Affiliations 

  • 1 MRC Centre for Global Infectious Disease Analysis, Department of Infectious Disease Epidemiology, Imperial College London, London, United Kingdom
  • 2 Institute for Medical Microbiology, National Reference Center for Streptococci, University Hospital RWTH Aachen, Aachen, Germany
  • 3 Respiratory Diseases Branch, Centers for Disease Control and Prevention, Atlanta, United States
  • 4 Laboratory of Molecular Genetics, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa, Oeiras, Portugal
  • 5 Cambodia Oxford Medical Research Unit, Angkor Hospital for Children, Siem Reap, Cambodia
  • 6 Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea
  • 7 Parasites & Microbes, Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, United Kingdom
  • 8 Laboratory of Molecular Microbiology of Human Pathogens, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa, Oeiras, Portugal
  • 9 Center for Communicable Disease Dynamics, Harvard T.H. Chan School of Public Health, Boston, United States
  • 10 Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, United States
Elife, 2021 Jul 14;10.
PMID: 34259624 DOI: 10.7554/eLife.67113

Abstract

Multidrug-resistant Streptococcus pneumoniae emerge through the modification of core genome loci by interspecies homologous recombinations, and acquisition of gene cassettes. Both occurred in the otherwise contrasting histories of the antibiotic-resistant S. pneumoniae lineages PMEN3 and PMEN9. A single PMEN3 clade spread globally, evading vaccine-induced immunity through frequent serotype switching, whereas locally circulating PMEN9 clades independently gained resistance. Both lineages repeatedly integrated Tn916-type and Tn1207.1-type elements, conferring tetracycline and macrolide resistance, respectively, through homologous recombination importing sequences originating in other species. A species-wide dataset found over 100 instances of such interspecific acquisitions of resistance cassettes and flanking homologous arms. Phylodynamic analysis of the most commonly sampled Tn1207.1-type insertion in PMEN9, originating from a commensal and disrupting a competence gene, suggested its expansion across Germany was driven by a high ratio of macrolide-to-β-lactam consumption. Hence, selection from antibiotic consumption was sufficient for these atypically large recombinations to overcome species boundaries across the pneumococcal chromosome.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.