Register for an account

X

Enter your name and email address below.

Your email address is used to log in and will not be shared or sold. Read our privacy policy.

X

Website access code

Enter your access code into the form field below.

If you are a Zinio, Nook, Kindle, Apple, or Google Play subscriber, you can enter your website access code to gain subscriber access. Your website access code is located in the upper right corner of the Table of Contents page of your digital edition.

Health

Superbugs Emerge From the School of Hard Knocks

“It’s the bacterial equivalent of ‘That which doesn’t kill you makes you stronger,’” says biomedical engineer Jim Collins.

By Valerie RossNovember 22, 2010 6:00 AM
superbug.jpg
Mutant strains of bacteria — the yellow colonies here — can acquire drug resistance from environmental changes. | Hemantha Kulasekara

Newsletter

Sign up for our email newsletter for the latest science news

The rise of superbugs that can survive multiple antibiotics—such as MRSA, the notorious “flesh-eating bacterium”—has turned once-trivial infections into persistent problems. To fight back, we need better information about how bacteria acquire this unsettling power. Two recent reports are providing just that.

Doctors have long known that an incomplete course of antibiotics can promote resistance, which is why pill bottles often carry a stern warning to “finish all this medication.” Boston University biomedical engineer Jim Collins and colleagues have identified one way in which such resistance can develop. They found that when E. coli were treated with doses of ampicillin too low to kill all of the cells, some of those left alive suffered DNA damage that was hastily—and often inaccurately—patched up. The sloppy repair job left behind mutations, and just by chance, a few of these gave the bugs resistance not only to ampicillin but to two other antibiotics they had never encountered. On the basis of these findings, he plans to search for molecules that can block bacteria’s efforts to patch up their genes.

Meanwhile, pediatric pulmonologist Luke Hoffman at the University of Washington has found that some bacteria can develop drug resistance in response to an environmental change, without exposure to any antibiotics. He examined Pseudomonas aeruginosa, a microbe that inhabits the mucus clogging the airways of cystic fibrosis patients. To his surprise, he found that mutations allowing the bacterium to adapt to low-oxygen conditions in the mucus also decrease its susceptibility to antibiotics. Many antibiotics work by disrupting bacterial metabolism, so adjustments to how the germs process oxygen can also strengthen their resistance to drugs. The findings help explain why lung infections in cystic fibrosis patients are so hard to treat. Identifying bacteria with these mutations may allow doctors to select alternative antibiotics that exploit other ways to kill them.

2 Free Articles Left

Want it all? Get unlimited access when you subscribe.

Subscribe

Already a subscriber? Register or Log In

Want unlimited access?

Subscribe today and save 70%

Subscribe

Already a subscriber? Register or Log In