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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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