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Infection and Immunity, November 1999, p. 5994-6001, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
A Genomic Island, Termed High-Pathogenicity Island,
Is Present in Certain Non-O157 Shiga Toxin-Producing
Escherichia coli Clonal Lineages
H.
Karch,1,*
S.
Schubert,2
D.
Zhang,3
W.
Zhang,1
H.
Schmidt,1
T.
Ölschläger,3 and
J.
Hacker3
Institut für Hygiene und Mikrobiologie,
D-97080 Würzburg,1
Max-von-Pettenkofer-Institut für Hygiene und
Mikrobiologie, 80336 München,2 and
Institut für Molekulare Infektionsbiologie, 97070 Würzburg,3 Germany
Received 19 May 1999/Returned for modification 28 July
1999/Accepted 2 September 1999
Shiga toxin-producing Escherichia coli (STEC) strains
cause a wide spectrum of diseases in humans. In this study, we tested 206 STEC strains isolated from patients for potential virulence genes
including stx, eae, and enterohemorrhagic
E. coli hly. In addition, all strains were examined for the
presence of another genetic element, the high-pathogenicity island
(HPI). The HPI was first described in pathogenic Yersinia
species and encodes the pesticin receptor FyuA and the siderophore
yersiniabactin. The HPI was found in the genome of distinct clonal
lineages of STEC, including all 31 eae-positive
O26:H11/H
strains and 7 of 12 eae-negative
O128:H2/H
strains. In total, the HPI was found in 56 (27.2%) of 206 STEC strains. However, it was absent from the genome of
all 37 O157:H7/H
, 14 O111:H
, 13 O103:H2,
and 13 O145:H
STEC isolates, all of which were positive
for eae. Polypeptides encoded by the fyuA gene
located on the HPI could be detected by using immunoblot analysis in
most of the HPI-positive STEC strains, suggesting the presence of a
functional yersiniabactin system. The HPI in STEC was located next to
the tRNA gene asnT. In contrast to the HPI of other
pathogenic enterobacteria, the HPI of O26 STEC strains shows a deletion
at its left junction, leading to a truncated integrase gene
int. We conclude from this study that the
Yersinia HPI is disseminated among certain clonal subgroups
of STEC strains. The hypothesis that the HPI in STEC contributes to the
fitness of the strains in certain ecological niches rather than to
their pathogenic potential is discussed.
*
Corresponding author. Mailing address: Institut
für Hygiene und Mikrobiologie/Universität Würzburg,
Josef-Schneider-Straße 2, 97080 Würzburg, Germany. Phone:
49-931-2015162. Fax: 49-931-2015166. E-mail:
hkarch{at}hygiene.uni-wuerzburg.de.
Infection and Immunity, November 1999, p. 5994-6001, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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