An interesting new Italian study has identified the mcr-1 gene, a plasmid-mediated colistin resistance gene, in 8% of environmental Enterobacteriaceae isolates. This suggests that environmental Enterobacteriaceae and perhaps even environmental surfaces themselves could be important reservoirs in the spread of mcr-1 and colistin resistance.
Plasmid-mediated colistin resistant genes are not common everywhere – in one of our recent studies in London, we found no mcr-1 in sight but plenty of colistin resistance due to various chromosomal mutations. However, in other parts of the world, the prevalence of mcr-1 colistin resistance genes in Enterobacteriaceae is alarming – up to 2% of human isolates and up to 10% or more in animal isolates (quoting figures from this paper). What is driving the spread of these plasmids? The relatively high prevalence in animal isolates suggests a flow of plasmids from animal to human populations. But what is the role of surfaces and environmental Enterobacteriaceae in the spread of these plasmids?
The study team went fishing for mcr-1 in an existing library of 300 environmental Enterobacteriaceae collected from 8 Italian hospitals in 2016-17. 25 (8.3%) of these bacteria harboured mcr-1. I’m slightly confused as to why Acinetobacter and Pseudomonas appear in the list of Enterobacteriaceae (because they’re not). But that nerdy technicality aside, these findings suggest that environmental Gram-negative bacteria can be a reservoir for mcr-1.
We know that the inanimate environment is a breeding ground for antibiotic resistance genes; it’s a meeting place for clinical and non-clinical isolates. But we need more work to understand the relative importance of animal vs. humans vs. environmental reservoirs for mcr-1 and other colistin resistance determinants.