Enteropathogenic Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 79

association of CDT-producing EPEC with diarrheal patients in the Republic of
Korea ( Kim et al., 2009 ). The E2348/69 strain does not encode CDT.
Other fimbriae and pili
Some EPEC strains elaborate pili or fimbriae other than or in addition to BFP
( Bradley and Thompson, 1992 ; Girón et al., 1993 ). Atypical EPEC strains lack-
ing BFP have been shown to express other fimbrial genes that could potentially
aid in adherence to epithelial cells ( Hernandes et al., 2011 ). The E. coli common
pilus (ECP) has been implicated in the LA of aEPEC ( Scaletsky et al., 2010b ).
The expression of the long, fine fimbriae; rigid bent fimbriae; and short, fine
fimbriae is ablated in a ler mutant of the EPEC strain E2348/69 ( Elliott et al.,
2000 ).
Flagella have also been shown to be involved in EPEC adherence to epithe-
lial cells. A mutation in the flagella gene, fliC , severely decreased the ability of
EPEC to adhere to and form microcolonies on host cells. Adherence was also
blocked by purified EPEC flagella and anti-flagellum antibodies ( Girón et al.,
2002 ). This ∆ fliC phenotype was restored upon growth in preconditioned tissue
culture media, suggesting that a signal from the mammalian cells influences
flagella production.
Type I pili of EPEC have been found to be antigenic in volunteer studies
( Karch et al., 1987 ). While type I pili do not have a role in adherence on epi-
thelial cells in vitro ( Elliott and Kaper, 1997 ), they have been associated with
biofilm development at low temperatures in aEPEC O55:H7 ( Weiss-Muszkat
et al., 2010 ).
Adherence and invasion
Localized adherence
Typical EPEC strains adhere to HeLa, HEp-2, and other cell lines, and to
organ cultures in vitro , in a distinctive pattern of three-dimensional clus-
ters or microcolonies ( Clausen and Christie, 1982 ; Scaletsky et al., 1984 ;
Knutton et al., 1987a,b ; Nataro et al., 1985, 1987 ; Yamamoto et al., 1992 ;
Hicks et al., 1998 ). The LA pattern is a characteristic specific to EPEC
strains and therefore has been used widely as a diagnostic tool ( Figure 4.1 A).
A similar adherence pattern had been observed on tissue biopsies from
EPEC-infected infants ( Rothbaum et al., 1982, 1983 ). LA is due to the
production of BFP by the bacterium. BFP binds to specific receptors on the
host cell surface. Different investigators have found that LA can be inhibited
by various sugar moieties, including galactose ( Vanmaele and Armstrong,
1997 ), N-acetylgalactosamine ( Scaletsky et al., 1988 ), N-acetyllactosamine
( Vanmaele et al., 1999 ), and fucosylated oligosaccharides and gangliosides
from milk ( Jagannatha et al., 1991 ; Costa-Carvalho et al., 1994 ). These
saccharides could be moieties of host cell glycolipids or glycoproteins that
serve as EPEC receptors ( Vanmaele et al., 1995 ; Manjarrez-Hernandez et al.,