Pseudomonas aeruginosa, a common pathogen known for causing difficult-to-treat hospital infections, has evolved a taste for plastic. But not just any plastic. It can break down polycaprolactone (PCL) — a biodegradable polymer widely used in medical implants — and use it as fuel to grow more powerful.

This means that in the very environments meant to heal us, some microbes may be learning to thrive on the materials designed to restore our bodies.

As if superbugs weren’t already dangerous enough

Hospitals are awash in plastic — from ventilator tubes and catheters to sutures and surgical meshes. Many of these devices are made with PCL because it’s biocompatible, biodegradable, and easy to mold through 3D printing. These very properties may be backfiring now.

P. aeruginosa is already infamous in intensive care units for causing ventilator-associated pneumonia and catheter-related infections. According to the World Health Organization, it poses one of the greatest threats to humans in terms of antibiotic resistance. But it may be even worse than we thought.

A team of scientists at Brunel University London has suspected that P. aeruginosa was capable of consuming plastic. The team, led by Ronan R. McCarthy, discovered a clinical wound isolate of P. aeruginosa — dubbed PA-W23 — that possesses a novel enzyme called Pap1. This enzyme breaks down PCL by as much as 78% in just seven days. It seems to be able to feed on this plastic, using it as its only carbon source.

But there’s more. When P. aeruginosa breaks down PCL, it releases a specific compound called 6-hydroxyhexanoic acid (6OH-HA). This byproduct is then incorporated into the biofilm matrix, the sticky mix of sugars, proteins, and DNA that holds the bacteria together and protects them. In other words, P. aeruginosa is not just digesting plastic for survival—it’s weaponizing it for its own survival.

The biofilm is a sticky defensive fortress

Biofilms are slimy microbial communities that act as fortresses against antibiotics and immune defenses. In the presence of plastic, PA-W23 didn’t just survive — it built thicker biofilms. These biofilms also seemed to be more virulent.

Researchers tested plastic and non-plastic biofilms on unfortunate moth larvae; the larvae were much more likely to be killed by biofilms from bacteria that had consumed plastic.

The team also analyzed whether this Pap1 enzyme could function in other strains. They inserted the specific gene into E. Coli and found that E. Coli can also get plastic-degrading abilities.

Even more alarmingly, their screening of pathogen genomes found other plastic-degrading enzyme candidates in species like Streptococcus pneumoniae and Acinetobacter baumannii. This hints at a broader, hidden reservoir of microbial plastic-eaters in clinical settings.

What does this all mean for patients?

Antibiotic resistance is one of the biggest threats to the human species. We forget just how vulnerable we were before the advent of antibiotics, and we underestimate how much these pathogens can adapt and change.

We know that medical devices are at risk of contamination. Bacteria can colonize them, forming biofilms that resist antibiotics and persist in the body. But if pathogens can also degrade the very materials these devices are made of, then a whole new risk emerges.

The discovery has implications for how we design, monitor, and regulate medical implants. For starters, screening for plastic-degrading enzymes in nosocomial pathogens may become a necessary precaution. If your sutures can be metabolized by bacteria, then that’s not just a failure of the material, it’s a doorway to infection.

There’s also an urgent call to revisit implant materials. While PCL’s biodegradability is normally an asset, here it becomes a liability. One possible solution may be to incorporate antimicrobial agents like silver or copper nanoparticles into PCL-based devices. Early efforts in this direction are already underway, the authors note.

Much remains unknown. We don’t know if Pap1 degrade other plastics like PET or polyurethane, nor how widespread this trait is in hospital bacteria. We may be able to stop it from spreading, or it may already be common.

There’s also a silver lining to this study. In recent years, scientists have looked to microbes as allies in breaking down plastic waste. Enzymes like the one used by these bacteria could be used to help us reduce some of our plastic pollution problems.

The study was published in Cell.