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Vibrio cholerae as a predator: lessons from evolutionary principles

Diarrheal diseases are the second-most common cause of death among children under the age of five worldwide. Cholera alone, caused by the marine bacterium Vibrio cholerae, is responsible for several million cases and over 120,000 deaths annually. When contaminated water is ingested, V. cholerae pass...

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Detalles Bibliográficos
Autores principales: Pukatzki, Stefan, Provenzano, Daniele
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3857921/
https://www.ncbi.nlm.nih.gov/pubmed/24368907
http://dx.doi.org/10.3389/fmicb.2013.00384
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author Pukatzki, Stefan
Provenzano, Daniele
author_facet Pukatzki, Stefan
Provenzano, Daniele
author_sort Pukatzki, Stefan
collection PubMed
description Diarrheal diseases are the second-most common cause of death among children under the age of five worldwide. Cholera alone, caused by the marine bacterium Vibrio cholerae, is responsible for several million cases and over 120,000 deaths annually. When contaminated water is ingested, V. cholerae passes through the gastric acid barrier, penetrates the mucin layer of the small intestine, and adheres to the underlying epithelial lining. V. cholerae multiplies rapidly, secretes cholera toxin, and exits the human host in vast numbers during diarrheal purges. How V. cholerae rapidly reaches such high numbers during each purge is not clearly understood. We propose that V. cholerae employs its bactericidal type VI secretion system to engage in intraspecies and intraguild predation for nutrient acquisition to support rapid growth and multiplication.
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spelling pubmed-38579212013-12-24 Vibrio cholerae as a predator: lessons from evolutionary principles Pukatzki, Stefan Provenzano, Daniele Front Microbiol Microbiology Diarrheal diseases are the second-most common cause of death among children under the age of five worldwide. Cholera alone, caused by the marine bacterium Vibrio cholerae, is responsible for several million cases and over 120,000 deaths annually. When contaminated water is ingested, V. cholerae passes through the gastric acid barrier, penetrates the mucin layer of the small intestine, and adheres to the underlying epithelial lining. V. cholerae multiplies rapidly, secretes cholera toxin, and exits the human host in vast numbers during diarrheal purges. How V. cholerae rapidly reaches such high numbers during each purge is not clearly understood. We propose that V. cholerae employs its bactericidal type VI secretion system to engage in intraspecies and intraguild predation for nutrient acquisition to support rapid growth and multiplication. Frontiers Media S.A. 2013-12-10 /pmc/articles/PMC3857921/ /pubmed/24368907 http://dx.doi.org/10.3389/fmicb.2013.00384 Text en Copyright © 2013 Pukatzki and Provenzano. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Pukatzki, Stefan
Provenzano, Daniele
Vibrio cholerae as a predator: lessons from evolutionary principles
title Vibrio cholerae as a predator: lessons from evolutionary principles
title_full Vibrio cholerae as a predator: lessons from evolutionary principles
title_fullStr Vibrio cholerae as a predator: lessons from evolutionary principles
title_full_unstemmed Vibrio cholerae as a predator: lessons from evolutionary principles
title_short Vibrio cholerae as a predator: lessons from evolutionary principles
title_sort vibrio cholerae as a predator: lessons from evolutionary principles
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3857921/
https://www.ncbi.nlm.nih.gov/pubmed/24368907
http://dx.doi.org/10.3389/fmicb.2013.00384
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