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Infection and Immunity, September 1999, p. 4879-4885, Vol. 67, No. 9
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Contribution of Salmonella typhimurium Virulence Factors to Diarrheal Disease in Calves

Renée M. Tsolis,1 L. Garry Adams,1 Thomas A. Ficht,1 and Andreas J. Bäumler2,*

Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station, Texas 77843-4467,1 and Department of Medical Microbiology and Immunology, College of Medicine, Texas A&M University Health Science Center, College Station, Texas 77843-11142

Received 20 April 1999/Returned for modification 26 May 1999/Accepted 16 June 1999

Limited knowledge is available about the virulence mechanisms responsible for diarrheal disease caused by Salmonella typhimurium. To assess the contribution to diarrheal disease of virulence determinants identified in models of infection, we tested a collection of S. typhimurium mutants for their ability to cause enteritis in calves. S. typhimurium strains carrying mutations in the virulence plasmid (spvR), Salmonella pathogenicity island 2 (SPI-2) (spiB), or SPI-5 (sopB) caused mortality and acute diarrhea in calves. An S. typhimurium rfaJ mutant, which is defective for lipopolysaccharide outer core biosynthesis, was of intermediate virulence. Mutations in SPI-1 (hilA and prgH) or aroA markedly reduced virulence and the severity of diarrhea. Furthermore, histopathological examination of calves infected with SPI-1 or aroA mutants revealed a marked reduction or absence of intestinal lesions. These data suggest that virulence factors, such as SPI-1, which are required during intestinal colonization are more important for pathogenicity in calves than are genes required during the systemic phase of S. typhimurium infection, including SPI-2 or the spv operon. This is in contrast to the degree of attenuation caused by these mutations in the mouse.

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

Infection and Immunity, September 1999, p. 4879-4885, Vol. 67, No. 9
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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