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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #147873
Title: COMPARATIVE PATHOGENICITY OF ESCHERICHIA COLI O157 AND INTIMIN-NEGATIVE NON-O157 SHIGA TOXIN-PRODUCING E. COLI STRAINS IN NEONATAL PIGS

Author
item NYSTROM, EVELYN
item MELTON-CELSA, A - UNIF SRVCS UNIV HLTH SCI
item POHLENZ, J - INST PATHOLOGY, GERMANY
item MOON, H - IOWA STATE UNIVERSITY
item O'BRIEN, A - UNIF SRVCS UNIV HLTH SCI

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/15/2003
Publication Date: 11/20/2003
Citation: NYSTROM, E.A., MELTON-CELSA, A.R., POHLENZ, J., MOON, H.W., O'BRIEN, A.D. COMPARATIVE PATHOGENICITY OF ESCHERICHIA COLI O157 AND INTIMIN-NEGATIVE NON-O157 SHIGA TOXIN-PRODUCING E. COLI STRAINS IN NEONATAL PIGS. INFECTION AND IMMUNITY. 2003. v. 71. p. 6526-6533.

Interpretive Summary: Shiga toxin-producing strains of Escherichia coli (STEC) are foodborne pathogens that cause severe diarrhea and sometimes kidney failure and death in humans. Although STEC O157:H7 strains (also called hamburger E. coli) are the most common type of STEC that cause disease in humans, non-O157 STEC strains also cause severe disease in humans. In this study, we compared the abilities of O157:H7 STEC and non-O157 STEC strains to cause disease in neonatal pigs. Unlike the STEC O157:H7 strains we tested, the non-O157 STED did not produce intimin (a bacterial protein that promotes the binding of bacteria to intestinal tissues). The STEC strains also produced different types of Shiga toxin 2. We showed that, unlike STEC O157:H7 strains, the non-O157 STEC strains did not require intimin to cause disease in neonatal pigs. We also showed that all types of Shiga toxin 2 produced by strains tested in this study caused similar disease and brain lesions in neonatal CDCD pigs, but that different types of Shiga toxin caused different types of lesions in the large intestines of these animals. These results indicate that non-O157-STEC use proteins other than intimin to stick to intestinal tissues and show that the intestinal barrier is an early target of Shiga toxin-mediated tissue damage. This critical new information about how STEC cause infections and disease in pigs, will facilitate the development of strategies to identify and reduce STEC infections in food animals, and thus help reduce the incidence of STEC disease in humans.

Technical Abstract: We compared the pathogenicity of intimin-negative non-O157:H7 Shiga toxin (Stx)-producing E. coli (STEC) O91:H21 and O104:H21 strains with 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 evoked CNS signs or comparable 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 in pigs inoculated with non-O157 versus those 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 and the severity of lesions.