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.
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