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INTRODUCTION

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Cholera is an acute life-threatening disease characterized by enormous loss of fluid and electrolytes due to profuse diarrhea and vomiting. This waterborne disease has been responsible for global scourges for centuries; it is often seen in the wake of disaster situations, both manmade and natural.

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PATHOGENESIS AND EPIDEMIOLOGY

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Vibrio cholerae is an oxidase-positive, gram-negative, highly mobile, curved bacillus with a single polar flagellum. It is a slow lactose fermenter and also ferments glucose and sucrose. It grows easily in alkaline media in the presence of bile salts and is exquisitely sensitive to acid and to drying. The organism can be isolated on a variety of culture media, but a selective media, such as thiosulfate-citrate-bile salt sucrose (TCBS) agar, is recommended. On TCBS agar, V cholerae appear as 2- to 4-mm large, smooth, round, yellow colonies with opaque centers and translucent edges that contrast with the blue-green agar. Suspicious colonies can be rapidly identified by agglutination tests using specific V cholerae O1 and O139 antisera. Nontoxigenic strains of V cholerae are occasionally isolated from patients with diarrhea or sepsis.

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There are at least 200 somatic serogroups based on somatic (O) antigens. The strains of only 2 serogroups, O1 and O139, have been associated with epidemic cholera. Other non-O1/O139 V cholerae serogroups result in sporadic diarrhea and occasionally cause a variety of severe extraintestinal infections including wound infections and sepsis, especially among patients with liver disease or immunosuppression. The V cholerae O1 are divided into 3 serotypes, Ogawa, Inaba, and Hikojima, based on specific antigenic determinants. The V cholerae O1 are further divided into 2 biotypes, classical and El Tor. V cholerae O139, first identified in 1993, originated from V cholerae O1 El Tor strain through a mutation in the O1 antigen leading to the substitution of O139 antigen.

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Several genes are responsible for the virulence of V cholerae. Only epidemic strains of V cholerae O1 and V cholerae O139 possess the ctxA and ctxB genes that encode for enterotoxin subunits A and B. The B subunits bind to GM1 ganglioside receptors on enterocytes, after which the A subunit enters the cell. The A subunit irreversibly activates the adenylate cyclase system in the mucosa, leaving it in the “on” position, leading to increases in the intracellular concentration of cyclic adenosine monophosphate, which results in sodium and water loss. Thus, the active secretion of sodium and chloride into the gut lumen with water following it passively results in secretion of isotonic fluid into the small intestine surpassing the absorptive capacity of the colon. This results in volume depletion and shock. Loss of bicarbonate and potassium also occurs, and this leads to metabolic acidosis and hypokalemia.

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The current characterization of the ecology of cholera includes global weather patterns, aquatic reservoirs, bacteriophages, zooplankton, the collective behavior of surface-attached cells, an adaptable genome, and the deep sea, together with the bacterium ...

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