PLoS One published a paper by Walsh and Duffy that reports the following:
- Culturable soil bacteria are all antibiotic resistant at the > 20 ug/ml level
- 80% are multi-drug resistant
- Efflux pumps and innate resistance are the predominant mechanisms
- The genes and enzymes responsible for clinical resistance don't seem to be in evidence
So it appears at first glance that soil is not acting as a reservoir of antibiotic resistance genes waiting to be recruited by clinical strains. Given that nearly all clinical antibiotics are derived from soil microbes, this is something of a surprise. It would have been a nice tidy story if Walsh and Duffy had shown that we get antibiotic resistance from the same place we get antibiotics.
So where do resistance genes come from? It seems unlikely that they could have arisen de novo in the clinic in the last 70 years - it is much more plausible that there is a well-established environmental reservoir that serves as a resistance bank from which clinical strains have been making withdrawals.
The best bet is still the soil, as that's where the antibiotics are. Walsh and Duffy did not want to make any assumptions about enzymes or genes, so they ran a phenotypic screen: they exposed soil bacteria to antibiotics and asked if they still grew as well in their presence as they did in their absence. The weakness of this approach, as the authors acknowledge, is that only about 1% of bacterial strains will grow as pure cultures under lab conditions. The rest require more complex conditions for growth, most especially including other microbes that form a community. It's these community-loving bacteria - the 99% - that are the most like source of current and future resistance genes.
For more on the sources of resistance in the environment, see this paper
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