The number of MRSA infections is among the highest of all antibiotic-resistant threats. The Centers for Disease Control and Prevention estimates more than 80,000 invasive MRSA infections and more than 11,000 related deaths occurred in 2011, the last year for which data is available.

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The scientists said their find represents the first known example of a new class of antibiotics. That’s particularly welcome news given the urgent global problem of antibiotic-resistant superbugs and the dwindling arsenal of drugs to replace ones that no longer work.

Until now, conventional antibiotic discovery has focused on looking for compounds from bacteria living in dirt. But identifying novel compound structures from soil microbes has been getting harder. The new research, from Andreas Peschel and colleagues at the University of Tübingen, suggests that the immense variety of microorganisms living in the human body, particularly in the nose, may be a potential source of new antibiotics.

“These organisms, or the antibiotics they produce, might serve as drug-discovery leads,” Kim Lewis of Northeastern University in Boston wrote in an accompanying commentary. Lewis, who was not involved in the study, directs Northeastern’s Antimicrobial Discovery Center and was part of the team that last year identified teixobactin, a new class of antibiotic in dirt that fights bacteria in a way that prevents bacteria from becoming resistant to it.

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The German researchers said lugdunin also is not prone to causing S. aureus to develop resistance. They are not exactly sure how it works, and clinical development is many years away and will require partners from the pharmaceutical industry, they said.

It’s possible that lugdunin disrupts the target bacteria’s cell membranes, but that could also make it harder to develop as a drug for injection because of its potential for also disrupting animal membranes, Lewis wrote.

Asked during a media briefing Tuesday why others had not looked within the human microbiome for similar leads, Peschel said that perhaps they looked in the wrong places.

“Or maybe we are just lucky,” he said.

Bacteria that live in the human body number more than a thousand species. Many compete for space and nutrients. Perhaps the pathogen residing in the nose developed the mechanism to produce an antibiotic that knocks out other bacterial species, allowing it to survive in a “nutrient-poor” environment filled with “soggy fluids,” Peschel said.

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Microbiologist Richard Novick of the New York University School of Medicine, who is one of the leading experts on S. aureus and was not involved in the latest research, called the findings “enormously interesting.” It’s long been known that bacteria make compounds — called bacteriocin — that attack or inhibit other bacteria in such places as the human intestine, he said.

“But no one thought about bacterial warfare in the nose,” Novick said. “That’s novel.”

This nostril-dwelling bacterium is also a species of Staphylococcus bacteria called S. lugdunensis. It’s a nasty pathogen in its own right. While the compound it produces “may be fantastic,” Novick said, “you wouldn’t want to colonize people with Staph lugdunensis because it causes lots of infections.”

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The German researchers examined nasal swabs from 187 hospitalized patients and found that of the people who carried S. lugdunensis, only about 6 percent also carried S. aureus, compared with 34 percent in individuals without the nasal bacteria. Those differences are evidence that bacteria in the nose help keep S. aureus at bay, according to the study.

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S. lugdunensis is present in only about 10 percent of humans, while S. aureus is found in about 30 percent of the population. There are probably more antibiotics yet to be discovered that may explain why the remaining 70 percent of humans do not carry the S. aureus bacteria, Lewis wrote.

In testing the lugdunin on mice that had skin infections caused by S. aureus, the researchers said some of the infections were completely cleared and others dramatically reduced. In two mice, the infection was not cured.

“Some mice just licked off the antibiotic,” Peschel said.