Modelling environmental antibiotic-resistance gene abundance: A meta-analysis

Abstract

The successful treatment of infectious diseases heavily relies on the therapeutic usage of antibiotics. However, the high use of antibiotics in humans and animals leads to increasing pressure on bacterial populations in favour of resistant phenotypes. Antibiotics reach the environment from a variety of emission sources and are being detected at relatively low concentrations. Given the possibility of selective pressure to occur at sub-inhibitory concentrations, the ecological impact of environmental antibiotic levels on microbial communities and resistance levels is vastly unknown. Quantification of antibiotic-resistance genes (ARG) and of antibiotic concentrations is becoming commonplace. Yet, these two parameters are often assessed separately and in a specific spatiotemporal context, thus missing the opportunity to investigate how antibiotics and ARGs relate. Furthermore, antibiotic (multi)resistance has been receiving ever growing attention from researchers, policy-makers, businesses and civil society. Our aim was to collect the limited data on antibiotic concentrations and ARG abundance currently available to explore if a relationship could be defined in surface waters, sediments and wastewaters. A metric of antibiotic selective pressure, i.e. the sum of concentrations corrected for microbial inhibition potency, was used to correlate the presence of antibiotics in the environment to total relative abundance of ARG while controlling for basic sources of non-independent variability, such as country, year, study, sample and antibiotic class. The results of this meta-analysis show a significant statistical effect of antibiotic pressure and type of environmental compartment on the increase of ARG abundance even at very low levels. If global environmental antibiotic pollution continues, ARG abundance is expected to continue as well. Moreover, our analysis emphasizes the importance of integrating existing information particularly when attempting to describe complex relationships with limited mechanistic understanding.

Keywords: Antibiotic pollution; Antibiotic resistance; Environmental risk; Gene abundance; Linear mixed-effects models.