Introduction to Foodborne Pathogens
535
As noted above, molecular genetic data suggest that the genera Escherichia and Salmonella arose
from a common ancestor, and thus it should not be surprising that virulence genes were exchanged
between them via horizontal transfer. The pathogenicity island on the chromosome of EHEC and
EPEC includes LEE, which contains the eae gene that encodes the intimin protein that is essential for
attachment–effacement (A/E).
12 The eae gene and LEE apparently were transferred horizontally within
EHEC.
12 EPEC strains contain the EPEC-secreted protein (espB) that makes them similar to EHEC.
It appears that EHEC strains evolved from EPEC via acquisition of phage-encoded Shiga toxins.
80
Evidence has been presented showing how EHEC evolved sequentially from an EPEC O55:H7 ancestor
by first acquiring the Stx2 gene and then by diverting into two branches.
43 The strains in one branch
are β-glucuronidase and sorbitol negative (the O157:H7 clone) and in the other are nonmotile but
sorbitol and glucuronidase positive (the O157:H7 clone). These investigators came to this conclusion
by, among other methods, subjecting EPEC and EHEC strains to multilocus enzyme electrophoresis
(see Chapter 11). They postulated that the Stx2 gene was acquired early and has been evolving in the
O157:H7 genome for a longer time than other virulence factors. Acid resistance was also acquired
early on, but whether it preceded Stx2 is unclear. In addition to the Stx genes, adhesins also appear to
have been acquired via horizontal transfer.
104
EHEC strains require intimin for colonization but it alone is not sufficient to cause A/E. The
possible use of intimin-based vaccines to protect cattle against EHEC infections has been suggested.
32
The pathogenicity of EHEC is due to the possession of Stx toxins, endotoxins, and host-derived
cytokines such as tumor necrosis factor alpha (TNF-a) and interleukin-1β. Stx1 and Stx2 toxins
inhibit protein synthesis in endothelial cells, and their receptor is globotriasylceramide (Gb3). Human
renal tissue contains large amounts of Gb3 and thus it is highly sensitive to the Stx toxins.
57 Stx2 toxin
has been found to be more toxic than Stx1 to human intestinal microvascular endothelial cells, and
this finding may be relevant to the preponderance of Stx2-producing EHEC in hemorrhagic colitis
infection.
57
EPEC strains require the plasmid-borne type IV bundle-forming pili (bfp) for adherence and autoagglutination. Mutants that lacked bfp caused less severe diarrhea and were about 200-fold less
virulent in human volunteers.
10 The A/E lesion and “pedestals” of densely clustered cytoskeletal
protein (including actin) are regarded as the hallmarks of EPEC infection.
41 The A/E lesion begins
as a nonintimate attachment of the bacterium, followed by the injection of type III proteins, which
effect cytoskeletal changes and effacement of microvilli. Intimin is required for the latter event.
37
Although they are not proven foodborne pathogens, some strains of Citrobacter freundii and Hafnia
alvei produce A/E, especially in certain animals.
89
Yersiniae
Y. enterocolitica (and some other yersiniae) possess a chromosomal determinant that is involved in
iron uptake, which is mediated by the siderophore yersiniabactin, and it is regarded as a pathogenicity
island (PI). This PI is also found in EAggEC strains but rarely in EPEC, EIEC, and ETEC; it is absent
from the EHEC, salmonellae, and shigellae strains tested.
90 It was probably acquired horizontally
between Y. pestis and some strains of E. coli.
90
The most significant pathogenic mechanism of Y. enterocolitica is contained in the yersiniae outer
protein (Yop) virulon (see Exhibit 22–3), which is also possessed in Y. pestis and Y. pseudotuberculosis. This virulon allows yersiniae to survive and multiply in host lymphoid tissue, and it consists
of four components as noted in Exhibit 22–3. Yop is encoded by a 70-kb plasmid, pYV, and it possesses high-pathogenicity island 1 that is necessary for virulence expression, and it determines Ca
2+
dependency.
4,25
535
As noted above, molecular genetic data suggest that the genera Escherichia and Salmonella arose
from a common ancestor, and thus it should not be surprising that virulence genes were exchanged
between them via horizontal transfer. The pathogenicity island on the chromosome of EHEC and
EPEC includes LEE, which contains the eae gene that encodes the intimin protein that is essential for
attachment–effacement (A/E).
12 The eae gene and LEE apparently were transferred horizontally within
EHEC.
12 EPEC strains contain the EPEC-secreted protein (espB) that makes them similar to EHEC.
It appears that EHEC strains evolved from EPEC via acquisition of phage-encoded Shiga toxins.
80
Evidence has been presented showing how EHEC evolved sequentially from an EPEC O55:H7 ancestor
by first acquiring the Stx2 gene and then by diverting into two branches.
43 The strains in one branch
are β-glucuronidase and sorbitol negative (the O157:H7 clone) and in the other are nonmotile but
sorbitol and glucuronidase positive (the O157:H7 clone). These investigators came to this conclusion
by, among other methods, subjecting EPEC and EHEC strains to multilocus enzyme electrophoresis
(see Chapter 11). They postulated that the Stx2 gene was acquired early and has been evolving in the
O157:H7 genome for a longer time than other virulence factors. Acid resistance was also acquired
early on, but whether it preceded Stx2 is unclear. In addition to the Stx genes, adhesins also appear to
have been acquired via horizontal transfer.
104
EHEC strains require intimin for colonization but it alone is not sufficient to cause A/E. The
possible use of intimin-based vaccines to protect cattle against EHEC infections has been suggested.
32
The pathogenicity of EHEC is due to the possession of Stx toxins, endotoxins, and host-derived
cytokines such as tumor necrosis factor alpha (TNF-a) and interleukin-1β. Stx1 and Stx2 toxins
inhibit protein synthesis in endothelial cells, and their receptor is globotriasylceramide (Gb3). Human
renal tissue contains large amounts of Gb3 and thus it is highly sensitive to the Stx toxins.
57 Stx2 toxin
has been found to be more toxic than Stx1 to human intestinal microvascular endothelial cells, and
this finding may be relevant to the preponderance of Stx2-producing EHEC in hemorrhagic colitis
infection.
57
EPEC strains require the plasmid-borne type IV bundle-forming pili (bfp) for adherence and autoagglutination. Mutants that lacked bfp caused less severe diarrhea and were about 200-fold less
virulent in human volunteers.
10 The A/E lesion and “pedestals” of densely clustered cytoskeletal
protein (including actin) are regarded as the hallmarks of EPEC infection.
41 The A/E lesion begins
as a nonintimate attachment of the bacterium, followed by the injection of type III proteins, which
effect cytoskeletal changes and effacement of microvilli. Intimin is required for the latter event.
37
Although they are not proven foodborne pathogens, some strains of Citrobacter freundii and Hafnia
alvei produce A/E, especially in certain animals.
89
Yersiniae
Y. enterocolitica (and some other yersiniae) possess a chromosomal determinant that is involved in
iron uptake, which is mediated by the siderophore yersiniabactin, and it is regarded as a pathogenicity
island (PI). This PI is also found in EAggEC strains but rarely in EPEC, EIEC, and ETEC; it is absent
from the EHEC, salmonellae, and shigellae strains tested.
90 It was probably acquired horizontally
between Y. pestis and some strains of E. coli.
90
The most significant pathogenic mechanism of Y. enterocolitica is contained in the yersiniae outer
protein (Yop) virulon (see Exhibit 22–3), which is also possessed in Y. pestis and Y. pseudotuberculosis. This virulon allows yersiniae to survive and multiply in host lymphoid tissue, and it consists
of four components as noted in Exhibit 22–3. Yop is encoded by a 70-kb plasmid, pYV, and it possesses high-pathogenicity island 1 that is necessary for virulence expression, and it determines Ca
2+
dependency.
4,25