Let’s say you have a problem at your hospital with carbapenemases.
One of the obvious solutions would be to reduce the use of carbapenems in order to reduce the selection pressure.
However even if you stopped carbapenem usage altogether the carbapenemases would not necessarily disappear…
This is because carbapenemases are often plasmid borne, and there are often antibiotic resistance genes for other antibiotics, e.g. A, B & C sitting on the same plasmid.
As long as the (high) usage of antibiotics A, B & C continued then the selection pressure would favour plasmid retention in the bacterium, and thus allowing persistence of the carbapenemase.
Selection pressure by proxy.
Are we all doomed?
A gene expressing one antimicrobial resistance determinant comes at an energy cost to a bacterial cell. Plasmids expressing multiple resistance genes come at even more energy cost to the cell. You can be sure if it did not need the plasmid to ensure its survival, it would be mercilessly dumped, and probably sooner rather than later.
Therefore even a modest reduction in carbapenem usage, along with a reduction in antibiotics A, B & C may go a long way to solving your problem.
Advances in molecular methods and whole genome sequencing over the next decade will mean that it will become much easier to work out exactly which resistance genes are contained in the plasmids circulating in our local hospitals, and anti-microbial stewardship can thus be optimised accordingly.
Sounds space age?
Not really, we just need to be aware that resistant bacteria are very smart in an evolutionary sense, and we need to stay alert, and not give them the niches they are looking for…
Illustration courtesy of www.biologyfun.blogspot.co.nz