LONDON - More than 700,000 people die every year because they are infected with microbes – bacteria, viruses, fungi or parasites – that have become resistant to most known drugs.

Antimicrobial resistance (AMR) is already a major public health problem around the world, though its effects are felt unequally: while an estimated 17% of infections in OECD countries are caused by drug-resistant microbes, 40%-60% of infections in Brazil, Indonesia and Russia are caused by such microbes.

Left unchecked, AMR threatens to become one of the world’s biggest health problems, surpassing diabetes and cancer. If more bugs become drug resistant, common infections could become untreatable, and routine treatments – chemotherapy, caesareans, hip replacements – too risky to carry out.

In 2019, a UN report estimated that drug-resistant microbes could lead to ten million deaths per year, and cost the world $100trn, by 2050. The Wellcome Trust has called AMR a “slow-moving pandemic”.


How do microbes become resistant?


Because of evolution by natural selection. Each time living things reproduce, their genetic code mutates. Often those mutations have little impact on the next generation. But sometimes they confer a survival advantage – perhaps the new generation of microbes need less food or water to survive, or maybe they are unaffected by the drugs that used to kill their ancestors.

Anti-microbial drugs increase the selection pressure: newer, resistant bugs survive and reproduce further. Over time, the only microbes that are left are the ones resistant to common drugs.

The most infamous examples of so-called “superbugs” are methicillin-resistant Staphylococcus aureus (MRSA) and drug-resistant tuberculosis – both caused by bacteria that are very difficult to treat with existing medicines. Drug resistance is nothing new, but the rate at which resistant bugs are appearing is growing fast and, worryingly, the supply of new drugs with which to treat them is drying up.


MRSA: the arms race


Alexander Fleming was studying Staphylococcus aureus – a bacterium that causes boils, abscesses, pneumonia and infections of surgical wounds and blood, sometimes causing fatal sepsis – when he discovered penicillin in 1928.

Penicillin revolutionised the treatment of staphylococcal (and other) infections, but its power soon began to wane: the first penicillin-resistant staphylococci were seen in 1942; they had evolved to make penicillinase, a penicillin-destroying enzyme.

In response, methicillin was developed – an antibiotic that was resistant to penicillinase. Soon after that, in 1961, scientists noticed the first methicillin-resistant Staphylococcus aureus (MRSA). In 1963, the first recorded outbreak occurred, in a Surrey hospital.

Since then, MRSA has spread around the world, evolving independently, generally in hospitals, in places from the US to Taiwan. By 2005, it was killing more Americans than HIV. About one in 30 healthy people in industrialised nations are now “colonised” by MRSA, living harmlessly on their skin or nose. Its resistance to traditional antibiotics makes infections difficult to treat. About half of cases respond to the “last resort” antibiotic vancomycin, but its use has in turn created a vancomycin-resistant strain: VRSA.


Why are more resistant bugs appearing?


Largely because of the overuse and misuse of antibiotics – antimicrobial drugs that work against bacteria – which drives the evolution of resistance. Doctors will often prescribe antibiotics based only on a patient’s symptoms, instead of knowing there is a bacterium causing the illness.

 

 

 

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