Researchers in Texas have discovered a new way to fight ‘superbugs’ – multidrug-resistant bacteria; by blinding them rather than killing them.
A study in rats conducted at the University of Texas (UT) Southwestern Medical Center in Dallas proved highly effective in a model of burn injuries, which are commonly associated with infections.
Co-senior author Dr Steven Wolf said: “Rather than killing the bacteria, we blinded them so they could not find the places where they normally stick to the host (body’s) cells. If bacteria cannot bind, they cannot grow.”
Texas, and particularly the University of Texas, is increasingly being recognised as a premier hub of superbug research. Earlier this year the John P. and Kathrine G. McGovern Medical School at University of Texas Health Science Center at Houston (UT Health) opened a new research center to address the global health threat posed by antibiotic-resistant bacteria. The UT Center for Antimicrobial Resistance and Microbial Genomics (CARMiG) is led by internationally-recognised superbug researcher Dr Cesar Arias. He also heads the Cluster for Antimicrobial Resistance at the Gulf Coast Consortia (GCC), a seven-member partnership of leading academic biomedical institutions in the Texas Medical Center that focuses on shared training initiatives, collaborative research and core facilities.
Back at UT Southwestern, co-senior author Dr Kim Orth, Professor of Molecular Biology and Biochemistry and head of the Orth lab, which is focused on the virulence factors from pathogenic bacteria, said: “Antibiotic-resistant bacteria are an increasingly prevalent problem in the clinic and hospital, so new ways to prevent and treat infections are direly needed. Antibiotics work by killing bacteria, which places microbes under extreme pressure to develop antibiotic resistance.
“Our approach doesn’t target bacterial survival; rather it targets the microbes’ ability to damage the host – its virulence. There is no reason for the bacteria to become resistant to this approach. Being unable to bind to wounded tissue is an inconvenience, and the bacteria move on. If all the parking spaces are filled, then the bacteria have no place to park.”
The study targeted one of the most lethal pathogens, multidrug-resistant Pseudomonas aeruginosa, which is found in 59 per cent of extensive burns, with the use of an engineered adhesion inhibitor molecule – Multivalent Adhesion Molecule 7 (MAM7). It works by hampering the activity of adhesive molecules that certain types of bacteria use to bind to cells and kickstart infections. Topical application of MAM7 substantially decreased the bacterial levels in wounds in the first 24 hours and prevented the spread of the infection to adjacent tissue for three more days. In addition, the experimental molecule aided wound healing.
The MAM7 molecule was developed in the Orth laboratory and grew out of the postdoctoral research project of the study’s third senior author, Dr Anne-Marie Krachler, now with the McGovern Medical School at UT Health.
“Antibiotics are amazing drugs, and they have saved countless lives since their discovery more than 80 years ago. But there is a challenge – the challenge of antibiotic resistance that has made many antibiotics ineffective. A material that targets virulence instead of killing bacteria could be a way to treat infections that are resistant to antibiotics,” she said. “This is a trial in rats. A future goal is to use this strategy in patients.”
Additional steps will include testing whether the anti-adhesion strategy might also block infection of bacteria that can cause lethal infections during surgery.
(Via UTSouthwestern, UTHealth, NewAtlas)
Featured image: (left to right) Dr. Steven Wolf, Dr. Kim Orth, and Dr. Ryan Huebinger Credit: UT Southwestern