial College, London, United Kingdom.

Infection and Immunity, June 1999, p. 2815-2821, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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