The Info List - Vibrio Cholerae

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_VIBRIO CHOLERAE_ is a Gram-negative, comma-shaped bacterium . The bacterium's natural habitat is brackish or saltwater. Some strains of _V. cholerae_ cause the disease cholera . _V. cholerae_ is a facultative anaerobe and has a flagellum at one cell pole as well as pili . _V. cholerae_ can undergo respiratory and fermentative metabolism. When ingested, _V. cholerae_ can cause diarrhea and vomiting in a host within several hours to 2–3 days of ingestion. _V. cholerae_ was first isolated as the cause of cholera by Italian anatomist Filippo Paciniin 1854, but his discovery was not widely known until Robert Koch
Robert Koch
, working independently 30 years later, publicized the knowledge and the means of fighting the disease.


* 1 Characteristics * 2 Pathogenesis * 3 Preventative measures

* 4 Genome

* 4.1 Bacteriophage
CTXφ * 4.2 _Vibrio_ pathogenicity island

* 5 Ecology and epidemiology * 6 Diversity and evolution * 7 Natural genetic transformation * 8 Gallery * 9 See also * 10 References * 11 External links


_V. cholerae_ is Gram-negativeand comma-shaped. Initial isolates are slightly curved, whereas they can appear as straight rods upon laboratory culturing. The bacterium has a flagellum at one cell pole as well as pili . _V. cholerae_ is a facultative anaerobe , and can undergo respiratory and fermentative metabolism.


_V. cholerae_ pathogenicity genes code for proteins directly or indirectly involved in the virulence of the bacteria. During infection, _V. cholerae_ secretes cholera toxin , a protein that causes profuse, watery diarrhea (known as "rice-water stool"). Colonization of the small intestine also requires the toxin coregulated pilus (TCP), a thin, flexible, filamentous appendage on the surface of bacterial cells. _V. cholerae_ can cause syndromes ranging from asymptomatic to cholera gravis. In endemic areas, 75% of cases are asymptomatic, 20% are mild to moderate, and 2-5% are severe forms such as cholera gravis. Symptoms include abrupt onset of watery diarrhea (a grey and cloudy liquid), occasional vomiting , and abdominal cramps. Dehydration
ensues, with symptoms and signs such as thirst, dry mucous membranes, decreased skin turgor, sunken eyes, hypotension , weak or absent radial pulse , tachycardia , tachypnea , hoarse voice, oliguria , cramps, renal failure , seizures , somnolence , coma, and death. Death due to dehydration can occur in a few hours to days in untreated children. The disease is also particularly dangerous for pregnant women and their fetuses during late pregnancy, as it may cause premature labor and fetal death. In cases of cholera gravis involving severe dehydration, up to 60% of patients can die; however, less than 1% of cases treated with rehydration therapy are fatal. The disease typically lasts 4–6 days. Worldwide, diarrhoeal disease , caused by cholera and many other pathogens, is the second-leading cause of death for children under the age of 5 and at least 120,000 deaths are estimated to be caused by cholera each year. In 2002, the WHO deemed that the case fatality ratio for cholera was about 3.95%.


When visiting areas with epidemic cholera, the following precautions should be observed: drink and use bottled water; wash hands often with soap and safe water; use chemical toilets or bury feces if no restroom is available; do not defecate in any body of water and cook food thoroughly.


_V. cholerae_ has two circular chromosomes , together totalling 4 million base pairs of DNA
sequence and 3,885 predicted genes . The genes for cholera toxin are carried by CTXphi (CTXφ), a temperate bacteriophage inserted into the _V. cholerae_ genome. CTXφ can transmit cholera toxin genes from one _V. cholerae_ strain to another, one form of horizontal gene transfer . The genes for toxin coregulated pilus are coded by the VPI pathogenicity island (VPI). The entire genome of the virulent strain _V. cholerae_ El TorN16961 has been sequenced, and contains two circular chromosomes. 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. The larger first chromosome contains the crucial genes for toxicity, regulation of toxicity, and important cellular functions, such as transcription and translation .

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, which are ribosomal subunit genes used to track evolutionary relationships between bacteria. Also relevant in determining if the replicon is a chromosome is whether it represents a significant percentage of the genome, and chromosome 2 is 40% by size of the entire genome. And, unlike plasmids, chromosomes are not self-transmissible. However, the second chromosome may have once been a megaplasmid because it contains some genes usually found on plasmids.

_V. cholerae_ contains a genomic island of pathogenicity and is lysogenized with phage DNA. That means that the genes of a virus were integrated into the bacterial genome and made the bacteria pathogenic. The molecular pathway involved in expression of virulence is discussed in the pathology and current research sections below.


CTXφ (also called CTXphi) is a filamentous phage that contains the genes for cholera toxin . Infectious CTXφ particles are produced when _V. cholerae_ infects humans. Phage
particles are secreted from bacterial cells without lysis . When CTXφ infects _V. cholerae_ cells, it integrates into specific sites on either chromosome. These sites often contain tandem arrays of integrated CTXφ prophage . In addition to the _ctxA_ and _ctxB_ genes encoding cholera toxin, CTXφ contains eight genes involved in phage reproduction, packaging, secretion, integration, and regulation. The CTXφ genome is 6.9 kb long.


The _Vibrio_ pathogenicity island (VPI) contains genes primarily involved in the production of toxin coregulated pilus (TCP). It is a large genetic element (about 40 kb) flanked by two repetitive regions (_att_-like sites), resembling a phage genome in structure. The VPI contains two gene clusters, the TCP cluster, and the ACF cluster, along with several other genes. The _acf_ cluster is composed of four genes: _acfABCD_. The _tcp_ cluster is composed of 15 genes: _tcpABCDEFHIJPQRST_ and regulatory gene _toxT_.


The main reservoirs of _V. cholerae_ are people and aquatic sources such as brackish water and estuaries , often in association with copepods or other zooplankton , shellfish , and aquatic plants.

infections are most commonly acquired from drinking water in which _V. cholerae_ is found naturally or into which it has been introduced from the feces of an infected person. Other common vehicles include contaminated fish and shellfish, produce, or leftover cooked grains that have not been properly reheated. Transmission from person to person, even to health care workers during epidemics, is rarely documented. _V. cholerae_ thrives in a aquatic environment , particularly in surface water. The primary connection between humans and pathogenic strains is through water, particularly in economically reduced areas that do not have good water purification systems.

Nonpathogenic strains are also present in water ecologies. The wide variety of pathogenic and nonpathogenic strains that co-exist in aquatic environments are thought to allow for so many genetic varieties. Gene transferis fairly common amongst bacteria, and recombination of different _V. cholerae_ genes can lead to new virulent strains.

A symbiotic relationship between _V. cholerae_ and _Ruminococcus obeum_ has been determined. _R. obeum_ autoinducer represses the expression of several _V. cholerae_ virulence factors . This inhibitory mechanism is likely to be present in other gut microbiota species which opens the way to mine the gut microbiota of members in specific communities which may utilize autoinducers or other mechanisms in order to restrict colonization by V.cholerae or other enteropathogens .


Two serogroups of _V. cholerae_, O1 and O139, cause outbreaks of cholera. O1 causes the majority of outbreaks, while O139 – first identified in Bangladesh
in 1992 – is confined to Southeast Asia. Many other serogroups of _V. cholerae_, with or without the cholera toxin gene (including the nontoxigenic strains of the O1 and O139 serogroups), can cause a cholera-like illness. Only toxigenic strains of serogroups O1 and O139 have caused widespread epidemics.

_V. cholerae_ O1 has two biotypes, classical and El Tor, and each biotype has two distinct serotypes, Inaba and Ogawa. The symptoms of infection are indistinguishable, although more people infected with the El Torbiotype remain asymptomatic or have only a mild illness. In recent years, infections with the classical biotype of _V. cholerae_ O1 have become rare and are limited to parts of Bangladesh
and India
. Recently, new variant strains have been detected in several parts of Asia and Africa. Observations suggest these strains cause more severe cholera with higher case fatality rates.


_V. cholerae_ can be induced to become competent for natural genetic transformation when grown on chitin , a biopolymer that is abundant in aquatic habitats (e.g. from crustacean exoskeletons). Natural genetic transformation is a sexual process involving DNA
transfer from one bacterial cell to another through the intervening medium, and the integration of the donor sequence into the recipient genome by homologous recombination . Transformation competence in _V. cholerae_ is stimulated by increasing cell density accompanied by nutrient limitation, a decline in growth rate, or stress. The _V. cholerae_ uptake machinery involves a competence -induced pilus , and a conserved DNA
binding protein that acts as a ratchet to reel DNA
into the cytoplasm.



_ Vibrio
cholerae_ bacteria *

Diagram of the bacterium, _V. cholerae_


* Molecular and Cellular Biology portal

* Drinking water
Drinking water
* Haiti cholera outbreak


* ^ _A_ _B_ _C_ _D_ _E_ _F_ _G_ "Laboratory Methods for the Diagnosis of Vibrio
cholerae" (PDF). Centre for Disease Control. Retrieved 29 October 2013.

* ^ See:

* Filippo Pacini(1854) "Osservazioni microscopiche e deduzioni patologiche sul cholera asiatico" (Microscopic observations and pathological deductions on Asiatic cholera), _Gazzetta by tiadwe Medica Italiana: Toscana_, 2nd series, 4 (50) : 397-401 ; 4 (51) : 405-412. The term "vibrio cholera" appears on page 411. * Reprinted (more legibly) as a pamphlet.

* ^ Bentivoglio, M; Pacini, P (1995). "Filippo Pacini: A determined observer". _Brain Research Bulletin_. 38 (2): 161–5. PMID 7583342 . doi :10.1016/0361-9230(95)00083-Q . * ^ _A_ _B_ _C_ _D_ _E_ _F_ _G_ _H_ _I_ Howard-Jones, N (1984). " Robert Koch
Robert Koch
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