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Gnotobiotic Piglets Develop Thrombotic Microangiopathy After Oral Infection With Enterohemorrhagic Escherichia coli

Florian Gunzer MD, Isabel Hennig-Pauka DVM, Karl-Heinz Waldmann DVM, Roger Sandhoff PhD, Hermann-Josef Gröne MD, Hans-Heinrich Kreipe MD, Andreas Matussek, Michael Mengel MD
DOI: http://dx.doi.org/10.1309/UMW9-D06Q-M94Q-JGH2 364-375 First published online: 1 September 2002


Oral infection with enterohemorrhagic Escherichia coli (EHEC) may cause severe enteritis, followed in up to 10% of cases by an extraintestinal complication, the hemolytic uremic syndrome (HUS). HUS is characterized by a triad of symptoms: anemia, thrombocytopenia, and acute renal failure due to thrombotic microangiopathy. EHEC produces several virulence factors, among which a family of phage-encoded cytotoxins, called Shiga toxin 1 and Shiga toxin 2, seems to be most important. However, since an appropriate animal model is not available, pathogenicity of these emerging enteric pathogens is still poorly understood. Germ-free gnotobiotic piglets infected orally with an O157:H7 or an O26:H11 EHEC wild-type isolate, both producing Shiga toxin 2, developed intestinal and extraintestinal manifestations of EHEC disease, including thrombotic microangiopathy in the kidneys, the morphologic hallmark of HUS in humans. Thus, gnotobiotic piglets are suitable to further study the pathophysiology of EHEC-induced HUS. It can be expected that data obtained from this animal model will improve our current standard of knowledge about this emerging infectious disease.

Key Words:
  • Escherichia coli
  • Shiga toxin
  • Hemolytic uremic syndrome
  • Endothelium
  • Thrombotic microangiopathy
  • Disease models, animal