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article · Nature Communications

An African Salmonella Typhimurium ST313 sublineage with extensive drug-resistance and signatures of host adaptation

2019135 citationsOpen accessUniversité de Kinshasa (UNIKIN)

In plain language

Bloodstream infections caused by Salmonella enterica serovar Typhimurium present a substantial health burden across sub-Saharan Africa. These invasive non-typhoidal infections are predominantly driven by sequence type 313. Research has now identified the emergence of ST313 sublineage II.1 in the Democratic Republic of the Congo. This sublineage displays extensive drug resistance, combining conventional multidrug resistance with extended spectrum beta-lactamase production and azithromycin resistance. The isolates carry a specific IncHI2 plasmid named pSTm-ST313-II.1, and decreased ciprofloxacin susceptibility was noted in one isolate. Whole genome sequencing demonstrates that sublineage II.1 has accumulated genetic signatures associated with altered pathogenicity and host adaptation, which correspond to observed shifts in metabolic capacity and biofilm formation. Having originated at the turn of the century, this sublineage remains involved in ongoing outbreaks and demonstrates continuous evolution in regional bloodstream pathogens.

Key takeaways

  • A newly described Salmonella Typhimurium ST313 sublineage, termed II.1, has emerged in the Democratic Republic of the Congo and is involved in active outbreaks.
  • The sublineage displays extensive drug resistance encompassing multidrug resistance, extended spectrum beta-lactamase production, and resistance to azithromycin.
  • Isolates harbour an IncHI2 plasmid designated pSTm-ST313-II.1, with one sample also exhibiting reduced susceptibility to ciprofloxacin.
  • Genomic data show markers of host adaptation and altered pathogenicity linked to modifications in biofilm formation and metabolic function.

Why it matters

Invasive non-typhoidal Salmonella infections represent a critical cause of severe bloodstream illness in sub-Saharan Africa. The emergence of strains showing extensive resistance to essential antimicrobial classes, including azithromycin and beta-lactams, severely limits clinical treatment choices. Understanding the genetic evolution and adaptations of these lineages provides vital information for public health surveillance and tracking hospital- and community-acquired bacterial outbreaks.

Commercialisation angle

The abstract does not indicate a direct commercial application pathway. The genomic signatures and plasmid profiles identified constitute early-stage research data that could inform diagnostic developers creating specialised molecular surveillance tools for drug-resistant pathogens. Any translation into clinical diagnostic tests or therapeutic guidance would require substantial applied development and validation.

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Abstract

Bloodstream infections by Salmonella enterica serovar Typhimurium constitute a major health burden in sub-Saharan Africa (SSA). These invasive non-typhoidal (iNTS) infections are dominated by isolates of the antibiotic resistance-associated sequence type (ST) 313. Here, we report emergence of ST313 sublineage II.1 in the Democratic Republic of the Congo. Sublineage II.1 exhibits extensive drug resistance, involving a combination of multidrug resistance, extended spectrum β-lactamase production and azithromycin resistance. ST313 lineage II.1 isolates harbour an IncHI2 plasmid we name pSTm-ST313-II.1, with one isolate also exhibiting decreased ciprofloxacin susceptibility. Whole genome sequencing reveals that ST313 II.1 isolates have accumulated genetic signatures potentially associated with altered pathogenicity and host adaptation, related to changes observed in biofilm formation and metabolic capacity. Sublineage II.1 emerged at the beginning of the 21st century and is involved in on-going outbreaks. Our data provide evidence of further evolution within the ST313 clade associated with iNTS in SSA.

Research topics

  • Salmonella and Campylobacter epidemiology
  • Vibrio bacteria research studies
  • Antibiotic Resistance in Bacteria

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DOI: 10.1038/s41467-019-11844-z

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