Antibiotic resistance is supercharging dangerous gut bacteria to withstand even hospital-grade disinfectants intended to kill them.
New research from Monash University, published in Nature Communications, reveals the bacteria Clostridioides difficile has picked up a key gene that gives its dormant spores a free pass against antibiotics and cleaning products.
Its spores act like plant seeds, waiting patiently to activate and spread in the right environment, like the human gut.
This is particularly dangerous given this bacterium is commonly found in hospitals and causes diarrhea that can be deadly for already unwell patients.
Lead researcher Professor Dena Lyras, Interim Dean of the Monash Sub-Faculty of Biomedical and Psychological Sciences and Director of Monash Biomedicine Discovery Institute, said the new research is a crucial step forward in what is a dynamic race against antimicrobial resistance.
“Antibiotics are helping bacteria evolve in ways we hadn’t anticipated,” Professor Lyras said.
“Our new research shows just how sophisticated their evolution is, with the potential to have disastrous impacts on humans.
“They are not only better at building tolerance to drugs we develop, but making new versions of themselves that can survive better in particular environments, like surfaces where cleaning products are commonly applied.”
Antimicrobial resistance occurs when bacteria stop responding to antibiotics leading to infections that can be hard or impossible to treat.
The World Health Organization lists this phenomenon as a major global health threat and estimates that it contributes to millions of deaths every year.
This new research, the first to uncover a link between antibiotic resistance and bacterial spores, shows that when Clostridioides difficile picks up this antibiotic resistance gene, the antibiotic block no longer works.
Instead, the bacteria is able to make even tougher spores that can survive hospital grade cleaning products and high laundry temperatures.
The antibiotic resistance gene produces a protein that replaces a key spore-building protein, allowing the bacteria to keep making spores.
First author Dr Yogitha Srikhanta, a Post-Doctoral Research Fellow at Monash Biomedicine Discovery Institute, said targeting the spores could be the key to unlocking a solution.
“Spore survival matters because spores are the main way these pathogens spread between people and through hospitals, homes, and the environment,” Dr Srikhanta said.
