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Updated: Mar 12, 2026

Testing the Role of Multicopy Plasmids in the Evolution of Antibiotic Resistance
Published on: May 2, 2018
Bacterial viruses enable their host to acquire antibiotic resistance genes from neighbouring cells
Jakob Haaber1, Jørgen J Leisner1, Marianne T Cohn1
1Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Stigboejlen 4, DK-1870 Frederiksberg, Denmark.
Abstract:
Prophages are quiescent viruses located in the chromosomes of bacteria. In the human pathogen, Staphylococcus aureus, prophages are omnipresent and are believed to be responsible for the spread of some antibiotic resistance genes. Here we demonstrate that release of phages from a subpopulation of S. aureus cells enables the intact, prophage-containing population to acquire beneficial genes from competing, phage-susceptible strains present in the same environment. Phage infection kills competitor cells and bits of their DNA are occasionally captured in viral transducing particles. Return of such particles to the prophage-containing population can drive the transfer of genes encoding potentially useful traits such as antibiotic resistance. This process, which can be viewed as 'auto-transduction', allows S. aureus to efficiently acquire antibiotic resistance both in vitro and in an in vivo virulence model (wax moth larvae) and enables it to proliferate under strong antibiotic selection pressure. Our results may help to explain the rapid exchange of antibiotic resistance genes observed in S. aureus.
Insights
Bacteriophages (viruses that infect bacteria) aid Staphylococcus aureus in acquiring antibiotic resistance genes from competitors. This "auto-transduction" process helps bacteria survive antibiotic pressure.
Area of Science:
- Microbiology
- Bacteriology
- Genetics
Background:
- Prophages, viral DNA integrated into bacterial genomes, are common in Staphylococcus aureus.
- These prophages are suspected to facilitate the spread of antibiotic resistance genes.
Purpose of the Study:
- To investigate the role of prophage release in Staphylococcus aureus's acquisition of beneficial genes.
- To understand the mechanism of antibiotic resistance gene transfer in S. aureus.
Main Methods:
- Studied gene transfer in Staphylococcus aureus populations under varying conditions.
- Utilized in vitro and in vivo (wax moth larvae) models.
- Analyzed phage-mediated DNA transfer and its impact on antibiotic resistance.
Main Results:
- Prophage release from a bacterial subpopulation enables gene acquisition by the remaining population.
- Phages transfer DNA fragments from killed competitor cells, including antibiotic resistance genes.
- This 'auto-transduction' mechanism enhances S. aureus's ability to gain antibiotic resistance.
Conclusions:
- Prophage activity facilitates the acquisition of antibiotic resistance in Staphylococcus aureus.
- Auto-transduction is a significant mechanism for bacterial adaptation and survival under antibiotic pressure.
- This process may explain the rapid dissemination of antibiotic resistance in S. aureus.
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