IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Herd, M.
Right arrow Articles by Kocks, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Herd, M.
Right arrow Articles by Kocks, C.

 Previous Article  |  Next Article 

Infection and Immunity, June 2001, p. 3972-3979, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3972-3979.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Gene Fragments Distinguishing an Epidemic-Associated Strain from a Virulent Prototype Strain of Listeria monocytogenes Belong to a Distinct Functional Subset of Genes and Partially Cross-Hybridize with Other Listeria Species

Martin Herd and Christine Kocks*

Institute for Genetics, University of Cologne, D-50674 Cologne, Germany

Received 16 November 2000/Returned for modification 6 February 2001/Accepted 13 March 2001

Most major food-borne outbreaks of listeriosis in Europe and in the United States have been caused by genetically closely related Listeria monocytogenes strains of serotype 4b. In order to assess whether genomic loci exist that could underlie this increased epidemic potential, we subtracted the genome of the virulent prototype L. monocytogenes strain EGD from a prototype epidemic strain. A total of 39 DNA fragments corresponding to 20% of an estimated total of 150 to 190 kb of differential genome material were isolated. For 21 of these fragments, no function on the basis of homology could be predicted. Of the remaining 18 fragments, 15 had homologies to bacterial surface proteins, some of which have been implicated in virulence mechanisms such as cell invasion, adhesion, or immune escape. Southern hybridization of arrays containing the epidemic-clone-specific DNA segments with genomic DNA of different L. monocytogenes strains was consistent with the current lineage division. Surprisingly, however, some of the fragments hybridized in a mosaic-like fashion to genomes of two other Listeria species, the animal pathogen L. ivanovii and the nonpathogen L. innocua. Taken together, our results provide a starting point for the identification of epidemic-trait-associated genes.


* Corresponding author. Mailing address: Institute for Genetics, University of Cologne, Zuelpicher Str. 47, D-50674 Cologne, Germany. Phone: 49 221 470 4857. Fax: 49 221 470 5172. E-mail: Christine.Kocks{at}uni-koeln.de.


Infection and Immunity, June 2001, p. 3972-3979, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3972-3979.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2001 by the American Society for Microbiology. All rights reserved.