Scientists from The University of Manchester have discovered that 'lonely' microbes are more likely to mutate, resulting in higher rates of antibiotic resistance.

The study, published today in Nature Communications and jointly funded by The Wellcome Trust and Engineering and Physical Sciences Research Council, explored the mutation rates of E. coli.

Researchers found out that the rate of mutation varied according to how many of the bacteria there were. Surprisingly, they discovered that more bacteria gave fewer mutations.

Meanwhile more 'lonely' bacteria developed greater resistance to the well-known antibiotic Rifampicin, used to treat tuberculosis.

Dr Chris Knight joint lead author on the study with Dr. Rok Krašovec from The University of Manchester, said: "What we were looking for was a connection between the environment and the ability of bacteria to develop the resistance to antibiotics. We discovered that the rate at which E. coli mutates depends upon how many 'friends' it has around. It seems that more lonely organisms are more likely to mutate."

This change of the mutation rate is controlled by a form of social communication known as quorum sensing – this is the way bacteria communicate to let each other know how much of a crowd there is. This involves the release of signalling molecules by bacteria when in a dense population to help the organisms understand their surrounding environment and coordinate behaviour to improve their defence mechanisms and adapt to the availability of nutrients.

Dr. Krašovec said: "We were able to change their mutation rates by changing who they shared a test tube with, which could mean that bacteria manipulate each other's mutation rates. It also suggests that mutation rates could be affected when bacteria are put at low densities for instance by a person taking antibiotics."

The rate of mutation was found to be dependent on the gene luxS which is known to be involved in quorum sensing in a wide range of bacteria.

The team now hopes to find ways to control this signalling for medical applications in a future study funded by the Biotechnology and Biological Sciences Research Council.

"Eventually this might lead to interventions to control mutation rates, for instance to minimise the evolution of antibiotic resistance, allowing antibiotics to work better," said Dr Knight.

Dr Mike Turner, Head of Infection and Immunobiology at the Wellcome Trust said: "Antibiotic resistance is a real threat to disease control and public health today. Any insight into the origins of such resistance is valuable in the fight to prevent it. Chris Knight and his team have gained a fundamental understanding of bacterial communication and the development of mutations which in the long run could contribute to more potent antibiotics and better control of bacterial disease".

There's new hope for development of an antibiotic that can put down a lethal "superbug" bacteria linked to the deaths of hundreds of hospital patients around the world, including a recent case at Edmonton's Royal Alexandra Hospital.

Researchers from the University of Alberta-based Alberta Glycomics Centre found a chink in the molecular armour of the pathogen Acinetobacter baumannii. The bacteria first appeared in the 1970s and in the last decade it has developed a resistance to most antibiotics.
U of A microbiologist Mario Feldman identified a mechanism that allows Acinetobacter baumannii to cover its surface with molecules known as glycoproteins. That led the researchers to another discovery. "If the superbug cannot produce glycoproteins they become less virulent and less capable of forming biofilms," said Feldman. "The biofilm protects the bacteria from antibiotics."
Acinetobacter baumannii is a particularly insidious and contagious pathogenic bacteria that has plagued hospitals around the world. It spreads from one person to another by physical contact. The bacteria can live on hard surfaces for several days and can cling to hospital equipment like catheter tubes and inhalers. Acinetobacter infection is also spread by coughing and sneezing.
Hospital patients whose immune systems are already worn down are the most susceptible to the bacteria. It infects wounds and can spread to the lungs, blood and brain.
The researchers say more work is required to understand how the bacteria produce glycoproteins. "We're hopeful our work will enable future development of drugs to interrupt the production of glycoproteins to weaken or eliminate the bacteria's shield against antibiotics," said Feldman.
Feldman is a principal investigator for the Alberta Glycomics Centre at the U of A. The list of coauthors includes U of A graduate students Jeremy Iwashkiw and Brent Weber, and research colleagues in Ottawa, Austria and Australia. Their work was published June 7 in the journal PLoS Pathogens.

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Details: Bacteriological Peptone it is an standardized peptone for the preparation of bacteriological culture media. The Nitrogen it contains is perfectly available for the bacterial growth requirements. It is completely soluble giving a transparent solution at the concentrations used in culture media.

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