Evolution of pathogenic Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 58

clonal lineages of E. coli that primarily cause urinary infections (mostly of B2
phylogenetic group - see Figure 3.2 ) ( Moreno et al., 2008 ). Thus, it is unlikely
that the primary, intestinal colonization of ExPEC depends on the ability to
cause the opportunistic infection. Therefore, the urovirulence factors that allow
the infections to be initiated are most likely to be of the pre-adapted nature.
Indeed, horizontally transferred virulence factors of uropathogenic E. coli such
as di-galactose-specific P fimbriae were proposed to be important for the intes-
tinal colonization of E. coli in humans with certain blood types ( Herias et al.,
1995 ).
By the same token, it has been shown that in the course of urinary tract
infections, bacteria can adapt there by mutating, among other traits, FimH adhe-
sin, LPS, flagella ( Weissman et al., 2003 ). Thus, at least some of the virulence
traits are selected for in the virulence habitat and, therefore, are of an adapted
nature. In fact, some of the clearest examples of pathoadaptive mutations in
the course of infection come from the UPEC. The dual nature of the virulence
factors in the opportunistic pathogens (i.e . being both pre-adapted and adapted)
makes this category complex from evolutionary model perspectives described
in detail below.
EVOLUTIONARY MODELS, SOURCE-SINKS, AND PARADOXES
Concepts of virulence evolution
The diversity of trajectories that are taken by evolution of E. coli pathotypes
provides illustrations of all three major models of virulence evolution: (i) viru-
lence is increasing fitness of (i.e. adaptive for) the pathogen, (ii) virulence is a
coincidental by-product of commensal evolution, and (iii) virulence is a result
of a shortsighted positive selection ( Levin and Bull, 1994 ).
According to the first model, i.e. virulence is adaptive for the pathogens,
there are two main sub-models: (a) benefit-of-virulence; and (b) cost-of-
virulence ( Sokurenko et al., 1999 ). Under the benefit-of-virulence model, dis-
ease is the primary mode of the host-bacteria interaction and transmission, even
when asymptomatic colonization is a more common outcome of it. In contrast,
under the cost-of-virulence model, the primary form of the pathogen's existence
is asymptomatic colonization, but disease is a relatively commonly associated
outcome of it at the early stages of encountering the new host. Most likely, the
professional pathogens like Shigella /EIEC, EPEC and ETEC could ostensibly
fit this model.
According to the second model, virulence is the coincidental outcome of
adaptation to a commensal or environmental habitat. In other words, virulence
had evolved under conditions different from the disease and, thus, pathogenicity
is a pure chance and not an evolutionary pre-determined property. In this case,
the virulence factors are pre-adapted. Both accidental and opportunistic patho-
gens fit this model.