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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 #166368
Title: SHIGA-TOXIGENIC ESCHERICHIA COLI-INOCULATED NEONATAL PIGLETS DEVELOP KIDNEY LESIONS THAT ARE COMPARABLE TO THOSE IN HUMANS WITH HEMOLYTIC-UREMIC SYNDROME

Author
item POHLENZ, J - HANNOVER VET SCHOOL
item WINTER, K - IOWA STATE UNIVERSITY
item NYSTROM, EVELYN

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/20/2004
Publication Date: 1/20/2005
Citation: Pohlenz, J.F., Winter, K.R., Nystrom, E.A. 2005. Shiga-toxigenic Escherichia coli-inoculated neonatal piglets develop kidney lesions that are comparable to those in humans with hemolytic-uremic syndrome. Infection and Immunity. 73(1):612-616.

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. STEC O157:H7 strains (also called hamburger E. coli) are the most common type of STEC that cause disease in humans, but other non-O157 STEC strains also cause severe disease in humans. The objective of this retrospective histological examination of kidney tissues obtained from STEC-infected and control neonatal piglets from previously reported and ongoing STEC infection experiments was to describe Stx-induced lesions. Neonatal piglets were necropsied at 1 to 11 days after inoculation with 10**10 or 10**6 colony forming units (CFU) of an STEC O157:H7 or non-O157:H7 STEC strain associated with a human outbreak, an Stx-negative E. coli O157:H7 strain, or a non-pathogenic E. coli control strain. Kidney lesions were seen in all groups of STEC-inoculated piglets (82/122 piglets) but not in any of 29 control pigs. STEC caused epithelial and vascular lesions in the kidneys of neonatal piglets as early as 18 hours after inoculation, and these lesions were similar to those found in humans with hemolytic uremic syndrome. These findings extend the evidence that Shiga toxins may be directly toxic for kidney epithelial cells. We conclude that our neonatal pig STEC infection model is an excellent model for studying the mechanisms of STEC disease in humans.

Technical Abstract: The main objective of this retrospective histological examination of kidney tissues obtained from Shiga toxin (Stx)-producing E. coli (STEC)-infected and control neonatal piglets from previously reported and ongoing STEC infection experiments was to describe Stx-induced lesions and compare lesions in neonatal piglets with those in humans with STEC-mediated hemolytic uremic syndrome (HUS). Neonatal piglets were necropsied at 1 to 11 days after inoculation with 10**10 or 10**6 colony forming units (CFU) of an STEC O157:H7 or non-O157:H7 STEC strain associated with a human outbreak, an Stx-negative E. coli O157:H7 strain, or a non-pathogenic E. coli control strain. All STEC-infected piglets in the higher dose groups were necropsied within 1-3 days PI because they developed early and severe central nervous signs. Kidney lesions were seen in all groups of STEC-inoculated piglets (82/122 piglets) but not in any of 29 control piglets. STEC caused tubular and vascular lesions in the kidneys of neonatal piglets. These lesions occurred early and simultaneously, and were similar to those found in humans with HUS. The location of lesions in porcine kidneys matched the locations where Stx2 binding and Gb3 (receptors for Stx) were identified by immunohistochemical staining. We concluded that the neonatal piglet STEC infection model is an excellent model for studying the mechanisms of Stx-mediated disease.