ArticleNature communications2024
Population genomics of Streptococcus mitis in UK and Ireland bloodstream infection and infective endocarditis cases.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The Clinical Significance ofOpen forum infectious diseases · 2026Article
- Clinical and genomic features of mitis group streptococcal bacteremia in patients with febrile neutropenia.BMC infectious diseases · 2026Article
- Gut microbiome-dependent IL-1 signaling is a mediator of ACVR1bioRxiv : the preprint server for biology · 2026Article
- Article
- An Unusual Case ofInfection and drug resistance · 2026Article
- Genomic identification and characterization of Streptococcus oralis group that causes intraamniotic infection.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025Article
- Encapsulation of Disease-Causing and Commensal Mitis Group Non-Pneumococcal Streptococci.Pathogens (Basel, Switzerland) · 2025Article
- Streptococcal endocarditis: a meta-analysis of species dependant risk.EClinicalMedicine · 2025Article
- Analysis of Clinical Characteristics and Antimicrobial Resistance in 249 Isolates ofPolish journal of microbiology · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Streptococcus mitis is a leading cause of infective endocarditis (IE). However, our understanding of the genomic epidemiology and pathogenicity of IE-associated S. mitis is hampered by low IE incidence. Here we use whole genome sequencing of 129 S. mitis bloodstream infection (BSI) isolates collected between 2001-2016 from clinically diagnosed IE cases in the UK to investigate genetic diversity, antimicrobial resistance, and pathogenicity. We show high genetic diversity of IE-associated S. mitis with virtually all isolates belonging to distinct lineages indicating no predominance of specific lineages. Additionally, we find a highly variable distribution of known pneumococcal virulence genes among the isolates, some of which are overrepresented in disease when compared to carriage strains. Our findings suggest that S. mitis in patients with clinically diagnosed IE is not primarily caused by specific hypervirulent or antimicrobial resistant lineages, highlighting the accidental pathogenic nature of S. mitis in patients with clinically diagnosed IE.
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