New method to combat antibiotic resistance in the works

New treatments that disarm disease-causing bacteria instead of killing them are currently in the works. These treatments are set to pave the way in combating the growing problem of antibiotic resistance.

Published in the journal 'Nature Structure and Molecular Biology', a study shows that disarming bacteria would deprive them of their molecular weaponry which in turn disables the disease process.

Research led by Monash University shows that a protein complex called the Translocation and Assembly Module (TAM) formed a type of molecular pump in bacteria.

The TAM allows bacteria to shuttle key disease-causing molecules from inside the bacterial cell where they are made, to the outside surface, priming the bacteria for infection.

Lead author and PhD student Joel Selkrig of the Department of Biochemistry and Molecular Biology at Monash said that the TAM was discovered in many disease-causing bacteria, from micro-organisms that cause whooping cough and meningitis, to hospital-acquired bacteria that are developing resistance to current antibiotics.

"By allowing bacteria to stay alive after antibiotic treatment, we believe we can also prevent the emergence of antibiotic resistance, which is fast becoming a major problem worldwide."

The Monash team, led by Professor Trevor Lithgow from the Department of Biochemistry and Molecular Biology, showed the TAM was made of two protein parts, TamA and TamB, which function together to form a machine of molecular scale.

Together with colleagues at the University of Melbourne, they compared normal virulent bacteria to mutant strains of bacteria engineered to have no TAM.

"We noticed that proteins important for disease were missing in the outer membrane of the mutant bacteria," Mr Selkrig said.

"The absent proteins help bacteria to adhere to our bodies and perform disease-related functions."

The next step for the group is to dissect the molecular mechanism of how the TAM complex functions and design an antibiotic that inhibits the TAM in bacteria, said Mr Selkrig.