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Letters to Nature

Nature 417, 642-645 (6 June 2002) | doi:10.1038/nature00778; Received 18 March 2002; Accepted 22 April 2002

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Host-induced epidemic spread of the cholera bacterium

D. Scott Merrell1,2, Susan M. Butler1, Firdausi Qadri3, Nadia A. Dolganov4, Ahsfaqul Alam3, Mitchell B. Cohen5, Stephen B. Calderwood6, Gary K. Schoolnik4 & Andrew Camilli1

  1. Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
  2. International Centre for Diarrhoeal Disease Research, Mohakhali, Dhaka 1212, Bangladesh
  3. Stanford Medical School, Beckman Center, Room 241, Stanford, California 94305, USA
  4. Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA
  5. Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts 02114, and Harvard Medical School, Boston, Massachusetts 02115, USA
  6. Present address: Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, California 94305, USA.

Correspondence to: Andrew Camilli1 Correspondence and requests for materials should be addressed to A.C. (e-mail: Email: Andrew.Camilli@Tufts.edu).

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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.