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EPEC (aEPEC) ( Kaper et al., 2004 ). The bundle forming pilus creates a network
of filaments that bind the bacteria together into what is known as a microcolony.
Both tEPEC and aEPEC have been associated with diarrheal disease ( Trabulsi
et al., 2002 ), which suggests that the BFP is not absolutely required for EPEC
virulence. Indeed, volunteer studies demonstrate that loss of the EAF plasmid
or mutation of bfp genes reduces, but does not eliminate pathogenicity ( Levine
et al., 1985 ; Bieber et al., 1998 ). Phylogenetic analysis based on concatenated
multilocus sequence typing (MLST) genes demonstrated that tEPEC are found
in two primary lineages (EPEC1 and EPEC2), although several smaller clades
have been identified ( Orskov et al., 1990 ; Lacher et al., 2007 ). This diversity
suggests that the acquisition of LEE and the EAF plasmid have occurred on
multiple, independent occasions.
The genomic landscape of EPEC is as follows: The first two EPEC genomes
sequenced were B171 and E110019 ( Rasko et al., 2008 ); B171 is a tEPEC iso-
late from the EPEC2 lineage ( Giron et al., 1991 ) and E110019 is an aEPEC that
was the etiological agent of a large outbreak in Finland in 1990 ( Viljanen et al.,
1990 ). A comparative analysis revealed that although 200 unique genes were
identified in the two EPEC genomes, compared to other sequenced genomes, few
( n = 9) pathovar-specific genes were identified ( Rasko et al., 2008 ). The proto-
type EPEC isolate E2348/69, which is part of the EPEC1 clade, was sequenced
in 2009 ( Iguchi et al., 2009 ). A comparative analysis demonstrated greater than
400 unique genes in this isolate. Furthermore, only 21 secreted effectors were
identified in the genome of E2348/69 compared to approximately 50 described
in the genomes of O157:H7 isolates ( Tobe et al., 1999 ).
The diversity of EPEC has been previously determined by the typing of
intimin variants ( Lacher et al., 2006 ); the intimin gene ( eae ) is encoded by the
LEE. In a study of 151 eae -positive isolates, 26 distinct profiles were observed
using fluorescent restriction fragment length polymorphism. Phylogenetic anal-
yses of EPEC have typically been performed from concatenated MLST markers
( Lacher et al., 2006 ). Phylogenies inferred from whole genome sequence data
have demonstrated that trees inferred from concatenated MLST markers do a
poor job at recapitulating the whole genome phylogeny ( Leopold et al., 2011 ;
Sahl et al., 2011 ). Thus whole genome phylogeny will help better understand
the phylogenetic history of EPEC isolates in the broader context of all E. coli
and Shigella genomes.
The sequencing of additional EPEC genomes, as part of the GSCID project
( http://gscid.igs.umaryland.edu/wp.php?wp=emerging_diarrheal_pathogens ),
has provided additional information on the evolution of EPEC. For example,
some BFP-positive EPEC are closely related to BFP-negative EPEC phyloge-
netically ( Hazen et al., 2012 ); this may be due to the loss of the EAF plas-
mid prior to or during lab passage. Previous studies have demonstrated that
in E2348/69, the prototype EPEC isolate, the plasmid is very stable ( Levine
et al., 1985 ; Donnenberg et al., 1993 ). However, as more isolates are sequenced
and investigated, the existing dogma is increasingly challenged. For example,
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