The spread of resistant bacteria and resistance genes depends on different factors but the major pressure is
Fig. 3. Long-term impacts of a 7 day clindamycin administration on the human faecal microbiome. Faecal samples were collected before antibiotic administration (day 0), on the last day of antibiotic administration (day 7), 2 weeks after cessation of treatment (day 21), subsequently every 3 months for 1 year post-administration, and 18 months and 2 years postadministration. (a) Correspondence analysis (COA) plots of T-RFLP fingerprints over time from one subject exposed to clindamycin, showing shifts in the dominant members of the bacterial community (i) and the Bacteroides community (ii). (b) Normalized relative gene abundance of three specific erm genes compared with day 0. Representatives of one clindamycinexposed subject (i) and one non-exposed subject (ii) are shown. (c) Bacteroides isolates from one clindamycin-exposed subject that were clonally typed using Rep-PCR. Bars with hatched lines represent clones susceptible to clindamycin and bars with solid lines represent resistant clones. This figure is adapted from a previous paper (Jernberg et al., 2007).
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antibiotic usage. Additional factors include the ability of resistant strains to colonize the gut, their relative fitness, mutation rates and efficiencies of horizontal transfer of resistance genes. Under the selective pressure of an antibiotic, a bacterium that acquires a resistance gene is often conferred with a benefit. When this selective pressure is no longer present, the resistant strain could have a lower fitness compared with its susceptible counterpart. However, this less competitive clone might compensate for this loss of fitness by acquiring compensatory mutations. The review by Andersson & Hughes (2010) discusses the fitness costs and mechanisms by which the bacterium can reduce these costs.