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Abstract

The factors that enhance the transmission of pathogens during epidemic spread are ill defined. Water-borne spread of the diarrhoeal disease cholera occurs rapidly in nature, whereas infection of human volunteers with bacteria grown in vitro is difficult in the absence of stomach acid buffering1. It is unclear, however, whether stomach acidity is a principal factor contributing to epidemic spread2. Here we report that characterization of Vibrio cholerae from human stools supports a model whereby human colonization creates a hyperinfectious bacterial state that is maintained after dissemination and that may contribute to epidemic spread of cholera. Transcriptional profiling of V. cholerae from stool samples revealed a unique physiological and behavioural state characterized by high expression levels of genes required for nutrient acquisition and motility, and low expression levels of genes required for bacterial chemotaxis.

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Acknowledgements

We thank E. A. Joyce, M. K. Waldor and A. L. Sonenshein for comments and discussion of the manuscript, C. C. Kim for help with statistical analysis, and S. Falkow and J. J. Mekalanos for critical discussions. This research was supported by grants from the National Institutes of Health. The ICDDR at Bangladesh is supported by agencies and countries that share its concern for the health problems of the developing world.

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Author notes

    • D. Scott Merrell

    Present address: Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, California, 94305, USA

Affiliations

  1. Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, 02111, USA

    • D. Scott Merrell
    • , Susan M. Butler
    •  & Andrew Camilli
  2. International Centre for Diarrhoeal Disease Research, Dhaka, Mohakhali, 1212, Bangladesh

    • Firdausi Qadri
    •  & Ahsfaqul Alam
  3. Stanford Medical School, Beckman Center, Room 241, Stanford, California, 94305, USA

    • Nadia A. Dolganov
    •  & Gary K. Schoolnik
  4. Children's Hospital Medical Center, Cincinnati, Ohio, 45229, USA

    • Mitchell B. Cohen
  5. Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, 02114

    • Stephen B. Calderwood
  6. Harvard Medical School, Boston, Massachusetts, 02115, USA

    • Stephen B. Calderwood

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The authors declare that they have no competing financial interests.

Corresponding author

Correspondence to Andrew Camilli.

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https://doi.org/10.1038/nature00778

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