Antibiotics make E.coli grow FASTER than if the bug were left alone
- E.coli bacteria growth is stimulated by antibiotics, a study claims
- Treating the bacteria with antibiotics multiplied them up to three times larger
- When the drugs were taken away, the changes to the E.coli were not undone
- Experts say bacteria can quickly rearrange their DNA to stop drugs from working
Antibiotics can make superbugs grow faster than if they were left untouched, a new study has found.
In an alarming set of experiments, scientists saw that E.coli - the 'food poisoning' bacteria which causes severe stomach pain, diarrhea and kidney failure in humans - increased in antibiotic resistance with each dose of treatment.
When researchers took the drug away, the bug maintained its newly-developed strength.
The ominous finding comes amid a rise in antibiotic resistance, with scientists scrambling to find new treatments that fight drug-resistant bacterial infections.
Escheria coli (E.coli) bacteria grew and multiplied up to three times larger when treated with antibiotics, a new study claims. Here, E.coli smeared on an agar plate shows the drug resistant bacteria (green) and the non-resistant (blue)
In the study, performed at the University of Exeter in England, researchers exposed E.coli bacteria to eight rounds of antibiotic treatment over four days.
Not only did the bug increase its antibiotic resistance with each treatment, but the mutated E.coli reproduced faster than before encountering the drugs.
It 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.
Lead author Professor Robert Beardmore said: 'Our research suggests there could be added benefits for E.coli bacteria when they evolve resistance to clinical levels of antibiotics.
'It's often said that Darwinian evolution is slow, but nothing could be further from the truth, particularly when bacteria are exposed to antibiotics.
'Bacteria have a remarkable ability to rearrange their DNA and this can stop drugs working, sometimes in a matter of days.
'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.'
The researchers tested the effects of the antibiotic doxycycline - used to treat many different bacterial infections such as acne, urinary tract infections, gonorrhea, and others - on the E.coli to study DNA changes brought about by drugs.
The E.coli 'uber-bug' that subsequently evolved was safely frozen at -112F (-80C) and the scientists used genetic sequencing to find out which DNA changes were responsible for its unusual evolution.
Some of the changes were well-known and have been seen in clinical patients, like E.coli producing more antibiotic pumps, which bacteria exploit to push antibiotics out of the cell.
Another change seen was the loss of DNA that is known to describe a dormant virus.
Co-author Dr Carlos Reding said: '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.'
'This creates an evolutionary force for change on two regions of the E.coli genome.
'Normally, self-destruction can help bacteria colonize surfaces through the production of biofilms. You see biofilms in a dirty sink when you look down the plughole.
'But our study used liquid conditions, a bit like the bloodstream, so the E.coli could give up on its biofilm lifestyle in favor of increasing cell production.'
Dr Mark Hewlett, also of the University of Exeter, 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.
'This shows it's important to use the right antibiotic on patients as soon as possible so we don't see adaptations like these in the clinic.'
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