Justin Sonnenburg, PhD, assistant professor of microbiology and immunology at the Stanford University School of Medicine and the senior author of the study said that the study specifically supports the suggestion that our resident microbes hold pathogens at bay by competing for nutrients.
The particular nutrients Sonnenburg's team looked at were sialic acid and fucose, a couple of members of the sugar family.
Researchers experimented on mice that had been born and bred in a germ-free environment. These mice's guts were devoid of bacteria, unlike normal mice, which harbour hundreds of bacterial species in their bowels just as humans do. Into these germ-free mice the investigators introduced a single bacterial strain, Bacteroides thetaiotaomicron.
In a series of separate experiments, the investigators introduced either S. typhimurium (a salmonella strain) or C. difficile in the B. theta-loaded experimental mice.
Introducing one friendly and one pathogenic bacterial strain into the guts of the formerly germ-free mice, the scientists were able to show that, in this approximation of an antibiotic-decimated gut-microbe ecosystem, the levels of sialic acid soared to high levels in the absence of a complete set of intestinal microbes that ordinarily would keep those levels from climbing.
In the presence of these sugars and absence of competition, both pathogens were able to replicate more rapidly. B. theta generated a sialic-acid surplus that, in the absence of the other hundreds of normal bacterial species, were bequeathed to the pathogenic strains.
When the researchers investigated the effects of antibiotics on mice with normal intestinal ecosystems, they saw the same sialic-acid spike- and pathogen population explosion- in the wake of the carnage.
The study was published in journal Nature.
--ANI (Posted on 02-09-2013)