期刊
JOURNAL OF CLINICAL MICROBIOLOGY
卷 55, 期 12, 页码 3374-3383出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JCM.01018-17
关键词
Neisseria gonorrhoeae; Neisseria meningitidis; bacterial genomics; urethritis
类别
资金
- Wellcome Trust
- Smith Family Foundation
- Harvard Global Health Institute
- Research Committee of Orebro County
- Orebro University Hospital Foundation, Orebro, Sweden
- Grants-in-Aid for Scientific Research [15K08485] Funding Source: KAKEN
Neisseria meningitidis, typically a resident of the oro- or nasopharynx and the causative agent of meningococcal meningitis and meningococcemia, is capable of invading and colonizing the urogenital tract. This can result in urethritis, akin to the syndrome caused by its sister species, N. gonorrhoeae, the etiologic agent of gonorrhea. Recently, meningococcal strains associated with outbreaks of urethritis were reported to share genetic characteristics with the 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 strains. Here, we analyzed the genomes of 39 diverse N. meningitidis isolates associated with urethritis, collected independently over a decade and across three continents. In particular, we characterized the diversity of the nitrite reductase gene (aniA), the factor H-binding protein gene (fHbp), and the capsule biosynthetic locus, all of which are loci previously suggested to be associated with urogenital colonization. We observed notable diversity, including frameshift variants, in aniA and fHbp and the presence of intact, disrupted, and absent capsule biosynthetic genes, indicating that urogenital colonization and urethritis caused by N. meningitidis are possible across a range of meningococcal genotypes. Previously identified allelic patterns in urethritis-associated N. meningitidis strains may reflect genetic diversity in the underlying meningococcal population rather than novel adaptation to the urogenital tract.
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