ArticleCommunications biology2024
The origins of haplotype 58 (H58) Salmonella enterica serovar Typhi.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Emergence of Genotype 2.3.1 Multidrug-Resistant Salmonella enterica Serovar Typhi Strain, West Africa, 2021-2025.Emerging infectious diseases · 2026Article
- A case for eliminating Widal testing for enteric fever, India.Bulletin of the World Health Organization · 2026Article
- Presence of globally prominent multidrug-resistant genotypes ofMicrobial genomics · 2026Article
- Genomic analysis ofMicrobial genomics · 2026Article
- The typhoid Mary legacy: Genomic epidemiology uncovers contemporary carriage dynamics across two decades of enteric fever surveillance in England and Wales.PLoS neglected tropical diseases · 2026Article
- Preclinical evaluation of a bivalent conjugate vaccine againstFrontiers in immunology · 2026Article
- Article
- ConfrontingInfection and drug resistance · 2026Review
- Genomic characterization of Salmonella enterica isolates causing typhoid among Ghanaian patients.PloS one · 2026Article
- Chemoinformatic Approaches to Identify Bioactive Inhibitors Against Type I Dehydroquinase (DHQ1) Enzyme of TyphoidalBioinformatics and biology insights · 2026Article
- High prevalence of multi-drug resistant H58 Salmonella Typhi and emerging fluoroquinolone resistance among febrile children in Nairobi County, Kenya.BMC infectious diseases · 2025Article
- Laboratory epidemiology ofOne health (Amsterdam, Netherlands) · 2025Article
- Comprehensive analysis of extensive drug-resistantMicrobiology spectrum · 2025Article
- Decoding pathogen evolution to curb antimicrobial resistance.Nature reviews. Microbiology · 2025Article
- Whole-genome sequencing for surveillance ofAfrican journal of laboratory medicine · 2025Article
- Emergence of carbapenem-resistantFrontiers in microbiology · 2025Article
- Exploring SNP filtering strategies: the influence of strict vs soft core.Microbial genomics · 2025Article
- An exploration of unusual antimicrobial resistance phenotypes in Salmonella Typhi from Blantyre, Malawi reveals the ongoing role of IncHI1 plasmids.Gates open research · 2024Article
- Assessing the global risk of typhoid outbreaks caused by extensively drug resistant Salmonella Typhi.Nature communications · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Antimicrobial resistance (AMR) poses a serious threat to the clinical management of typhoid fever. AMR in Salmonella Typhi (S. Typhi) is commonly associated with the H58 lineage, a lineage that arose comparatively recently before becoming globally disseminated. To better understand when and how H58 emerged and became dominant, we performed detailed phylogenetic analyses on contemporary genome sequences from S. Typhi isolated in the period spanning the emergence. Our dataset, which contains the earliest described H58 S. Typhi organism, indicates that ancestral H58 organisms were already multi-drug resistant (MDR). These organisms emerged spontaneously in India in 1987 and became radially distributed throughout South Asia and then globally in the ensuing years. These early organisms were associated with a single long branch, possessing mutations associated with increased bile tolerance, suggesting that the first H58 organism was generated during chronic carriage. The subsequent use of fluoroquinolones led to several independent mutations in gyrA. The ability of H58 to acquire and maintain AMR genes continues to pose a threat, as extensively drug-resistant (XDR; MDR plus resistance to ciprofloxacin and third generation cephalosporins) variants, have emerged recently in this lineage. Understanding where and how H58 S. Typhi originated and became successful is key to understand how AMR drives successful lineages of bacterial pathogens. Additionally, these data can inform optimal targeting of typhoid conjugate vaccines (TCVs) for reducing the potential for emergence and the impact of new drug-resistant variants. Emphasis should also be placed upon the prospective identification and treatment of chronic carriers to prevent the emergence of new drug resistant variants with the ability to spread efficiently.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.