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

Sam Haldenby, Christina Bronowski, Charlotte Nelson, John Kenny, Carmen Martinez-Rodriguez, Roy Chaudhuri, Nicola J. Williams, Ken Forbes, Norval J. Strachan, Jane Pulman, Ian N. Winstanley, Caroline E. Corless, Tom J. Humphrey, Frederick J. Bolton, Sarah J. O’Brien, Neil Hall, Christiane Hertz-Fowler, Craig Winstanley*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


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.

Original languageEnglish
Article numbere0227535
JournalPLoS ONE
Issue number1
Publication statusPublished - 1 Jan 2020
Externally publishedYes

Bibliographical note

Funding Information:
Funded by CW, RC, NJW, NH, SJO: Food Standards Agency, UK (FSA Project FS101072); SJO, KF, NJS, TJH, FJB, NH, CW: ENIGMA was funded by the Medical Research Council, Natural Environment Research Council, Economic and Social Research Council, Biotechnology and Biosciences Research Council and Food Standards Agency through the Environmental and Social Ecology of Human Infectious Diseases Initiative (ESEI) (Project no. G1100799/1); SJO, FJB, CHF, CW: INTEGRATE was funded by the Wellcome Trust and Department of Health through the Health Innovation Challenge Fund (HICF) (Grant Reference: HICF-T5-354); The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Publisher Copyright:
© 2020 Haldenby et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


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