Antibiotic Resistance: The Final Frontier

Forget Donald Trump, here is a nightmare scenario that is little thought about: you pick up an infection, perhaps after routine surgery or childbirth, and the doctors attempt to treat it with antibiotics. They go through them one by one. Nothing works. With alarm, the doctors realise that the bacteria infecting you is resistant to every antibiotic they have available. You will either fight it off on your own or die.

Most have heard of antibiotic resistance in the form of MRSA, methicillin-resistant Staphylococcus aureus, the bacteria which particularly plagues hospitals. Like its name suggests, MRSA is a bacteria which is resistant to the antibiotics which would normally treat such a staph infection. The problem with antibiotic resistant bacteria is that they can spread quickly, replacing the antibiotic susceptible members with rapid ease and making treating patients that much more difficult, or in the extreme case mentioned above, impossible.

Antibiotic resistance is a result of natural selection. Many would have heard about natural selection in school; when you set up an environment in which only certain members of the species can survive and reproduce, in the end you end up those selected and hence fitter members for that environment. In this case, the antibiotic is doing the selecting and the resistance allows particular bacteria to survive. Now, the antibiotic does not cause the resistance, it only selects for mutants in the population which can survive in its presence. A specific and well-known example is the enzyme called TEM-1 β-lactamase, which breaks down the antibiotic ampicillin. Bacteria with this enzyme will be resistant to the antibiotic ampicillin. The enzyme cannot usually break down so-called third generation cephalosporin antibiotics such as cefotaxime. However, mistakes, or mutations, occur every time a bacteria replicates and mistakes in the gene which encode the TEM-1 β-lactamase have an impact on the enzyme’s function. Usually, these mutations would be present in the general genetic diversity of the population, and as long as ampicillin is around then either the normal type outcompetes the mutants or mutants who can degrade ampicillin better than the normal type will reign supreme. However, now you start treating the patient with cefotaxime and since most of those bacteria carry the TEM-1 β-lactamase which cannot degrade it, they will die. The patient starts to feel better. But, there are mutant bacteria present which carry mutations in TEM-1 β-lactamase which allows them to degrade cefotaxime. The introduction of the antibiotic cefotaxime has now selected for these mutants and they replicate to become the dominant bacteria in the population.

There are aggravating factors which evidently speed-up the acquiring of resistance. Giving out antibiotics when they are not needed, such as in the case of colds or flu, or using antibiotics to fatten-up livestock will create opportunities to select for mutants which are resistant to that antibiotic. Even if they are not directly disease-causing, many bacteria carry antibiotic resistance genes on small circular DNA called plasmids which can be shuttled among many species of bacteria, the disease-causing ones included. We only have time to play with and yet we appear happy to squander that away as mentioned in the documentary Resistance.

We are in an arms race with disease-causing bacteria. The only weapons we have are new antibiotics which have to be continuously found before resistance accrues. It is incredibly shocking that we leave such an important endeavour as antibiotic discovery to pharmaceutical companies who spend so little on it, mostly due to its much smaller profit margins. There are alternative therapies such as phage therapy, using viruses which infect bacteria but not our eukaryotic cells, to kill disease-causing bacteria. Again, this does not negate the Darwinian war we are locked into. Mutants will eventually arise which will resist infection and destruction by said phages.

We need a reliable source of funding to find treatments for bacterial infections, whether antibiotic discovery or alternative treatments or a combination. This is too important to be left to the whims of the market place. After all, would you wish to be the one told by doctors that there is nothing to be done except wait and see?


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