The ecology of Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 7

as it represents a very large fraction of the sequence types in the E. coli MLST
database hosted by University College Cork.
Strains responsible for extraintestinal infection may originate from any of
the E. coli phylo-groups, although most isolates are members of phylo-groups
B2 and to a lesser extent, D. All of the available evidence indicates that the
main pathotypes responsible for intestinal disease have arisen from each of the
phylo-groups, often on multiple occasions ( Figure 1.1 ). Although for the intes-
tinal pathogens, phylo-group A, B1, D, and E strains were more likely to have
provided the ancestral lineages than phylo-group B2 strains ( Escobar-Páramo
et al., 2004 ; Yang et al., 2007 ). It is often also the case that a particular patho-
genic lineage has as its closest relative a non-pathogenic variant ( Figure 1.1 ).
WITHIN AND AMONG HOST E. COLI DIVERSITY
Studies based on non-selective plating (e.g. MacConkey) of fecal E. coli iso-
lates have revealed that typically one or two genotypes are recovered per host,
although as many as six or more may be detected ( Caugant et al., 1983 ; Alm
et al., 2011 ). However, such studies seldom use sample sizes that permit the
detection of genotypes occurring at a frequency of less than 5% of the total
E. coli population. Selective plating, usually for antibiotic-resistant variants,
almost always reveals the presence of additional genotypes that represent less
than 1% of the total E. coli population ( Gordon et al., 2002 ). E. coli have been
isolated from different regions of the small and large intestines of domestic
pigs and wild boars ( Dixit et al., 2004 ; Schierack et al., 2009 ). These studies
have revealed that the focus on fecal isolates underestimates the diversity of
isolates present in the gut. A similar outcome has been observed for O157:H7 in
cattle, where rectal swabs can result in significantly higher frequencies of posi-
tive animals than do fecal isolations ( Naylor et al., 2003 ). Significantly, the pig
studies have shown that there are isolates detected in the small intestine that are
not detected in the colon or feces. The reasons for this outcome are unknown
but probably reflect the fact that cell densities achieved in the small intestine
are from 100 to 1000 times lower than those achieved in the colon. Further,
there is experimental evidence to suggest that non-adherent E. coli cells do not
divide ( Poulsen et al., 1995 ). Hence non-adhering cells originating in the small
intestine would be significantly outnumbered in the feces. Although there are
very limited data, strains from different gut regions appear to have different
characteristics. For example, bacteriocin production was less frequent among
isolates from the duodenum as compared to isolates from downstream regions
and the kinds of bacteriocins produced differed between strains isolated from
the ileum and those taken from feces ( Abraham et al., 2012 ). Food transit times
are more rapid in the upper small intestine and nutrient concentrations high
compared to the lower intestinal tract ( Timm et al., 2011 ). Theoretical studies
indicate that bacteriocin producers should be disadvantaged under these condi-
tions compared to non-bacteriocin producers ( Frank, 1994 ; Barnes et al., 2007 ).