Drug-resistant superbugs appear to be more tenacious and resilient than we previously thought.
This flies in the face of the long-held belief that drug-resistant bacteria become weaker and less able to infect a host after acquiring resistance to antibiotics. Scientists had previously thought that the same mutations that slow the antibiotics’ uptake into cells would also block food and other ingredients necessary for survival.
This view has prevailed for years, even without much convincing evidence to back it up. The results of this new study, from Brigham and Women’s Hospital, offer a compelling challenge to this long-held belief.
“This is an exciting and unexpected discovery that questions the standard paradigm in the field,” Kim Lewis, director of the Antimicrobial Discovery Center at Northeastern University not involved with the study, told Tech Insider.
To understand how mutations in many different genes affect the “fitness,” or ability to survive in and make a host sick, the team infected mice with various strains of Pseudomonas aeruginosa, a particularly nasty bacteria that infects the nose, throat, lungs, and can lead to pneumonia and blood infections. Without treating the mice with any medications, they found that the mice infected with antibiotic-resistant strains of the bacteria were more likely to die than those infected with bacteria that were not resistant.
They also found that the antibiotic-resistant strains were better able to kill the host’s immune cells, the body’s natural defence system.
To confirm these findings, the team also infected mice and rabbits with
Acinetobacter baumannii, a multi-drug-resistant bacteria commonly found in healthcare settings, and
Vibrio cholerae, the bacteria responsible for cholera infections around the world. They found the same results: Those bacteria that had acquired resistance to antibiotics were stronger and more likely to cause illness than the bacteria that were not resistant.
“We got a very new signal,” study researcher David Skurnik, assistant professor of medicine at Brigham and Women’s Hospital, told Tech Insider. “When you improve antibiotic resistance, you improve fitness.”
So how does this change our approach to antibiotic resistance?
The study was in mice, not people, and it’s possible that antibiotic-resistant bacteria interact with the human immune system differently; further research will be needed to confirm these results. But the findings challenge the long-held notion that simply reducing the use of antibiotics will be enough to combat the growing problem of resistance. This study suggests that drug-resistant strains of bacteria might still be better able to survive the less-resistant bugs no matter what.
“There are the problems with antimicrobial resistance that everyone knows, but now the problem is even worse,” Skurnik said. “We have to really work on preventing infectious disease by improving hygiene, but in parallel we have to develop an alternative approach not based on antibiotics.”
Skurnik is already researching such alternatives, one of which may be the use of vaccines and antibodies that target proteins that bacteria express on the outside of their cells. If successful, this new approach will be an innovative step in stemming the tide of antibiotic resistant bacteria and their increasing threat to humans.
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