352 ◾ Fundamental Food Microbiology
Enterotoxigenic Escherichia coli (ETEC) 18,19
These strains are the major cause of diarrhea among travelers (also known as Traveler’s Diarrhea,
Montezuma’s Revenge, or Delhi belly) as well as in infants in many developing countries with
poor sanitation. It is estimated the 300,000–500,000 deaths are associated with ETEC in children under the age of five. The presence of disease is a result of the ability of the pathogens to
colonize by adhering to the intestinal epithelial cells using pili or colonization factor antigen
(CFA) and then producing either heat labile (LT) or heat stable (ST) or both LT and ST toxins. 18
LT toxin binds to a GM1 ganglioside receptor in enterocytes, and it does not cause any histological
changes in the mucosal layers. Little or no inflammation is observed in the intestine. The toxin(s)
induces intracellular cAMP levels, which, in turn, activate cystic fibrosis transmembrane receptor
(CFTR) chloride channel resulting in increased membrane permeability, electrolyte imbalance
(Na + , K + ), and severe fluid loss (watery diarrhea) (Figure 26.3).
The symptom is gastroenteritis, like a mild form of cholera. It is fatal in children because of excessive fluid loss and dehydration. In addition, other signs and symptoms include headache, fever, nausea,
and vomiting. The pathogen is spread directly or indirectly by human carriers. Both food and water
have been implicated in outbreaks and sporadic cases in humans. In 1983, imported Brie cheese contaminated with O27:H7 serotype caused outbreaks in several countries, including the United States.
Ingestion of large numbers of cells (10 8 –10 9 ) is necessary for an individual to develop the symptoms.
Enteropathogenic Escherichia coli (EPEC) 20,21
These strains are important in infant diarrhea worldwide, especially in places with poor sanitation.
Atypical EPEC (aEPEC) is more prevalent than the typical EPEC (tEPEC) in both developed and
developing countries. They are transmitted directly or indirectly through human carriers. Several
serotypes (O111:H12; O55:H6) are implicated in waterborne and foodborne disease outbreaks
in different countries. These pathogens do not produce any toxins, but they intimately attach to
the epithelial cells with the help of bundle-forming pili (bfp) and a virulence factor called the
attachment-effacement factor or Intimin. The Esc. coli attaching and effacing (eaeA) gene encodes
Intimin, which is responsible for intimate contact, resulting in severe lesions on the epithelial layer
called attachment-effacement lesions that destroys the absorptive villi, resulting in malabsorption
and diarrhea (Figure 26.3). The eaeA gene is located in the LEE (locus of enterocyte effacement)
pathogenicity island. One needs to ingest high numbers of cells (10 6 –10 9 ) to develop the symptoms, which could appear within three hours. The predominant symptoms are gastroenteritis,
profuse watery diarrhea, vomiting, and low-grade fever.
Although there is no clear differentiation for these four subgroups, both EIEC and EHEC
strains seem to fit with the enteric pathogens associated with foodborne infection. Thus these two
groups are discussed in this chapter. Both EPEC and ETEC groups are included in the chapter
discussing toxicoinfection (Chapter 27).
Enteroinvasive Escherichia coli (EIEC) 22
These strains are known to cause dysentery, like shigellosis. They first bind to epithelial cells and
invade and move from cell to cell spreading infection in the intestines (Figure 26.3). Cell damage
results in bloody mucoid diarrhea similar to bacillary dysentery caused by Shigella. Human carriers, directly or indirectly, spread the disease. Ingestion of as many as 10 6 cells may be necessary
for an individual to develop the symptoms. An outbreak in the United States as early as 1971 was
Enterotoxigenic Escherichia coli (ETEC) 18,19
These strains are the major cause of diarrhea among travelers (also known as Traveler’s Diarrhea,
Montezuma’s Revenge, or Delhi belly) as well as in infants in many developing countries with
poor sanitation. It is estimated the 300,000–500,000 deaths are associated with ETEC in children under the age of five. The presence of disease is a result of the ability of the pathogens to
colonize by adhering to the intestinal epithelial cells using pili or colonization factor antigen
(CFA) and then producing either heat labile (LT) or heat stable (ST) or both LT and ST toxins. 18
LT toxin binds to a GM1 ganglioside receptor in enterocytes, and it does not cause any histological
changes in the mucosal layers. Little or no inflammation is observed in the intestine. The toxin(s)
induces intracellular cAMP levels, which, in turn, activate cystic fibrosis transmembrane receptor
(CFTR) chloride channel resulting in increased membrane permeability, electrolyte imbalance
(Na + , K + ), and severe fluid loss (watery diarrhea) (Figure 26.3).
The symptom is gastroenteritis, like a mild form of cholera. It is fatal in children because of excessive fluid loss and dehydration. In addition, other signs and symptoms include headache, fever, nausea,
and vomiting. The pathogen is spread directly or indirectly by human carriers. Both food and water
have been implicated in outbreaks and sporadic cases in humans. In 1983, imported Brie cheese contaminated with O27:H7 serotype caused outbreaks in several countries, including the United States.
Ingestion of large numbers of cells (10 8 –10 9 ) is necessary for an individual to develop the symptoms.
Enteropathogenic Escherichia coli (EPEC) 20,21
These strains are important in infant diarrhea worldwide, especially in places with poor sanitation.
Atypical EPEC (aEPEC) is more prevalent than the typical EPEC (tEPEC) in both developed and
developing countries. They are transmitted directly or indirectly through human carriers. Several
serotypes (O111:H12; O55:H6) are implicated in waterborne and foodborne disease outbreaks
in different countries. These pathogens do not produce any toxins, but they intimately attach to
the epithelial cells with the help of bundle-forming pili (bfp) and a virulence factor called the
attachment-effacement factor or Intimin. The Esc. coli attaching and effacing (eaeA) gene encodes
Intimin, which is responsible for intimate contact, resulting in severe lesions on the epithelial layer
called attachment-effacement lesions that destroys the absorptive villi, resulting in malabsorption
and diarrhea (Figure 26.3). The eaeA gene is located in the LEE (locus of enterocyte effacement)
pathogenicity island. One needs to ingest high numbers of cells (10 6 –10 9 ) to develop the symptoms, which could appear within three hours. The predominant symptoms are gastroenteritis,
profuse watery diarrhea, vomiting, and low-grade fever.
Although there is no clear differentiation for these four subgroups, both EIEC and EHEC
strains seem to fit with the enteric pathogens associated with foodborne infection. Thus these two
groups are discussed in this chapter. Both EPEC and ETEC groups are included in the chapter
discussing toxicoinfection (Chapter 27).
Enteroinvasive Escherichia coli (EIEC) 22
These strains are known to cause dysentery, like shigellosis. They first bind to epithelial cells and
invade and move from cell to cell spreading infection in the intestines (Figure 26.3). Cell damage
results in bloody mucoid diarrhea similar to bacillary dysentery caused by Shigella. Human carriers, directly or indirectly, spread the disease. Ingestion of as many as 10 6 cells may be necessary
for an individual to develop the symptoms. An outbreak in the United States as early as 1971 was