Development of animal model for enterohemorrhagic Escherichia coli infection

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Infections due to Shiga toxin-producing Escherichia coli (STEC) are responsible for severe diarrheal diseases in humans, and these bacteria have recently emerged as a leading cause of renal failure and encephalitis in children and the aged. To develop rapid diagnosis methods or methods/medicines to treat patients infected with STEC, animal model are necessary. Conventional mice or rat are not sensitive for STEC. Gnotobiotic mice, antibiotics treated mice or malnutritional mice are used. Removal of the cecum from normal mice caused a major perturbation of the microbial ecology of the gastrointestinal tract. There was a permanent reduction in colonization resistance resulting in a 1,000-fold increase in the concentration of facultatively anaerobic coliform bacteria. Coincident with this increase in coliform counts was a decrease in the numbers of strictly anaerobic fusiform bacteria that dominate the rodent intestinal tract, resulting in reduced levels of volatile fatty acids. As the volatile fatty acids are major metabolic end products of anaerobic bacteria that colonize the rodent intestine and are produced mainly in the cecum, it was likely that the decrease in fatty acid levels was due to changes in the normal microbiota of the intestine. Cecectomized are likely to be a useful model for study of Intestinal pathogen that can not colonize in the intestine of normal mice. We succeeded to development of this model, though STEC challenged into cecectomized mice could not colonize and cause diarrea in challenged mice.