Sensationalist headlines predict the end of the world as killer bacteria wipe out the human race, unstoppable in their march thanks to resistance acquired from exposure to antibiotics that are flippantly over-used by hypercondriacs.
The theory that is used to justify these headlines is that more we use antibiotics, the more quickly bacteria evolve to resist them, and the faster the drugs stop working. Basically, an arms race where biology is pitted against technology, and where biology will be the inevitable winner as technology eventually runs out of ideas.
But is this really the case?
Well, we may indeed end up being wiped out by an unstoppable killer bacteria, but if that is our fate then it is our fate despite the use of antibiotics, not because of it.
One of the worst offenders is Dame Sally Davies, England’s chief medical officer who encourages the development of new antibiotics on the one hand (which is good), but who champions the training of NHS staff so that they “have the skills, knowledge and training to prescribe and administer antibiotics appropriately” – as though the prescription or non-prescription of these drugs makes any difference whatsoever to the spread of these “superbugs”.
Mutations are random and they happen all the time. The mutation that allowed early Europeans to produce lactase which enabled us to process lactose in milk was good. Mutations that turn previously healthy cells cancerous are bad. Neither mutation was caused by antibiotics.
The Lederberg experiment
In 1952, Esther and Joshua Lederberg set up an experiment. They hypothesised that antibiotic resistant strains of bacteria surviving an application of antibiotics had the resistance before they were exposed and not as a result of the exposure. This was what they did:
So the penicillin-resistant bacteria were present in the population before they encountered penicillin and did not evolve resistance in response to exposure to the antibiotic. Similarly, the bacteria that was not immune before exposure on the original plate continued not to be immune after exposure on the penicillin plate.
So instead of causing bacteria to become immune to antibiotics, what these drugs do is expose the already-resistant bacteria by destroying the organisms that are not immune, leaving only the resistant ones behind.
Therefore, preventing or slowing down the use of antibiotics will not prevent bacteria from becoming resistant to them as a given cell is either already resistant or is destined to become resistant due to random mutations that would occur both in the presence and absence of the drug.
Instead, the outcome of using antibiotics is that a resistant organism may thrive in a host if its non-resistant variant – effectively its competition – is wiped out by an antibiotic. That is, although the resistant organism might have existed within the host in any case, without antibiotics it may have been limited in concentration by the competition for resources from its non-resistant variants. With that competition removed, it is free to expand at will and is therefore more likely to be the variant passed on to someone else.
But whether this outcome is really a problem is debatable, because it’s impossible to know whether a variant that was wiped out by a given antibiotic today wouldn’t have gone on to evolve into something much worse than the resistant variant tomorrow. It’s all purely down to chance.