Shanghai researchers discover how bacteria develop antibiotic resistance

Medical researchers in Shanghai say they have discovered why certain types of disease-causing bacteria develop resistance to antibiotics, a development that could prolong the useful life of existing drugs without having to develop expensive replacements.

The over-prescription of antibiotics is widely blamed for the emergence of drug-resistant bacteria worldwide, and the mainland is one of the worst offenders - per capita consumption of the drugs was 138 grams a year in 2011, a survey by Peking University found. That's 10 times the global average, Xinhua reported in December, citing the State Food and Drug Administration.

Now researchers at Fudan University's Shanghai Medical College say they have uncovered an important mechanism leading to resistance. The team, led by Professor Alastair Murchie, a British molecular biologist, said in a paper in the peer-reviewed journal Cell last week, that they had found a special section of ribonucleic acid (RNA) in some infectious bacteria that could make antibiotics useless.

Specifically, the Fudan team discovered that a section of RNA, called a riboswitch, in bacteria that cause diseases like meningitis, pneumonia and bone joint inflammation, could control the bacteria's antibiotic-resistance. The riboswitch could recognise aminoglycoside antibiotics and release a protein to render the antibiotics inactive.

Murchie said that while aminoglycoside antibiotics accounted for only about 20 per cent of all antibiotics, the research was important because drug resistance remained a significant threat due to the way it evolved and emerged.

"It's important that we understand the underlying mechanism [of] why resistance happens, how are the bacteria so flexible and why do they respond so well to treatment by antibiotics?" Murchie said.

Another member of the team, Dr Chen Dongrong , said they had hypothesised at the start of the study that a riboswitch could play a role in antibiotic-resistance. The team then spent three years identifying the aminoglycoside antibiotic that triggered the response and were testing other antibiotics to prove their hypothesis.