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FIGURE 1.4 Change in the relative abundance of the main E. coli phylo-groups (A, B1, B2, D)
with respect to human host age. Data taken from Gordon et al. (2005) .
EAEC were detected in 3.1% of samples and atypical EPEC in 2.4% of sam-
ples ( Robins-Browne et al., 2004 ). All other pathotypes were detected in less
than 0.2% of the samples. Similarly, asymptomatic carriage in many mammal
species also seems to be rare. Few of almost 500 E. coli strains isolated from
native Australian mammals ( Gordon and Cowling, 2003 ) were found to possess
virulence factors associated with intestinal pathotypes. For example, eaeA was
detected in 5% of strains, either stx 1 or stx 2 were detected in 1% of strains, and
bfpA and aggR were not detected (unpublished data). A growing body of data
indicates there are strains present in the intestinal tract that are not detected in
fecal samples. This means that it is possible that in asymptomatic hosts, cells of
most pathotypes are shed at frequencies too low to be detected. The significance
of such hosts to the maintenance of the disease is unknown.
The minimum infectious dose is a significant component of a parasite's
basic reproductive value. The infectious dose for EIEC and EHEC is thought to
be in the order of hundreds of cells while the infectious dose for EPEC, ETEC,
and EAEC pathotypes is thought to be many orders of magnitude larger ( Nataro
and Kaper, 1998 ). It is, however, unclear whether these differences in infectious
dose reflect the site of infection, small (EIEC and EHEC) versus large bowel
(EPEC, ETEC, EAEC) or a dichotomy in the manner in which infectious dose is
measured; experimentally or epidemiologically. It is well accepted among peo-
ple working with commensal E. coli that it is virtually impossible to establish an
E. coli strain in a host with an existing E. coli population and such attempts will
only be successful when using germ-free or antibiotic-treated animals. How-
ever, these outcomes are at odds with the observation that international travelers
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