Article Text

P1.59 Genomic characterisation of urethritis-associated neisseria meningitidis
  1. Ma KC1,
  2. M Unemo2,
  3. S Jeverica3,
  4. RD Kirkcaldy4,
  5. M Ohnishi5,
  6. YH Grad1,6
  1. 1Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, USA
  2. 2WHO Collaborating Centre for Gonorrhoea and other STIs, National Reference Laboratory for Pathogenic Neisseria, Faculty of Medicine and Health, Örebro University, Örebro, Sweden
  3. 3Institute for Microbiology and Immunology, Medical Faculty, University of Ljubljana, Ljubljana, Slovenia
  4. 4Division of STD Prevention, National Centre for HIV/AIDS, Viral Hepatitis, STD and TB Prevention, CDC, Atlanta, Georgia, USA
  5. 5Department of Bacteriology I, National Institute of Infectious Diseases, Tokyo, Japan
  6. 6Division of Infectious Diseases, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA


Introduction Mainly case reports have shown that N. meningitidis, typically a resident of the oropharynx and the causative agent of meningococcal meningitis and meningococcemia, is capable of invading and colonising the urogenital tract. This can result in urethritis, akin to the syndrome caused by N. gonorrhoeae, the etiologic agent of gonorrhoea. Recently, meningococcal strains associated with outbreaks of urethritis were reported to share genetic characteristics with gonococcus, raising the question of the extent to which these strains contain features that promote adaptation to the genitourinary niche, making them “gonococcus-like” and distinguishing them from other N. meningitidis.

Methods A total of 31 urethritis-associated N. meningitidis, representing multiple serogroups and independently collected over a decade and 3 continents, underwent genome sequencing and analysis. The genomes were compared with serogroup-matched N. meningitidis strains isolated from carriage and invasive disease and N. gonorrhoeae strains isolated from men with urethritis.

Results Intact nitrite reductase (AniA), disrupted factor-H binding protein (fHbp), and the lack of capsule are features previously speculated to promote urogenital colonisation. However, we found that a considerable number (n=11) of meningococcal urethritis isolates harbour mutations in AniA predicted to result in truncated peptides and a minority (n=4) of these isolates contained alleles associated with frameshifted fHbp. We noted substantial diversity in the capsule biosynthetic locus, including intact, disrupted, and absent capsules, indicating urogenital colonisation is possible across a range of capsular phenotypes.

Conclusion The meningococcal urethritis strains in this study do not share the allelic patterns of AniA, fHbp, or the capsule locus previously reported for urethritis-associated N. meningitidis. The allelic patterns likely reflect diversity in the underlying meningococcal population, rather than novel adaptation to the urogenital tract.

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.