Abstract
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.
Highlights
Vibrio cholerae – the causative agent of the diarrheal disease cholera – is an ancient companion of human civilization
toxin co-regulated pilus (TCP) biosynthesis genes are encoded within a horizontally transferred mobile genetic element known as Virulence Pathogenicity Island I (VPI-I) that in addition to TCP and other accessory genes encodes several transcriptional activators and virulence factors required for pandemic spread of V. cholerae (Karaolis et al, 1998)
The contribution of CTX-φ to bacterial pathogenesis brought to light a remarkable example of mutualism between a bacteriophage and a bacterial pathogen, because only V. cholerae strains encoding cholera toxin (CT) are capable of pandemic spread (Waldor and Mekalanos, 1996)
Summary
Vibrio cholerae – the causative agent of the diarrheal disease cholera – is an ancient companion of human civilization. Mucin-supported growth may be important in the small intestine – the host environment colonized by V. cholerae. Perhaps V. cholerae’s ancestral role as a chitin degrader in marine environments is the reason for the ability of the cholera bacterium to bind mucin in the human intestine.
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