Cholera stool bacteria repress chemotaxis to increase infectivity

Authors

  • Susan M. Butler,

    1. Department of Molecular Biology and Microbiology, Tufts University School of Medicine and
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    • Present address: Department of Microbiology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.

  • Eric J. Nelson,

    1. Department of Molecular Biology and Microbiology, Tufts University School of Medicine and
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  • Nityananda Chowdhury,

    1. International Centre for Diarrhoeal Disease Research, Mohakhali, Dhaka 1212, Bangladesh.
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  • Shah M. Faruque,

    1. International Centre for Diarrhoeal Disease Research, Mohakhali, Dhaka 1212, Bangladesh.
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  • Stephen B. Calderwood,

    1. Division of Infectious Diseases, Massachusetts General Hospital, Boston, MA 02114, and Harvard Medical School, Boston, MA 02115, USA.
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  • Andrew Camilli

    Corresponding author
    1. Department of Molecular Biology and Microbiology, Tufts University School of Medicine and
    2. Howard Hughes Medical Institute, 136 Harrison Avenue, Boston, MA 02111, USA.
      *E-mail andrew.camilli@tufts.edu; Tel. (+1) 617 636 2144; Fax (+1) 617 636 2175.
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*E-mail andrew.camilli@tufts.edu; Tel. (+1) 617 636 2144; Fax (+1) 617 636 2175.

Summary

Factors that enhance the transmission of pathogens are poorly understood. We show that Vibrio cholerae shed in human ‘rice-water’ stools have a 10-fold lower oral infectious dose in an animal model than in vitro grown V. cholerae, which may aid in transmission during outbreaks. Furthermore, we identify a bacterial factor contributing to this enhanced infectivity: The achievement of a transient motile but chemotaxis-defective state upon shedding from humans. Rice-water stool V. cholerae have reduced levels of CheW-1, which is essential for chemotaxis, and were consequently shown to have a chemotaxis defect when tested in capillary assays. Through mutational analyses, such a state is known to enhance the infectivity of V. cholerae. This is the first report of a pathogen altering its chemotactic state in response to human infection in order to enhance its transmission.

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