This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Angelichio, M. J. Articles by Camilli, A. Search for Related Content PubMed PubMed Citation Articles by Angelichio, M. J. Articles by Camilli, A. Pubmed/NCBI databases Substance via MeSH

 Previous Article  |  Next Article 

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.

Spatiotemporal Analysis of Acid Adaptation-Mediated Vibrio cholerae Hyperinfectivity

Michael J. Angelichio,¹ D. Scott Merrell,² and Andrew Camilli^1*

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.

---

* Corresponding author. Mailing address: Department of Molecular Biology & Microbiology, Tufts University School of Medicine, Boston, MA 02111. Phone: (617) 636-2144. Fax: (617) 636-0337. E-mail: andrew.camilli{at}tufts.edu. Present address: Marine Biological Sciences, University of New England, Biddeford, ME 04005.

Editor: V. J. DiRita

---

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.

This article has been cited by other articles:

• Fisher, M. L., Castillo, C., Mecsas, J. (2007). Intranasal Inoculation of Mice with Yersinia pseudotuberculosis Causes a Lethal Lung Infection That Is Dependent on Yersinia Outer Proteins and PhoP. Infect. Immun. 75: 429-442 [Abstract] [Full Text]  
• Alam, A., LaRocque, R. C., Harris, J. B., Vanderspurt, C., Ryan, E. T., Qadri, F., Calderwood, S. B. (2005). Hyperinfectivity of Human-Passaged Vibrio cholerae Can Be Modeled by Growth in the Infant Mouse. Infect. Immun. 73: 6674-6679 [Abstract] [Full Text]  
• Rediers, H., Rainey, P. B., Vanderleyden, J., De Mot, R. (2005). Unraveling the Secret Lives of Bacteria: Use of In Vivo Expression Technology and Differential Fluorescence Induction Promoter Traps as Tools for Exploring Niche-Specific Gene Expression. Microbiol. Mol. Biol. Rev. 69: 217-261 [Abstract] [Full Text]