Don’t let the superbugs bite

But don't despair - we might be struggling but we are not beaten yet.

Evolution continues to be a bitch. Recently scientists gathered in Kensington, London, to have a good moan and to plan what can be done about it. “Superbugs and Superdrugs” is a great title for a meeting. Unfortunately the bugs seem to be more super than the drugs.

While that meeting went on, the US Centres for Disease Control and Prevention (CDC) issued a warning that we are entering a “nightmare” era. The CDC’s problem is a killer bacterium known as CRE, which is spreading in the US. Some strains of CRE are not only resistant to all antibiotics; they are also passing on that resistance to other bacteria, creating drug-resistant strains of E coli, for instance. On 11 March, Sally Davies, the UK government’s chief medical officer, asked the government to add the superbug problem to its “strategic risk register”, which highlights potentially catastrophic threats to the UK.

For a while, it all looked so good. When scientists discovered penicillin, then ever more weapons for our antibiotic arsenal, it seemed that bacteria had been defeated. The problem is, they fought back.

For all the worry over CRE, perhaps nowhere is this antibiotic resistance more evident than with tuberculosis. In the west, we won the war on TB so convincingly that receiving the BCG vaccine against it – once a waymark in British childhood – is no longer routine. Only in certain inner-city communities where migrant populations increase the likelihood of encountering the TB bacterium are children routinely immunised. However, in 2011, the World Health Organisation marked London out as the city with the highest TB infection rate in western Europe.

Many resistant bacteria originate in hospitals, where pharmaceutical regimes kill off the normal strains, making space in which bacteria that are naturally resistant can proliferate. Yet you can’t always blame the drugs. Research published at the end of February shows that drug resistance can arise even when the bacteria have never encountered a chemical meant to kill them.

In the study, E coli bacteria were made to suffer by exposing them to heat and restricting the nutrients in their environment. According to conventional wisdom, this should have kept proliferation in check – but it caused a spontaneous mutation that made the E coli resistant to rifampicin, one of the weapons in our antibiotic arsenal. What is worse is the observation that there was good reason for this mutation to arise: it made the stressful conditions more survivable. Bacteria with the mutation grew much faster.

Bacteria are survivors – if they can’t magic up a spontaneous mutation, they’ll pick one up in the street. A sampling of puddles in New Delhi showed that almost a third contain the genetic material that allows bacteria to produce an enzyme that destroys a swath of antibiotics. The NDM-1 gene is particularly evil. Its tricks include forcing itself into gut bacteria such as E coli that are incorporated into faeces; as a result, the resistant strains travel between hosts with ease.

Many infections involving a bacterium carrying NDM-1 are untreatable. GlaxoSmithKline is reportedly developing a drug to deal with it but it is years behind the curve. In the autumn, an EU project to mine the seabed for so far undiscovered antibiotics will start up, but it will take years for that, too, to bear fruit.

Let’s end on a positive note. Superbugs might be evolving in fiendish ways but they’re doing it blind and they’re up against evolution’s greatest invention – the human brain. We might be struggling but we are not beaten yet.

The EHEC bacteria. Image: Getty Images

Michael Brooks holds a PhD in quantum physics. He writes a weekly science column for the New Statesman, and his most recent book is At the Edge of Uncertainty: 11 Discoveries Taking Science by Surprise.

This article first appeared in the 25 March 2013 issue of the New Statesman, After God

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The answer to the antibiotics crisis might be inside your nose

The medical weapons we have equipped ourselves with are losing their power. But scientists scent an answer. 

They say there’s a hero in everyone. It turns out that actually, it resides within only about ten percent of us. Staphylococcus lugdunensis may be the species of bacteria that we arguably don’t deserve, but it is the one that we need.

Recently, experts have cautioned that we may be on the cusp of a post-antibiotic era. In fact, less than a month ago, the US Centres for Disease Control and Prevention released a report on a woman who died from a "pan-resistant" disease – one that survived the use of all available antibiotics. Back in 1945, the discoverer of penicillin, Alexander Fleming, warned during his Nobel Prize acceptance speech against the misuse of antibiotics. More recently, Britain's Chief Medical Officer Professor Dame Sally Davies has referred to anti-microbial resistance as “the greatest future threat to our civilisation”.

However, hope has appeared in the form of "lugdunin", a compound secreted by a species of bacteria found in a rather unlikely location – the human nose.

Governments and health campaigners alike may be assisted by a discovery by researchers at the University of Tubingen in Germany. According to a study published in Nature, the researchers had been studying Staphylococcus aureus. This is the bacteria which is responsible for so-called "superbug": MRSA. A strain of MRSA bacteria is not particularly virulent, but crucially, it is not susceptible to common antibiotics. This means that MRSA spreads quickly from crowded locations where residents have weaker immune systems, such as hospitals, before becoming endemic in the wider local community. In the UK, MRSA is a factor in hundreds of deaths a year. 

The researchers in question were investigating why S. aureus is not present in the noses of some people. They discovered that another bacteria, S. lugdunensis, was especially effective at wiping out its opposition, even MRSA. The researchers named the compound created and released by the S. lugdunensis "lugdunin".

In the animal testing stage, the researchers observed that the presence of lugdunin was successful in radically reducing and sometimes purging the infection. The researchers subsequently collected nasal swabs from 187 hospital patients, and found S. aureus on roughly a third of the swabs, and S. lugdunensis on up to 10 per cent of them. In accordance with previous results, samples that contained both species saw an 80 per cent decrease of the S. aureus population, in comparison to those without lugdunin.

Most notably, the in vitro (laboratory) testing phase provided evidence that the new discovery is also useful in eliminating other kinds of superbugs, none of which seemed to develop resistance to the new compound. The authors of the study hypothesised that lugdunin had evolved  “for the purpose of bacterial elimination in the human organism, implying that it is optimised for efficacy and tolerance at its physiological site of action". How it works, though, is not fully understood. 

The discovery of lugdunin as a potential new treatment is a breakthrough on its own. But that is not the end of the story. It holds implications for “a new concept of finding antibiotics”, according to Andreas Peschel, one of the bacteriologists behind the discovery.

The development of antibiotics has drastically slowed in recent years. In the last 50 years, only two new classes of this category of medication have been released to the market. This is due to the fact almost all antibiotics in use are derived from soil bacteria. By contrast, the new findings record the first occurrence of a strain of bacteria that exists within human bodies. Some researchers now suggest that the more hostile the environment to bacterial growth, the more likely it may be for novel antibiotics to be found. This could open up a new list of potential areas in which antibiotic research may be carried out.

When it comes to beating MRSA, there is hope that lugdunin will be our next great weapon. Peschel and his fellow collaborators are in talks with various companies about developing a medical treatment that uses lugdunin.

Meanwhile, in September 2016, the United Nations committed itself to opposing the spread of antibiotic resistance. Of the many points to which the UN signatories have agreed, possibly the most significant is their commitment to “encourage innovative ways to develop new antibiotics”. 

The initiative has the scope to achieve a lot, or dissolve into box ticking exercise. The discovery of lugdunin may well be the spark that drives it forward. Nothing to sniff about that. 

Anjuli R. K. Shere is a 2016/17 Wellcome Scholar and science intern at the New Statesman