Evolution of pathogenic Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 59

According to the third model, virulence results from short-sighted evolu-
tion during the course of infection itself, when selection improves fitness of the
pathogen, no matter how transient the infection is. Because fitness is the mea-
sure of improved survival resulting from reduced elimination and/or increased
reproduction rates in the habitat, the selection processes result in bacterial
organisms that cause more long-lasting and, sometimes, more damaging (clini-
cally severe) infection. Again, both accidental and opportunistic pathogens are
most likely to be subjected to such selective pressures. By being pre-adapted
for the ability to cause clinical infection, they are unlikely to be as optimally
adapted to the pathogenic lifestyle as are professional pathogens, thus providing
ample room for the action of positive selection.
Source-sink dynamics
Because evolution of accidental and opportunistic pathogens fits two differ-
ent models of virulence evolution, the models are not mutually exclusive. In
fact, combination of the coincidental and short-sighted virulence leads to a so-
called 'source-sink' dynamics of virulence evolution ( Sokurenko et al., 2006 ).
Source-sink has been originally developed as an ecological model, where a
species exists in two distinct types of habitats ( Pulliam 1988 ). The 'source' is
a continuously inhabited, stable, or reservoir habitat supporting the long-term
existence of the species. In contrast, 'sink' is an occasionally invaded unstable
habitat that can support the species survival only for a short period of time.
The evolutionary source-sink model implies that species continuously undergo
genetic adaption to the sink environment upon invasion from the source, result-
ing in increased fitness in the former ( Sokurenko et al., 2006 ). However, while
improving survival in the sink, the adaptive evolution there not only fails to
make the sink sustainable in the long term, but also reduces the fitness-of-sink-
adapted organisms in the source. This happens due to a trade-off effect of the
sink-adaptive changes in the source habitat.
When applied to the pathogens, the commensal colonization reservoir could
be defined as the source habitat and the infection as the sink habitat. Adaptation to
the sink is likely to happen only via mutations, because transferrable genetic ele-
ments are not readily available in the course of infections (that are usually mono-
infections, i.e. caused by a single strain). Clearly, loss-of-function pathoadaptive
mutations that result in inactivation of the commensal traits are maladaptive back
in the reservoir habitat. Mutations modifying gene function could also have the
trade-off effect with the original gene function. Thus, patho-adapted bacteria will
be under negative selection upon entering the original habitat.
The trade-off effect could be primarily noted with opportunistic pathogens
that can readily go back from the sink to the source. Indeed, pathoadaptive
mutations in, for example the FimH adhesin of uropathogenic E. coli , bear a
signature of being only recently evolved - the likely sign of their instability in a
long-term natural circulation ( Weissman et al., 2007 ).