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Author Notes:

Corresponding author Timothy D. Read, tread@emory.edu

Genome sequencing was performed at the Emory Genomics Center. We wish to thank Tauqeer Alam at Emory University, for advice on phylogenetic methods, and Sinisa Vidovic and Sidarath Dev from the Vaccine and Infectious Disease Orgarnization- International Vaccine center at the University of Saskatchewan, Canada for their help in antimicrobial susceptibility determination and preliminary genomic assessments.

We also thank the Broad Institute for pre-publication release of genomic data used in this study.

Competing Interests Richard F. Selden and Rosemary S. Turingan are employees of NetBio.

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Research Funding:

National Institutes of Health/National Institute of Allergy and Infectious Diseases (NIAD) AI09768R37 AI021150-29R43 AI097688. Medical Research Service of the Department of Veterans Affairs . Senior Research Career Scientist Award . Centers for Disease Control and Prevention 1H25PS004311. Saskatchewan Health Research Foundation #9127. Research Alliance for the Prevention of Infectious Disease [RAPID] . University of Saskatchewan .

Funding for this study was provided by the National Institutes of Health/National Institute of Allergy and Infectious Diseases (NIAD) grants number AI09768, R37 AI021150-29 (WMS) and R43 AI097688 (Timothy D. Read, Deborah Dean and Richard F. Selden), a VA Merit Award from the Medical Research Service of the Department of Veterans Affairs, a Senior Research Career Scientist Award from the VA Medical Research Service of the Department of Veterans Affairs (William M. Shafer) and the Centers for Disease Control and Prevention grant 1H25PS004311 (Carlos Del Rio).

This work was also supported by the Saskatchewan Health Research Foundation (Grant# 9127, Research Alliance for the Prevention of Infectious Disease [RAPID]), and funding to Jo-Anne R Dillon from the University of Saskatchewan.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Keywords:

  • Antimicrobial resistance
  • Genetic admixture
  • Population structure
  • Recombination
  • Whole genome sequence analysis

Population structure of Neisseria gonorrhoeae based on whole genome data and its relationship with antibiotic resistance.

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Journal Title:

PeerJ

Volume:

Volume 3

Publisher:

, Pages e806-e806

Type of Work:

Article | Final Publisher PDF

Abstract:

Neisseria gonorrhoeae is the causative agent of gonorrhea, a sexually transmitted infection (STI) of major importance. As a result of antibiotic resistance, there are now limited options for treating patients. We collected draft genome sequence data and associated metadata data on 76 N. gonorrhoeae strains from around the globe and searched for known determinants of antibiotics resistance within the strains. The population structure and evolutionary forces within the pathogen population were analyzed. Our results indicated a cosmopolitan gonoccocal population mainly made up of five subgroups. The estimated ratio of recombination to mutation (r/m = 2.2) from our data set indicates an appreciable level of recombination occurring in the population. Strains with resistance phenotypes to more recent antibiotics (azithromycin and cefixime) were mostly found in two of the five population subgroups.

Copyright information:

© 2015 Ezewudo et al.

This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits distribution of derivative works, making multiple copies, distribution, public display, and publicly performance, provided the original work is properly cited. This license requires copyright and license notices be kept intact, credit be given to copyright holder and/or author.

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