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; Andrew Camilli

doi:10.1038/nature00778

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, Andrew Camilli

Microbiology, Immunology, and Molecular Genetics

Research output: Contribution to journal › Article › peer-review

419 Scopus citations

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 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.

Original language	English
Pages (from-to)	642-645
Number of pages	4
Journal	Nature
Volume	417
Issue number	6889
DOIs	https://doi.org/10.1038/nature00778
State	Published - Jun 6 2002

Bibliographical note

Funding 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.

ASJC Scopus subject areas

General

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/nature00778

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title = "Host-induced epidemic spread of the cholera bacterium",

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 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.",

author = "Merrell, {D. Scott} and Butler, {Susan M.} and Firdausi Qadri and Dolganov, {Nadia A.} and Ahsfaqul Alam and Cohen, {Mitchell B.} and Calderwood, {Stephen B.} and Schoolnik, {Gary K.} and Andrew Camilli",

note = "Funding 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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doi = "10.1038/nature00778",

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AU - Merrell, D. Scott

AU - Butler, Susan M.

AU - Qadri, Firdausi

AU - Dolganov, Nadia A.

AU - Alam, Ahsfaqul

AU - Cohen, Mitchell B.

AU - Calderwood, Stephen B.

AU - Schoolnik, Gary K.

AU - Camilli, Andrew

N1 - Funding 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.

PY - 2002/6/6

Y1 - 2002/6/6

N2 - 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.

AB - 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.

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JO - Nature

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ER -

Host-induced epidemic spread of the cholera bacterium

Abstract

Bibliographical note

ASJC Scopus subject areas

UN SDGs

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