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2017 ; 17
(1
): 68
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Uropathogenic Escherichia coli pathogenicity islands and other ExPEC virulence
genes may contribute to the genome variability of enteroinvasive E coli
#MMPMID28302076
da Silva LC
; de Mello Santos AC
; Silva RM
BMC Microbiol
2017[Mar]; 17
(1
): 68
PMID28302076
show ga
BACKGROUND: Enteroinvasive Escherichia coli (EIEC) may be the causative agent of
part of those million cases of diarrhea illness reported worldwide every year and
attributable to Shigella. That is because both enteropathogens have many common
characteristics that difficult their identification either by traditional
microbiological methods or by molecular tools used in the clinical laboratory
settings. While Shigella has been extensively studied, EIEC remains barely
characterized at the molecular level. Recent EIEC important outbreaks, apparently
generating more life-threatening cases, have prompted us to screen EIEC for
virulence traits usually related to extraintestinal pathogenic E. coli (ExPEC).
That could explain the appearance of EIEC strains presenting higher virulence
potential. RESULTS: EIEC strains were distributed mainly in three phylogroups in
a serogroup-dependent manner. Serogroups O124, O136, O144, and O152 were
exclusively classified in phylogroup A; O143 in group E; and O28ac and O29 in
group B1. Only two serogroups showed diverse phylogenetic origin as follows: O164
was assigned to groups A, B1, C, and B2 (one strain each), and O167 in groups E
(five strains), and A (one strain) (Table 1). Eleven of 20 virulence genes (VGs)
searched were detected, and the majority of the 19 different VGs combinations
found were serogroup-specific. Uropathogenic E. coli (UPEC) PAI genetic markers
were detected in all EIEC strains. PAIs I(J96) and II(CFT073) were the most
frequent (92.1 and 80.4%, respectively). PAI IV(536) was restricted to some
serogroups from phylogroups A, B1 and E. PAI I(CFT073) was uniquely detected in
phylogroups B2 and E. A total of 45 (88%) strains presented multiple PAI markers
(two to four). PAIs I(J96) and II(CFT073) were found together in 80% of strains.
CONCLUSIONS: EIEC is a DEC pathovar that presents VGs and pathogenicity island
genetic markers typically associated with ExPEC, especially UPEC. These features
are distributed in a phylogenetic and serogroup-dependent manner suggesting the
existence of stable EIEC subclones. The presence of phylogroups B2 and E strains
allied to the presence of UPEC virulence-associated genes may underscore the
ongoing evolution of EIEC towards a hypervirulent pathotype.