Scientists at the University of Exeter have found that antibiotics can stimulate the growth of bacteria. When Escherichia coli bacteria was treated with eight rounds of antibiotics over the course of four days, the scientists found that antibiotic resistance increased with every round of treatment. While this was not an unexpected result, it was also found that mutated E coli were growing faster than they had been before drug treatment, and the resulting colony was three times as big, something only observed in microbes that had been treated with antibiotics. Removing the drug did not have any effect; the new characteristics of the bacteria were permanent. The work has been published in Nature Ecology & Evolution.
"Our research suggests there could be added benefits for E.coli bacteria when they evolve resistance to clinical levels of antibiotics," said Professor Robert Beardmore of the University of Exeter and the lead author of the report. "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."
To investigvate the effects of antibiotics on bacterial DNA, E.coli was exposed to doxycycline, which created a so-called E. coli "uber-bug" that was safely tucked away after its evolution. The researchers then utilized genetic sequencing to determine what changes to the DNA took place that resulted in this altered organism.
Such mutations to bacterial DNA are known after being observed and documents in patients in hospitals and clinics; for example E.coli will produce additional antibiotic pumps. Microbes take advantage of those pumps in order to remove antibiotic molecules from cells. Another change seen by the researchers was a loss of DNA that is understood to characterize 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 study researcher Dr. Carlos Reding.
"This creates an evolutionary force for change on two regions of the E.coli genome. 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, explained,” explained Reding. “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."
"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,” commented Dr. Mark Hewlett, also of the University of Exeter. "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."
Scientists have been using this methodology to study antibiotic resistant bacteria. In the video above, you can hear about how expert scientists can create highly resistant bacterial strains for use in the lab.