Date Published: 28 November 2013

Resistance protein in the superbug acinetobacter baumannii

Researchers at Leeds University (Yorkshire, England) together with colleagues at Macquarie University (Australia) have recently identified a resistance protein that allows bacteria (structure of a bacteria cell) to survive chlorhexidine, an antiseptic commonly used in wipes, cleansers and mouthwashes in hospitals.

A study showed how the superbug acinetobacter baumannii, which is prevalent among soldiers treated in medical facilities in Iraq and Afghanistan, can pump the antiseptic out of its system. This happens when a gene in the bacteria responds to *chlorhexidine by producing a so-called 'resistance protein' that then binds to the antiseptic, causing the chlorhexidine that has entered the cell to be removed from it.

*Early indications are that the protein specifically binds with chlorhexidine rather than other antibiotic molecules.

The resistance protein has been called Acinetobacter Chlorhexidine Efflux, abbreviated to 'Ace'.

The information revealed by this study is important for the design of new chemicals to combat the germ acinetobacter baumannii. This is important due to the serious threat posed by the emergence of such antibiotic-resistance bacteria. Concern about such bacteria was expressed by Sally Davies, the Chief Medical Officer for England, who stated in March 2013 that antibiotic resistance posed a "catastrophic threat" that could mean that even minor surgeries might carry deadly risks by the 2030s.

Acinetobacter baumannii is a good example of the development of antibiotic-resistant strains of bacteria because it used to be treatable with normal antibiotics and now it has been described as one of the most worrying superbugs threatening the medical system. Its ability to survive on disinfected artificial surfaces for long periods has allowed it to thrive and spread through the military and into the civilian medical system.

Comments from the research team:

Professor Peter Henderson of Leeds University's School of Biomedical Sciences said:

"The Australians saw that, in response to chlorhexidine, a gene becomes active and produces a protein they called Acinetobacter Chlorhexidine Efflux, or 'Ace' for short. Working together, we demonstrated that Ace binds to the antiseptic and effectively pumps the chlorhexidine that has leaked through the cell wall out again."

He also said that ...

"Identifying the resistance protein now allows us to look for a compound that will inhibit the protein's activity and form the basis of a new treatment against infection."

and ...

"There are very similar genes in other pathogenic organisms. Our next step will be to explore what these proteins do in those other organisms. In some cases, it is strongly suggested that they make the germ resistant to chlorhexidine, but in others it appears to be something else. We need to find out what that is."
... and added that "The bad news is that the bugs are winning. We can't devise new antibiotics nearly fast enough to find a new way of dealing with them and there is not enough funding to pursue the research. This project is typical of the sort of work that we have to do to win the fight against superbugs."

Professor Ian Paulsen at Macquarie University, Australia, said:

"Antiseptics and disinfectants are a key defence used to control the spread of these bacteria in hospitals particularly. Following this discovery, we plan to investigate ways to block this pump. Such work is important in ensuring that we can continue to use successfully this antiseptic to reduce rates of infection in hospitals."

Ref. to Paper:
Karl A. Hassan, Scott M. Jackson et.al., 'Transcriptomic and biochemical analyses identify a family of chlorhexidine efflux proteins' was published online by the journal Proceedings of the National Academy of Sciences (PNAS) at DOI: 10.1073/pnas.1317052110 on 25 Nov 2013. [Subscription reqd to access article.]

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