356 ◾ Fundamental Food Microbiology
epidemic outbreak, Shi. flexneri and Shi. sonnei cause endemic disease, and Shi. boydii causes rare
disease. Only humans and some primates serve as their hosts. The organisms are either transmitted
directly through fecal-oral routes or indirectly through fecal-contaminated food and water. While
in most developed countries transmission through drinking water has been reduced, in developing countries contaminated drinking water is a major cause of shigellosis or bacillary dysentery.
The disease is prevalent in some geographic locations, particularly in Asia, Mexico, and South
America. It occurs more frequently in places with poor sanitation. In the United States, shigellosis
occurs more among migrant workers, on Indian reservations, in poor urban institutions, and in
daycare centers. Children below five years of age are more affected. In developing countries, there
is a high fatality rate among children suffering from shigellosis. In the United States, before the
1950s, the predominant species was Shi. dysenteriae. At present, the predominant species is Shi.
sonnei. In the United States, between 1983 and 1987, there were 44 outbreaks, affecting 9971
people with two deaths. In one outbreak in 1987, several thousand people were affected by eating
commercial meals prepared under poor hygienic conditions that resulted in contamination of food
with Shi. sonnei. The CDC estimates Shigella spp. cause about 130,000 cases with 10 deaths annually in the United States. 29 In general, food service establishments have been implicated in more
outbreaks, and poor personal hygiene has been the major cause. The disease is more predominant
during late spring to early fall.
Characteristics
The cells of the species are Gram-negative, nonmotile, facultative anaerobic rods. They are generally catalase positive and oxidase and lactose negative. They ferment sugars, usually without
forming gas. On the basis of DNA homology, both Shigella and Escherichia can be included in one
genus, and because of many biochemical similarities, the separation between the two genera is not
clear. There are suggestions that Shigella species could be pathogenic variants of Esc. coli. They are
more like Shiga-toxin-producing Esc. coli with Shigella O antigen.
The strains grow between 7°C and 46°C with an optimum at 37°C. The cells are not as fragile as once thought. They survive for days under different physical and chemical stresses, such as
refrigeration, freezing, 5% NaCl, and pH 4.5. They are killed by pasteurization. The strains can
multiply in many types of food when stored in the growth temperature range.
Habitat
The intestine of humans and some primates are the only habitats known. Humans can carry the
organism in the intestine and shed it in the feces without showing any symptoms. Following
recovery from shigellosis, an individual can remain a carrier for months.
Toxins
The strains are believed to carry plasmid-encoded invasive traits that enable the shigellae cells to
invade epithelial mucosa of the small and large intestines. Once engulfed by the epithelial cells,
they produce an exotoxin that has an enterotoxigenic property. The toxin is designated as Shiga
toxin (Stx). The invasive trait is expressed at 37°C but not at 30°C. Shigellae cells growing at
30°C need a few hours of conditioning at 37°C before they can invade intestinal epithelial cells.
The engulfed shigellae cells kill the epithelial cells and then attack fresh cells, causing ulcers and
lesions.
epidemic outbreak, Shi. flexneri and Shi. sonnei cause endemic disease, and Shi. boydii causes rare
disease. Only humans and some primates serve as their hosts. The organisms are either transmitted
directly through fecal-oral routes or indirectly through fecal-contaminated food and water. While
in most developed countries transmission through drinking water has been reduced, in developing countries contaminated drinking water is a major cause of shigellosis or bacillary dysentery.
The disease is prevalent in some geographic locations, particularly in Asia, Mexico, and South
America. It occurs more frequently in places with poor sanitation. In the United States, shigellosis
occurs more among migrant workers, on Indian reservations, in poor urban institutions, and in
daycare centers. Children below five years of age are more affected. In developing countries, there
is a high fatality rate among children suffering from shigellosis. In the United States, before the
1950s, the predominant species was Shi. dysenteriae. At present, the predominant species is Shi.
sonnei. In the United States, between 1983 and 1987, there were 44 outbreaks, affecting 9971
people with two deaths. In one outbreak in 1987, several thousand people were affected by eating
commercial meals prepared under poor hygienic conditions that resulted in contamination of food
with Shi. sonnei. The CDC estimates Shigella spp. cause about 130,000 cases with 10 deaths annually in the United States. 29 In general, food service establishments have been implicated in more
outbreaks, and poor personal hygiene has been the major cause. The disease is more predominant
during late spring to early fall.
Characteristics
The cells of the species are Gram-negative, nonmotile, facultative anaerobic rods. They are generally catalase positive and oxidase and lactose negative. They ferment sugars, usually without
forming gas. On the basis of DNA homology, both Shigella and Escherichia can be included in one
genus, and because of many biochemical similarities, the separation between the two genera is not
clear. There are suggestions that Shigella species could be pathogenic variants of Esc. coli. They are
more like Shiga-toxin-producing Esc. coli with Shigella O antigen.
The strains grow between 7°C and 46°C with an optimum at 37°C. The cells are not as fragile as once thought. They survive for days under different physical and chemical stresses, such as
refrigeration, freezing, 5% NaCl, and pH 4.5. They are killed by pasteurization. The strains can
multiply in many types of food when stored in the growth temperature range.
Habitat
The intestine of humans and some primates are the only habitats known. Humans can carry the
organism in the intestine and shed it in the feces without showing any symptoms. Following
recovery from shigellosis, an individual can remain a carrier for months.
Toxins
The strains are believed to carry plasmid-encoded invasive traits that enable the shigellae cells to
invade epithelial mucosa of the small and large intestines. Once engulfed by the epithelial cells,
they produce an exotoxin that has an enterotoxigenic property. The toxin is designated as Shiga
toxin (Stx). The invasive trait is expressed at 37°C but not at 30°C. Shigellae cells growing at
30°C need a few hours of conditioning at 37°C before they can invade intestinal epithelial cells.
The engulfed shigellae cells kill the epithelial cells and then attack fresh cells, causing ulcers and
lesions.