Biology Reference
In-Depth Information
Chapter 5
Enterohemorrhagic and
other Shigatoxin-producing
Escherichia coli
Sivapriya Kailasan Vanaja
1
, Dakshina M. Jandhyala
2
, Emily M. Mallick
3
,
John M. Leong
1
, and Sowmya Balasubramanian
1
1
Tufts University School of Medicine, Boston, MA, USA,
2
Division of Geographic Medicine
and Infectious Disease Tufts-New England Medical Center, Boston, MA, USA,
3
University of
Massachusetts Medical School, Worcester, MA, USA
BACKGROUND
Definition and classification
Shiga toxin-producing
Escherichia coli
, known as STEC, produce a typical
AB
5
toxin, with a single A (enzymatically active) subunit and five B (binding)
subunits and characterized by its profound and irreversible cytopathic effect
on Vero cells (
Paton and Paton, 1998
). Enterohemorrhagic
E. coli
, known as
EHEC, is a subset of STEC that harbors additional virulence factors, such as a
type III secretion system (T3SS) that translocates bacterial effectors into mam-
malian cells, and a large virulence plasmid (
Levine, 1987
). In addition to the
characteristic virulence factor armament, EHEC are also defined by their abil-
ity to induce characteristic attaching and effacing (AE) lesions in the host cells
(see below) and to cause manifestations such as hemorrhagic colitis and hemo-
lytic uremic syndrome (HUS) in humans (
Croxen and Finlay, 2010
). Similar
to the related pathogen enteropathogenic
E. coli
(EPEC; Chapter 4), the T3SS
is encoded on the LEE (locus of enterocyte effacement) pathogenicity island,
and is responsible for the AE lesions induced by EHEC (
Elliott et al., 1998
;
Croxen and Finlay, 2010
).
E. coli
O157:H7 is the predominant serotype of
EHEC that causes human infections globally (
Tarr et al., 2005
;
Pennington,
2010
). The lack of β-glucuronidase activity (GUD
-
) and the inability to fer-
ment sorbitol (SOR
-
) differentiate STEC O157:H7 from other
E. coli
strains
(
Paton and Paton, 1998
).
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