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intestine. EHEC represent a classical example of virulence, being the result of
failure to establish commensal relationships with the host. Because bacteria
are being lysed during the phage activation, the toxin over-expression would
unlikely evolve as an adapted trait for bacteria and, thus, can be considered as a
pre-adapted virulence factor.
Examples of pathoadaptive mutations in EHEC could be mutations inactivat-
ing the type 1 fimbriae, the most ubiquitous mannose-binding adhesive trait in
E. coli
(
Shaikh et al., 2007
). Inactivating mutations are found both in the adhesin
protein FimH and the fimbrial expression switch, suggesting it occurred repeat-
edly and, thus, under the action of positive selection (
Leopold et al., 2009
). How-
ever, these mutations are found in both clinical and non-clinical isolates of O157
serotype, consistent with their pre-adapted nature in the latter. The role of the
fimbrial loss in either the human infection or bovine colonization is unclear yet.
Besides EHEC, some other infections caused by
E. coli
strains are eco-
logical dead-ends, e.g. meningitis or bloodstream infections, rendering them
as accidental pathogens. Therefore, their putative virulence factors, such
as cerebrospinal barrier (CSB)-binding, sialic-acid specific S-fimbriae of
meningitis-causing
E. coli
strains (
Ott et al., 1986
), could also be defined as
pre-adapted virulence traits.
Opportunistic pathogens
This type of pathogen represents the most diverse and, from evolutionary per-
spectives, ambiguous group of
E. coli
. Unlike professional pathogens, these
E. coli
appear to be able to continuously circulate only as human asymptom-
atic colonizers (commensals). They cause clinical infections only occasionally,
mostly in individuals with at least somewhat or transiently compromised defense
barriers. Unlike the accidental pathogens, however, the bacteria might be readily
able to return to their original environment (human intestine) while being shed
during the infection, sometimes in high numbers. Thus, the infectious process
does not impose an evolutionary dead-end scenario for the pathogen. Examples
of such
E. coli
are primarily the ExPEC pathotype that, in developed countries,
causes the vast majority of
E. coli
infections (
Johnson and Russo, 2002
). Just
the urinary tract infections alone (primarily bladder infection - cystitis), where
E. coli
is the main pathogen, affects over 7 million women each year in the USA
(
Foxman, 2002
). The infecting
E. coli
usually come from the intestinal micro-
biota, introduction of which into the bladder is facilitated by sexual intercourse,
diaphragm use, or bladder catheterization (
Brown and Foxman, 2000
). Bladder
infection commonly lasts 5-7 days, during which bacteria are shed with urine,
often more than 10
5
CFU per ml. In rare cases, bacteria from the bladder ascend
into kidney, resulting in a more serious clinical infection - pyelonephritis.
While the urinary tract infections are common, they affect primarily women
and, in terms of frequency and bacterial load, are minute in comparison to intes-
tinal colonization by
E. coli
in both men and women. This is true even for the
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