Listeria bacteria share DNA to increase antibiotic resistance

Biologists have identified a previously unknown mode of communication within bacterial cells that helps pathogens develop resistance to antibiotics. The findings show how these mechanisms drive antimicrobial resistance in Listeria monocytogenes, the foodborne bacteria responsible for listeriosis.  

The research is a collaboration between the University at Albany and the New York State Department of Health, with the hope that it will help to inform the development of new drugs and, potentially, future personalised medicine approaches. 

Unlocking the puzzle of antibiotic resistance

“Antibiotic resistance is on the rise globally,” said UAlbany’s Cheryl Andam, Associate Professor in the Department of Biological Sciences and Scientific Director of the Life Sciences Research. “Patients are acquiring infections that we used to be able to treat, but as bacterial strains are becoming increasingly virulent and resistant to multiple types of drugs, providers are running out of options. In the race to understand how this is happening, our latest findings unlock a critical piece of the puzzle: bacteria contain intricate communication networks and the players within them are able to talk and collaborate in ways that were previously unknown.” 

The findings suggest that bacteria collaborate via complex internal communication networks previously unknown to science, a discovery that Andam compares to realising that groups believed to lack a shared language are in fact communicating and learning from one another.

The cells contained mobile genetic elements, which are short fragments of DNA that store information and exist in many forms with distinct structures and functions. These elements are grouped into categories such as plasmids, phages and transposons based on their defining characteristics. While scientists had already known that mobile genetic elements of the same type could exchange genetic information within and between cells, this study revealed something entirely new: different types of elements are also able to swap pieces of DNA. This exchange allows pathogens to gain traits that increase drug resistance and transmissibility, significantly expanding understanding of how communication occurs within cells and how bacteria evolve to become more dangerous.

Mapping information pathways inside cells

While many foodborne pathogens are restricted to the digestive system, listeriosis can spread into normally sterile parts of the body, including blood and the brain, causing life threatening conditions such as sepsis, meningitis and encephalitis. The invasive form of the disease carries a mortality rate of 20-30 percent.  

In this study, the team examined how mobile genetic elements transfer DNA sequences, including antimicrobial resistance genes, in L. monocytogenes. They analysed bacterial genome sequences and mapped genetic connections between different types of mobile genetic elements.       

The researchers then studied DNA extracted from 936 L. monocytogenes samples collected from patients in New York State between 2000 and 2021. Using specialised computer programs, they identified a total of 2,332 mobile genetic elements, focusing on three main types: plasmids, phages and transposons.      

To trace DNA sharing, the team created network diagrams, representing each mobile genetic element as a dot and connections between elements sharing DNA sequences as lines. This allowed them to track how information moves across different types of elements, fundamentally changing our understanding of how traits like antimicrobial resistance spread.

Implications for medicine and public health

The transfer of DNA between different types of mobile genetic elements greatly expands how antimicrobial resistance and virulence genes are distributed and able to move between bacteria. When these elements exchange genetic material, they can generate new combinations of resistance genes, allowing a single element to accumulate multiple defences against antibiotics. Bacterial cells that acquire these elements can become resistant to several drugs at once, making infections increasingly difficult to treat.

“Understanding how bacteria become resistant to drugs that were once able to kill them is a critical question in biomedical research,” Andam said. “Someday, we hope our work could inform the development of new, more powerful drugs. It could also be put to use as a predictive strategy. As we learn more about the nuanced mechanisms at play inside different strains of a particular pathogen, it becomes possible to better predict which medication will be most effective at treating a given strain. This could help a provider identify the best treatment more efficiently, improving outcomes for the patient when time is of the essence.”