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Infection and Immunity, November 2003, p. 6526-6533, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6526-6533.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Comparative Pathogenicity of Escherichia coli O157 and Intimin-Negative Non-O157 Shiga Toxin-Producing E. coli Strains in Neonatal Pigs

Evelyn A. Dean-Nystrom,1* Angela R. Melton-Celsa,2 Joachim F. L. Pohlenz,3 Harley W. Moon,4 and Alison D. O'Brien2

Pre-Harvest Food Safety and Enteric Research Unit, National Animal Disease Center, USDA Agricultural Research Service, Ames, Iowa,1 Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, Bethesda, Maryland,2 Institute for Pathology, School of Veterinary Medicine, Hannover, Germany,3 Department of Veterinary Pathology, Iowa State University, Ames, Iowa4

Received 7 April 2003/ Returned for modification 21 May 2003/ Accepted 15 July 2003

We compared the pathogenicity of intimin-negative non-O157:H7 Shiga toxin (Stx)-producing Escherichia coli (STEC) O91:H21 and O104:H21 strains with the pathogenicity of intimin-positive O157:H7 and O157:H- strains in neonatal pigs. We also examined the role of Stx2d-activatable genes and the large hemolysin-encoding plasmid of O91:H21 strain B2F1 in the pathogenesis of STEC disease in pigs. We found that all E. coli strains that made wild-type levels of Stx caused systemic illness and histological lesions in the brain and intestinal crypts, whereas none of the control Stx-negative E. coli strains evoked comparable central nervous system signs or intestinal lesions. By contrast, the absence of intimin, hemolysin, or motility had little impact on the overall pathogenesis of systemic disease during STEC infection. The most striking differences between pigs inoculated with non-O157 STEC strains and pigs inoculated with O157 STEC strains were the absence of attaching and effacing intestinal lesions in pigs inoculated with non-O157:H7 strains and the apparent association between the level of Stx2d-activatable toxin produced by an STEC strain and the severity of lesions.

* Corresponding author. Mailing address: National Animal Disease Center, USDA ARS, P.O. Box 70, Ames, IA 50010-0070. Phone: (515) 663-7376. Fax: (515) 663-7458. E-mail: enystrom{at}nadc.ars.usda.gov.

Editor: B. B. Finlay

Infection and Immunity, November 2003, p. 6526-6533, Vol. 71, No. 11
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.11.6526-6533.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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