Research reveals new evolutive mechanism of bacteria that expands pathogenic potential

A group of nine researchers has just published new findings on the mechanisms that regulate how bacteria from the Staphylococcus aureus genus transfer genetic material, awarding them greater pathogenic virulence and resistance to antibiotics.

The study, which was just published in Nature Microbiology, was led by Professor José R. Penadés, a researcher from the Imperial College London who collaborated with the Biomedical Science Department of the CEU Cardenal Herrera University (CEU UCH) of Valencia.

In this study, the team of professor Penadés found a new mechanism that activates and transmits genetic material between the pathogenicity islands found in the chromosomes of bacteria and super bacteria, to award them greater virulence and resistance. This new evolutive mechanism has been identified in the Staphylococcus aureus genus, which is of critical priority for the WHO due to its multi-resistance to antibiotics and its ability to cause severe infections.

In 2019, professor Penadés published in Molecular Cell how these pathogenicity islands of the bacteria that cause more virulent infections "hijack" viruses to expand faster in the natural medium and turn harmless bacteria into virulent pathogens.

Until now, this was believed to be the only mechanism used to expand their pathogenic potential. But what we just detected is that, for Staphylococcus aureus, some pathogenicity islands, instead of hijacking a virus, hijack another pathogenicity island to transfer to it."

José R. Penadés,Professor and Researcher, Imperial College London

"This represents a level of parasitism that has not been described to date, as a pathogenicity island initially hijacks mechanisms of viruses to spread them, and when this happens, another island uses the mechanisms that the first hijacked from the virus for its own benefit. This cascade of activation allows the pathogenicity islands to transfer the genetic material that they have due to their high pathogenic capacity to other bacteria at previously unseen frequencies. This better explains the speed at which these genetic elements expand, awarding greater virulence and resistance to the Staphylococcus aureus strains that causes infections with the most severe and hard to treat clinical consequences, such as toxic shock syndrome, pneumonia or necrotizing fasciitis," says professor Penadés.

"With this finding, he adds, we have taken another step forward in the knowledge of the evolutive genetic mechanisms that turn bacteria and superbacteria into pathogens that cause extremely severe infections and which are resistant to the antibiotic treatments that we have today. Advancing the knowledge on these genetic mechanisms that take place in the most severe bacterial infections will make it possible to design new strategies to treat them in a more efficient way in the future."

Molecular bases of bacterial virulence

Professor Penadés has led, since July 2020, the MRC-CMBI Centre for Molecular Bacteriology & Infection at the Imperial College London, which has the largest group of researchers in the United Kingdom devoted to studying the biological bases and molecular mechanisms of bacterial infections.

The research of professor Penadés has focused on studying bacteriophages, the viruses that infect bacteria and replicate inside them, awarding them greater pathogenic capacity and resistance to antibiotics, as well as the mechanisms that these viruses use to transfer genetic material from one set of bacteria to others.

Thus, his most recent studies have made it possible to identify a new mechanism with which bacteria transmit their genes, lateral transduction, published in 2018 in Science. He also identified a new family of molecular parasitic viruses in bacteria, new mobile genetic elements involved in their evolution, resistance, and virulence, called PICIs (Phage-Inducible Chromosomal Islands), in a study published in 2019 in Molecular Cell.

In this article published in September in Nature Microbiology, professor José R. Penadés led researchers from the New York University School of Medicine, the Imperial College London, the University of Wroclaw, the National University of Singapore, and the University of Glasgow, along with researchers from the Valencian Institute of Biomedicine (IBV-CSIC) and the CIBERER, Francisca Gallego del Sol and Alberto Marina.