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Infection and Immunity, April 2004, p. 2405-2407, Vol. 72, No. 4
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.4.2405-2407.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Molecular Biology & Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111,1 Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, California 943052
Received 18 July 2003/ Returned for modification 1 September 2003/ Accepted 27 December 2003
Acid adaptation has previously been shown to increase the infectivity of Vibrio cholerae in the infant mouse model. To better understand this phenomenon, we monitored the spatial distribution and temporal changes in the ratios of acid-adapted cells to unadapted V. cholerae cells in the small intestine, as well as the timing of virulence factor expression. We found that the competitive advantage afforded by acid adaptation does not become manifest until greater than 3 h postinfection; thus, acid adaptation does not increase V. cholerae passage through the gastric acid barrier. Additionally, acid-adapted and unadapted V. cholerae cells colonize the same sections of the small intestine and show similar kinetics of transcriptional induction of the virulence genes tcpA and ctxA. These studies suggest that the increased infectivity of acid-adapted V. cholerae is due to a more rapid onset of multiplication and/or to an increased multiplication rate within the infant mouse intestine.
Present address: Marine Biological Sciences, University of New England, Biddeford, ME 04005.
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