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Infection and Immunity, April 2000, p. 2082-2095, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Molecular and Biological Analysis of Eight Genetic Islands That Distinguish Neisseria meningitidis from the Closely Related Pathogen Neisseria gonorrhoeae

Silke R. Klee,1 Xavier Nassif,2 Barica Kusecek,1 Petra Merker,1 Jean-Luc Beretti,2 Mark Achtman,1,* and Colin R. Tinsley2

Max-Planck Institut für Molekulare Genetik, 14195 Berlin, Germany,1 and Laboratoire de Microbiologie, INSERM Unité 411, Faculté de Médecine Necker-Enfants Malades, 75730 Paris Cedex 15, France2

Received 2 August 1999/Returned for modification 12 October 1999/Accepted 22 December 1999

The pathogenic species Neisseria meningitidis and Neisseria gonorrhoeae cause dramatically different diseases despite strong relatedness at the genetic and biochemical levels. N. meningitidis can cross the blood-brain barrier to cause meningitis and has a propensity for toxic septicemia unlike N. gonorrhoeae. We previously used subtractive hybridization to identify DNA sequences which might encode functions specific to bacteremia and invasion of the meninges because they are specific to N. meningitidis and absent from N. gonorrhoeae. In this report we show that these sequences mark eight genetic islands that range in size from 1.8 to 40 kb and whose chromosomal location is constant. Five of these genetic islands were conserved within a representative set of strains and/or carried genes with homologies to known virulence factors in other species. These were deleted, and the mutants were tested for correlates of virulence in vitro and in vivo. This strategy identified one island, region 8, which is needed to induce bacteremia in an infant rat model of meningococcal infection. Region 8 encodes a putative siderophore receptor and a disulfide oxidoreductase. None of the deleted mutants was modified in its resistance to the bactericidal effect of serum. Neither were the mutant strains altered in their ability to interact with endothelial cells, suggesting that such interactions are not encoded by large genetic islands in N. meningitidis.

* Corresponding author. Mailing address: Max-Planck Institut für molekulare Genetik, Ihnestrasse 73, 14195 Berlin, Germany. Phone: 49 30 8413 1262. Fax: 49 30 8413 1385. E-mail: achtman{at}molgen.mpg.de.

Infection and Immunity, April 2000, p. 2082-2095, Vol. 68, No. 4
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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