Sorry, kids. You may be doing your best at jamming your finger up your nose, digging tirelessly. But it seems scientists are the ones that have struck gold.
Sifting through the bacteria that inhabit our cavernous snouts, researchers came up with one that produces a new antibiotic—an antibiotic unlike any other bacteria-busting drug known to modern medicine. That prized chemical nugget can kill off Staphylococcus aureus strains, including the dastardly methicillin resistant kind called MRSA, plus other drug-resistant foes. Though it's still unclear how exactly the new drug slays nasal rivals, scientists are hopeful that the compound will be useful in treating deadly MRSA infections and even clearing out S. aureus from the nose before it has a chance to cause an infection.
“Nobody has found something like this before,” Bernhard Krismer, a bacteriologist at the University of Tübingen in Germany and a lead scientist for the research, said in a press briefing. The drug, along with its bacterial maker, have “a huge impact on the composition of the microbiota,” Krismer added. The full results of the nasal excavation appear in the July 28 issue of Nature.
Krismer and colleagues started mining for new antibiotics in the nose based on the simple fact that those booger-crusted cavities are barren landscapes for germs. Any wannabe nasal colonizers that periodically blow into schnozville have to put up quite a fight for scant resources. And some of the best weapons bacteria have to fight each other are antibiotics. So the researchers filtered through all of the staph isolates known to take up residence in the human nose, growing them all in the presence of S. aureus. That’s when they noticed S. lugdunensis, which clearly elbowed out S. aureus when they shared a petri dish full of food.
S. lugdunensis seemed to be making something that pushed back S. aureus. To figure out what it was, the researchers made a pile of mutant versions of S.lugdunensis, each one having a different segment of its DNA broken. The researchers hoped to independently break each and every bit of the bacteria’s genome to find the stretch responsible for the S. aureus*-slaughtering chemical. Examining all the mutants, they found one that could no longer fight off S. aureus, leading them to a group of broken genes that looked a little like an antibiotic-encoding cluster. With a bit of genetic engineering, the researchers created a S. lugdunensis strain that mass-produced whatever that group of genes held the blueprints for—an antibiotic they then isolated and dubbed lugdunin, it turned out.
Lugdunin has a chemical structure unlike any other antibiotic researchers had seen, an unusual cyclic peptide that includes five amino acids. But however weird-looking, the chemical did great in lab tests at killing off S. aureus and other drug-resistant human pathogens, including Enterococcus isolates resistant to a last-resort antibiotic called vancomycin.
On the wounded backs of shaved mice, a smear of lugdunin could fight off S. aureus, keeping it from causing an infection—except in two mice that apparently licked off all their lugdunin. When the researchers put S. lugdunensis and S. aureus together in the noses of rats, S. lugdunensis won out.
Those results echoed what researchers found when they peered into the dark crannies of 187 hospital patients’ noses. Though less than 10 percent of patients had S. lugdunensis in their noses, the rate of S. aureus colonization in those patients was 5.9 times lower than patients that didn’t have S. lugdunensis in their nose.
Based on the results, the researchers are optimistic that lugdunin could not only be used to treat MRSA and other infections, but that S. lugdunensis could be used as a probiotic. If people purposefully added the drug-pumping bug into their noses, they could keep S. aureus from ever getting a foot in the door. This might be really helpful because about 30 percent of the population naturally carries around S. aureus in their noses. While S. aureus only causes infections when the opportunity strikes, carrying it around certainly increases a person’s chances of getting an infection.
Scientists say the study also suggests that our microbiomes—the microbes that share our bodies with us—may be an untapped spring of new antibiotics. Or, in more drug development terms, they “might serve as drug-discovery leads,” according to microbiologist and antibiotic researchers Kim Lewis and Philip Strandwitz of Northeastern University, who were not involved in the study. Such new antibiotics are desperately needed to combat that rising number of highly drug-resistant bacteria.
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Originally Posted by Carlybee
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