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the most host adapted as, at least in humans, there are data to suggest they per-
sist longer in a host than strains of the other phylo-groups (
Nowrouzian et al.,
2005, 2006
). They are also competitively dominant, as hosts harboring a B2
strain have, on average, fewer detectable
E. coli
genotypes than hosts harboring
strains belonging to other phylo-groups (
Moreno et al., 2009
). There is also a
growing body of evidence to indicate that the transmission dynamics of strains
of the different phylo-groups also differs. For example, phylo-group A and B1
strains are over-represented in freshwater samples, whilst B2 and D strains are
rare in such samples (
Power et al., 2005
;
Walk et al., 2007
;
Ratajczak et al.,
2010
). The persistence of
E. coli
strains in soil also varies with their phylo-
group membership (
Bergholz et al., 2010
). A phenotype commonly linked to a
strain's ability to survive stressful conditions is the red dry and rough (rdar) phe-
notype, where cells produce an extracellular matrix composed of curli fimbriae
and a variety of polysaccharides, is more frequent in B1 strains than in strains
belonging to the other phylogroups (
White et al., 2011
).
While it is clear that strains belonging to the different phylo-groups of
E. coli
differ in their phenotypic, ecological and life-history characteristics, there is little
understanding of the underlying mechanisms leading to these differences. To a very
great extent this difficulty has arisen because of the enormous genetic diversity to
be found in
E. coli
(
Touchon et al., 2009
). A typical
E. coli
genome consists of
about 4700 genes, however, only about 2000 of these genes are common to all
E. coli
strains. The balance of the genes in the genome of a strain is drawn from a
gene pool that is in excess of 10 000 unique genes, after eliminating all transposable
elements and prophages. To date, there has been no systematic attempt to determine
whether or not any genes are over-represented in a particular phylo-group.
Strains of the various phylo-groups do vary in their phenotypic properties,
such as carbon source utilization patterns (
Gordon, 2004
) and their ability to
cause disease in a mouse model of extraintestinal infection (
Johnson et al.,
2006
). Strains of the various phylo-groups also differ in their gene content, with
phylo-group B2 strains in particular harboring a variety of traits, often at high
frequency, thought to enhance the ability of a strain to cause extraintestinal
disease. These same traits have been shown to be important determinants of a
strain's ability to colonize the intestine (
Diard et al., 2010
).
The hierarchical structure of
E. coli
extends beyond the species or phylo-
group level to clonal complexes and clonal lineages (MLST sequence type (ST)
or clonal complex (CC)) (
Figure 1.1
). Researchers studying
E. coli
responsi-
ble for intestinal infections have long recognized the significance of particular
clonal groups, for example, the infamous O157:H7 clonal group (ST 11). Par-
ticular clonal lineages are also often responsible for extraintestinal infections
such as the phylo-group D clonal group A strains (ST 69) (
Johnson et al., 2011
);
or the phylo-group B2 strains O1:K1:H7/NM (ST 95) (
Mora et al., 2009
).
Other lineages are less often responsible for extraintestinal infection, but very
commonly isolated from the feces of humans and other animals. The group of
strains related to
E. coli
K12, belonging to ST 10, is the best known of these
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