Scientists have discovered that a notorious hospital bacterium can digest the very plastics used in sutures, stents, and surgical mesh. By turning the polymer into food, the microbe may cling more stubbornly to devices and linger longer on ward surfaces.
Researchers from Brunel University London, working with a patient-derived strain of Pseudomonas aeruginosa, found that the pathogen dismantles polycaprolactone (PCL), a biodegradable plastic common in modern medicine.
The insight challenges the assumption that clinical polymers are immune to microbial attack.
The team traced the plastic-eating trick to a single enzyme, which they named Pap1. In laboratory tests, Pap1 reduced a thin PCL film by seventy-eight percent within seven days. The bacterium then used the liberated fragments as its sole carbon source.
“It means we need to reconsider how pathogens exist in the hospital environment,” said professor Ronan McCarthy, who led the study.
“Plastics, including plastic surfaces, could potentially be food for these bacteria. Pathogens with this ability could survive for longer in the hospital environment. It also means that any medical device or treatment that contains plastic could be susceptible to degradation by bacteria.”
PCL is prized because it bends without snapping, melts at low temperatures, and gradually dissolves in the body. Those traits make it ideal for resorbable sutures, drug-delivery patches, and soft tissue scaffolds.
Until now, surgeons assumed the material would vanish only through hydrolysis and harmless metabolic clearance. Pap1 shows that microbes can accelerate the process – and exploit it.
When P. aeruginosa chews up plastic, it gains more than nourishment. The broken polymer pieces help the cells weave tougher biofilms, those gluey communal layers that resist disinfectants, immune cells, and multiple classes of antibiotics.
Catheter-related urinary tract infections and ventilator-associated pneumonia already rank among the hardest hospital infections to treat. PCL degradation could fortify the culprit’s defenses, complicating therapy even further.
The World Health Organization lists P. aeruginosa among the top “critical” pathogens in need of new drugs. Its uncanny ability to evolve resistance and to thrive in damp, nutrient-poor niches makes it a frequent cause of persistent outbreaks.
The study showed that plastic may be an unexpected reservoir of calories, tipping survival odds further in the germ’s favor.
The researchers looked at genetic databases and spotted related enzyme blueprints in other bacteria known to haunt intensive-care units.
Though only PCL digestion was proven, the sequence hints suggest that plastics such as polyurethane or polyethylene terephthalate – used in everything from vascular grafts to wound dressings – might also be vulnerable.
“The bug’s plastic-eating ability is likely helping it survive on surfaces in hospitals, potentially driving hospital outbreaks. We should start to consider focusing on plastics that are harder for microbes to digest and potentially screening pathogens for these enzymes, especially in unexplained prolonged outbreaks,” McCarthy said.
That prospect affects far more than one operating theatre. Cardiac stents, breast implants, dental membranes and bone fillers all rely on polymers for flexibility and strength. If any of those materials can be metabolized, latent infections might smolder undetected until biofilms reach critical mass.
One response is to redesign polymers so their chemical bonds resist enzymatic cleavage. Another is to coat device surfaces with inert barriers or embedded antimicrobials that deny bacteria a foothold.
Any such solution must preserve the mechanical virtues that made PCL popular in the first place while preventing degradation inside the body.
Research chemists may also mine Pap1 itself for clues. By mapping its active site, they could predict which molecular motifs invite attack and which repel it. That information could steer the next generation of hospital plastics toward safer territory.
Hospitals already culture swabs from taps, beds, and keyboard covers. The new data suggest laboratories should add targeted searches for plastic-digesting enzymes.
Environmental isolates that test positive might explain outbreaks whose source has eluded standard surveillance. Cleaning protocols could likewise shift focus: scrubbing away visible grime is not enough if bacteria can tuck inside the polymer and nibble at its chains.
McCarthy emphasizes that the present work is an early step. It examined one strain, one enzyme, and one polymer under controlled conditions. Real-world environments mix many microbes, variable temperatures, and diverse materials.
“Plastic is everywhere in modern medicine, and it turns out some pathogens have adapted to degrade it, and we need to understand the impact this has on patient safety,” McCarthy said.
Future studies will test explanted devices for microscopic bite marks, track enzyme genes across hospital genomes and expose other medical plastics to potential degraders.
Animal models may reveal whether in-body digestion changes implant strength or releases inflammatory by-products. Parallel work on coatings and polymer chemistry will explore defenses.
For now, the image is sobering: a superbug perched on a catheter, slowly digesting the tube meant to heal, using the fragments to thicken its fortress and bide its time. The finding upends old assumptions and signals that in the quiet corners of a ward, plastic may not be inert at all – but a secret feast for the enemy within.
The study is published in the journal Cell Reports.
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