Biology Reference
In-Depth Information
EHEC interacts with the intestinal epithelium in a highly characteristic fashion,
manipulates many host cell functions by injecting dozens of bacterial effec-
tors, regulates gene expression by sensing products of both nearby bacteria and
mammalian cells, and causes life-threatening disease by the local production of
a potent cytotoxin that is absorbed systemically. One potential limitation of our
understanding of the pathogenesis of infection by EHEC is that the majority of
the findings discussed in this chapter are derived from studies of a few
E. coli
O157:H7 strains. Investigation of how broadly these pathogenic features are
shared by other EHEC may be a fruitful area of future investigation.
Entry
E. coli
O157:H7 and other STECs are primarily transmitted to humans
through consumption of contaminated foods (
Bell et al., 1994
;
Itoh et al.,
1998
;
Cody et al., 1999
;
Guh et al., 2010
;
Buchholz et al., 2011
). The infec-
tious dose of EHEC is extremely low (<100 organisms), indicating that it can
pass through the stomach with high efficiency (
Tilden et al., 1996
;
Nataro
and Kaper, 1998
;
Doyle and Pariza, 2001
;
Yoon and Hovde, 2008
). A critical
aspect of successful host entry by
E. coli
is its ability to withstand the highly
acidic (pH 1.5-3.0) gastric environment (
Waterman and Small, 1996
;
Large
et al., 2005
). EHEC possess at least three acid resistance (AR) systems (AR1,
AR2, and AR3) that regulate an acid resistance response (
Smith et al., 1992
;
Stim and Bennett, 1993
;
Lin et al., 1995
;
Hersh et al., 1996
;
Castanie-Cornet
et al., 1999
) (for review see
Foster (2004)
). In addition, the chaperone HdeA,
RNA polymerase-associated-protein SspA, small non-coding DsrA RNA, and
DNA-binding protein Dps have been shown to have a role in acid resistance
(
Lease et al., 2004
;
Hansen et al., 2005
;
Kern et al., 2007
;
Calhoun and Kwon,
2011
;
Hong et al., 2012
).
Adherence
Initial attachment
Upon transit through the stomach, EHEC must adhere to the luminal surface
of the large intestine in order to effectively colonize the host and compete with
normal microbiota. EHEC encodes a multitude of surface factors including fim-
brial and non-fimbrial adhesins (
Table 5.2
; for review, see
Torres et al. (2005)
and
Bardiau et al. (2010)
) that may mediate the initial interaction with the host
mucosa and promote colonization and disease (
La Ragione et al., 2000
;
Perna
et al., 2001
;
Cergole-Novella et al., 2007
).
The EHEC-specific long polar fimbriae (LPF) (
Torres et al., 2002a, 2004
)
was recently shown to be involved in intestinal colonization of infant rab-
bits (
Lloyd et al., 2012
). Additionally, bacteria deficient in production of
hemorrhagic coli pilus (HCP), a type IV pilus that EHEC shares with most
other
E. coli
(see Chapter 13), display a significant reduction in adherence
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