Antibiotic Resistance: The Real War on Drugs


Are we at risk of a disaster movie becoming reality?

Almost all of us have required antibiotics at some point in our lives, but do we really understand what they do? How they work? More importantly, do you know that we could be much closer to losing their amazing protective power altogether? To explain why, let me ask you a question…

Do you remember a time before flat screen TVs? How amazing they were when they first arrived? How about mobile phones, or the internet?

Over time, we adjust and become used to new things. Imagine going back to a big, chunky TV now, or having to wait until you got home or to a phone box to ring someone. Time has a habit of making us forget how difficult things used to be, generating a complacency that can put that more comfortable way of life at risk. The same is true with medicine.

Antibiotics, in one form or another, have existed since the early 20th century. The most prominent early example is a man called Alexander Fleming’s apparent “accidental” discovery of a well-known antibiotic. The story goes that Fleming left out a small dish of Staphylococcus bacteria (often a cause of food poisoning) on his lab bench before leaving for the summer, where it was by chance contaminated by mould. When Fleming returned, he investigated further, and found that the mould was stopping the growth of the bacteria by breaking them down. The mould turned out to be Penicillium notatum, the byproduct of which Fleming branded the now famous ‘Penicillin’.

So let your flatmates//spouse/pets know that if you leave plates of unfinished food on the kitchen top for weeks to gather mould, you are actually attempting to discover a new and potentially lifesaving treatment. Do not be perturbed by the modern pharmaceuticals industry either. Sure, they have hundreds of millions of pounds to potentially pour into researching new antibiotic treatments, but there is not as much progress there as you’d expect. In fact, there have been almost no new antibiotics produced in the last 30 years. Why?


“I’ll throw it away first thing tomorrow, I swear!” – The words of a genius biologist.

The worrying answer is that antibiotic use is seen as a big risk for healthcare professionals and policy makers. There is not much money to be made in something that hardly ever gets used. But why is antibiotic use so sparse?

Throughout modern medicine, antibiotics efficiency in dealing with bacterial infection has never been in question, but with extended use on such a large scale, a biological battle began to rage, unseen by most. A battle of resistance.



A rare picture of the bacteria known as ‘flagstaph-ylococcus’

Antibiotics, from penicillin to the most recently discovered, were becoming non-functional, and the battle still rages on today.

How did this happen? Surely what killed bacteria 50 years ago should have exactly the same effect then as it does now?

For an explanation, we need to go to the frontlines of the war: the inside of your body. Like actual war, the technology has progressed, and the humble penicillin takes on new shapes, with a whole family of antibiotics to its name (with well-known examples including amoxicillin and ampicillin.)


“Fight not to scale, as you’ll see soon”

Bacteria are the main cause of infection in broken skin, mainly because they’re already all over your skin before it breaks (don’t think about it too much). They have 2 layers of protection: an outer thick cell wall, made of proteins known as peptidoglycans, as well as a thin and wobbly inner cell membrane. The wall gives them a solid shape whilst also protecting from damage. It is a key part of their structure, without which the bacteria will die.


There are other smaller bits of the cell wall, but peptidoglycans are the thing that gives it strength and structure.

The reason the penicillin family of antibiotics has been so successful in treating these sorts of infections is that it can block the production of this cell wall. So how does it do this?

Here is where the art of microbial war becomes interesting. Penicillin does not attack this very sturdy cell wall head-on, instead, it sneaks into the bacteria itself, behind enemy lines, where it finds an enzyme known as transpeptidase. These enzymes are the builders and repairers of the cell wall. Think of them as the ones who put the mortar between the bricks that are peptidoglycans.


“It’s transpeptidase time” just doesn’t have the same ring to it.

Penicillin binds to these transpeptidases, blocking them from being able to maintain the walls strength as the bacteria grows. This results in a breakdown of the wall, and a rather embarrassed and weak bacteria.



When you take penicillin, you’re sending waves and waves of these medical molecules to fight back the bacterial infection. After a few weeks, all that’s left are a few gutsy bacteria, they may be the most resilient, but even they cannot outlast the offensive power of penicillin much longer.



“Where are our reinforcements?” “Why hasn’t the general sent any?”

The general here, of course, is you. Every year thousands of people leave their antibiotic courses unfinished in the UK. Even though there are not enough bacteria for you to feel ill, they still exist inside you, and you’ve just given them the respite they need.

So why is this a problem? There are only a few bacteria left, and you don’t feel ill anymore! If it starts to get bad again you can just go back to the doctor for more medicine if you get ill, right? Unfortunately not. If the disease returned a month or so later, you may find the same treatment will not be as effective.

It turns out that the few remaining bacteria the first time had survived because they, out of all the other bacteria, were the only ones to possess a molecule called B-lactamase, which breaks down penicillin, keeping the transpeptidase builders safe.


I did not want to show graphic molecule on molecule violence, so use your imagination to what happens to penicillin after this.

Not only that, but this time all of the bacteria, not just the strongest few, have this ability. How can this be?

The issue comes from the way bacteria multiply. They divide. If the penicillin course remains unfinished, all bacteria in the infection will then be children of the remaining penicillin-breaking bacteria. Bacteria that have already proved their resistance and resilience. Some bacteria can divide into two every half an hour, growing from just a single cell to over a million in only twelve hours.


The bacteria don’t actually get smaller, its just the only way to fit them all in the picture.

This is obviously a problem on an individual level, but the resistance dilemma does not end there. Bacteria do not only transfer their ability when they divide, but can also transfer this ability to other nearby bacteria, even if they aren’t the same species. This is because they have a small circle of DNA encoding genes for this resistance. This little genetic instruction manual is passed between close-by bacteria, spreading the knowledge of how to prevent the damage caused by penicillin.


Never has a book club been so terrifying.

The combination of dividing bacteria and this trading of information means that anywhere with a high number of people, antibiotics and infectious diseases is going to be on the front line of this resistance war. Hospitals now have to fight against strains of bacteria that are resistant not just to penicillin, but to many different drugs. MRSA, the super-bug, is short for Methicillin-Resistant Staphylococcus Aureus, and has been a threat to patients both hospital bound and visiting for years. It is the stronger and harder version of the bacteria you see fighting the penicillin above. Over 44,000 people die of sepsis a year in the UK (more than lung cancer), and many of these are due to antibiotic-resistant infections.

This is why there are so many guidelines in place to help combat this growing resistance. Antibiotics are only given when absolutely necessary, and only in bacterial infections. If you have a cold or cough, these may be viral infections. Viruses hide inside our own cells, reproducing there, so antibiotics will have no effect at all. It would be like treating a splinter with a bandage, you aren’t going to get anything out and it’ll most likely just make things worse.

In terms of what you can do, it is advised that you take all of the medication the doctor gives you, and especially for the length of time the medical professional states. This is to ensure you finish off the strongest of the bacteria and avoid creating even more resistant strains. Feel free to discuss why this is with your doctor, they’re normally more than happy to talk about it.

There is another problem, not just outside of hospitals, but outside of humans altogether. Livestock. The World Health Organisation (WHO) states that in some countries over 80% of antibiotic use is in animals. Many farms across the world including Europe and the US are still using antibiotics in animals even when they are not ill. This sort of preventative care would be devastating for humans, and yet this is occurring in food that ends up in our bodies anyway. Marks and Spencer’s took an important step to help combat this less than a week ago, stating they will begin to publish data on antibiotics used in their supply chain. This will hopefully encourage others to do the same, and allow consumers to see what is being put into their food.


“I hear you work for big farmer”

These bacteria have no concerns jumping from livestock to humans and there were already cases last year of MRSA existing in livestock within Europe. We are using the same drugs on animals as we use ourselves, meaning we are sacrificing their potential medical use even quicker than necessary.

We’re putting all of our eggs in one basket, and we’re running out of eggs.

The second World health organisation (WHO) World Antibiotic Awareness week has just passed (14th-20th November). This annual event aims to help educate people, both public and professional, on the risks of antibiotic overuse. WHO are also advising farmers to only use antibiotics that are categorised as “least important to human health” in livestock.

In terms of what we as individuals can do, we can, on a personal level, ensure that we follow the doctor’s advice with how often we take our antibiotics, and advise everyone else that they do the same. We can spread the WHO’s message that current antibiotic use in animals is a ticking clock, and if it is not more carefully controlled we stand to lose a precious medical resource.

When they are turned to sparingly, and used appropriately, antibiotics can be an extremely effective tool against infections that would have previously been fatal. But without this control, we may risk living in what WHO describes as “the post-antibiotic era”. Like TV, phones and the internet, most of us have not experienced a world where antibiotics don’t exist, and one glance at history tells us that we don’t ever want to.


If you want to read more about how genes affect humans as well as cells, read my previous blog: “Genetics: The Real Book of Life.

The shape of knowledge: squares, cones and needles


So, are you a square, a cone, or a needle?

I suppose the correct response is: ‘What on earth are you talking about?’ and I guess you’d be right. It is up to me to elaborate on what I mean. But first I’ll have to explain how I came up with this question in the first place…

When you start university, the subjects, or rather sub-subjects you can specialise into are laid out before you in different ‘fields’. This is an appropriate word, considering how immense the number of choices seems. You are presented with more information and specialties than you can shake an overpriced textbook at, and it’s up to you to narrow it all down to one or two if you want to progress.

If you’d taken an overall measurement of knowledge at the start of mine and anyone else’s university education, it would probably look something like this…

  • sqyare

    An innocent square, unburdened by student loans, deadlines, and the thought that education must end and you have to start adulting.

I believe, in terms of knowledge breadth (how many things you know about) and knowledge depth (how much you know about said things) that most people start higher education fairly similar in both, while we may be more drawn to or naturally talented in certain areas of study, the inherent structure of A-levels or other post-school education tends to leave our knowledge bases about even across the board. But what happens after the beginning of university?

Starting a degree is the first time most people feel they are developing what I’m going to refer to as a “cone of knowledge”. A phenomenon by which you begin to specialise in one core topic, at the expense of knowledge about the surrounding ones, your square will begin to taper, and end up becoming a bit more…coney.


Symptoms include being picky over the use of the word ‘significant’ and beginning sentences with “current consensus shows…”

For example, at the end of second year, a bright-eyed and bushy-tailed me uttered the words, “Oh, Genetics looks fun, I guess I’ll choose that”. Suddenly, a class of 350 trainee scientists was pulled in different disciplinary directions, with mine whittled down to just 16. Each discipline allowed students to evolve themselves in different ways. As a budding geneticist, I occasionally worried we’d picked the educational equivalent of an evolutionary dead end.

Thankfully, me and the rest of the genetics course fell into the ‘platypus’ category of oddity, instead of, for example, the ‘dodo’ variety. The knowledge and interest I gained on genes, DNA, evolution and inheritance is most likely going to make up or be involved in a large portion of the things I talk about in the future.

So after my bachelors, having finally found a subject I felt confident and settled in, with a few months lab experience under my belt, I made the logical decision and continued in this subject area switched to a completely different field. Neuroscience.

This wasn’t a completely random decision. Like genes, brains are something I’ve always been interested in. I seem to be unstoppable drawn towards things that are irreducibly complex or complicated, or at least that’s what I tell myself while trying to untangle the wires from beneath my desk.

I had hoped, going into it, there would be some overlap between the two subjects. I knew it was possible, as my undergraduate project had involved looking at gene expression in the developing brain. But I quickly found that just because neuroscience plays by the same scientific rules, it doesn’t mean it is in anyway the same game.

Genes, as some of you may know, are small individual units of heredity made up by DNA, that tend to code for a specific protein (except when they don’t, but that’s a caveat for another time). Each one can be described as a tiny little instruction manual for one building block of an entire organism, and like tiny little instruction manuals, the directions can be difficult to read. However, science has taken great leaps in the past decade and a half in learning to decipher it.

Brains, on the other hand, pose an entirely different problem. They raise the mind boggling question of whether it is possible to understand the very thing that powers understanding. It’s the sort of thing that leads to fellow neuroscientists narrowing their eyes at each other and saying things like ‘You better not be talking about philosophy’.

To compare to genes, trying to understand the brain’s instructions may be like opening the first page and reading “To understand this manual you must have first read the manual”. It could just be something we can never achieve, due to our lack of an outsiders point of view. In other words, it feels like the darned thing won’t sit still long enough for us to work it out.

To pull this back to the shapes I’ve been mentioning, my ‘cone of knowledge’ had definitely narrowed, and was becoming more of a pointed triangle by this point. It amazed me how quickly you can put on intellectual blinkers to other subject areas when you’re in a lab environment. Sometimes it’s simply necessary to get through the volume of information on your specific topic, and I think this is why you get the occasional ‘needle’ in a lab environment.


Disclaimer: The look of horror and general scruffiness is my personal experience of a needly lifestyle, and is not indicative of the needle population at large.

A needle tends to be the one who would perfect their topic on mastermind or university challenge but shrugs on the general knowledge round in a pub quiz because they simply don’t have time for keeping up with daily events.

Don’t get me wrong, the overwhelming number of people I’ve met in science have somehow managed to hang on to their random facts and niche interests despite the sometimes frustratingly specific information they encounter. Everyone acts a bit square at times, and everyone can get a bit needley.

But science needs those needles, it needs those finely tuned points of specificity to pop the never-ending balloons of ignorance. And if you put enough of those sharp folks together, you get a figurative bed of nails, a carpet of points that together is strong enough to hold up the weight of human advancement.

I’ve now left the world of academic research, and I’ve noticed that the switch from ‘studying’ to ‘studied’ in regards to my relationship with genetics and neuroscience has unsettled me. It sounds too historic, too final. I can feel my knowledge on the subjects fading, and I think if I don’t do something about it it will become nothing but a passing interest, something for me to regurgitate a few facts about in polite conversation.

That’s the reason I set up this blog, to hopefully preserve a knowledge of science and research that I have always enjoyed and been interested in, while also presenting it in a form people can read and (in exceptional cases) enjoy.

So while I find myself trying to fix my cone, I salute to all those people who know exactly what their shape should be.


This entry is a bit longer than I’ll be aiming for in future weeks (although I’m aware I’m now making it longer discussing it) and this blog post began as a 200-word section for the ‘About page’. So when I try to write an actual first blog post you can expect the novel out early 2017…