Cholera is a potentially epidemic and life-threatening secretory diarrhea characterized by numerous, voluminous watery stools, often accompanied by vomiting, and resulting in hypovolemic shock and acidosis. It is caused by certain members of the species Vibrio cholerae which can also cause mild or inapparent infections. Other members of the species may occasionally cause isolated outbreaks of milder diarrhea whereas others—the vast majority—are free-living and not associated with disease.
? Structure, Classification, and Antigenic Types
Vibrios are Gram-negative, highly motile curved rods with a single polar flagellum. They tolerate alkaline media that kill most intestinal commensals, but they are sensitive to acid. Numerous free-living vibrios are known, some potentially pathogenic. Until 1992, cholera was caused by only two serotypes, Inaba (AC) and Ogawa (AB), and two biotypes, classical and El Tor, of toxigenic O group 1 V cholerae. These organisms may be identified by agglutination in O group 1-specific antiserum directed against the lipopolysaccharide component of the cell wall and by demonstration of their enterotoxigenicity. In 1992, cholera caused by serogroup O139 (synonym ?Bengal? the 139th and latest serogroup of V cholerae to be identified) emerged in epidemic proportions in India and Bangladesh. This serovar is identified by 1) absence of agglutination in O group 1 specific antiserum; 2) by agglutination in O group 139 specific antiserum; and 3) by the presence of a capsule.
? Pathogenesis
Cholera is transmitted by the fecal-oral route. Vibrios are sensitive to acid, and most die in the stomach. Surviving virulent organisms may adhere to and colonize the small bowel, where they secrete the potent cholera enterotoxin (CT, also called ?choleragen?). This toxin binds to the plasma membrane of intestinal epithelial cells and releases an enzymatically active subunit that causes a rise in cyclic adenosine 51-monophosphate (cAMP) production. The resulting high intracellular cAMP level causes massive secretion of electrolytes and water into the intestinal lumen.Copyright © 1996
The University of Texas Medical Branch at Galveston