Economics and evolution help scientists identify new strategy to control antibiotic resistance

Mar 18, 2011

A team of scientists from the University of Oxford, U.K. have taken lessons from Adam Smith and Charles Darwin to devise a new strategy that could one day slow, possibly even prevent, the spread of drug-resistant bacteria. In a new research report published in the March 2011 issue of GENETICS, the scientists show that bacterial gene mutations that lead to drug resistance come at a biological cost not borne by nonresistant strains. They speculate that by altering the bacterial environment in such a way to make these costs too great to bear, drug-resistant strains would eventually be unable to compete with their nonresistant neighbors and die off.

"Bacteria have evolved resistance to every major class of antibiotics, and new antibiotics are being developed very slowly; prolonging the effectiveness of existing drugs is therefore crucial for our ability to treat infections," said Alex Hall, Ph.D., a researcher involved in the work from the Department of Zoology at the University of Oxford. "Our study shows that concepts and tools from and genetics can give us a boost in this area by identifying novel ways to control the spread of resistance."

The research team measured the growth rates of resistant and susceptible Pseudomonas aeruginosa bacteria in a wide range of laboratory conditions. They found that the cost of has a cost to bacteria, and can be eliminated by adding chemical inhibitors of the enzyme responsible for resistance to the drug. Leveling the playing field increased the ability of resistant bacteria to compete effectively against sensitive strains in the absence of antibiotics. Given that the cost of plays an important role in preventing the spread of resistant bacteria, manipulating the cost of resistance may make it possible to prevent resistant bacteria from persisting after the conclusion of antibiotic treatment. For instance, new additives or treatments could render antibiotic resistance more costly for bacteria, making it less likely that the will persist at the end of treatment.

"If we've learned one thing about microscopic organisms over the past century, it's that they evolve quickly, and that we can't stop the process," said Mark Johnston, Editor-in-Chief of the journal GENETICS. "This research turns this fact against the bacteria. This is an entirely new strategy for extending the useful life of antibiotics, and possibly for improving the potency of old ones."

Explore further: Mutations from Mars: Researchers explain why genetic fertility problems can persist in a population

More information: The Fitness Cost of Rifampicin Resistance in Pseudomonas aeruginosa Depends on Demand for RNA Polymerase, Hall et al. 2011, www.genetics.org/cgi/content/abstract/187/3/817

Provided by Genetics Society of America

5 /5 (2 votes)
add to favorites email to friend print save as pdf

Related Stories

Resistant gut bacteria will not go away by themselves

Jun 19, 2007

E. coli bacteria that have developed resistance to antibiotics will probably still be around even if we stop using antibiotics, as these strains have the same good chance as other bacteria of continuing to colonise the gut, ...

Probing Question: How does antibiotic resistance happen?

Mar 05, 2009

Before Alexander Fleming's discovery of penicillin in 1928, there were any number of unpleasant ways that bacteria could kill you. Countless women died from infection after childbirth, and a simple chest cold could turn into ...

New antibiotic beats superbugs at their own game

Jul 03, 2008

The problem with antibiotics is that, eventually, bacteria outsmart them and become resistant. But by targeting the gene that confers such resistance, a new drug may be able to finally outwit them. Rockefeller ...

Recommended for you

Gene research targets scarring process

7 hours ago

Scientists have identified three genes that may be the key to preventing scar formation after burn injury, and even healing existing scars.

Researchers find new mechanism for neurodegeneration

Jul 24, 2014

A research team led by Jackson Laboratory Professor and Howard Hughes Investigator Susan Ackerman, Ph.D., have pinpointed a surprising mechanism behind neurodegeneration in mice, one that involves a defect in a key component ...

User comments : 0