Uropathogenic Escherichia coli - Escherichia coli: Pathotypes and Principles of Pathogenesis - page 265

Chapter 9
Uropathogenic Escherichia coli
Rachel R. Spurbeck and Harry L.T. Mobley
University of Michigan Medical School, Ann Arbor, MI, USA
BACKGROUND
Classification and evolution of uropathogenic E. coli
Uropathogenic Escherichia coli (UPEC) are a heterogeneous group of strains
within the broader classification of extraintestinal pathogenic E. coli . There is
no core set of virulence factors shared by all UPEC. Most UPEC belong to B2
and D phylogroups (Chapter 1) and can be classified based on the O (lipopoly-
saccharide) serotype into uropathogenic clones, with 58% of UPEC isolates
belonging to one of eight serogroups (O1, O2, O4, O6, O8, O9, O18, and O83)
( Blanco et al., 1994, 1996 ). UPEC can be classified by the type or severity of
infection from which the bacteria are isolated. Pyelonephritis or urosepsis iso-
lates cause the most severe UTI, infecting the kidneys and allowing access to the
bloodstream. Cystitis isolates cause bladder infections, and asymptomatic bac-
teriuria (ABU) strains stably colonize the urinary tract without causing disease
symptoms in an almost commensal state. Comparative genomic hybridization
comparing the genomic content of ten UPEC strains and four fecal/commensal
strains revealed 10 pathogen-specific genomic islands comprising 13% of the
genome of pyelonephritis isolate E. coli CFT073 ( Lloyd et al., 2007 ). Three
islands were known pathogenicity islands containing P fimbriae and other char-
acterized virulence factors. Furthermore, 52% of the genome is shared among
UPEC and commensal isolates, and only 131 genes of the 5379 genes present in
E. coli CFT073 were UPEC-specific ( Lloyd et al., 2007 ).
ABU isolates, like UPEC isolates that cause symptomatic disease, have
expanded genomes when compared to fecal commensal E. coli . However, a
study of 112 ABU isolates, in which bacteriuria lasted from 1-74 days with at
least one urine culture of ≥10 5 CFU/ml, suggests that ABU isolates have under-
gone reductive evolution within human hosts. Point mutations and deletions in
genes encoding virulence factors reduce the virulence of the ABU isolates over
time ( Salvador et al., 2012 ). Therefore, UPEC acquired virulence through hori-
zontal gene transfer events, such as acquisition of PAIs, but reductive evolution
attenuates ABU strains into a more commensal-like state.