How medicine created a bacteria problem

Unfortunately, we have used too many antibiotics too freely, and so Staphylococcus aureus has mutated to beat them

On a warm afternoon in summer we were sitting in the lecture theatre, learning about germs. A microbiologist was showing us slides of enormously magnified bacteria (“God, this is like bug Imax!” said the girl behind me). The lecturer had a cold; he was coughing dramatically. After a prolonged bout he hawked into his coffee cup. “Now that’s how TB spreads,” he said, studying the contents. “God, that’s absolutely disgusting,” said my neighbour.

Later on, in the lab, we had to behave more decorously. “Try not to splutter everywhere,” said the microbiologist, handing out Petri dishes. We were going to grow some germs. After a week, we were able to view the harvest. There were streptococci, chains of circular bacteria, easily remembered as looking like the queues of sweets in a packet of Strepsils. And there was Staphylococcus aureus, forming the round, golden colonies that its name suggests, one of the most common bacteria that coexists with humans, and now one of the most problematic.

Staphylococcus aureus (or “staph” as it is often called) lives on skin and mucus membranes. Our skin is covered in commensal bacteria – germs causing no harm – and staph is often a part of this population. It is only if the staph breaches the skin and multiplies that it becomes a problem. S.aureus causes many common skin infections, including boils, abscesses and styes. You can sometimes see evidence of its presence in, for example, impetigo, a skin infection common in children that produces a rash with a tell-tale golden crust. If S.aureus gets into the blood stream it can also cause more serious infections. Invasive staph can affect the joints, bones, lungs, coverings of the brain and the heart.

Staph used to be treated with penicillin (Alexander Fleming’s chance Penicillium mould killed a colony of S.aureus), but the bacteria evolved, and in most cases it now produces an enzyme that can break the ring structure of penicillin, rendering it useless. This means we have to use one of penicillin’s descendants instead: a drug such as methicillin or flucloxacillin. Unfortunately, we have used too many antibiotics too freely, and S.aureus has mutated again, which is how we ended up with the strain called Methicillin-resistant Staphylococcus aureus, or MRSA.

It is a problem that medicine has created. Like regular staph, MRSA can live as a harmless commensal, but if it becomes invasive the consequences can be deadly. You’re more at risk if you’re already ill, if your immune system is suppressed, or if you’ve recently had surgery. Treating invasive MRSA infections requires ever-more powerful (and expensive) antibiotics with serious side effects. Options such as vancomycin, teicoplanin and linezolid are all lumped together under the general term, “Domestos”. Frighteningly, VRSA already exists.

The best defence against MRSA is not to get it, which is why hospitals are dotted with alcohol-gel dispensers and forlorn notices requesting doctors and visitors not to sit on the beds. (MRSA as been found on sheets, door handles, chairs and hospital curtains, among other things.) Staph is a relatively sturdy germ and MRSA can survive outside the body for considerable periods of time. This is why the first event when you’re admitted to hospital is someone sticking a cotton swab up your nose, to check if you’re a carrier. And why the most ostensibly revolting things – such as coughing into coffee cups – are not the most dangerous, after all.

Sophie Harrison is a hospital doctor in South Yorkshire

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