354 ◾ Fundamental Food Microbiology
serotypes, such as those that belong to O55, O26, O113, and O117. One of the main characteristics of these pathotypes is the production of Shiga-toxin (Stx), which is an important virulence factor, responsible for HUS. Because all EHEC produce Stx, they are also known as Shiga-toxigenic
Esc. coli (STEC) or verotoxigenic Esc. coli (VTEC) resulting from cytotoxic effects on Vero cells
(the African Green Monkey kidney cell line). Because Stx production has been attributed to be
the major virulence factor, recent emphasis is on classifying organisms based on their ability to
produce Stx; hence they are called STEC. In 2011, the U.S. Department of Agriculture identified
seven major STEC serovars, including O26, O45, O103, O111, O121, O145, and O157, as adulterants, and meats contaminated with any of these serovars cannot be sold for human consumption.
Animals, particularly dairy and beef cattle, are thought to be the carriers. Ingestion of as few as
10–100 cells can produce the disease, especially in sensitive individuals.
Gastroenteritis Resulting from EHEC/STEC 25
Characteristics
The principal serotype associated with enterohemorrhagic colitis is Esc. coli O157:H7. In contrast to
other Esc. coli, it generally does not ferment sorbitol or have glucuronidase activity. Like other Esc. coli, it
grows rapidly at 30°C–42°C, grows poorly at 44°C–45°C, and does not grow at 10°C or below. Strains
resistant to pH 4.5 or below have been identified. The organism is destroyed by pasteurization temperatures and time and killed at 64.3°C in 9.6 seconds. The cells survive well in food at –20°C.
Toxins
Esc. coli O157:H7 produces Verotoxins (VT) or Shiga-like toxins (Stx). There are two distinct Stx:
Stx1 and Stx2. A single STEC can produce Stx1 only, Stx2 only, or both. Stx2 is more potent than
Stx1 and is thought to be responsible for pathogenesis. Stx binds to a specific glycolipid receptor,
globotriaosylceramide (Gb3) located in intestinal and kidney cells and leukocytes. The toxin is
also called verotoxin (VT) because of its cytotoxic effect on Vero cells. The toxin then blocks
protein synthesis, resulting in cell death. EHEC also produces an intimate adhesion factor called
Intimin encoded by the eaeA gene, which is responsible for attachment/effacement (A/E) lesion
in the intestine similar to EPEC. EHEC also produces enterohemolysin, which is encoded in a
60-MDa plasmid and translocated intimin receptor (TIR), which serves as a host cell receptor for
Intimin.
Disease and Symptoms
Upon consumption of contaminated food or water, the bacteria first colonize in the intestine
by adhering to the epithelial cells. The protein Intimin facilitates intimate adhesion forming a
pedestal-like structure on the microvilli, producing the characteristic A/E lesion. This destroys the
absorptive vili resulting in malabsorption, and the lesion resembles EPEC-mediated destruction
(Figure 26.3). Bacteria then produce toxins (Stx) that damage colon epithelial cells, resulting in
hemorrhagic colitis. Toxins (Stx1 or Stx2) are also absorbed into the bloodstream and damage the
small blood vessels in the intestine, kidneys, and brain and also damage the kidney tubules. This
results in hemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP).
Symptoms occur three to nine days after ingestion and generally last for 4–10 days. The colitis
symptoms include a sudden onset of abdominal cramps, watery diarrhea (which in 35%–75% of
serotypes, such as those that belong to O55, O26, O113, and O117. One of the main characteristics of these pathotypes is the production of Shiga-toxin (Stx), which is an important virulence factor, responsible for HUS. Because all EHEC produce Stx, they are also known as Shiga-toxigenic
Esc. coli (STEC) or verotoxigenic Esc. coli (VTEC) resulting from cytotoxic effects on Vero cells
(the African Green Monkey kidney cell line). Because Stx production has been attributed to be
the major virulence factor, recent emphasis is on classifying organisms based on their ability to
produce Stx; hence they are called STEC. In 2011, the U.S. Department of Agriculture identified
seven major STEC serovars, including O26, O45, O103, O111, O121, O145, and O157, as adulterants, and meats contaminated with any of these serovars cannot be sold for human consumption.
Animals, particularly dairy and beef cattle, are thought to be the carriers. Ingestion of as few as
10–100 cells can produce the disease, especially in sensitive individuals.
Gastroenteritis Resulting from EHEC/STEC 25
Characteristics
The principal serotype associated with enterohemorrhagic colitis is Esc. coli O157:H7. In contrast to
other Esc. coli, it generally does not ferment sorbitol or have glucuronidase activity. Like other Esc. coli, it
grows rapidly at 30°C–42°C, grows poorly at 44°C–45°C, and does not grow at 10°C or below. Strains
resistant to pH 4.5 or below have been identified. The organism is destroyed by pasteurization temperatures and time and killed at 64.3°C in 9.6 seconds. The cells survive well in food at –20°C.
Toxins
Esc. coli O157:H7 produces Verotoxins (VT) or Shiga-like toxins (Stx). There are two distinct Stx:
Stx1 and Stx2. A single STEC can produce Stx1 only, Stx2 only, or both. Stx2 is more potent than
Stx1 and is thought to be responsible for pathogenesis. Stx binds to a specific glycolipid receptor,
globotriaosylceramide (Gb3) located in intestinal and kidney cells and leukocytes. The toxin is
also called verotoxin (VT) because of its cytotoxic effect on Vero cells. The toxin then blocks
protein synthesis, resulting in cell death. EHEC also produces an intimate adhesion factor called
Intimin encoded by the eaeA gene, which is responsible for attachment/effacement (A/E) lesion
in the intestine similar to EPEC. EHEC also produces enterohemolysin, which is encoded in a
60-MDa plasmid and translocated intimin receptor (TIR), which serves as a host cell receptor for
Intimin.
Disease and Symptoms
Upon consumption of contaminated food or water, the bacteria first colonize in the intestine
by adhering to the epithelial cells. The protein Intimin facilitates intimate adhesion forming a
pedestal-like structure on the microvilli, producing the characteristic A/E lesion. This destroys the
absorptive vili resulting in malabsorption, and the lesion resembles EPEC-mediated destruction
(Figure 26.3). Bacteria then produce toxins (Stx) that damage colon epithelial cells, resulting in
hemorrhagic colitis. Toxins (Stx1 or Stx2) are also absorbed into the bloodstream and damage the
small blood vessels in the intestine, kidneys, and brain and also damage the kidney tubules. This
results in hemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP).
Symptoms occur three to nine days after ingestion and generally last for 4–10 days. The colitis
symptoms include a sudden onset of abdominal cramps, watery diarrhea (which in 35%–75% of