Foodborne Toxico-Infections ◾ 379
cholera cases (also designated as non-O1 gastroenteritis) in the United States and other countries.
Non-O1 strains were previously thought to be incapable of causing large epidemics, but in 1992,
a non-O1 serotype, non-O139, was involved in large epidemics in Bangladesh and India. In 2011,
CDC reported that annually 84 people are infected by foodborne Vib. cholerae each year in the
United States without any fatality. 3
Characteristics
Vib. cholerae, like other vibrios, is a gram-negative motile, curved rod, and often carry a single
polar flagellum. The species has many serogroups. Strains in O1 and O139 are associated with epidemic cholera. The non-O1/non-O139 are rarely toxigenic and also seldom involved in outbreak.
The O1 serotype is further characterized by biotype and serotype. 12 The type currently associated
with cholera epidemics worldwide is of the El Tor biotype. The O1 serotype is again classified into
Inaba, Ogawa, and Hikojima. O1 serotype does not have a capsule while O139 carries a capsule.
Non-O1 serotypes do not agglutinate with antibodies prepared against O1 antigens. Also, nonO1 serotypes, similar to O1 serotypes, are not sensitive to trimethoprim-sulfamethoxazole with
furazolidone. Both types are sensitive to heat and are killed by the temperature used for cooking.
Improper heating (at lower temperatures for a shorter time) may not be able to kill all the cells
present in a food. The optimum temperature of growth is between 30°C and 37°C. The growth
rate is very rapid, even at room temperature. The cells do not multiply in contaminated live crabs,
oysters, or fish. However, in cooked seafoods, rapid growth can occur at 25°C–35°C. Alkaline
foods facilitate rapid growth. Survival of cells is better in cooked foods at 5°C–10°C.
Habitat
Cholera is a human disease. The disease results from the ingestion of infective doses of Vib. cholerae cells
through food and water contaminated with feces of humans suffering from the disease. Chronic carriers are rare and may not be important in large epidemics. Marine environments may serve as long-term
reservoirs. Both serotypes, especially non-O1, have been isolated from water in the U.S. Gulf Coast
states (Florida, Louisiana, and Texas), in Chesapeake Bay, and along California coasts. Seafoods (crab,
oysters, and finfish) harvested from these areas can carry contamination and provide the infective dose.
Contaminated water can also be the source of the disease.
Toxins and Toxin Production 12
The pathogenic strains (O1 and O139 serotypes) harbor a cholera toxin prophage (CTXΦ) that
carries the genes that encode the cholera toxin (CT), which is responsible for the major clinical
symptoms of the disease. CT is an 85-kDa cytotoxic protein, heat labile, and it is also called A-B
toxin. The B subunit binds to a specific cell receptor (GM1) on host enterocytes, and the toxin
is internalized, stimulates adenylate cyclase, leading to elevated intracellular cAMP levels, and
resulting in a major loss of water and electrolytes in profuse secretory diarrhea. There is a massive
secretion of water along with chloride, potassium, and bicarbonate in the lining of the intestine.
In addition, bacteria also produce pili called toxin coregulated pilus (TCP) and chitin binding
protein that help colonization in the gut. The non-O1 and O139 serotypes produce a cytotoxin
and a hemolysin but seldom cause outbreak. Following ingestion of Vib. cholerae cells in sufficient
numbers, the cells colonize the small intestine and multiply rapidly and produce toxins. When the
cells die and lyse, the toxins are released into the intestine.
cholera cases (also designated as non-O1 gastroenteritis) in the United States and other countries.
Non-O1 strains were previously thought to be incapable of causing large epidemics, but in 1992,
a non-O1 serotype, non-O139, was involved in large epidemics in Bangladesh and India. In 2011,
CDC reported that annually 84 people are infected by foodborne Vib. cholerae each year in the
United States without any fatality. 3
Characteristics
Vib. cholerae, like other vibrios, is a gram-negative motile, curved rod, and often carry a single
polar flagellum. The species has many serogroups. Strains in O1 and O139 are associated with epidemic cholera. The non-O1/non-O139 are rarely toxigenic and also seldom involved in outbreak.
The O1 serotype is further characterized by biotype and serotype. 12 The type currently associated
with cholera epidemics worldwide is of the El Tor biotype. The O1 serotype is again classified into
Inaba, Ogawa, and Hikojima. O1 serotype does not have a capsule while O139 carries a capsule.
Non-O1 serotypes do not agglutinate with antibodies prepared against O1 antigens. Also, nonO1 serotypes, similar to O1 serotypes, are not sensitive to trimethoprim-sulfamethoxazole with
furazolidone. Both types are sensitive to heat and are killed by the temperature used for cooking.
Improper heating (at lower temperatures for a shorter time) may not be able to kill all the cells
present in a food. The optimum temperature of growth is between 30°C and 37°C. The growth
rate is very rapid, even at room temperature. The cells do not multiply in contaminated live crabs,
oysters, or fish. However, in cooked seafoods, rapid growth can occur at 25°C–35°C. Alkaline
foods facilitate rapid growth. Survival of cells is better in cooked foods at 5°C–10°C.
Habitat
Cholera is a human disease. The disease results from the ingestion of infective doses of Vib. cholerae cells
through food and water contaminated with feces of humans suffering from the disease. Chronic carriers are rare and may not be important in large epidemics. Marine environments may serve as long-term
reservoirs. Both serotypes, especially non-O1, have been isolated from water in the U.S. Gulf Coast
states (Florida, Louisiana, and Texas), in Chesapeake Bay, and along California coasts. Seafoods (crab,
oysters, and finfish) harvested from these areas can carry contamination and provide the infective dose.
Contaminated water can also be the source of the disease.
Toxins and Toxin Production 12
The pathogenic strains (O1 and O139 serotypes) harbor a cholera toxin prophage (CTXΦ) that
carries the genes that encode the cholera toxin (CT), which is responsible for the major clinical
symptoms of the disease. CT is an 85-kDa cytotoxic protein, heat labile, and it is also called A-B
toxin. The B subunit binds to a specific cell receptor (GM1) on host enterocytes, and the toxin
is internalized, stimulates adenylate cyclase, leading to elevated intracellular cAMP levels, and
resulting in a major loss of water and electrolytes in profuse secretory diarrhea. There is a massive
secretion of water along with chloride, potassium, and bicarbonate in the lining of the intestine.
In addition, bacteria also produce pili called toxin coregulated pilus (TCP) and chitin binding
protein that help colonization in the gut. The non-O1 and O139 serotypes produce a cytotoxin
and a hemolysin but seldom cause outbreak. Following ingestion of Vib. cholerae cells in sufficient
numbers, the cells colonize the small intestine and multiply rapidly and produce toxins. When the
cells die and lyse, the toxins are released into the intestine.