Evolution of pathogenic Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 44

FIGURE 3.1 Phylogenetic tree (phylogram) of 22 E. coli isolates with fully assembled genomes.
The tree is based on 7-loci Multi-Locus Sequence Type (MLST) profiles, using E. fergusonii as
an outgroup. Core genes are present in all 22 isolates, mosaics are present in multiple but not all
isolates, and unique genes are present in one isolate only.
Thus, the genomic differences between strains from different pathotypes are
even more pronounced than on average strain-to-strain, making the search for
pathotype-specific traits difficult.
Interestingly, however, at least in some cases, clonally related strains with
the same ST could be drastically different in their virulence ( Weissman et al.,
2012 ). For example, the probiotic strain Nissle-1917 that was isolated from the
feces of a healthy individual almost a century ago has the same ST profile as
model pathogenic E. coli strain CFT073 isolated from a patient with urosep-
sis in the 1980s ( Vejborg et al., 2010 ). The vast majority of genes are shared
between Nissle and CFT073, and only about 17% of genes are different. On
the nucleotide level, there are about 100-fold fewer mutational differences than
found between clonally unrelated strains. Thus, comparing clonally related
strains might facilitate the search for the genetic basis of differential virulence
and the evolutionary mechanisms of virulence acquisition.
GENETIC MECHANISMS OF VIRULENCE EVOLUTION
To gather insights on the microevolution of virulence in E. coli , the first step
is to understand the genetic mechanisms the species adopt to achieve their