I came to ECCMID 2017 with a very specific question: do we need to think beyond ‘same-bug-same-gene’ horizontal transmission from a practical IPC view point in order to address the threat of IPC? The answer, unfortuantely, is yes!
This is a summary of my take-home messages from a session on the threat of horizontal antimicrobial resistance plasmid transmission delivered expertly by Robeto Melano, Amy Mathers, Surbhi Malhotra-Kumar, and Henrik Hasman.
- Plasmids are seriously cool bits of kit – any engineers reading this would swoon over their simple, effective design, which allow independent replication and recombination in response to various triggers.
- The idea of inter-species plasmid transfer of AMR genes isn’t new, and was investigated in the 1970s regarding gentamicin-resistance.
- We now have the molecular tools to test the hypothesis of whether inter-species plasmid transfer occurs – all you need is a laptop, a minION sequencer (and a purified plasmid).
- There are several convincing individual case reports and small outbreaks where it is clear that inter-species plasmid transfer of AMR genes has occurred in Gram-negative bacteria. In one plasmid outbreak, multiple carbapennemases were dealt out like a pack of cards to multiple Enterobacteriaceae species from a single index patient. More broadly, the population structure of KPC-producing K. pneumoniae is consistent with horizontal gene transfer
- However, the picture is not straightforward:
- It is not clear how similar a plasmid has to be to be considered a smoking gun of horizontal gene transfer! Multiple plasmids are often involved simultaneously, which have a habit of recombining!
- Complex bacterial factors are at work. Amy Mathers said “It seems like something is wrong with this Kleb pneumo – it keeps hoovering up KPC plasmids”. This could be bacteria adapting to adopt plasmid DNA more efficiently to gain a selective advantage!
- Environmental factors are at play too: temperature and substrate affect bacterial transduction rate.
- The inanimate environment is likely to be one of the places where plasmid ‘dealing’ happens.
- The interventions that work to prevent ‘same-bug-same-gene’ horizontal transmission may not prevent plasmid transmission.
It seems that plasmid outbreaks are upon us. So, I think it is time for us to look at our CPE epi curve with fresh eyes to see whether we are looking at a plasmid outbreak. Also, we need to find ways to track and interrupt plasmid transmission going forwards.
Image: addgene.
Excellent blog of talks that I missed. This (https://www.ncbi.nlm.nih.gov/pubmed/24626209) was a clear example of a plasmid-outbreak in the Netherlands (see also: https://www.ncbi.nlm.nih.gov/pubmed/26485437) in which screening was actually directed towards identifying the OXA48 gene (rather than the bug in which it resided). We also learned dat about 1% of the Rotterdam population harbors Schewanella (with chromosome-based OXA48).
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This may also explain why measures and disinfectants used to kill germs (e.g. in sinks) do not work against pieces of DNA (plasmids).
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