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FIGURE 8.2
The basic features of EAEC pathogenesis. Stages 1-3 highlighted in yellow illus-
trate the three main steps in EAEC pathogenesis. See text for discussion.
Modified after
Harrington
et al. (2006)
.
mucosal inflammation (
Steiner et al., 1998
,
2000
;
Bouckenooghe et al., 2000
;
Jiang et al., 2002
;
Harrington et al., 2005
) (
Figure 8.2
).
Virulence determinants
Several putative virulence factors have been identified in EAEC (
Table 8.1
),
including enterotoxins and cytotoxins, secreted proteins and many more. The
virulence factors so far described are encoded either on the large virulence plas-
mid of EAEC called pAA, or on the chromosome. The clinical roles of these
factors remain uncertain (Nataro, 2005).
The best-studied EAEC factor is AggR, putatively the master regulator of
EAEC virulence. AggR is a member of the AraC/XylS family of transcriptional
activators with its nearest neighbors being Rns of ETEC and RegA of
Citrobac-
ter rodentium
, while ToxT of
Vibrio cholerae
is a distant relative.
Virulence factors regulated by AggR
AggR controls expression of adherence factors, a dispersin surface coat protein
and a large cluster of genes encoded on the EAEC chromosome.
Nataro (2005)
have therefore suggested that a 'package' of plasmid-borne and chromosomal
virulence factors for EAEC are required to execute pathogenesis, and that this
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