Infection and Immunity, July 2000, p. 3808-3814, Vol. 68, No. 7
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


Department of Microbiology, Molecular Biology, and Biochemistry,3 Department of Food Science and Toxicology,1 Division of Statistics,4 and Department of Animal and Veterinary Science,5 University of Idaho, Moscow, Idaho 83844, and Field Disease Investigation Unit, Department of Clinical Veterinary Sciences, Washington State University, Pullman, Washington 991642
Received 19 January 2000/Returned for modification 17 March 2000/Accepted 6 April 2000
Human infections with Escherichia coli O157:H7 cause hemorrhagic colitis that can progress to a life-threatening sequelae. The most common mode of disease transmission is ingestion of contaminated bovine food products, and it is well established that E. coli O157:H7 is a transient member of the bovine microbiota. However, the conditions that induce acquisition and subsequent clearance of this bacterium from the ruminant gastrointestinal tract (GIT) are not understood. Evidence that the rates of epithelial cell proliferation in the lower GIT of cattle are associated with the duration animals remained E. coli O157:H7 culture positive is presented. Cattle with slower rates of intestinal cell proliferation in the cecum and the distal colon were culture positive significantly longer than cohort cattle with faster cell proliferation rates. Cell death rates (apoptotic indices) between the short- and long-term culture-positive animals were not different. Typical grain-based finishing diets and forage-based growing diets did not effect GIT cell proliferation or the duration animals remained E. coli O157:H7 culture positive. To identify a dietary intervention that would effect GIT cell proliferation, we used sheep as a model ruminant. A fasting-refeeding regime that increased the rate of GIT cell proliferation was developed. The fasting-refeeding protocol was used in cattle to test the hypothesis that feeding interventions that increase the rate of GIT cell proliferation induce the clearance of E. coli O157:H7 from the bovine GIT.
Present address: Department of Nutrition and Food Science,
University of Maryland, College Park, MD 20742.
Present address: Department of Medicine, Massachusetts General
Hospital, Harvard University, Boston, MA 02114.
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