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of the virulence genes might have preferably occurred in strains of a similar
genomic background.
To answer the question about the driving force behind the emergence of
pathogenic lineages of
E. coli
, it is necessary to examine whether the ability
of
E. coli
to cause disease contributes to its continuous survival in nature. It
appears that any of the pathogenic
E. coli
are capable of asymptomatic coloni-
zation of humans or non-human hosts. By definition, however, all pathogenic
E. coli
can enter protected compartments and cause clinical infection. The key dif-
ference between different pathogens is how much they depend on the conditions
asymptomatic for human habitats to maintain themselves in nature. Considering
the dual habitats of pathogenic
E. coli
, from the ecological and evolutionary
perspectives
E. coli
pathotypes could be subdivided into three general categories -
professional, accidental, and opportunistic pathogens (
Figure 3.3
).
Professional pathogens
In these
E. coli
their ability to cause disease is essential for continuous circula-
tion in nature, with pathotypes like
Shigella
and enteroinvasive
E. coli
(EIEC)
being the great examples. While they can colonize humans asymptomatically,
the asymptomatic carriers are predominantly individuals who recovered from
symptomatic infection by the same strain (
Zdziarski et al., 2010
). The profes-
sional pathogens can also effectively transmit during the active infection to form
new infections, i.e. from patient to patient (
Stewart et al., 2003
). Thus, virulence
factors of
Shigella
and EIEC are likely to be maintained specifically to cause the
infection or to be transmitted as a pathogen, i.e. to be of the adapted nature. This
relates to both mechanisms of virulence evolution, horizontal gene transfer, and
pathoadaptive mutations (
Figure 3.3
). Among the former category is a large
virulence plasmid that encodes genes for expression of characteristic
Shigella
virulence such as invasion, intracellular replication, intercellular spread, and
induction of an inflammatory response (
Pupo et al., 2000
). Among pathoadap-
tive mutations the leading role is played by the loss-of-function mutations, with
the classic example of deletion of
cadA
and
ompT
antivirulence genes that inter-
fere with the function or secretion of the enterotoxin (
Day et al., 2001
). Also,
among different
E. coli
pathotypes,
Shigella
/EIEC carry the largest amount of
point mutational changes (variations) in the core genes, a bulk of which could
be pathoadaptive in nature (
Chattopadhyay et al., 2009
).
Other
E. coli
pathotypes that could represent professional pathogens are
ETEC and EPEC, where diarrhea might be a prerequisite for establishing
asymptomatic intestinal colonization in new human hosts. These new hosts are
primarily individuals that did not encounter the pathogen before - either chil-
dren or newcomers to the community ('travelers') (
von Sonnenburg et al., 2000
).
However, ETEC and EPEC appear to circulate as a commensal within the com-
munity having built-up immunity against them. It is also possible that domesti-
cated animals are primary reservoirs for some of these pathotypes (see Chapter 1).
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