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 Pacini
in 1854, but his discovery was not widely known until Robert Koch,
working independently 30 years later, publicized the knowledge and the
means of fighting the disease.
3 Preventative measures
Vibrio pathogenicity island
5 Ecology and epidemiology
6 Diversity and evolution
7 Natural genetic transformation
9 See also
11 External links
V. cholerae is
Gram-negative and 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
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; frequently wash hands
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. A single dose vaccine is available for those
traveling to an area where cholera is common.
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
Vibrio pathogenicity island (VPI).
The entire genome of the virulent strain V. cholerae
El Tor N16961 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
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.
Vibrio pathogenicity island
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.
Ecology and epidemiology
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.
Cholera 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
Gene transfer is fairly common amongst bacteria, and
recombination of different V. cholerae genes can lead to new virulent
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.
Diversity and evolution
Two serogroups of V. cholerae, O1 and O139, cause outbreaks of
cholera. O1 causes the majority of outbreaks, while O139 – first
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
El Tor biotype 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.
Natural genetic transformation
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
Vibrio cholerae bacteria
Diagram of the bacterium, V. cholerae
Microscope slide with a sample of "colera asiaticus", prepared by
Pacini in 1854
Molecular and Cellular Biology portal
Haiti cholera outbreak
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Wikimedia Commons has media related to
Wikispecies has information related to
Copepods and cholera in untreated water
El Tor N16961 Genome Page
Type strain of
Vibrio cholerae at
BacDive - the Bacterial Diversity
Strains: El Tor
Discovery: 1854 Broad Street cholera outbreak
Oral rehydration therapy
Cholera pandemics: 1817–24 cholera pandemic
1829–51 cholera pandemic
1852–60 cholera pandemic
1863–75 cholera pandemic
1881–96 cholera pandemic
1899–1923 cholera pandemic
1961–75 cholera pandemic
Other outbreaks: 1854 Broad Street cholera outbreak
2007 Iraq cholera outbreak
2008 Congo cholera outbreak
2008 Zimbabwean cholera outbreak
2010 Haiti cholera outbreak
2012 Sierra Leonean cholera outbreak
2014–15 African cholera outbreak
2016–17 Yemen cholera outbreak
Bacterial disease: Proteobacterial G−
primarily A00–A79, 001–041, 080–109
Epidemic typhus, Brill–Zinsser disease, Flying squirrel typhus
Rocky Mountain spotted fever
Japanese spotted fever
North Asian tick typhus
Queensland tick typhus
Flinders Island spotted fever
African tick bite fever
American tick bite fever
Rickettsia aeschlimannii infection
Flea-borne spotted fever
Ehrlichiosis: Anaplasma phagocytophilum
Human granulocytic anaplasmosis, Anaplasmosis
Human monocytotropic ehrlichiosis
Ehrlichiosis ewingii infection
Bartonellosis: Bartonella henselae
Either B. henselae or B. quintana
Carrion's disease, Verruga peruana
Meningococcal disease, Waterhouse–Friderichsen syndrome,
Eikenella corrodens/Kingella kingae
Burkholderia cepacia complex
Bordetella pertussis/Bordetella parapertussis
Rhinoscleroma, Klebsiella pneumonia
Escherichia coli: Enterotoxigenic
Enterobacter aerogenes/Enterobacter cloacae
Citrobacter koseri/Citrobacter freundii
Typhoid fever, Paratyphoid fever, Salmonellosis
Shigellosis, Bacillary dysentery
Proteus mirabilis/Proteus vulgaris
Far East scarlet-like fever
Brazilian purpuric fever
Legionella pneumophila/Legionella longbeachae
Aeromonas hydrophila/Aeromonas veronii
Campylobacteriosis, Guillain–Barré syndrome
Peptic ulcer, MALT lymphoma, Gastric cancer