Bacteria use antimicrobial agent to kill competition

Scientists studied antibiotic-resistant Enterococcus bacteria, which can cause lethal infections if they get into the bloodstream.CDC/ Janice Haney Carr

Hospitalized patients are often given antibiotics, which reduces the diversity of bacteria in their microbiomes. It also allows drug-resistant strains to gain a foothold and take over. Enterococcus faecium is a gut bacterium that can cause lethal infections if it gets into the bloodstream. Vancomycin-resistant E. faecium (VREfm), which is resistant to vancomycin and multiple other antibiotics, is a growing problem in healthcare settings. Populations of VREfm within healthcare systems are known to change over time. But the factors driving these changes aren’t well understood.

NIH-supported researchers at the University of Pittsburgh Medical Center have been collecting and sequencing bacterial DNA from hospitalized patients through the Enhanced Detection System for Healthcare-Associated Transmission (EDS-HAT). This helps clinicians to recognize and stop potential outbreaks. As part of this effort, researchers collected more than 700 VREfm samples between 2017 and 2022. A team at the university, led by Dr. Daria Van Tyne, used data from these samples to track VREfm evolution. Their findings appeared in Nature Microbiology on March 21, 2025.

Genome sequencing of the samples identified 42 different genetic lineages, or strains, of VREfm. Almost half of the samples were closely related to at least one other sample. This suggests a high level of transmission within the hospital. Before 2020, about a third of the samples belonged to the strain ST17. From 2020 onward, two new strains, ST80 and ST117, began to take over. By the end of 2022, these two strains made up more than 80% of all samples, while ST17 was not detected.

The researchers found that ST80 and ST117 could kill ST17, but not vice versa. Further examination revealed that ST80 and ST117, but not ST17, produce an antimicrobial peptide (a short chain of amino acids) called bacteriocin T8. Both in laboratory cultures and the guts of mice, strains that made bacteriocin T8 outcompeted strains that didn’t.

Next, the team analyzed more than 15,000 publicly available VREfm genomes collected worldwide between 2002 and 2022. They saw the same trend, with ST17 replaced by ST80 and ST117. This suggests that the changes observed in a single hospital reflected global trends.

The results suggest that bacteriocin T8 gives certain VREfm strains an advantage over others. These strains use the compound to kill competing strains, allowing them to take over. This competitive advantage is driving T8-producing strains to become dominant worldwide. The new VREfm strains don’t appear to make patients any sicker than the earlier strains, so the finding doesn’t have immediate clinical consequences. But it could have implications for the development of new therapies.

“The diversity of the VREfm population appears to be narrowing from lots of different types causing infection to only a few. That means we may soon have only one single target for which to design therapeutics,” Van Tyne says. “It also suggests that bacteriocins are very potent and perhaps we could weaponize them for our own purposes.”

The findings also highlight the utility of collecting and sequencing bacterial strains to track how healthcare-associated infections evolve over time.

—by Brian Doctrow, Ph.D.