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 buffering. It is unclear, however, whether stomach acidity is a principal factor contributing to epidemic spread. 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.
|Number of pages||4|
|State||Published - Jun 6 2002|
Bibliographical noteFunding Information:
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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