Horizontal antimicrobial resistance transfer drives epidemics of multiple Shigella species

Kate S. Baker*, Tim Dallman, Nigel Field, Tristan Childs, Holly Mitchell, Martin Day, François Xavier Weill, Sophie Lefèvre, Mathieu Tourdjman, Gwenda Hughes, Claire Jenkins, Nicholas Thomson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

47 Citations (Scopus)


Horizontal gene transfer has played a role in developing the global public health crisis of antimicrobial resistance (AMR). However, the dynamics of AMR transfer through bacterial populations and its direct impact on human disease is poorly elucidated. Here, we study parallel epidemic emergences of multiple Shigella species, a priority AMR organism, in men who have sex with men to gain insight into AMR emergence and spread. Using genomic epidemiology, we show that repeated horizontal transfer of a single AMR plasmid among Shigella enhanced existing and facilitated new epidemics. These epidemic patterns contrasted with slighter, slower increases in disease caused by organisms with vertically inherited (chromosomally encoded) AMR. This demonstrates that horizontal transfer of AMR directly affects epidemiological outcomes of globally important AMR pathogens and highlights the need for integration of genomic analyses into all areas of AMR research, surveillance and management.

Original languageEnglish
Article number1462
JournalNature Communications
Issue number1
Publication statusPublished - 1 Dec 2018

Bibliographical note

Funding Information:
The authors are grateful to the administrative, sequencing and pathogen informatics teams at the Wellcome Trust Sanger Institute as well as Dr John Lees for discussions regarding genome-wide association study, and other helpful scientists who commented on the work in progress during formal and informal presentations. The authors also thank John Were for his contribution to managing epidemiological data and Vivienne DoNascimento for her technical assistance in susceptibility testing. This work was supported by Wellcome Trust grant number 206194, and KSB is supported by a Wellcome Trust Clinical Research Career Development Fellowship (106690/A/14/Z).


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