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Vibrio cholerae is a species of Gram-negative, facultative anaerobe and Vibrio bacteria. The bacteria naturally live in Brackish water or saltwater where they attach themselves easily to the chitin-containing shells of crabs, shrimp, and other shellfish. Some strains of V. cholerae are pathogenic to humans and cause a deadly disease called cholera, which can be derived from the consumption of undercooked or raw marine life species or drinking contaminated water.
V. cholerae was first described by Félix-Archimède Pouchet in 1849 as some kind of protozoa. Filippo Pacini correctly identified it as a bacterium and from him, the scientific name is adopted. The bacterium as the cause of cholera was discovered by Robert Koch in 1884. Sambhu Nath De isolated the cholera toxin and demonstrated the toxin as the cause of cholera in 1959.
The bacterium has a flagellum (a tail like structure) at one pole and several Pilus throughout its cell surface. It undergoes respiratory and fermentative metabolism. Two serotype called O1NCBI: Vibrio cholerae O1 (serogroup) and O139NCBI: Vibrio cholerae O139 (serogroup) are responsible for cholera outbreaks. Infection is mainly through drinking contaminated water or ingestion of food contaminated with faecal matter from an infected person, therefore is linked to sanitation and hygiene. When ingested, it invades the intestinal mucosa which can cause diarrhea and vomiting in a host within several hours to 2–3 days of ingestion. Ringers lactate and Oral rehydration solution combined with antibiotics such as fluoroquinolones and are the common treatment methods in severe cases.
V. cholerae has two circular chromosomes. One chromosomes produces the cholera toxin (CT), a protein that causes profuse, watery diarrhea (known as "rice-water stool"). But the DNA does not directly code for the toxin as the genes for cholera toxin are carried by CTXphi (CTXφ), a temperate bacteriophage (virus). The virus only produces the toxin when inserted into the bacterial DNA. Quorum sensing in V. cholerae is well studied and it activates host immune signaling and prolongs host survival, by limiting the bacterial intake of nutrients, such as tryptophan, which further is converted to serotonin. As such, quorum sensing allows a Commensalism interaction between host and pathogenic bacteria.
V. cholerae was first observed and recognized under microscope by the French zoologist Félix-Archimède Pouchet. In 1849, Pouchet examined the stool samples of four people having cholera. His presentation before the French Academy of Sciences on 23 April was recorded as: "Pouchet could verify that there existed in these cholera dejecta an immense quantity of microscopic infusoria." As summarised in the Gazette medicale de Paris (1849, p 327), in a letter read at the 23 April 1849 meeting of the Paris Academy of Sciences, Pouchet announced that the organisms were infusoria, a name then used for microscopic protists, naming them as the 'Vibrio rugula of Mueller and Shrank', a species of protozoa described by Danish naturalist Otto Friedrich Müller in 1786.
Although Koch was convinced that the bacterium was the cholera pathogen, he could not entirely procure critical evidence that the bacterium produced the symptoms in healthy subjects (an important element in what was later known as Koch's postulates). His experiment on animals using his pure bacteria culture did not lead to the appearance of the disease in any of the subjects, and he correctly deduced that animals are immune to the human pathogen. The bacterium was by then known as "the comma bacillus." It was only in 1959, in Calcutta, that Indian physician Sambhu Nath De isolated the cholera toxin and showed that it caused cholera in healthy subjects, hence fully proving the bacterium-cholera relationship.
During infection, V. cholerae secretes cholera toxin (CT), a protein that causes profuse, watery diarrhea (known as "rice-water stool"). This cholera toxin contains 5 B subunits that plays a role in attaching to the intestinal epithelial cells and 1 A subunit that plays a role in toxin activity . Colonization of the small intestine also requires the toxin coregulated pilus (TCP), a thin, flexible, filamentous appendage on the surface of bacterial cells. Expression of both CT and TCP is mediated by two component systems (TCS), which typically consist of a membrane-bound histidine kinase and an intracellular response element. TCS enable bacteria to respond to changing environments. In V. cholerae several TCS have been identified to be important in colonization, biofilm production and virulence. Quorum regulatory small RNAs (Qrr RNA) have been identified as targets of V. cholerae TCS. Here, the small RNA (sRNA) molecules bind to mRNA to block translation or induce degradation of inhibitors of expression of virulence or colonization genes. In V. cholerae the TCS EnvZ/OmpR alters gene expression via the sRNA coaR in response to changes in osmolarity and pH. An important target of coaR is tcpI, which negatively regulates expression of the major subunit of the TCP encoding gene ( tcpA). When tcpI is bound by coaR it is no longer able to repress expression tcpA, leading to an increased colonization ability. Expression of coaR is upregulated by EnvZ/OmpR at a pH of 6,5, which is the normal pH of the intestinal lumen, but is low at higher pH values. V. cholerae in the intestinal lumen utilizes the TCP to attach to the intestinal mucosa, not invading the mucosa. After doing so it secretes cholerae toxin causing its symptoms. This then increases cyclic AMP or cAMP by binding (cholerae toxin) to adenylyl cyclase activating the GS pathway which leads to efflux of water and sodium into the intestinal lumen causing watery stools or rice watery stools.
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, kidney failure, , 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. A study done by the Centers for Disease Control (CDC) in Haiti found that in pregnant women who contracted the disease, 16% of 900 women had fetal death. Risk factors for these deaths include: third trimester, younger maternal age, severe dehydration, and vomiting Dehydration poses the biggest health risk to pregnant women in countries that there are high rates of cholera. 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%.
There is a V. cholerae vaccine available to prevent disease spread. The vaccine is known as the, "oral cholera vaccine" (OCV). There are three types of OCV available for prevention: Dukoral®, Shanchol™, and Euvichol-Plus®. All three OCVs require two doses to be fully effective. Countries who are endemic or have an epidemic status are eligible to receive the vaccine based on several criteria: Risk of cholera, Severity of cholera, WASH conditions and capacity to improve, Healthcare conditions and capacity to improve, Capacity to implement OCV campaigns, Capacity to conduct M&E activities, Commitment at national and local level"Oral Cholera Vaccines." World Health Organization, World Health Organization, 17 May 2018, www.who.int/cholera/vaccines/en/. Since May the start of the OCV program to May 2018 over 25 million vaccines have been distributed to countries who meet the above criteria.
The larger first chromosome is 3 Mbp long with 2,770 open reading frames (ORFs). It contains the crucial genes for toxicity, regulation of toxicity, and important cellular functions, such as transcription and translation.
The second chromosome is 1 Mbp long with 1115 ORFs. It 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, including a P1 plastid-like origin of replication.
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. Cholera is most likely to be found and spread in places with inadequate water treatment, poor sanitation, and inadequate hygiene. Other common vehicles include raw or undercooked fish and shellfish. Transmission from person to person is very unlikely, and casual contact with an infected person is not a risk for becoming ill. V. cholerae thrives in an 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 transfer is 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. Autoinducers, specifically with V. cholerae, can develop biofilms and control virulence in response to extracellular quorum-sensing molecules.
Outbreaks of Cholera cause an estimated 120,000 deaths annually worldwide. There has been roughly seven pandemics since 1817, the first. These pandemics first arose in the Indian subcontinent and spread.
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 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.
Bacteriophage CTXφ
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 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.
Ecology and epidemiology
The main reservoirs of V. cholerae are aquatic sources such as , , and estuaries, often in association with copepods or other zooplankton, shellfish, and aquatic plants.
Diversity and evolution
Two serotype 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.
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 cytoplasm. There are two models of genetic transformation, sex hypothesis and competent bacteria.
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