Apocalypse Now (no, really)

I woke up yesterday morning to a litany of death… because Pete has changed the radio station to BBC4.

Every single story was death; refugees fleeing death, a child found dead, babies dying unexpectedly, and people, all of us, who are going to die because complete antibiotic resistance has been found and it’s just a matter of time before it spreads and kills us all.

I’ve changed the radio station (thank you BBC6).

The scientific paper portending antibiotic-resistance doom, is this one:

Emergence of plasmid-mediated colistin resistance mechanism MCR-1 in animals and human beings in China: a microbiological and molecular biological study

Snappily named, but what does that mean, and should BBC4 be scaring me at 7am? Is the fear-mongering justified? What did the research actually find, and what is the context?

Some of these scientists were carrying out a routine surveillance project on antimicrobial resistance in commensal Escherichia coli from food animals in China.

Antimicrobial resistance is when microorganisms which cause infections are not killed or their growth is not stopped by a medicine that would normally kill or stop them.

Commensal is from medieval Latin commensalis, from com- ‘sharing’ + mensa ‘a table’; these E.coli bacteria obtain food from the food animals, without affecting the food animal.

E coli Ag Res Mag

Food animals (simply, but oddly named) are animals bred to become human food.

So the scientists were checking, as they routinely do, to see if any E. coli living with (but not hurting) animals for our food, are not killed by medication that they are normally killed by.

They found an increase in the number of colistin resistant microorganisms in their food animals, and isolated (from a pig) a strain of E. coli with colistin resistance that could be transferred to another strain of E. coli that was not previously resistant.

Colistin is an antibiotic, first derived from bacteria in 1949. It’s a type of antibiotic called a Polymyxin. We don’t use it to treat infections in humans (unless we have to) due to its nephrotoxicity (from the Greek for kidney ‘nephros’) – it poisons kidneys. It is a last resort antibiotic for treating some bacterial infections which are resistant to other less harmful (to humans) antibiotics.

So they found more E. coli than they have found before, that are resistant to colisitin.

Resistance to colistin isn’t new – it was first described in vitro in 1960, and although it is rare in infections affecting humans, one paper last year described 13 cases in India. It is the mechanism of spread of resistance to colistin that is new here – that resistance can be transferred from one strain of E. coli to another, via horizontal gene transfer. Vertical gene transfer would be parent E.coli to baby E.coli, which we would expect. Horizontal gene transfer is parent E.coli straight to another parent E.coli. Before now, resistance to polymyxin antibiotics, including colistin, via horizontal gene transfer, has never been found.

Having found this resistance, and the pattern in which it could be transmitted, the researchers tried to identify how resistance was transmitted.

They found a plasmid-mediated resistance mechanism, MCR-1.

MCR-1 is a gene in a plasmid (a plasmid is a small DNA molecule, separate from the chromosomal DNA, that can replicate independently; they are commonly found in bacteria). This gene in the plasmid, in the E.coli bacteria, living happily in the pig, is responsible for the resistance to colistin.


This gene can be transferred to other bacteria, Klebsiella pneumoniae and Pseudomonas aeruginosa, and stay in these organisms, which leads to the theory that the gene might be (without our interference) transferring to other organisms and spreading in those populations too.

So why is this such as big deal?

Because we are running out of tools to treat infectious diseases. It isn’t just these cases, or these bacteria, or these drugs. People have been trying to raise awareness of this problem and the consequences for years. We know that we have resistance to antimicrobials in many diseases caused by infectious agents, including parasites, bacteria, viruses and fungi. Malaria. Tuberculosis. HIV. Candida. MRSA. Gonorrhea. Pneumonia. Cystitis. We know that resistance to more drugs is increasing. We know that resistance is spreading geographically. As antimicrobial resistance increases and spreads, we won’t be able to successfully treat these diseases. We are developing new antimicrobials, and finding new ways to discover them, but this progress needs to outpace resistance, and currently, it doesn’t.

Without effective antimicrobial agents we won’t be able to treat many diseases that are currently, rarely fatal. We won’t be able to continue to control the spread of diseases – currently contained(ish) disease will spread more quickly and widely.

It’s not just people with infectious diseases that this will affect. We won’t be able to undergo surgery safely, as any post-surgical infections may be fatal. Giving birth will become very dangerous. Some people – those at high risk of infection, and those who are unable to fight off of infections (babies, older people etc.) will be much less likely to survive.

There are many ways we could decrease the development and spread of antimicrobial resistance but we’re simply not doing many of them. We are all responsible for these actions. Preventing transmission by washing our hands, using condoms, and getting our vaccinations. Not demanding antibiotics from doctors unless they are effective against our illness, and always finishing a full course of antibiotics. Not prescribing antibiotics to keep your patients quiet, and keeping up with best clinical practise for reducing development of drug resistance. Not eating meat that has been routinely fed antibiotics. Supporting campaigns and research that will preserve and develop treatment options.

We’re not all doomed yet, but we will be unless we change. BBC4 should be scaring all of us at 7am. It isn’t fear-mongering. We all need to change the way we use antimicrobials.


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