Antibiotics may cause bacteria to mutate into "uber-bugs" which reproduce much faster, say scientists who found that a bug which causes severe stomach pain, diarrhoea and kidney failure in humans had increased resistance after each round of drug treatment.

Researchers at University of Exeter in the UK exposed E coli bacteria to eight rounds of antibiotic treatment.

They found that mutated E coli reproduced faster than before encountering the drugs and formed populations that were three times larger because of the mutations.

This was only seen in bacteria exposed to antibiotics and when researchers took the drug away, the evolutionary changes were not undone and the new-found abilities remained.

"Our research suggests there could be added benefits for E coli bacteria when they evolve resistance to clinical levels of antibiotics," said Robert Beardmore, Professor at University of Exeter.

"Bacteria have a remarkable ability to rearrange their DNA and this can stop drugs working, sometimes in a matter of days," said Beardmore.

"While rapid DNA change can be dangerous to a human cell, to a bacterium like E coli it can have multiple benefits, provided they hit on the right changes," he added.

The researchers tested the effects of the antibiotic doxycycline on E coli as part of a study of DNA changes brought about by antibiotics.

The E coli "uber-bug" that subsequently evolved was safely frozen at minus 80 degrees Celsius and the scientists used genetic sequencing to find out which DNA changes were responsible for its unusual evolution.

Some changes are well known and have been seen in clinical patients, like E coli producing more antibiotic pumps that bacteria exploit to push antibiotics out of the cell.

Another change saw the loss of DNA that is known to describe a dormant virus.

"Our best guess is that losing viral DNA stops the E coli destroying itself, so we see more bacterial cells growing once the increase in pump DNA allows them to resist the antibiotic in the first place," said Carlos Reding, from University of Exeter.

"This creates an evolutionary force for change on two regions of the E coli genome," Reding said.

"Normally, self-destruction can help bacteria colonise surfaces through the production of biofilms. You see biofilms in a dirty sink when you look down the plughole," he said.

"But our study used liquid conditions, a bit like the bloodstream, so the E coli could give up on its biofilm lifestyle in favour of increasing cell production," he added.

"It is said by some that drug resistance evolution doesn't take place at high dosages but our paper shows that it can and that bacteria can change in ways that would not be beneficial for the treatment of certain types of infection," said Mark Hewlett of the University of Exeter.

The research was published in the journal Nature Ecology and Evolution.