Vibrio cholerae

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A Microbial Biorealm page on the genus Vibrio cholerae

Vibrio cholerae with its single polar flagellum. Electron Micrograph of Vibrio cholerae by Leodotia Pope, Department of Microbiology, University of Texas at Austin.

Classification

Higher order taxa

Bacteria; Proteobacteria; Gammaproteobacteria; Vibrionales; Vibrionaceae; Vibrio

Species

NCBI: Taxonomy

Vibrio cholerae

Description and significance

Gram-stain of Vibrio comma bacteria, a strain of V. cholerae. CDC Public Health Image Library (PHIL). 1979. Click to enlarge.

Vibrio cholerae is a "comma" shaped gram negative1 bacteria with a single, polar flagellum for movement. There are numerous strains of V. cholerae, some of which are pathogenic and some of which are not.


The most wide sweeping pathogenic strain is the Vibrio cholerae serotype O1 El Tor N16961 strain that causes the pandemic disease cholera.2 The latest pathogenic serotype O139 was discovered in 1992. The El Tor strain was active in the seventh and most recent pandemic of cholera from 1960's-1970's, as well as in the early 1990's along with serotype O139, both displaying resistance to multiple drugs.7


The bacteria infects the intestine and increases mucous production causing diarrhea and vomiting which result in extreme dehydration and, if not treated, death. It is usually transmitted through the feces of an infected person, often by way of unclean drinking water or contaminated food.2 Since water treatment and sanitation is more advanced in the United States, cholera is not nearly as high of a public health threat in the US as it is in densely populated, economically reduced areas like India or sub-Saharan Africa where water and sewage treatment technology is low.2


It is for this great risk to human health that makes it so worthy of studying and sequencing. And because of the variety of strains, it could be possible to determine the pathogenicity of new strains by comparing their genomes to strains of known pathogenic status.


Click to enlarge.

Filippo Pacini first discovered V. cholereae in Italy in 1854, though it was originally believed to be Robert Koch who discovered it thirty years later in Berlin in 1884.Italians at that time believed that diseases like cholera came from "bad air" or the greek term "miasma." John Snow, a doctor known as the father of epidemiology, did a study during the London cholera epidemic of 1854 from which he concluded that cholera was not passed by bad air but by contaminated water, and discovered that a well that provided water to the public was collecting the leachings of a bacteria laden cesspit. Snow had the handle removed from a water pump that was found to be the neighborhood's source of the contaminated water, and immediately the epidemic began to subside.4, 5


Genome structure

Chromosome 1 (bottom) and chromosome 2 (top) of V. cholerae El Tor N16961 strain. (Heidelberg, J.F., et al.) Click to enlarge.

The entire genome of the virulent strain V. cholerae El Tor N16961 has been sequenced,1 and contains two circular chromosomes.3 Chromosome 1 has 2,961,149 base pairs with 2,770 open reading frames (ORF’s) and chromosome 2 has 1,072,315 base pairs, 1,115 ORF’s. It is the larger first chromosome that contains the crucial genes for toxicity, regulation of toxicity and important cellular functions, such as transcription and translation.1


The second chromosome is determined to be different from a plasmid or megaplasmid due to the inclusion of housekeeping and other essential genes in the genome, including essential genes for metabolism, heat-shock proteins and 16S rRNA genes. Also relevant in determining if the replicon is a chromosome is whether it represents a significant percentage of the genome. And, unlike plasmids, chromosomes are not self-transmissable.3 However it is believed that the second chromosome may have once been a megaplasmid because it contains some genes that are usually found on plasmids.1


Cell structure and metabolism

Describe any interesting features and/or cell structures; how it gains energy; what important molecules it produces.

When V. cholerae are growing during the logarithmic phase there is little or no change to the cellular envelope. However, towards the end of logarithmic phase and into the begining of stationary phase cholera toxin is produced, which is accompanied by internal swelling of the cell and permeability changes to the cellular envelope.6


Ecology

Describe any interactions with other organisms (included eukaryotes), contributions to the environment, effect on environment, etc.

Pathology

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

Cholera toxin (CT) is an enterotoxin made up of five B-subunits that form a pore to fits one A-subunit.8 CT is made from phage genes from a filamentous phage, CTXphi.9 A phage gene is also responsible for another virulence factor of V. cholerae, which is toxin co-regulated pilus (TCP), which acts as a receptor for CTXphi.10

Application to Biotechnology

Does this organism produce any useful compounds or enzymes? What are they and how are they used?

The non-toxic B-units of cholera toxin are used for several purposes in cellular and molecular biology.

Current Research

V. cholerae communicate with each other through a system called quorum sensing. Autoinducers are molecules that cells use to communicate, and to coordinate a specific function or gene expression as a group. Quorum sensing in V. cholerae has been paralleled to a well known system in V. harveyi, a bacteria that is pathogenic to tiger prawns but not to humans.11


V. harveyi use quorum sensing to bioluminesce by expression of lux gene. Some V. cholerae strains that are not pathogenic are also known to bioluminesce. It was shown that luxO represses lux as mutant V. harveyi missing luxO bioluminesced without decreasing in brightness, and that luxR expresses lux as mutant V. harveyi missing luxR did not bioluminesce at all.11


References

1. Heidelberg, J.F., Eisen, J.A., Nelson, W.C., et al. DNA sequence of both chromosomes of the cholera pathogen Vibrio cholerae. Nature. (2000);406 (6795), 477-483.

2. Center for Disease Control, Coordinating Center for Infectious Diseases / Division of Bacterial and Mycotic Diseases, October 6, 2005. http://www.cdc.gov/ncidod/dbmd/diseaseinfo/cholera_g.htm

3. Trucksis, M., Michalski, J., Deng, Y.K., Kaper, J.B. The Vibrio cholerae genome contains two unique circular chromosomes. Proc. Natl Acad. Sci. USA (1998);95, 14464-14469.

4. Bentivoglio, M., Pacini, P. Filippo Pacini: a determined observer. Brain Res Bull. (1995);38(2):161-5.

5. Howard-Jones N. Robert Koch and the cholera vibrio: a centenary. British Medical Journal. (1984);288, 379-381.

6. Kennedy, J.R., Stephen, H.R. Fine Structure of Vibrio cholerae During Toxin Production. J Bacteriol. (December 1969);100(3): 1393–1401.

7. Ingole, K.V., Jalgaonkar, S.V., Fule, C., Fule, R.P. Changing pattern of Vibrio cholerae serotype EL TOR and 0139 in Yavatmal (Maharashtra, India) during 1992 to 1994. Indian J Pathol Microbiol. (July 1997);40(3):369-71.

8. Zhang R., Scott D., Westbrook M., Nance S., Spangler B., Shipley G., Westbrook E. (1995). The three-dimensional crystal structure of cholera toxin. J Mol Biol 251 (4): 563-73.

9. Davis B., Waldor M. Filamentous phages linked to virulence of Vibrio cholerae. Curr Opin Microbiol. (2003);6 (1): 35-42.

10. Boyd, E.F., Waldor, M.K. Evolutionary and functional analyses of variants of the toxin-coregulated pilus protein TcpA from toxigenic Vibrio cholerae non-O1/non-O139 serogroup isolates. Microbiology. (2002);148, 1655-1666.

10. Miller, M.B., Skorupski, K., Lenz, D.H., Taylor, R.K., Bassler, B.L. Parallel quorum sensing systems converge to regulate virulence in Vibrio cholerae. Cell. (2002);110, 303-314.

Edited by Sasha Gardner, student of Rachel Larsen