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Portrait of Antibiotic resistance

Science · Biology

Antibiotic resistance

Biology — microbiology and public health

Antibiotic resistance is the evolution of bacteria that survive drugs designed to kill them — by pumping the drug out, altering its target, or making enzymes that destroy it. It is natural selection in fast motion, accelerated by overuse in medicine and agriculture and spread between species by plasmids carrying resistance genes. Alexander Fleming warned of it in his 1945 Nobel lecture; a 2022 Lancet study attributed 1.27 million deaths in 2019 directly to it, and the 2016 O'Neill review projected 10 million a year by 2050.

How to spot them

  • ▸Natural selection acting on bacteria under drug pressure
  • ▸Spread between unrelated species by plasmids and horizontal gene transfer
  • ▸MRSA, VRE, CRE and the ESKAPE pathogens
  • ▸Warned about by Alexander Fleming in his 1945 Nobel lecture
  • ▸Projected by the O'Neill review to kill 10 million people a year by 2050

Key facts

Alexander Fleming warned of it in his 1945 Nobel lecture, telling listeners it was easy to underdose a microbe and make it resistant (1945)

He shared the prize with Howard Florey and Ernst Chain.

Abraham and Chain described a bacterial enzyme that destroys penicillin in 1940, before the drug was even in clinical use (1940)

Penicillinase, the first beta-lactamase.

Its best-known hospital acronym begins with 'methicillin-' and names a staphylococcus

MRSA — methicillin-resistant Staphylococcus aureus, first identified in Britain in 1961.

Plasmids and horizontal gene transfer let it spread between unrelated bacterial species, not just from parent to offspring

Conjugation, transformation and transduction all move the genes about.

Jim O'Neill's 2016 review for the UK government projected 10 million deaths a year by 2050 (2016)

More than cancer currently kills annually; the economic cost was put at 100 trillion US dollars.

A 2022 Lancet study by the GRAM project attributed 1.27 million deaths in 2019 directly to it (2022)

It was associated with 4.95 million deaths in total — more than HIV/AIDS or malaria.

The mcr-1 gene, found in Chinese pigs in 2015, undermined colistin, the drug kept back as a last resort (2015)

Worse still, mcr-1 sits on a plasmid, so it transfers readily between species.

Doctors are told to finish the course, use narrow-spectrum drugs and rotate them — 'stewardship' against this problem

Agriculture matters too: much of the world's antibiotic tonnage goes to farm animals, often as growth promoters.

Key ideas

  • Mechanisms fall into four families: destroy the drug (beta-lactamases), pump it out (efflux pumps), change the target (altered penicillin-binding proteins in MRSA), or restrict entry through the cell wall.
  • Resistance genes are ancient — they have been recovered from 30,000-year-old permafrost — because microbes have been chemically warring with one another for billions of years. Antibiotic use does not create them; it selects for them.

Quick-fire facts

  • •Selman Waksman coined the word 'antibiotic' and discovered streptomycin, winning the 1952 Nobel Prize in Physiology or Medicine.
  • •Fleming discovered penicillin in 1928 at St Mary's Hospital, London; he has his own GoDeep entry as a scientist.
  • •MRSA was first identified in 1961, just two years after methicillin was introduced.
  • •The ESKAPE pathogens — Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter species — are the priority list of escape artists.
  • •The WHO declared it one of the top ten global public health threats facing humanity.
  • •Almost no genuinely new classes reached the clinic between 1962 and 2000, a gap called the discovery void; teixobactin, reported in 2015, was the first promising new class in decades.
  • •Tuberculosis has multi-drug-resistant (MDR-TB) and extensively drug-resistant (XDR-TB) forms requiring treatment for many months.
  • •Gonorrhoea has worked its way through penicillin, tetracycline, ciprofloxacin and now threatens the last dependable option, ceftriaxone.
  • •Common misconception: it is not the patient who becomes resistant, but the bacteria; and it happens in untreated people too, since resistant strains spread by ordinary contagion.

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