Antibiotics work by killing not only the harmful bacteria, but also the beneficial bacteria. It is relatively common for antibiotics to lead to gut infections that arise because potentially pathogenic bacteria are no longer kept in check by the beneficial microbes that inhabit the gut. “Antibiotics open the door for these pathogens to take hold. But how, exactly, that occurs hasn’t been well understood,” noted Justin Sonnenburg, PhD, lead author of a recent study published in the journal Nature  that examined more closely just how antibiotics put us at risk for intestinal infections.

The cells that line the inside of the intestine are covered in a mucous layer that is made up of a variety of sugars that can be used by gut microbes as food. “Our gut microbes have become very adept at eating mucus,” Sonnenburg said.

The researchers used an animal model to introduce a single bacterial strain—Bacteroides thetaiotamicron, known to be an important constituent of a healthy gut—into the digestive tracts of mice that were otherwise germ free, or without microbes, a similar state as when antibiotics are administered. B. theta is known to break off two particular sugars from the mucosal lining—sialic acid and fucose, little-known sugars that are produced in the gut. B. theta does not use the sugars, but other bacteria can use them once they are broken off.

The researchers introduced either Clostridium difficile or Staphylococcus typhimurium, both known pathogens, into the guts of these mice, knowing that both of these bacteria feed on sialic acid. Each of these pathogenic bacteria greatly increased in number. “The bad guys in the gut are scavenging nutrients that were liberated by the good guys, who are casualties of the collateral damage incurred by antibiotics,” said Sonnenburg. “Antibiotics cause our friendly gut bacteria to unwittingly help these pathogens.”

“We believe that bacterial pathogens in the gut cause disease in two steps,” he continued. “Others have shown that once these pathogens attain sufficient numbers, they use inflammation-triggering tricks to wipe out our resident friendly microbes—at no cost to the pathogens themselves, because they’ve evolved ways to deal with it. But first, they have to surmount a critical hurdle: In the absence of the inflammation they’re trying to induce, they have to somehow reach that critical mass. Our work shows how they go about it after a dose of antibiotics. They take advantage of a temporary spike in available sugars liberated from intestinal mucus left behind by slain commensal microbes.”

Sonnenburg thinks that this research may someday lead to drugs or, alternately, probiotics, developed to inhibit the release of these sugars when taken along with an antibiotic. More research is needed, but this is an interesting study that helps us get closer to understanding how our gut balance is affected by antibiotics.