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Powerful, Promising New Molecule May Snuff Antibiotic Resistant Bacteria

ByR.A. BeckerNOVA NextNOVA Next

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Antibiotic resistant bacteria pose one of greatest threats to public health. Without new weapons in our arsenal, these bugs could cause 10 million deaths and cost nearly $100 trillion worldwide each year by the year 2050, according to a recent study commissioned by the British government.

But just this week, scientists announced that they have discovered a potent new weapon hiding in the ground beneath our feet—a molecule that kills drug resistant bacteria and might itself be resistant to resistance. The team published their results Wednesday in the journal Nature.

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Scanning electron micrograph of methicillin-resistant Staphylococcus aureus and a dead human neutrophil
Methicillin-resistant staph surround human immune cell.

Scientists have been coopting the arsenal of soil-dwelling microorganisms for some time, said Kim Lewis, professor at Northeastern University and senior investigator of the study. Earth-bound bacteria live tightly packed in an intensely competitive environment, which has led to a bacterial arms race. “The ones that can kill their neighbors are going to have an advantage,” Lewis said. “So they go to war with each other with antibiotics, and then we borrow their weapons to fight our own pathogens.”

However, by the 1960s, the returns from these efforts were dwindling. Not all bacteria that grow in the soil are easy to culture in the lab, and so antibiotic discovery slowed. Lewis attributes this to the interdependence of many soil-dwelling microbes, which makes it difficult to grow only one strain in the lab when it has been separated from its neighbors. “They kill some, and then they depend on some others. It’s very complex, just like in the human community,” he said.

But a new device called the iChip, developed by Lewis’s team in collaboration with NovoBiotic Pharmaceuticals and colleagues at the University of Bonn, enables researchers to isolate bacteria reluctant to grow in the lab and cultivate them instead where they’re comfortable—in the soil.

Carl Nathan, chairman of microbiology and immunology at Weill Cornell Medical School and co-author of a recent New England Journal of Medicine commentary about the growing threat of antibiotic resistance, called the team’s discovery “welcome,” adding that it illustrates a point that Lewis has been making for several years, that soil’s well of antibiotic-producing microorganisms “is not tapped out.”

The researchers began by growing colonies of formerly un-culturable bacteria on their home turf and then evaluating their antimicrobial defenses. They discovered that one bacterium in particular, which they named

Eleftheria terrae , makes a molecule known as teixobactin which kills several different kinds of bacteria, including the ones that cause tuberculosis, anthrax, and even drug resistant staph infections.

Teixobactin isn’t the first promising new antibiotic candidate, but it does have one quality that sets it apart from others. In many cases, even if a new antibiotic is able to kill bacteria resistant to our current roster of drugs, it may eventually succumb to the same resistance that felled its predecessors. (Resistance occurs when the few bacteria strong enough to evade a drug’s killing effects multiply and pass on their genes.)

Unlike current antibiotic options, though, teixobactin attacks two lipid building blocks of the cell wall, which many bacteria strains can’t live without. By attacking such a key part of the cell, it becomes harder for a bacterium to mutate to escape being killed.

“This is very hopeful,” Nathan said. “It makes sense that the frequency of resistance would be very low because there’s more than one essential target.” He added, however, that given the many ways in which bacteria can avoid being killed by pharmaceuticals, “Is this drug one against which no resistance will arise? I don’t think that’s actually proved.”

Teixobactin has not yet been tested in humans. Lewis said the next steps will be to conduct detailed preclinical studies as well as work on improving teixobactin’s molecular structure to solve several practical problems. One they hope to address, for example, is its poor solubility; another is that it isn’t readily absorbed when given orally—as is, it will have to be administered via injection.

While Lewis predicts that the drug will not be available for at least five years, this new method offers a promising new avenue of drug discovery. Nathan agrees, though he cautions it’s too soon to claim victory. The message of this recent finding, he said, “is not that the problem of antibiotic resistance has been solved and we can stop worrying about it. Instead it’s to say that there’s hope.”

Photo credit: NIAID

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