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Thus, epidemiological data supporting the essential role of virulence in the cir-
culation of ETEC and EPEC are not as strong as for the strictly human-adapted
Shigella
/EIEC.
Accidental pathogens
In these
E. coli
pathotypes, the virulence habitat is an ecological accident and
evolutionary dead-end (
Figure 3.3
). Causing the clinical infection in humans
does not usually promote their transmission to another person or into the origi-
nal host environment. EHEC strains are a good example of an accidental human
pathogen by being a zoonotic pathogen (
Caprioli et al., 2005
). Upon ingestion
of contaminated food, this pathotype causes diarrhea, sometimes accompanied
by a characteristic and devastating hemolytic-uremic syndrome (
Levine et al.,
1987
). The most notorious lineage of EHEC is comprised of strains with the
O157:H7 serotype, though lately several other serotypes have become promi-
nent as well (
Riley et al., 1983
). Individuals may shed EHEC for 30 days or
more following infection and child-to-child transmission at home or day care
centers might contribute to the outbreaks (
Swerdlow and Griffin, 1997
). How-
ever, such outbreaks die out relatively quickly despite potential person-person
transmission and the low infectious dose. Thus, EHEC clearly cannot rely on
human-human transmission to be sustained in nature. At the same time, EHEC
are commonly and continuously isolated from domesticated animals (cows),
which they seemingly colonize asymptomatically (
Caprioli et al., 2005
).
Because there is a sufficient ecological separation between humans and domes-
ticated animals, there is no significant transmission from the former to the lat-
ter even if bacteria are being shed in considerable numbers during the clinical
infection. Although, due to low infectious dose, they are spread from human to
human frequently leading to outbreaks, such bursts do not sustain for prolonged
periods (
Bell et al., 1994
). Thus, EHEC lineages could not evolve specifically
to cause infection in humans, and the outcome is just accidental for both the
bacteria and the human host.
Because of the accidental nature of the pathogen, most EHEC virulence fac-
tors should be considered to be of the pre-adapted nature, i.e. did not evolve for
virulence per se, at least not in humans. One of the critical virulence factors of
EHEC is Shiga-like toxin encoded by prophage (
Sandvig, 2001
). The toxin is
apparently expressed and secreted even without the phage activation and has
powerful toxicity against human cells (
Bielaszewska et al., 2006
). However,
it likely evolved as a weapon against protozoan predators of bacteria rather
than to induce human tissue damage (
Steinberg and Levin, 2007
). It has been
proposed that Shiga-toxin in EHEC is over-expressed or released in an overly
large amount during the human infection due to activation of the prophage
(
Mellmann et al., 2009
). The latter could be the result of stress imposed on bac-
teria in human intestine as it tries to establish colonization there. The nature of
the stress is unclear but it appears to be absent during the colonization of bovine
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