The standard treatment strategy for a bacterial infection is to hit ‘em fast and hit ‘em hard with a combination of antibiotics to keep bacterial cells from multiplying and the infection from spreading. 

But new research from the University of Exeter in the UK and Kiel University in Germany says that may be the wrong approach.

The study, published today in PLOS Biology, states that using highly potent, combined antibiotic treatments could speed up bacteria’s resistance to these drugs, which is an increasing health concern worldwide.

The U.S. Centers for Disease Control and Prevention (CDC) says that controlling and combating the spread of life-threatening bacteria, such as methicillin-resistant Staphylococcus aureus (MRSA), remains one of their top priorities.

How Bacteria Evolve in Response to Drugs

In a laboratory setting, Exeter and Kiel researchers gave E. coli bacteria both single and combination antibiotic treatments. They found that the stronger treatments sped up drug resistance, and that the most effective treatments worked on the first day but could become ineffective as quickly as day two and nearly useless by day five. 

Researchers found that drug-resistant bacteria replicate fastest when competing bacteria are eliminated by the aggressive antibiotic therapies. In essence, bacteria behave like any other invasive species in nature: remove the competition and they will flourish.

“We were concerned by how quickly the bacteria evolved resistance,” lead study author Robert Beardmore, professor of mathematical biosciences at the University of Exeter, said in a press release. “We nearly stopped the experiments because we didn't think some of the treatments should be losing potency that fast; sometimes within a day.”

Beardmore's team soon learned that the bacteria that remained after the initial antibiotic treatment quickly replicated their treatment-resistant genes, and that the copies of those genes appeared more quickly with a combination treatment, “resulting in the rapid evolution of very resistant bacteria,” Beardmore said.

His team also used mathematical modeling and whole-genome analysis—a laboratory process to decode all of the E. coli bacteria’s DNA—and determined that current antibiotic prescribing practices don’t account for the speed at which treatment resistance occurs and “may not represent the optimal course of action.” 

“The interesting thing is that the bacteria didn’t just make copies of the genes they needed,” study co-author Hinrich Schulenburg, professor of zoology at Kiel University, said in a press release. “Just in case, they copied other genes as well, increasing resistance to antibiotics that they weren't even treated with.”

The Scary Reality of Antibiotic Resistance

The World Economic Forum has called antibiotic resistance “arguably the greatest risk” to human health. 

Both the over-prescription of antibiotics—to treat the common cold and other viral infections—and the use of antibiotics in livestock have been linked to the increased ineffectiveness of current antibiotic treatments in humans.

In 2009, more than 6.5 million pounds of antibiotics were administered to U.S. patients, and in 2010, 28.6 million pounds were given to animals, according to perspective paper published earlier this year in The New England Journal of Medicine.

A study published earlier this year that documented the spread of MRSA from livestock to humans was evidence enough for U.S. Rep. Louise Slaughter (D-N.Y.) to again propose a bill that would reduce the use of antibiotics in animals and humans. The bill is currently before the House Energy and Commerce Committee.

But there is still reason to hope. Earlier this month, researchers from Rockefeller University said they’d found a weak point in bacteria’s armor, which could allow viruses called phages to kill even treatment-resistant bacteria. 

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