Evolution of pathogenic Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 42

Chapter 3
Evolution of pathogenic
Escherichia coli
Sujay Chattopadhyay and Evgeni V. Sokurenko
University of Washington, Seattle, WA, USA
INTRODUCTION
As with evolution in general, bacterial evolution happens through the action
of selection and drift on random genetic variations, affecting their frequency
in nature, in space and in time. The evolution of virulence is viewed from the
host's perspective, where evolution of microbial genomes results in the abil-
ity of the microorganism to cause clinically manifested damage of the host.
The ability to cause disease reflects the microbial fitness (i.e. ability to survive
and reproduce) during the infection itself. To understand the driving forces and
mechanisms behind the evolution of microbial virulence, one might compare
the genomic content of organisms that are able to cause the disease to those that
are unable to do so. There are relatively few (<200) bacterial species that are
isolated as the cause of human infections, among which less than a dozen cause
the vast majority of the infections. It is possible to compare these species to
the species that do not act as common pathogens. While this approach is valid,
the high level of genomic diversity between even closely related species makes
such a strategy difficult. Frequent horizontal gene transfer between prokaryotic
species results in a high level of genome mosaicism, which adds to the genome
plasticity along with intragenomic variations, like point mutations, gene dele-
tion/amplification, or genomic rearrangements. It is easier to compare organ-
isms from the same bacterial species that differ significantly in their ability to
cause disease. Escherichia coli offers an ideal example of such within-species
virulence diversity.
WITHIN-SPECIES DIVERSITY OF PATHOGENIC E. COLI
There is a huge diversity of phenotypic traits across E. coli strains, both quanti-
tatively or qualitatively, which allow these strains to differ in their appearance,
behavior, metabolism, as well as in their ability to cause disease in humans. At
one end, commensal strains, the vast majority of E. coli population, have adapted