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from other E. coli strains by their SOR - and GUD - phenotype. The O55:H7 SOR +
GUD + strains evolved from ancestral EPEC-like strains through the acquisition of
the LEE pathogenicity island ( Figure 5.1 ). This was followed by the acquisition
of Stx2 phage through transduction of a toxin-converting bacteriophage. The next
step was marked by the gain of the EHEC virulence plasmid and an antigenic shift
from O55 to O157. In further steps, E. coli O157:H7 acquired Stx1 phage and lost
Current O157:H7 with LEE, Stx1, Stx2, and pO157
O157:H7 SOR-GUD-
Loss of GUD+
O157:H7 SOR-GUD+
Stx1
phage
Loss of SOR+
O157:H7 SOR+GUD+
Antigenic shift
O55 to O157
pO157
plasmid
O55:H7 SOR+GUD+
Stx2
phage
O55:H7 SOR+GUD+
(Ancestral atypical EPEC with LEE)
FIGURE 5.1 Step-wise model of E. coli O157:H7 evolution. In the first step, anatypical EPEC-
like O55:H7 SOR + GUD + strain carrying the LEE pathogenicity island acquired Stx2 phage through
transduction of a toxin-converting bacteriophage. In the next step EHEC virulence plasmid was
gained and an antigenic shift occurred from O55 to O157. Subsequently, O157:H7 acquired Stx1
phage and lost the SOR fermentation and GUD activities, resulting in the current O157:H7 GUD -
SOR - strain containing Stx1, Stx2, and the EHEC plasmid (Modified from Kaper et al., 2004 ).
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