In the high-stakes world of infectious disease, it’s a microscopic arms race. And the latest twist? One deadly bacterium has leveled up in a shocking way—by turning against its own kind. Scientists at the University of Pittsburgh School of Medicine have uncovered a disturbing new strategy in the battle for bacterial dominance: a drug-resistant strain of Enterococcus faecium has evolved to weaponize a genetic tool that eliminates its bacterial cousins. The discovery, published in Nature Microbiology, opens new possibilities—and new questions—in the fight against some of the world’s deadliest hospital-acquired infections.
The Rise of a Ruthless Bacterial Overlord
Hospitals have long been battlegrounds for life-threatening infections. Now, vancomycin-resistant Enterococcus faecium (VREfm)—already a notorious villain—has added a ruthless tactic to its arsenal. Once a diverse population of bacterial strains coexisted in relative equilibrium. But within the last several years, two hyper-aggressive strains of VREfm have emerged as global dominators, outcompeting and wiping out their rivals in the gut microbiomes of vulnerable hospital patients.
At the heart of this bacterial coup is a molecular weapon called a bacteriocin—a type of antimicrobial compound that bacteria produce to attack and kill closely related competitors. Think of bacteriocins as microscopic daggers: potent, precise, and deadly. In this case, the two emergent VREfm strains have evolved to manufacture their own bacteriocin, effectively declaring war on their bacterial relatives and monopolizing resources in the process.
The result? A near-monopoly. What was once a balanced playing field with eight major strains of VREfm vying for survival has narrowed to just two. By 2022, these strains were responsible for a staggering 80% of all patient infections studied in the University of Pittsburgh Medical Center (UPMC) system.
But the real shocker? This isn’t just a Pittsburgh problem. Lead researcher Emma Mills and her team found the same bacterial takeover happening across the globe.
How Scientists Uncovered the Plot
This discovery wasn’t the product of a targeted investigation—it started as routine surveillance. Using a powerful new tool called the Enhanced Detection System for Health Care-Associated Transmission (EDS-HAT), scientists at Pitt and UPMC were monitoring genetic patterns in hospital infections in real time. EDS-HAT, which combines genomic sequencing with sophisticated computer algorithms, was originally designed to spot outbreaks and enable clinicians to stop them before they spread.
But while reviewing years of data, Mills noticed a curious trend. The once-diverse landscape of VREfm infections was shrinking. Intrigued, she zoomed out and analyzed 710 VREfm infection samples collected over six years from patients in Pittsburgh-area hospitals.
What she found was astonishing. Beginning in 2018, two strains began to outcompete all others. They weren’t just winning—they were annihilating the competition.
Mills dug deeper. By analyzing the genomic sequences of these dominant strains, she discovered they had acquired genes coding for bacteriocins. These genes gave the strains the ability to directly attack and kill other VREfm variants within the gut. Imagine two rival gangs vying for control of a neighborhood, and then one suddenly gets access to a secret weapon that wipes out the other gang entirely. That’s the brutal efficiency of bacteriocins in action.
A Global Takeover
Was this microbial massacre unique to Pittsburgh? Mills wanted to find out. She scoured a vast library of over 15,000 VREfm genomes collected from across the globe between 2002 and 2022. The answer: no. What she saw locally was a small piece of a much larger puzzle.
The same two bacteriocin-producing strains were turning up everywhere, from Europe to Asia to North America. They weren’t just surviving—they were thriving, dominating hospital settings on an international scale. These strains had evolved a winning formula, and they were spreading it like wildfire.
“This was a completely unexpected discovery,” said Mills. “I was surprised to see such a dramatic signal. Once these strains are in an institutional setting—such as a hospital—and are matched up against other strains of VRE in a patient’s gut, they take over. It’s a ‘kill your buddies and eat their food’ scenario.”
What Does This Mean for Patients?
The good news: so far, these aggressive strains aren’t making patients any sicker than their less-dominant predecessors. The mortality rate for VREfm infections still hovers around 40%, particularly among immunocompromised individuals whose microbiomes are already weakened by antibiotic use.
The bad news: VREfm is already notoriously difficult to treat. Resistant to vancomycin—a frontline antibiotic in many hospital infections—VREfm thrives in settings where antibiotics suppress other, less resilient bacteria. If these bacteriocin-producing strains become the default version of VREfm worldwide, treatment options could become even more limited.
But there’s also a potential silver lining. According to Dr. Daria Van Tyne, senior author of the study and associate professor at Pitt’s Division of Infectious Diseases, the narrowing of VREfm diversity could offer an opportunity for targeted treatment strategies.
“If the diversity of the VRE population continues to shrink, we may soon have only one or two dominant strains to focus on,” said Van Tyne. “That makes it easier to design specific therapeutics—whether antibiotics or phage therapy—that target these specific strains.”
Turning Bacteriocins Into a Weapon for Humans?
One of the most exciting implications of the discovery is the potential use of bacteriocins themselves as weapons against bacterial infections. Unlike broad-spectrum antibiotics, which can wipe out beneficial bacteria along with harmful ones, bacteriocins are highly selective. They only target closely related strains, leaving the rest of the microbiome intact.
Van Tyne suggests that scientists could weaponize bacteriocins to help fight antibiotic-resistant bacteria. “Bacteriocins are very potent, and perhaps we could harness them for our own purposes,” she said.
Pharmaceutical companies and biotech firms are already exploring bacteriocins as the basis for a new generation of narrow-spectrum antibiotics. Unlike conventional drugs, which often face resistance as bacteria evolve, bacteriocins may offer a more sustainable alternative—especially if they’re customized to target emerging superbugs like the dominant VREfm strains.
The Broader Battle Against Superbugs
The discovery underscores just how adaptive and opportunistic bacteria can be, especially in high-stress environments like hospitals, where antibiotics are in heavy use. “Our lab has a front row seat to the parade of pathogens that move through the hospital setting,” said Van Tyne. “And when we took a step back and zoomed out, it quickly became apparent that big changes were afoot with one of the world’s more difficult-to-treat bacteria.”
Antibiotic resistance is one of the most pressing public health threats of the 21st century. The Centers for Disease Control and Prevention (CDC) estimates that at least 2.8 million antibiotic-resistant infections occur in the U.S. each year, resulting in more than 35,000 deaths. VREfm is on the CDC’s list of urgent threats.
The findings from Pittsburgh highlight how bacteria are constantly evolving—and how public health systems need to stay one step ahead. Tools like EDS-HAT offer a new line of defense by tracking bacterial evolution in real time, but developing effective treatments will require continued innovation, vigilance, and global collaboration.
What Comes Next?
For now, the discovery of bacteriocin-wielding VREfm strains is a wake-up call for infectious disease specialists and researchers worldwide. The fact that these strains have independently emerged and spread across continents suggests a powerful evolutionary advantage—one we’re only just beginning to understand.
Future research will focus on:
- Understanding how bacteriocin genes are acquired and shared between bacterial populations.
- Investigating whether bacteriocins can be engineered or modified for therapeutic use.
- Monitoring the continued spread and dominance of these aggressive VREfm strains in hospitals worldwide.
- Developing targeted interventions, whether through new antibiotics, bacteriophage therapies, or microbiome-based treatments.
For Emma Mills, this unexpected discovery has opened a fascinating new chapter in the story of antibiotic resistance. “This is what makes science so exciting,” she said. “You think you’re looking for one thing, and then you find something completely different—something that changes the way we understand these infections and how we might fight them.”
A Final Thought
The microscopic world is full of surprises—and not all of them are welcome. But with cutting-edge tools like EDS-HAT, innovative thinking, and a little bit of luck, we might just turn the tide in humanity’s battle against the superbugs of tomorrow. For now, the discovery of bacteriocin-wielding VREfm is a stark reminder that nature is always a few steps ahead. Our job is to catch up—and stay there.
Reference: ‘Bacteriocin production facilitates nosocomial emergence of vancomycin-resistant Enterococcus faecium’, Nature Microbiology (2025). DOI: 10.1038/s41564-025-01958-0