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Infection and Immunity, October 2005, p. 6674-6679, Vol. 73, No. 10
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.10.6674-6679.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh,1 Division of Infectious Diseases, Massachusetts General Hospital,2 Department of Immunology and Infectious Diseases, Harvard School of Public Health,5 Department of Medicine,3 Department of Pediatrics,4 Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts6
Received 26 April 2005/ Returned for modification 16 May 2005/ Accepted 9 July 2005
It has previously been shown that passage of Vibrio cholerae through the human intestine imparts a transient hyperinfectious phenotype that may contribute to the epidemic spread of cholera. The mechanism underlying this human-passaged hyperinfectivity is incompletely understood, in part due to inherent difficulties in recovering and studying organisms that are freshly passed in human stool. Here, we demonstrate that passage of V. cholerae through the infant mouse intestine leads to an equivalent degree of hyperinfectivity as passage through the human host. We have used this infant mouse model of host-passaged hyperinfectivity to characterize the timing and the anatomic location of the competitive advantage of mouse-passaged V. cholerae as well as the contribution of three type IV pili to the phenotype.
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