What Drives The Global Spread of Antimicrobial Resistance: New Research

Antimicrobial Resistance

An international research team has discovered new information on what causes the global development of antimicrobial resistance (AMR) genes in bacteria.

The project, conducted by researchers from the Quadram Institute and the University of East Anglia, brought together specialists from France, Canada, Germany, and the United Kingdom and will bring fresh insights to tackle the worldwide threat of AMR.

Researchers published the study, “Dynamics of extended-spectrum cephalosporin resistance genes in Escherichia coli from Europe and North America” in Nature Communications.

Discovered the AMR genes

The scientists discovered that various AMR genes had different temporal dynamics by studying the genome sequences of roughly two thousand resistant bacteria, mainly Escherichia coli, collected between 2008 and 2016. Some, for example, were discovered in North America and spread to Europe, whilst others spread from Europe to North America.

The study examined bacteria from several geographic locations as well as varied hosts such as people, animals, food (meat), and the environment (wastewater) to determine how these distinct but linked elements affected the development and spread of AMR. Understanding this interconnection is crucial to understanding transmission dynamics and the processes through which resistance genes are propagated.

The Joint Programming Initiative on Antimicrobial Resistance (JPIAMR), a worldwide cooperation spanning 29 nations and the European Commission charged with turning the tide on AMR, funded the study. Without worldwide collaboration, AMR will surely expose millions more individuals to diseases caused by bacteria and other microbes that can now be treated with antimicrobials.

The experimental section of the research

The researchers concentrated on resistance to a specific class of antimicrobials known as extended-spectrum cephalosporins (ESCs). The World Health Organization has classified these antimicrobials as crucial because they are a “last option” therapy for multidrug-resistant bacteria. Nonetheless, effectiveness has diminished since their introduction as bacteria have evolved resistance.

Bacteria that are resistant to ESCs accomplish this by producing specialised enzymes known as beta-lactamases, which are capable of inactivating ESCs.

These enzymes’ instructions are encoded in genes, specifically two types of genes: extended-spectrum beta-lactamases (ESBLs) and AmpC beta-lactamases (AmpCs).

These genes can be located on bacteria’s chromosomes, where they are handed down to progeny during clonal multiplication, or on plasmids, which are tiny DNA molecules that exist independently of the bacterium’s primary chromosome. Plasmids are mobile and may migrate across bacteria, providing an alternate method of sharing genetic material.

This study discovered how certain resistance genes spread by clonal proliferation of especially effective bacterial subtypes, while others spread directly on epidemic plasmids across multiple hosts and nations.

Researchers’ view on this research

Understanding AMR transmission and the worldwide development of resistance requires an understanding of the transfer of genetic information within and across bacterial populations. This understanding will help design critical treatments that can prevent Antimicrobial Resistance (AMR) in the real world, where bacteria from various hosts and environmental niches interact, and international travel and commerce imply that these interactions are not geographically confined.

Professor Alison Mather of the Quadram Institute and the University of East Anglia stated: “We were able to uncover the essential genes imparting resistance to these vital medications by compiling such a huge and diverse sample of genomes. We were also able to demonstrate that the bulk of the resistance to extended-spectrum cephalosporins is propagated by a small number of dominant plasmids and bacterial lineages; knowing the transmission processes is critical for designing treatments to minimise AMR spread.”

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