Introduction to Foodborne Pathogens
537
Yops are synthesized at 37
◦ C and translocated into mammalian cells upon contact. Gram-positive
bacteria can secrete proteins directly out of their cell since there is no outer membrane. In the type I
secretory system of Gram-negative bacteria, bacterial proteins are secreted directly from the cytoplasm
to the environment by two cytoplasmic and one outer membrane proteins. However, in a type III
secretion system, the bacterial proteins need a specialized apparatus to exit the producing cells, and
Yops is an example of such apparatus.
The yersiniae secretion apparatus is normally kept closed at the outer membrane by YopN, which
acts as a cork. YopN can be removed (system uncorked) by removing Ca
2+ , at which time Yops
are secreted from the cytoplasm to the outside. YopP is responsible for the suppression of TNF-α
release by infected macrophages.
13 When Yops contact a eucaryotic cell, a microinjection device is
formed that allows Yops to pass via the type III secretion system and directly into the eucaryotic
cell.
41 This process has been described by Silhavy
92 as death of macrophages by lethal injection.
Falkow
41 has stated that “shigellae cause the macrophage to commit suicide.” The type III secretion
system in S. Typhimurium has been described as a supramolecular structure that spans the inner and
outer membranes.
66 Type III systems are also possessed by the plant pathogenic strains of Erwinia,
Xanthomonas, Pseudomonas, and Ralstonia.
2 As noted in Exhibit 22–3, a type IV system is possessed
by the plant pathogen, Agrobacterium tumefaciens.
Shigellae
The M cells of Peyer’s patches in the terminal ileum are invaded by shigellae as well as some salmonellae, some EPEC, and some viruses.
41 Shigellae invade macrophages of the colonic and rectal M cells
and the macrophages die by apoptosis. The result is an acute inflammatory response with dysentery.
This is especially true for invasive strains of S. flexneri.
110 This type of damage leads to the loss of
blood and mucus in the intestinal lumen. Since colonic absorption of water is inhibited, the result is
the passage of scanty (squirts) dysenteric stools. When shigellosis is accompanied by watery diarrhea,
it is due to the transient multiplication of the organisms as they pass through the jejunum. Of the
shigellae species, S. sonnei causes diarrhea most often. As to minimum infectious dose, as few as 10
cells caused disease in 10% of volunteers, and when using 500 cells, 50% became infected.
39
The Shiga toxin of S. dysenteriae type 1 binds to galabiose and begins the inhibition of mammalian
protein synthesis. Although hemolytic uremic syndrome (HUS) is most often associated with EHEC
strains of E. coli, it may also be caused by S. dysenteriae.
Vibrios
In contrast to the Gram-negative bacteria discussed above, vibrios are not members of the family
Enterobacteriaceae, and those associated with foodborne illness are also noninvasive. In the case of
V. parahaemolyticus, its pathogenesis is associated with the production of a 46-kDa homodimer—
thermostable direct hemolysin (TDH). The latter appears to be responsible for the following events:
hemolysis, pore-forming capacity, cytotoxic effects, lethality in small animals, and enterotoxigenicity
as assessed by its activity in ileal loops. For more details on TDH, see Chapter 28.
The 01 strains of V. cholerae colonize the epithelium of the small intestine with preference to M cells,
and this leads to profuse diarrhea. The two primary virulence factors of this organism are (1) toxincoregulated pili (TCP) that are required for intestinal colonization, and (2) cholera toxin (CT) that is
an enterotoxin.
98 The CT genes (ctxAB) are part of a larger genetic element, CTX, which constitutes
the genome of a filamentous bacteriophage designated CTXø.
42,98 The latter can be propagated in
recipient V. cholerae strains in which it either integrates chromosomally to form stable lysogens or
537
Yops are synthesized at 37
◦ C and translocated into mammalian cells upon contact. Gram-positive
bacteria can secrete proteins directly out of their cell since there is no outer membrane. In the type I
secretory system of Gram-negative bacteria, bacterial proteins are secreted directly from the cytoplasm
to the environment by two cytoplasmic and one outer membrane proteins. However, in a type III
secretion system, the bacterial proteins need a specialized apparatus to exit the producing cells, and
Yops is an example of such apparatus.
The yersiniae secretion apparatus is normally kept closed at the outer membrane by YopN, which
acts as a cork. YopN can be removed (system uncorked) by removing Ca
2+ , at which time Yops
are secreted from the cytoplasm to the outside. YopP is responsible for the suppression of TNF-α
release by infected macrophages.
13 When Yops contact a eucaryotic cell, a microinjection device is
formed that allows Yops to pass via the type III secretion system and directly into the eucaryotic
cell.
41 This process has been described by Silhavy
92 as death of macrophages by lethal injection.
Falkow
41 has stated that “shigellae cause the macrophage to commit suicide.” The type III secretion
system in S. Typhimurium has been described as a supramolecular structure that spans the inner and
outer membranes.
66 Type III systems are also possessed by the plant pathogenic strains of Erwinia,
Xanthomonas, Pseudomonas, and Ralstonia.
2 As noted in Exhibit 22–3, a type IV system is possessed
by the plant pathogen, Agrobacterium tumefaciens.
Shigellae
The M cells of Peyer’s patches in the terminal ileum are invaded by shigellae as well as some salmonellae, some EPEC, and some viruses.
41 Shigellae invade macrophages of the colonic and rectal M cells
and the macrophages die by apoptosis. The result is an acute inflammatory response with dysentery.
This is especially true for invasive strains of S. flexneri.
110 This type of damage leads to the loss of
blood and mucus in the intestinal lumen. Since colonic absorption of water is inhibited, the result is
the passage of scanty (squirts) dysenteric stools. When shigellosis is accompanied by watery diarrhea,
it is due to the transient multiplication of the organisms as they pass through the jejunum. Of the
shigellae species, S. sonnei causes diarrhea most often. As to minimum infectious dose, as few as 10
cells caused disease in 10% of volunteers, and when using 500 cells, 50% became infected.
39
The Shiga toxin of S. dysenteriae type 1 binds to galabiose and begins the inhibition of mammalian
protein synthesis. Although hemolytic uremic syndrome (HUS) is most often associated with EHEC
strains of E. coli, it may also be caused by S. dysenteriae.
Vibrios
In contrast to the Gram-negative bacteria discussed above, vibrios are not members of the family
Enterobacteriaceae, and those associated with foodborne illness are also noninvasive. In the case of
V. parahaemolyticus, its pathogenesis is associated with the production of a 46-kDa homodimer—
thermostable direct hemolysin (TDH). The latter appears to be responsible for the following events:
hemolysis, pore-forming capacity, cytotoxic effects, lethality in small animals, and enterotoxigenicity
as assessed by its activity in ileal loops. For more details on TDH, see Chapter 28.
The 01 strains of V. cholerae colonize the epithelium of the small intestine with preference to M cells,
and this leads to profuse diarrhea. The two primary virulence factors of this organism are (1) toxincoregulated pili (TCP) that are required for intestinal colonization, and (2) cholera toxin (CT) that is
an enterotoxin.
98 The CT genes (ctxAB) are part of a larger genetic element, CTX, which constitutes
the genome of a filamentous bacteriophage designated CTXø.
42,98 The latter can be propagated in
recipient V. cholerae strains in which it either integrates chromosomally to form stable lysogens or