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approximately 80 kb of MG1655-specific sequences, resulting in approximately
713 kb larger chromosome size in RS218. This difference is 160 kb larger than the
previously estimated genome size difference between RS218 and MG1655 (
Rode
et al., 1999
). Previous studies using comparative macrorestriction mapping and
subtractive hybridization of the chromosomes of meningitis-causing
E. coli
K1
(e.g. 018:K1 strains RS218 and C5, belonging to phylogenetic group B2) com-
pared to non-pathogenic
E. coli
have identified 500 kb spread over at least 12
chromosome loci specific to
E. coli
K1 (
Bloch et al., 1996
;
Bonacorsi et al., 2000
).
Mapping studies reveal that those
E. coli
loci are located at different regions of
the
E. coli
chromosome. Twenty-two RDIs have also been shown to be located at
different regions of the
E. coli
K1 RS218 chromosome (
Xie et al., 2006a,b
).
Using RDI deletion mutants constructed from strain RS218, eight RDIs
have been shown to be involved in the pathogenesis of meningitis (i.e. induc-
tion of a high degree of bacteremia, HBMEC binding, and invasion). Two RDIs
include a P4-family integrase and are directly adjacent to tRNAs (RDI 4-
serX
and RDI 21-
leuX
) and four RDIs have markedly lower GC percentages com-
pared to the whole RS218 genome (
Xie et al., 2006a,b
), suggesting that these
RDIs are acquired through horizontal gene transfer. Further identification and
characterization of microbial factors from those RDIs that are involved in the
pathogenesis of
E. coli
meningitis should help in elucidating microbial factors
involved in meningitis.
At present, the microbial factors identified from prototypic meningitis-caus-
ing 018:K1
E. coli
strains (e.g. strains RS218 and C5) have been used to under-
stand the pathogenesis of
E. coli
meningitis (
Kim, 2001, 2002, 2003, 2008
;
Xie
et al., 2006a,b
;
Yao et al., 2006
), but it is unclear whether the information derived
from these
E. coli
K1 strains is relevant to other
E. coli
K1 strains isolated from
CSF. We have conducted a comparative genomic hybridization (CGH) with an
E. coli
DNA microarray to examine the basis of meningitis caused by representa-
tive
E. coli
K1 strains isolated from CSF, belonging to phlyogenetic groups B2
and D (
Yao et al., 2006
). These strains include RS218 (O18:K1, B2 group), C5
(18:K1, B2 group), IHE3034 (O18:K1, B2 group), EC10 (O7:K1, D group), A90
(O1:K1, B2 group), RS168 (O1:K1, D group), RS167 (O16:K1, B2 group), S88
(O45:K1, B2 group), and S95 (O45:K1, Be group). Our hierarchical clustering
revealed that these strains can be categorized into two groups. Group 1 includes
strains RS218, C5, IHE3034, A90, RS167, S88, and S95, while strains EC10 and
RS168 belong to group 2. All group 1 strains belong to the phylogenetic group
B2, which is predominant in CSF isolates, and group 2 strains belong to less
common phylogenetic groups A and D (
Yao et al., 2006
). Of interest, a type III
secretion system was found to be present in group 2 strains of
E. coli
but not in
group 1 strains, isolated from neonatal meningitis, and was shown to contribute
to
E. coli
invasion of HBMEC and intracellular survival (
Yao et al., 2009
). The
existence of a type III secretion system as well as its effectors and homologs was
verified by genome sequencing of strain EC10 (
Lu et al., 2011
). This is the first
demonstration of a type III secretion system in meningitis-causing
E. coli
, but its
underlying mechanisms involved in
E. coli
meningitis remain to be established.
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