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The genus Vibrio consists of Gram-negative straight or curved rods, motile by means of a single polar flagellum. Vibrios are capable of both respiratory and fermentative metabolism. O₂ is a universal electron acceptor; they do not denitrify. Most species are oxidase-positive. In most ways vibrios are related to enteric bacteria, but they share some properties with pseudomonads a well. The Family Vibrionaceae is found in the "Facultatively Anaerobic Gram-negative Rods" in Bergey's Manual (1986), on the level with the Family Enterobacteriaceae. In the revisionist taxonomy of 2001 (Bergey's Manual), based on phylogenetic analysis, Vibrionaceae, Pseudomonadaceae and Enterobacteriaceae are all landed in the  Gammaproteobacteria. Vibrios are distinguished from enterics by being oxidase-positive and motile by means of polar flagella. Vibrios are distinguished from pseudomonads by being fermentative as well as oxidative in their metabolism. Of the vibrios that are clinically significant to humans, Vibrio cholerae,the agent of cholera, is the most important.

Most vibrios have relatively simple growth factor requirements and will grow in synthetic media with glucose as a sole source of carbon and energy. However, since vibrios are typically marine organisms, most species require 2-3% NaCl or a sea water base for optimal growth. Vibrios vary in their nutritional versatility, but some species will grow on more than 150 different organic compounds as carbon and energy sources, occupying the same level of metabolic versatility as Pseudomonas. In liquid media vibrios are motile by polar flagella that are enclosed in a sheath continuous with the outer membrane of the cell wall. On solid media they may synthesize numerous lateral flagella which are not sheathed.

Vibrios are one of the most common organisms in surface waters of the world. They occur in both marine and freshwater habitats and in associations with aquatic animals. Some species are bioluminescent and live in mutualistic associations with fish and other marine life. Other species are pathogenic for fish, eels, and frogs, as well as other vertebrates and invertebrates.

V. cholerae and V. parahaemolyticus are pathogens of humans. Both produce diarrhea, but in ways that are entirely different. V. parahaemolyticus is an invasive organism affecting primarily the colon; V. cholerae is noninvasive, affecting the small intestine through secretion of an enterotoxin. Vibrio vulnificus is an emerging pathogen of humans. This organism causes wound infections, gastroenteritis, or a syndrome known as "primary septicemia."

Campylobacter jejuni (formerly Vibrio fetus), is now moved to the class Epsilonproteobacteria in the the family Campylobacteraceae. Campylobacter jejuni has been associated with dysentery-like gastroenteritis, as well as with other types of infection, including bacteremic and central nervous system infections in humans. Another vibrio-like organism, Helicobacter pylori causes duodenal and gastric ulcers and gastric cancer. It is also reclassified into the class Epsilonproteobacteria family Helicobacteraceae.


Vibrio cholerae

Cholera

Cholera (frequently called Asiatic cholera or epidemic cholera) is a severe diarrheal disease caused by the bacterium Vibrio cholerae. Transmission to humans is by water or food. The natural reservoir of the organism is not known. It was long assumed to be humans, but some evidence suggests that it is the aquatic environment.

V. cholerae produces cholera toxin, the model for enterotoxins, whose action on the mucosal epithelium is responsible for the characteristic diarrhea of the disease cholera. In its extreme manifestation, cholera is one of the most rapidly fatal illnesses known. A healthy person may become hypotensive within an hour of the onset of symptoms and may die within 2-3 hours if no treatment is provided. More commonly, the disease progresses from the first liquid stool to shock in 4-12 hours, with death following in 18 hours to several days.

The clinical description of cholera begins with sudden onset of massive diarrhea. The patient may lose gallons of protein-free fluid and associated electrolytes, bicarbonates and ions within a day or two. This results from the activity of the cholera enterotoxin which activates the adenylate cyclase enzyme in the intestinal cells, converting them into pumps which extract water and electrolytes from blood and tissues and pump it into the lumen of the intestine. This loss of fluid leads to dehydration, anuria, acidosis and shock. The watery diarrhea is speckled with flakes of mucus and epithelial cells ("rice-water stool") and contains enormous numbers of vibrios. The loss of potassium ions may result in cardiac complications and circulatory failure. Untreated cholera frequently results in high (50-60%) mortality rates.

Treatment of cholera involves the rapid intravenous replacement of the lost fluid and ions. Following this replacement, administration of isotonic maintenance solution should continue until the diarrhea ceases. If glucose is added to the maintenance solution it may be administered orally, thereby eliminating the need for sterility and iv. administration. By this simple treatment regimen, patients on the brink of death seem to be miraculously cured and the mortality rate of cholera can be reduced more than ten-fold. Most antibiotics and chemotherapeutic agents have no value in cholera therapy, although a few (e.g. tetracyclines) may shorten the duration of diarrhea and reduce fluid loss.