It is not uncommon that scientists, especially researchers active within the environmental field, view antibiotic resistance genes (ARGs) as pollutants (e.g. Pruden et al. 2006). While there are practical benefits of doing so, especially when explaining the threat of antibiotic resistance to politicians and the public, this generalization is a little bit problematic from a scientific view. There are several reasons why this view is not as straightforward as one might think.

The first is that ARGs does not spread the same way as pollutants do. ARGs are carried in bacteria. This means that ARGs cannot readily be transferred into, e.g. the human body by themselves. They need to be carried by a bacterial host (ARGs present on free DNA floating around is of course possible, but likely not a major source of ARG transmission into new systems). Therefore, when we find resistance genes in an environment, that is an extremely strong indication of that we also have resistant bacteria. Also, finding ARGs is not necessarily an indication of high levels of antibiotics, as the resistance genes can remain present in the bacterial genome for extended periods of time after exposure (Andersson & Hughes 2011).

The second reason why ARGs should not be viewed as pollutants is that they are not. If anything, the ARGs contribute to the resilience of the ecosystem towards the actual toxicants, which are the antibiotics themselves. Having a resistance gene is an insurance that you will survive antibiotic perturbations. Calling ARGs pollutants just deflects attention from the real problem to nature’s response to our contaminant.

What we have to do is not to try to defeat the resistance itself, but to try to minimize the spread of it. This means that we need to constantly monitor our usage and possible emissions of antibiotics and try to reduce risk environments as much as possible. Emissions from sewage treatment plants (Karthikeyan & Meyer 2006; Lindberg et al. 2007), hospitals (Lindberg et al. 2004), production facilities (Larsson et al. 2007; Fick et al. 2009) and food production (Davis et al. 2011) are obvious starting points, but we need to continuously monitor sources of antibiotic pollutions. Of course, this is only my view of the problem, but I believe that while the problem for our society lies within the resistance genes, the cause lies within the actual pollutants – the antibiotics we use and abuse.

References

  1. Andersson, D.I. & Hughes, D., 2011. Persistence of antibiotic resistance in bacterial populations. FEMS Microbiology Reviews, 35(5), pp.901–911.
  2. Davis, M.F. et al., 2011. An ecological perspective on U.S. industrial poultry production: the role of anthropogenic ecosystems on the emergence of drug-resistant bacteria from agricultural environments. Current Opinion in Microbiology, 14(3), pp.244–250.
  3. Fick, J. et al., 2009. Contamination of surface, ground, and drinking water from pharmaceutical production. Environmental toxicology and chemistry / SETAC, 28(12), pp.2522–2527.
  4. Karthikeyan, K.G. & Meyer, M.T., 2006. Occurrence of antibiotics in wastewater treatment facilities in Wisconsin, USA. The Science of the total environment, 361(1-3), pp.196–207.
  5. Larsson, D.G.J., de Pedro, C. & Paxeus, N., 2007. Effluent from drug manufactures contains extremely high levels of pharmaceuticals. Journal of hazardous materials, 148(3), pp.751–755.
  6. Lindberg, R. et al., 2004. Determination of antibiotic substances in hospital sewage water using solid phase extraction and liquid chromatography/mass spectrometry and group analogue internal standards. Chemosphere, 57(10), pp.1479–1488.
  7. Lindberg, R.H. et al., 2007. Environmental risk assessment of antibiotics in the Swedish environment with emphasis on sewage treatment plants. Water research, 41(3), pp.613–619.
  8. Pruden, A. et al., 2006. Antibiotic resistance genes as emerging contaminants: studies in northern Colorado. Environmental Science & Technology, 40(23), pp.7445–7450.