Increasing prevalence of a fluoroquinolone resistance mutation amongst Campylobacter jejuni isolates from four human infectious intestinal disease studies in the United Kingdom.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2020
Historique:
received: 11 06 2019
accepted: 20 12 2019
entrez: 31 1 2020
pubmed: 31 1 2020
medline: 11 4 2020
Statut: epublish

Résumé

Campylobacter jejuni is the most common bacterial cause of human infectious intestinal disease. We genome sequenced 601 human C. jejuni isolates, obtained from two large prospective studies of infectious intestinal disease (IID1 [isolates from 1993-1996; n = 293] and IID2 [isolates from 2008-2009; n = 93]), the INTEGRATE project [isolates from 2016-2017; n = 52] and the ENIGMA project [isolates from 2017; n = 163]. There was a significant increase in the prevalence of the T86I mutation conferring resistance to fluoroquinolone between each of the three later studies (IID2, INTEGRATE and ENIGMA) and IID1. Although the distribution of major multilocus sequence types (STs) was similar between the studies, there were changes in both the abundance of minority STs associated with the T86I mutation, and the abundance of clones within single STs associated with the T86I mutation. Four population-based studies of community diarrhoea over a 25 year period revealed an increase over time in the prevalence of the T86I amongst isolates of C. jejuni associated with human gastrointestinal disease in the UK. Although associated with many STs, much of the increase is due to the expansion of clones associated with the resistance mutation.

Sections du résumé

BACKGROUND
Campylobacter jejuni is the most common bacterial cause of human infectious intestinal disease.
METHODS
We genome sequenced 601 human C. jejuni isolates, obtained from two large prospective studies of infectious intestinal disease (IID1 [isolates from 1993-1996; n = 293] and IID2 [isolates from 2008-2009; n = 93]), the INTEGRATE project [isolates from 2016-2017; n = 52] and the ENIGMA project [isolates from 2017; n = 163].
RESULTS
There was a significant increase in the prevalence of the T86I mutation conferring resistance to fluoroquinolone between each of the three later studies (IID2, INTEGRATE and ENIGMA) and IID1. Although the distribution of major multilocus sequence types (STs) was similar between the studies, there were changes in both the abundance of minority STs associated with the T86I mutation, and the abundance of clones within single STs associated with the T86I mutation.
DISCUSSION
Four population-based studies of community diarrhoea over a 25 year period revealed an increase over time in the prevalence of the T86I amongst isolates of C. jejuni associated with human gastrointestinal disease in the UK. Although associated with many STs, much of the increase is due to the expansion of clones associated with the resistance mutation.

Identifiants

pubmed: 31999701
doi: 10.1371/journal.pone.0227535
pii: PONE-D-19-16518
pmc: PMC6992184
doi:

Substances chimiques

Fluoroquinolones 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0227535

Subventions

Organisme : Medical Research Council
ID : G1100799
Pays : United Kingdom
Organisme : Wellcome Trust
ID : HICF-T5-354
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_U122785837
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom
Organisme : Biotechnology and Biological Sciences Research Council
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0900753
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Sam Haldenby (S)

Centre for Genomic Research, University of Liverpool, Liverpool, United Kingdom.

Christina Bronowski (C)

Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom.

Charlotte Nelson (C)

Centre for Genomic Research, University of Liverpool, Liverpool, United Kingdom.

John Kenny (J)

Centre for Genomic Research, University of Liverpool, Liverpool, United Kingdom.

Carmen Martinez-Rodriguez (C)

Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom.

Roy Chaudhuri (R)

Department of Biology and Biotechnology, University of Sheffield, Sheffield, United Kingdom.

Nicola J Williams (NJ)

Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom.

Ken Forbes (K)

School of Medicine, Medical Sciences & Nutrition, Foresterhill, University of Aberdeen, Aberdeen, United Kingdom.

Norval J Strachan (NJ)

School of Biological Sciences, University of Aberdeen, Aberdeen, United Kingdom.

Jane Pulman (J)

Centre for Genomic Research, University of Liverpool, Liverpool, United Kingdom.

Ian N Winstanley (IN)

Centre for Genomic Research, University of Liverpool, Liverpool, United Kingdom.

Caroline E Corless (CE)

Infection and Immunity, Liverpool Clinical Laboratories, Royal Liverpool and Broadgreen University Hospitals NHS Trust, Liverpool, United Kingdom.

Tom J Humphrey (TJ)

Medical Microbiology and Infectious Diseases, School of Medicine, Swansea University, Swansea, United Kingdom.

Frederick J Bolton (FJ)

Department of Public Health and Policy, Institute of Population Health Sciences, University of Liverpool, Liverpool, United Kingdom.
NIHR Health Protection Research Unit in Gastrointestinal Infections, University of Liverpool, Liverpool, United Kingdom.

Sarah J O'Brien (SJ)

Department of Public Health and Policy, Institute of Population Health Sciences, University of Liverpool, Liverpool, United Kingdom.
NIHR Health Protection Research Unit in Gastrointestinal Infections, University of Liverpool, Liverpool, United Kingdom.

Neil Hall (N)

The Earlham Institute, Norwich Research Park, Norwich, United Kingdom.
School of Biological Sciences, University of East Anglia, Norwich, United Kingdom.

Christiane Hertz-Fowler (C)

Centre for Genomic Research, University of Liverpool, Liverpool, United Kingdom.

Craig Winstanley (C)

Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom.

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