[1] The bacteria naturally live in brackish or saltwater where they attach themselves easily to the chitin-containing shells of crabs, shrimp, and other shellfish.

Ringers lactate and Oral rehydration solution combined with antibiotics such as fluoroquinolones and tetracyclines are the common treatment methods in severe cases.

One chromosomes produces the cholera toxin (CT), a protein that causes profuse, watery diarrhea (known as "rice-water stool").

The English physician John Snow was the first to give convincing evidence in London in 1854 that cholera was spread from drinking water – a contagion, not miasma.

[10] His presentation before the French Academy of Sciences on 23 April was recorded as: "[Pouchet] could verify that there existed in these [cholera patients] 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.

An Italian physician, Filippo Pacini, while investigating cholera outbreak in Florence in the late 1854, identified the causative pathogen as a new type of bacterium.

[12][13] Reporting his discovery before the Società Medico-Fisica Fiorentina (Medico-Physician Society of Florence) on 10 December, and published in the 12 December issue of the Gazzetta Medica Italiana (Medical Gazette of Italy), Pacini stated:Le poche materie del vomito che ho potuto esaminare nel secondo e terzo caso di cholera ... e di più trovai degli ammassi granulosi appianati, simili a quelli che si formano alla superficie delle acque corrotte, quando sono per svilupparsi dei vibrioni; dei quali di fatto ne trovai alcuni del genere Bacterium, mentre la massima parte, per la loro estrema piccolezza, erano stati eliminati con la decantazione del fluido.

[From the few samples of vomit that I was able to examine in the second and third cases of cholera ... and in addition I found smoothed granular masses, similar to those which form on the surface of dirty waters, when they are about to develop vibrios; of which in fact I found some of the genus Bacterium, while the greatest part, because of their extreme smallness, had been eliminated with the removal of the liquid.

[14]]Pacini thus introduced the name vibrioni (Latin vībro means "to move rapidly to and fro, to shake, to agitate").

Pacini also stated that there was no reason to say that the bacterium caused the disease since he failed to create a pure culture and perform experiments, which was necessary 'to attribute the quality of contagion to cholera'.

[17] The medical importance and relationship between the bacterium and the cholera disease was discovered by German physician Robert Koch.

[18] Koch found that the intestinal mucosa of people who died of cholera always had the bacterium, yet he could not confirm if it was the causative agent.

But an Italian bacteriologist Vittore Trevisan published in 1884 that Koch's bacterium was the same as that of Pacini's and introduced the name Bacillus cholerae.

[31] V. cholerae pathogenicity genes code for proteins directly or indirectly involved in the virulence of the bacteria.

To adapt the host intestinal environment and to avoid being attacked by bile acids and antimicrobial peptides, V. cholera uses its outer membrane vesicles (OMVs).

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.

[34][35] 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).

[37] Symptoms include abrupt onset of watery diarrhea (a grey and cloudy liquid), occasional vomiting, and abdominal cramps.

[1][37] 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, seizures, somnolence, coma, and death.

The disease is also particularly dangerous for pregnant women and their fetuses during late pregnancy, as it may cause premature labor and fetal death.

The major symptoms include: watery diarrhea, vomiting, rapid heart rate, loss of skin elasticity, low blood pressure, thirst, and muscle cramps.

[48] When patients are severely dehydrated and unable to take in the proper amount of ORS, IV fluid treatment is generally pursued.

[48] V. cholerae (and Vibrionaceae in general)[51] has two circular chromosomes, together totalling 4 million base pairs of DNA sequence and 3,885 predicted genes.

Autoinducers, specifically with V. cholerae, can develop biofilms and control virulence in response to extracellular quorum-sensing molecules.

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).

[58] 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.