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      Neisseria gonorrhoeae host-adaptation and pathogenesis

      research-article
      ,
      Nature reviews. Microbiology
      Biological sciences / Microbiology / Bacteriology [URI /631/326/1320], Biological sciences / Microbiology / Pathogens [URI /631/326/421], Biological sciences / Microbiology / Bacteria / Bacterial pathogenesis [URI /631/326/41/2531], Biological sciences / Microbiology / Bacteria / Bacterial immune evasion [URI /631/326/41/2534], Biological sciences / Microbiology / Bacteria / Bacterial host response [URI /631/326/41/2533], Biological sciences / Microbiology / Bacteria / Bacterial physiology [URI /631/326/41/1969], Biological sciences / Microbiology / Bacteria / Bacterial physiology / Antibacterial drug resistance [URI /631/326/41/1969/2038] , Biological sciences / Microbiology / Clinical microbiology [URI /631/326/107], Biological sciences / Ecology / Microbial ecology [URI /631/158/855], Health sciences / Diseases / Infectious diseases / Bacterial infection [URI /692/699/255/1318]

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          Abstract

          The host-adapted human pathogen Neisseria gonorrhoeae is the causative agent of gonorrhea. Consistent with its proposed evolution from an ancestral commensal bacterium, N. gonorrhoeae has retained features that are common in commensals, but it has also developed unique features that are crucial to its pathogenesis. The continued worldwide incidence of gonorrheal infection, coupled with the rising resistance to antimicrobials, and with the difficulties in controlling the disease in developing countries, highlights the need to better understand the molecular basis of N. gonorrhoeae infection. This knowledge will facilitate disease prevention, surveillance and control, improve diagnostics and may help to facilitate the development of effective vaccines or new therapeutics. In this Review, we discuss gender-related symptomatic gonorrheal disease, and provide an overview of the bacterial factors that are important for the different stages of pathogenesis, including transmission, colonization and immune evasion, and discuss the problem of antibiotic resistance.

          Table of contents blurb

          The host-adapted human pathogen Neisseria gonorrhoeae is the causative agent of gonorrhea. In this Review, Quillin and Seifert provide an overview of the bacterial factors that are important for the different stages of pathogenesis, including transmission, colonization and immune evasion, and discuss the problem of antibiotic resistance.

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          Most cited references143

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          Antimicrobial resistance in Neisseria gonorrhoeae in the 21st century: past, evolution, and future.

          Neisseria gonorrhoeae is evolving into a superbug with resistance to previously and currently recommended antimicrobials for treatment of gonorrhea, which is a major public health concern globally. Given the global nature of gonorrhea, the high rate of usage of antimicrobials, suboptimal control and monitoring of antimicrobial resistance (AMR) and treatment failures, slow update of treatment guidelines in most geographical settings, and the extraordinary capacity of the gonococci to develop and retain AMR, it is likely that the global problem of gonococcal AMR will worsen in the foreseeable future and that the severe complications of gonorrhea will emerge as a silent epidemic. By understanding the evolution, emergence, and spread of AMR in N. gonorrhoeae, including its molecular and phenotypic mechanisms, resistance to antimicrobials used clinically can be anticipated, future methods for genetic testing for AMR might permit region-specific and tailor-made antimicrobial therapy, and the design of novel antimicrobials to circumvent the resistance problems can be undertaken more rationally. This review focuses on the history and evolution of gonorrhea treatment regimens and emerging resistance to them, on genetic and phenotypic determinants of gonococcal resistance to previously and currently recommended antimicrobials, including biological costs or benefits; and on crucial actions and future advances necessary to detect and treat resistant gonococcal strains and, ultimately, retain gonorrhea as a treatable infection. Copyright © 2014, American Society for Microbiology. All Rights Reserved.
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            Nutritional immunity beyond iron: a role for manganese and zinc.

            Vertebrates sequester iron from invading pathogens, and conversely, pathogens express a variety of factors to steal iron from the host. Recent work has demonstrated that in addition to iron, vertebrates sequester zinc and manganese both intracellularly and extracellularly to protect against infection. Intracellularly, vertebrates utilize the ZIP/ZnT families of transporters to manipulate zinc levels, as well as Nramp1 to manipulate manganese levels. Extracellularly, the S100 protein calprotectin sequesters manganese and potentially zinc to inhibit microbial growth. To circumvent these defenses, bacteria possess high affinity transporters to import specific nutrient metals. Limiting the availability of zinc and manganese as a mechanism to defend against infection expands the spectrum of nutritional immunity and further establishes metal sequestration as a key defense against microbial invaders. Copyright 2009 Elsevier Ltd. All rights reserved.
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              The novel 2016 WHO Neisseria gonorrhoeae reference strains for global quality assurance of laboratory investigations: phenotypic, genetic and reference genome characterization.

              Gonorrhoea and MDR Neisseria gonorrhoeae remain public health concerns globally. Enhanced, quality-assured, gonococcal antimicrobial resistance (AMR) surveillance is essential worldwide. The WHO global Gonococcal Antimicrobial Surveillance Programme (GASP) was relaunched in 2009. We describe the phenotypic, genetic and reference genome characteristics of the 2016 WHO gonococcal reference strains intended for quality assurance in the WHO global GASP, other GASPs, diagnostics and research worldwide.
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                Author and article information

                Journal
                101190261
                31733
                Nat Rev Microbiol
                Nat. Rev. Microbiol.
                Nature reviews. Microbiology
                1740-1526
                1740-1534
                25 December 2018
                12 February 2018
                April 2018
                11 January 2019
                : 16
                : 4
                : 226-240
                Affiliations
                Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
                Author notes
                Correspondence to H.S.S. h-seifert@ 123456northwestern.edu

                Author contributions

                S.J.Q. and H.S.S. contributed to researching data for article. S.J.Q. and H.S.S. substantially contributed to the discussion of content. S.J.Q. and H.S.S. wrote the article. S.J.Q. and H.S.S. reviewed and edited the manuscript before submission.

                Article
                PMC6329377 PMC6329377 6329377 nihpa1003492
                10.1038/nrmicro.2017.169
                6329377
                29430011
                c8aa6c36-cfcd-4a9b-b761-bd39deac2e5d
                History
                Categories
                Article

                Biological sciences / Microbiology / Bacteria / Bacterial host response [URI /631/326/41/2533],Biological sciences / Microbiology / Bacteriology [URI /631/326/1320],Biological sciences / Microbiology / Pathogens [URI /631/326/421],Biological sciences / Microbiology / Bacteria / Bacterial pathogenesis [URI /631/326/41/2531],Biological sciences / Microbiology / Bacteria / Bacterial immune evasion [URI /631/326/41/2534],Biological sciences / Microbiology / Bacteria / Bacterial physiology [URI /631/326/41/1969],Biological sciences / Microbiology / Bacteria / Bacterial physiology / Antibacterial drug resistance [URI /631/326/41/1969/2038],Biological sciences / Microbiology / Clinical microbiology [URI /631/326/107],Biological sciences / Ecology / Microbial ecology [URI /631/158/855],Health sciences / Diseases / Infectious diseases / Bacterial infection [URI /692/699/255/1318]

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