Skip to main content
ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #151096
Title: SHIGATOXIGENIC ESCHERICHIA COLI (STEC) INDUCE KIDNEY LESIONS IN NEONATAL PIGLETS THAT ARE COMPARABLE TO THOSE SEEN IN HUMANS SUFFERING FROM COMPLICATIONS OF ENTEROHEMORRHAGIC COLITIS

Author
item POHLENZ, J - VISITING SCI, GERMANY
item WINTER, K - IOWA STATE UNIVERSITY
item Nystrom, Evelyn

Submitted to: International Conference on Emerging Zoonoses
Publication Type: Abstract Only
Publication Acceptance Date: 9/18/2003
Publication Date: 9/18/2003
Citation: POHLENZ, J.F., WINTER, K.R., NYSTROM, E.A. SHIGATOXIGENIC ESCHERICHIA COLI (STEC) INDUCE KIDNEY LESIONS IN NEONATAL PIGLETS THAT ARE COMPARABLE TO THOSE SEEN IN HUMANS SUFFERING FROM COMPLICATIONS OF ENTEROHEMORRHAGIC COLITIS. INTERNATIONAL CONFERENCE ON EMERGING ZOONOSES. 2003. ABSTRACT p. 87.

Interpretive Summary:

Technical Abstract: Enterohemorrhagic Escherichia coli strains (EHEC) are zoonotic foodborne bacterial pathogens that cause hemorrhagic colitis and the hemolytic uremic syndrome (HUS) in humans. EHEC-induced CNS and intestinal lesions in experimentally infected piglets have been described previously. In this retrospective study, kidney tissues obtained from STEC-infected neonatal piglets and matched controls from previously reported and ongoing STEC infection experiments were histologically examined and compared. Neonatal (less than or equal to 8 hours of age) colostrum-fed (suckling) piglets or cesarean-derived, colostrum-deprived (CDCD) piglets were inoculated with 10**10 (high dose) or 10**6 (low dose) colony forming units (CFU) of an STEC O157:H7 strain isolated from a human outbreak (strain 86-24 or strain 933), or with either Shiga toxin-negative E. coli O157:H7 strain 87-23 or non-pathogenic control E. coli strain 123. Because STEC-infected piglets in the high dose groups developed early and severe central nervous symptoms (including somnolence, recumbency, paddling), they were all necropsied within 1-2 days PI. Some STEC piglets in the low dose groups remained clinically normal and were kept until 11 days PI. No lesions were seen in any of the 29 control pigs inoculated with either Shiga toxin-negative strain 87-23 or control strain 123. Kidney lesions were seen in both suckling and CDCD piglets and in both high and low dose groups. Four predominant types of lesions were seen: focal to multifocal tubular necrosis; capillary impairment of glomeruli; arterial constriction; and thrombus formation and arterial and glomerular sclerosis. Nuclear fragmentation consistent with apoptosis was also noted. Kidney lesions were seen in 25/28 and 29/43 piglets inoculated with 10**10 and 10**6 STEC, respectively. The location of lesions in the kidneys matched the locations where Gb3 receptors and Stx2 binding sites were identified by immunohistochemistry on frozen tissue sections. We conclude that EHEC cause tissue damage in kidneys of neonatal pigs, that kidney damage occurs early after exposure to Shiga toxin, and that damage occurs simultaneously in tubular epithelial cells and endothelial cells/arterioles. The presence of EHEC-induced lesions in the kidneys, as well as in the CNS and intestines, the early and simultaneous occurrence of lesions in tubules and blood vessels, and the similarity of lesions in neonatal piglets to those in humans with severe EHEC disease (i.e., HUS) make the neonatal piglet EHEC infection model ideal for studying the mechanisms of EHEC pathogenesis.