Throughout recorded history cholera [Greek chole, bile] has caused seven pandemics in various areas of the world, especially in Asia, the Middle East, and Africa. The disease has been rare in the United States since the 1800s, but an endemic focus is believed to exist on the gulf coast of Louisiana and Texas.
Cholera is caused by the gram-negative Vibrio cholerae bacterium of the family Vibrionaceae. Although there are many serogroups, only O1 and O139 have exhibited the ability to cause epidemics. V. cholerae O1 is divided into two serotypes, Inaba and Ogawa, and two biotypes, classic and E1 Tor. Cholera is acquired by ingesting food or water contaminated by fecal material from patients or carriers. (Shellfish and copepods are natural reservoirs.) In 1961 the E1 Tor biotype emerged as an important cause of cholera pandemics, and in 1992 the newly identified strain V. cholerae O139 emerged in Asia. This novel toxigenic strain does not agglutinate with O1 antiserum but possesses epidemic and pandemic potential. In Calcutta, India, serogroup O139 of Vibrio cholerae has displaced E1 Tor V. cholerae serogroup O1, an event that has never happened in the recorded history of cholera.
Once the bacteria enter the body, the incubation period is from 24 to 72 hours. The bacteria adhere to the intestinal mucosa of the small intestine, where they are not invasive but secrete choleragen, a cholera toxin.
Choleragen is a protein composed of two functional units, an enzymatic A subunit and an intestinal receptor-binding B subunit. The A subunit enters the intestinal epithelial cells and activates the enzyme adenylate cyclase by the addition of an ADP-ribosyl group in a way similar to that employed by diphtheria toxin. As a result choleragen stimulates hypersecrection of water and chloride ions while inhibiting absorption of sodium ions. The patient loses massive quantities of fluid and electrolytes, which is associated with abdominal muscle cramps, vomiting, fever, and watery diarrhea. The diarrhea can be so profuse that a person can lose 10 to 15 liters of fluid during the infection. Death may result from the elevated concentrations of blood proteins, caused by reduced fluid levels, which leads to circulatory shock and collapse. There is now evidence that the cholera toxin gene is carried by the CTX filamentous bacteriophage. The phage binds to the pilus used to colonize the host’s gut, enters the bacterium, and incorporates its genes into the bacterial chromosome.
Recent evidence indicates that passage through the human host enhances infectivity. Before V. cholerae exits the body in watery stools, the intestinal environment stimulates the activity of certain genes. These genes, in turn, seem to prepare the bacteria for ever more effective colonization of their next victims, possibly fueling epidemics.
Laboratory diagnosis is by culture of the bacterium from feces and subsequent identification by agglutination reactions with specific antisera. Treatment is by oral rehydration therapy with NaCl plus glucose to stimulate water uptake by the intestine; the antibiotics of choice are a tetracycline, trimethoprim-sulfamethoxazole, or ciprofloxacin. The most reliable control methods are based on proper sanitation, especially of water supplies. The mortality rate without treatment is often over 50%; with treatment and supportive care, it is less than 1%. Fewer than 20 cases of cholera are reported each year in the United States.
(Prescott, L.M., Harley, J.P., Klein, D.A. 2005. Microbiology, 6th ed. New York: McGraw-Hill)