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one that was acquired/evolved and maintained to perform a specific function in
a specific environment. By using a kitchenware analogy, a vegetable knife is
adapted (designed) to chop vegetables, a salad fork to pick them up on the plate
and a soupspoon to fish them out in the bowl. In contrast, pre-adapted traits are
those that might fit to perform a specific function though they are not designed
to do so. By the same kitchenware analogy (but not so peaceful), the vegetable
knife can easily be adapted as a deadly weapon in most hands. The salad fork
can also be adapted as a weapon (but in rather skillful hands), while it is difficult
to make use of a soupspoon for that purpose in virtually any hands.
Thus, virulence traits should be defined as adapted when they were acquired/
evolved specifically to increase the ability of a pathogen to survive in the course
of infection. In contrast, pre-adapted virulence traits are those that also increase
the pathogenic fitness but are originally adapted for a function that is unrelated
to the virulence, e.g. evolved as a trait for commensal colonization of humans or
non-human hosts. Defining whether or not a virulence factor is adapted or pre-
adapted might seem a purely intellectual exercise from practical perspectives.
Indeed, why should a patient, physician, or even medical researcher care whether
or not the pathogen had
evolved
to impose the misery of infection or just be able
to do it? As described below, however, to define the virulence trait as adapted or
pre-adapted is essential for answering the most important question from evolu-
tionary perspectives: what is the driving force behind the emergence and mainte-
nance of the pathogenic
E. coli
? This, in turn, could help us to pinpoint what the
critical virulence factors in a pathogen are, whatever nature they are.
WHY DID
E. COLI
EVOLVE TO BE PATHOGENIC?
It is likely that some
E. coli
strains just lack specific traits or their combination
that would allow them to cause infection in humans, i.e. to sustain themselves
long enough in protected compartments and to induce clinically manifested
tissue damage. So, they can be defined as non-pathogens that can exist only
asymptomatically to the human habitats (
Figure 3.3
). These strains are confined
to either non-human hosts only or commensal colonization of healthy humans.
It appears that, from evolutionary perspectives, the non-pathogenic
E. coli
lineages are original to the species and gave rise to different pathotypes of
E. coli
and not vice versa. First, non-pathogens constitute the bulk of
E. coli
organisms in nature. Second, the clonal diversity of non-clinical
E. coli
is signif-
icantly higher than of any type of clinical isolate (
Kohler and Dobrindt, 2011
),
implying that the latter are expanded subsets of the former and, thus, derived
(evolved) from them. Thirdly, many traits that can be defined as virulence factors
in pathogens (either adapted or pre-adapted) are recently acquired from evolu-
tionary perspectives. Pathogenic strains have horizontally transferred genes on
plasmids, prophages, or chromosomal islands that are missing in most of the
non-clinical strains. While theoretically non-pathogens could have mostly lost
these highly mobile elements, phylogenetic analysis of their distribution argues
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