_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
Filippo Paciniin 1854, but his discovery was not widely
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
* 4.2 _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
Dehydrationensues, 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
_V. cholerae_ has two circular chromosomes , together totalling 4
million base pairs of
DNAsequence 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
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.
Phageparticles 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
_VIBRIO_ PATHOGENICITY ISLAND
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_.
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.
Cholerainfections 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 transferis fairly common amongst bacteria, and
recombination of different _V. cholerae_ genes can lead to new
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
DIVERSITY AND EVOLUTION
Two serogroups of _V. cholerae_, O1 and O139, cause outbreaks of
cholera. O1 causes the majority of outbreaks, while O139 – first
Bangladeshin 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 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
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
DNAtransfer 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
DNAbinding protein that acts as a ratchet to reel
Diagram of the bacterium, _V. cholerae_
* Molecular and Cellular Biology portal
Haiti cholera outbreak
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