Enterotoxigenic Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 181

TABLE 6.1 Modulation of virulence determinants by CRP

Gene(s)/
operon

cAMP-CRP
modulation

Reference(s)

eltAB - Bodero and Munson, 2009

estA + Bodero and Munson, 2009

fliC + Chilcott and Hughes, 2000

CS1-3 + Evans et al., 1991

CFA/I + Karjalainen et al., 1991

tibDBCA + Espert et al., 2011

tolC + * Hantke et al., 2011 ; Zheng et al., 2004

imA - Muller et al., 2009

luxS − Wang et al., 2005

*Indirect via activation of marRAB ( Zheng et al., 2004 ).

a number of other genes, including those encoding several other colonization
factors ( Pilonieta et al., 2007 ) ( Table 6.2 ).
Not surprisingly, ETEC appear to be programmed to respond to other small
molecules that may be found in the small intestine such as those contained in
bile. Recent array studies indicate that bile can induce production of both ST
and LT ( Sahl and Rasko, 2012 ). Therefore, expression of virulence factors by
ETEC likely reflects the integration of multiple signals as these organisms make
their way through different environments culminating in epithelial attachment
and toxin delivery to the host cell.

Adherence and invasion

Colonization factors
A principal focus of ETEC pathogenesis has been the study of factors which pro-
mote colonization of the small intestine. Here, colonization of the intestinal mucosa
is thought to be required for efficient delivery of ST and LT ( Zafriri et al., 1987 ;
Ofek et al., 1990 ). Fimbrial structures known as colonization factors (CFs) were
among the earliest virulence factors to be identified in ETEC ( Evans et al., 1975 ).
Early ETEC volunteer challenge studies demonstrated that a strain cured of a
plasmid encoding CFA/I failed to cause diarrheal illness ( Figure 6.2 a) ( Evans et al.,
1978 ; Satterwhite et al., 1978 ), and recipients of the CFA/I-negative strain had sig-
nificant reductions in fecal shedding. However, the reduced pathogenicity observed
in these studies likely was not simply due to absence of CFA/I as other important
determinants are now known to be encoded on this plasmid ( Figure 6.2 b).