Prevalence of the "high-pathogenicity island" of Yersinia species among Escherichia coli strains that are pathogenic to humans - PubMed (original) (raw)

Prevalence of the "high-pathogenicity island" of Yersinia species among Escherichia coli strains that are pathogenic to humans

S Schubert et al. Infect Immun. 1998 Feb.

Abstract

The fyuA-irp gene cluster contributes to the virulence of highly pathogenic Yersinia (Yersinia pestis, Yersinia pseudotuberculosis, and Yersinia enterocolitica 1B). The cluster encodes an iron uptake system mediated by the siderophore yersiniabactin and reveals features of a pathogenicity island. Two evolutionary lineages of this "high pathogenicity island" (HPI) can be distinguished on the basis of DNA sequence comparison: a Y. pestis group and a Y. enterocolitica group. In this study we demonstrate that the HPI of the Y. pestis evolutionary group is disseminated among species of the family Enterobacteriaceae which are pathogenic to humans. It prevails in enteroaggregative Escherichia coli and in E. coli blood culture isolates (93 and 80%, respectively), but is rarely found in enteropathogenic E. coli, enteroinvasive E. coli, and enterotoxigenic E. coli isolates. In contrast, the HPI was absent from enterohemorrhagic E. coli, Shigella, and Salmonella enterica strains investigated. Polypeptides encoded by the fyuA, irp1, and irp2 genes located on the HPI could be detected in E. coli strains pathogenic to humans. However, these E. coli strains showed a reduced sensitivity to the bacteriocin pesticin, whose uptake is mediated by the FyuA receptor. Escherichia strains do not possess the hms gene locus thought to be a part of the HPI of Y. pestis. Deletions of the juA-irp gene cluster affecting solely the fyuA part of the HPI were identified in 3% of the E. coli strains tested. These results suggest horizontal transfer of the HPI between Y. pestis and some pathogenic E. coli strains.

PubMed Disclaimer

Figures

FIG. 1

Physical map of the HPI of Y. enterocolitica O8 WA-C with the presumed 5′ and 3′ borders of the HPI. Horizontal lines below the restriction map represent different subcloned DNA fragments (E6, E8.8, E3.5, and Cl8) which were used as probes in hybridization assays. Arrows and bars within the restriction map indicate the locations of the identified genes and repeated sequence (RS) elements, respectively. E, _Eco_RI; C, _Cla_I; p12H2 and p17A11, cosmid clones. The locations of the 5′-HPI probe and the adjacent asnT tRNA are indicated. The asterisk indicates an additional internal _Eco_RI site found only in the irp2 genes of Y. enterocolitica biotype 1B strains.

FIG. 2

Southern hybridizations of _Eco_RI-digested genomic DNA of Y. enterocolitica and different E. coli strains with four DNA fragments, E6, E8.8, E3.5, and Cl8 (as shown in Fig. 1), representing the central part of the Yersinia HPI. Lane 1, E. coli DH5α; lane 2, Y. enterocolitica O8 WA-C; lane 3, Y. pseudotuberculosis O1; lane 4, EAEC 17-2 (HPI positive); lane 5, EPEC 12-1; (HPI positive); lane 6, EIEC E12860 (HPI positive); lane 7, ETEC H488/84 (HPI positive); lane 8, E. coli 14094/96 from blood culture; (HPI positive); lane 9, EAEC DMI 155 (HPI positive); lane 10, EIEC H823/88 (HPI positive); lane 11, EHEC 1249/87 (HPI negative); and lane 12, EAEC 4827/94; (HPI negative).

FIG. 3

Immunoblot of outer membrane proteins probed with anti-FyuA rabbit serum. Lane 1, Y. enterocolitica O8 WA-C; lane 2, E. coli 14094/96 from blood culture (HPI positive); lane 3, EAEC 17-2 (HPI positive); and lane 4, EAEC 4827/94 (HPI negative).

FIG. 4

(A) Immunoblot of outer membrane proteins probed with anti-HMWP1 and anti-HMWP2 mouse serum. Lanes: 1, Y. enterocolitica O8 WA-C; 2, Y. pseudotuberculosis O1; 3, E. coli DH5α; 4, EAEC 4827/94 (HPI negative); 5, EPEC 2403/85 (HPI negative); 6, EAEC 17-2 (HPI positive); 7, EPEC 12-1 (HPI positive); 8, EIEC E12860 (HPI positive); 9, ETEC H488/84 (HPI positive); 10, E. coli 14094/96 from blood culture (HPI positive); and 11, EHEC 1249/87 (HPI negative). (B) Fluorographs of a polyacrylamide gel containing 35S-labeled proteins from E. coli DH5α (lane 1), Y. enterocolitica O8 WA-C (lane 2), EPEC 2403/85 (HPI positive) (lane 3), EIEC E12860 (HPI positive) (lane 4), EAEC 17-2 (HPI positive) (lane 5), and EAEC 4827/94 (HPI negative) (lane 6).

References

1. Ausubel F M, Brent R, Kingston R E, Moore D D, Seidman J G, Smith J A, Struhl K. Current protocols in molecular biology. New York, N.Y: John Wiley & Sons; 1989.
1. Autenrieth I B, Hantke K, Heesemann J. Immunosuppression of the host and delivery of iron to the pathogen: a possible dual role of siderophores in the pathogenesis of microbial infections? Med Microbiol Immunol. 1991;180:135–141. - PubMed
1. Bagg A, Neilands J B. Molecular mechanism of regulation of siderophore-mediated iron assimilation. Microbiol Rev. 1987;51:509–518. - PMC - PubMed
1. Bearden S W, Fetherston J D, Perry R D. Genetic organization of the yersiniabactin biosynthetic region and construction of avirulent mutants in Yersinia pestis. Infect Immun. 1997;65:1659–1668. - PMC - PubMed
1. Bettelheim K A, Hanna N, Smith D L, Dwyer B W. Evaluation of the Phadebact ETEC-LT test for the heat-labile enterotoxin of Escherichia coli. Int J Med Microbiol. 1989;271:70–76. - PubMed

Prevalence of the "high-pathogenicity island" of Yersinia species among Escherichia coli strains that are pathogenic to humans - PubMed (original) (raw)