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and analyzed (
Sahl et al., 2011
). A whole genome analysis demonstrated that
these genomes fell into phylogroups B1 and A. A comparative genomic analysis
demonstrated that ETEC genomes share more chromosomal sequence with one
another than they do with non-ETEC
E. coli
genomes (
Sahl et al., 2011
).
Decreasing sequencing costs have allowed the sequencing and comparison
of a large number of clinical ETEC isolates. In a single study, 71 ETEC iso-
lates were sequenced; 38 isolates were taken from patients with active diarrheal
disease and 33 isolates were taken from patients with no diarrheal symptoms
(
Sahl et al., 2012
). A whole genome phylogeny demonstrated that ETEC are
distributed across the
E. coli
phylogeny. This result is not unanticipated because
the acquisition of the virulence plasmid that harbors the LT and/or ST genes is
all that is required to be typed as an ETEC. A comparative analysis of diarrheal-
associated and asymptomatic isolates demonstrated that several genes were
differentially conserved in each group irrespective of their phylogroup mem-
bership. In addition, an analysis was performed by which the genomic content
of ETEC and non-ETEC genomes in phylogroups A and B1 were compared.
The results demonstrate that greater than 100 non-plasmid-associated genes
were differentially conserved in ETEC isolates. Therefore, a genomic back-
ground in ETEC appears to exist beyond the simple acquisition and expression
of an ETEC virulence plasmid. Additional large-scale projects are underway
with hundreds of isolates being sequenced (
http://gscid.igs. umaryland.edu/
lates_from_infections_of_different_clinical_severity
). Genomics has changed
the understanding of ETEC evolution, gene content, and pathogenesis. Genomic
comparative analyses have identified putative virulence factors (
Sahl and
Rasko, 2012
) that will help focus functional characterization studies. A global
understanding of the genomic diversity of an entire pathovar will help move
beyond the limitations of single-isolate, prototypical analyses. With these types
of studies underway, we can begin to apply epidemiological principles to the
identification of genomic regions that are associated with isolates from health,
colonization, and disease presentations. The application of genomics in this way
is termed genomic epidemiology.
ENTEROAGGREGATIVE
E. COLI
(EAEC)
Enteroaggregative
E. coli
(EAEC) are characterized by the phenotypic 'stacked
brick' attachment to host cells. EAEC isolates cannot be defined by a single
molecular marker that distinguishes all isolates of this pathovar (
Kaper et al.,
2004
), which presents a challenge for surveillance of potential outbreak events.
However, the aggregative adherence (AA) phenotype appears to be encoded by
genes harbored on the pAA virulence plasmid (
Vial et al., 1988
). Whole genome
analysis has demonstrated that the genetic composition of pAA plasmids can
differ dramatically between divergent EAEC isolates (
Rasko et al., 2011
). The
original definition of the EAEC was predicated on the lack of the ST or LT of
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