Trillions of microbes in the intestine aid human health, including digestion of breast milk, breaking down fiber and helping control the immune system. However, Antibiotic Treatment is known to disrupt the community structure of these microbes -- 500 to 1,000 bacterial species that have a mainly beneficial influence.
A study at the University of Alabama at Birmingham now has tracked this disruption at the level of a Strain of microbes replacing another strain of the same species in 30 individuals -- all of them young, healthy adults who would be expected to have stable microbial communities.
The UAB study used bioinformatic toolsto analyze a previously described study of 18 individuals who had been given a single antibiotic, cefprozil, for a week. Their fecal samples were collected at pre-treatment, at the end of antibiotic treatment and at three months post-treatment. The UAB study also analyzed previously described data of 12 individuals who were given a combination of three antibiotics -- meropenem, gentamicin and vancomycin -- for four days. Their fecal samples were collected at pretreatment; at end of treatment; and at four, 38 and 176 days post-treatment. Six control individuals who did not receive antibiotics were also analyzed.
In general, the UAB researchers found that strains of the 10 most abundant species remained stable in controls. In the single antibiotic treatment individuals, 15 of 18 individuals had transient new strains post-treatment that, in turn, were replaced by the original strain by three months post-treatment.
In contrast, the triple-antibiotics individuals showed a significant increase of new strains that persisted as long as six months after treatment, as compared to the single antibiotic and the control individuals. Furthermore, the fraction of transient strains was also significantly higher in the multiple antibiotics individuals. This suggested a long-term change to an alternative stable microbiome state, Morrow says. These changes were not due to a difference in growth rates.
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Posted by Dr. Tim Sandle, Pharmaceutical Microbiology
