Whole genome sequence analysis of Salmonella Typhi in Papua New Guinea reveals an established population of genotype 2.1.7 sensitive to antimicrobials.


Journal

PLoS neglected tropical diseases
ISSN: 1935-2735
Titre abrégé: PLoS Negl Trop Dis
Pays: United States
ID NLM: 101291488

Informations de publication

Date de publication:
03 2022
Historique:
received: 26 09 2021
accepted: 05 03 2022
revised: 07 04 2022
pubmed: 29 3 2022
medline: 12 4 2022
entrez: 28 3 2022
Statut: epublish

Résumé

Typhoid fever, a systemic infection caused by Salmonella enterica serovar Typhi, remains a considerable public health threat in impoverished regions within many low- and middle-income settings. However, we still lack a detailed understanding of the emergence, population structure, molecular mechanisms of antimicrobial resistance (AMR), and transmission dynamics of S. Typhi across many settings, particularly throughout the Asia-Pacific islands. Here we present a comprehensive whole genome sequence (WGS) based overview of S. Typhi populations circulating in Papua New Guinea (PNG) over 30 years. Bioinformatic analysis of 86 S. Typhi isolates collected between 1980-2010 demonstrated that the population structure of PNG is dominated by a single genotype (2.1.7) that appears to have emerged in the Indonesian archipelago in the mid-twentieth century with minimal evidence of inter-country transmission. Genotypic and phenotypic data demonstrated that the PNG S. Typhi population appears to be susceptible to former first line drugs for treating typhoid fever (chloramphenicol, ampicillin and co-trimoxazole), as well as fluoroquinolones, third generation cephalosporins, and macrolides. PNG genotype 2.1.7 was genetically conserved, with very few deletions, and no evidence of plasmid or prophage acquisition. Genetic variation among this population was attributed to either single point mutations, or homologous recombination adjacent to repetitive ribosomal RNA operons. Antimicrobials remain an effective option for the treatment of typhoid fever in PNG, along with other intervention strategies including improvements to water, sanitation and hygiene (WaSH) related infrastructure and potentially the introduction of Vi-conjugate vaccines. However, continued genomic surveillance is warranted to monitor for the emergence of AMR within local populations, or the introduction of AMR associated genotypes of S. Typhi in this setting.

Sections du résumé

BACKGROUND
Typhoid fever, a systemic infection caused by Salmonella enterica serovar Typhi, remains a considerable public health threat in impoverished regions within many low- and middle-income settings. However, we still lack a detailed understanding of the emergence, population structure, molecular mechanisms of antimicrobial resistance (AMR), and transmission dynamics of S. Typhi across many settings, particularly throughout the Asia-Pacific islands. Here we present a comprehensive whole genome sequence (WGS) based overview of S. Typhi populations circulating in Papua New Guinea (PNG) over 30 years.
PRINCIPLE FINDINGS
Bioinformatic analysis of 86 S. Typhi isolates collected between 1980-2010 demonstrated that the population structure of PNG is dominated by a single genotype (2.1.7) that appears to have emerged in the Indonesian archipelago in the mid-twentieth century with minimal evidence of inter-country transmission. Genotypic and phenotypic data demonstrated that the PNG S. Typhi population appears to be susceptible to former first line drugs for treating typhoid fever (chloramphenicol, ampicillin and co-trimoxazole), as well as fluoroquinolones, third generation cephalosporins, and macrolides. PNG genotype 2.1.7 was genetically conserved, with very few deletions, and no evidence of plasmid or prophage acquisition. Genetic variation among this population was attributed to either single point mutations, or homologous recombination adjacent to repetitive ribosomal RNA operons.
SIGNIFICANCE
Antimicrobials remain an effective option for the treatment of typhoid fever in PNG, along with other intervention strategies including improvements to water, sanitation and hygiene (WaSH) related infrastructure and potentially the introduction of Vi-conjugate vaccines. However, continued genomic surveillance is warranted to monitor for the emergence of AMR within local populations, or the introduction of AMR associated genotypes of S. Typhi in this setting.

Identifiants

pubmed: 35344544
doi: 10.1371/journal.pntd.0010306
pii: PNTD-D-21-01426
pmc: PMC8989336
doi:

Substances chimiques

Anti-Bacterial Agents 0

Types de publication

Journal Article Review Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0010306

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 106158/Z/14/Z
Pays : United Kingdom

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Zoe Anne Dyson (ZA)

London School of Hygiene & Tropical Medicine, London, United Kingdom.
Department of Infectious Diseases, Central Clinical School, Monash University, Melbourne, Australia.
Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Department of Medicine, University of Cambridge, Cambridge, United Kingdom.
Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, United Kingdom.

Elisheba Malau (E)

School of Science, Psychology and Sport, Federation University, Churchill, Australia.

Paul F Horwood (PF)

College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, Australia.

Rebecca Ford (R)

Papua New Guinea Institute of Medical Research, Goroka, Papua New Guinea.

Valentine Siba (V)

Papua New Guinea Institute of Medical Research, Goroka, Papua New Guinea.

Mition Yoannes (M)

Papua New Guinea Institute of Medical Research, Goroka, Papua New Guinea.

William Pomat (W)

Papua New Guinea Institute of Medical Research, Goroka, Papua New Guinea.

Megan Passey (M)

University Centre for Rural Health, Faculty of Medicine and Health, University of Sydney, Lismore, Australia.

Louise M Judd (LM)

Department of Infectious Diseases, Central Clinical School, Monash University, Melbourne, Australia.

Danielle J Ingle (DJ)

Department of Microbiology and Immunology, The University of Melbourne at The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia.

Deborah A Williamson (DA)

Department of Microbiology and Immunology, The University of Melbourne at The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia.
Microbiological Diagnostic Unit Public Health Laboratory, Department of Microbiology and Immunology, The University of Melbourne at The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia.

Gordon Dougan (G)

Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Department of Medicine, University of Cambridge, Cambridge, United Kingdom.

Andrew R Greenhill (AR)

School of Science, Psychology and Sport, Federation University, Churchill, Australia.

Kathryn E Holt (KE)

London School of Hygiene & Tropical Medicine, London, United Kingdom.
Department of Infectious Diseases, Central Clinical School, Monash University, Melbourne, Australia.

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