Host-induced epidemic spread of the cholera bacterium

D. Scott Merrell, Susan M. Butler, Firdausi Qadri, Nadia A. Dolganov, Ahsfaqul Alam, Mitchell B. Cohen, Stephen B. Calderwood, Gary K. Schoolnik and Andrew Camilli ()
Additional contact information
D. Scott Merrell: Tufts University School of Medicine
Susan M. Butler: Tufts University School of Medicine
Firdausi Qadri: International Centre for Diarrhoeal Disease Research
Nadia A. Dolganov: Stanford Medical School, Beckman Center, Room 241
Ahsfaqul Alam: International Centre for Diarrhoeal Disease Research
Mitchell B. Cohen: Children's Hospital Medical Center
Stephen B. Calderwood: Massachusetts General Hospital
Gary K. Schoolnik: Stanford Medical School, Beckman Center, Room 241
Andrew Camilli: Tufts University School of Medicine

Nature, 2002, vol. 417, issue 6889, 642-645

Abstract: 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.

Date: 2002
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DOI: 10.1038/nature00778

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