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Antimicrobial resistance

How microbes escape antimicrobials, how resistance spreads between them and between countries, and how surveillance and stewardship slow it.

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Antimicrobial resistance (AMR) happens when bacteria, viruses, fungi or parasites no longer respond to medicines that used to work. It makes infections harder to treat and makes surgery, cancer treatment and intensive care riskier. WHO estimates that bacterial AMR was associated with more than 4.7 million deaths worldwide in 2021.

Mechanisms

  • Enzymes: β-lactamases, including ESBLs (destroy most penicillins and cephalosporins) and carbapenemases (KPC, NDM, OXA-48 types); aminoglycoside-modifying enzymes
  • Target change: PBP2a in MRSA (encoded by mecA); D-Ala-D-Lac cell-wall precursors in vancomycin-resistant enterococci; mutated DNA gyrase in fluoroquinolone resistance
  • Reduced entry: loss of outer-membrane porins in Gram-negative bacteria
  • Efflux pumps that export several drug classes at once
  • Bypass: an alternative enzyme, as in trimethoprim resistance

How resistance arises and spreads

Random mutations arise in large bacterial populations; an antibiotic kills the susceptible ones and leaves the resistant ones to grow. Horizontal gene transfer (plasmids, transposons, integrons) then shares resistance genes between strains and species. Resistant organisms spread from patient to patient through hands, equipment and the environment, and between countries with travel, food and animals. This is why AMR is a One Health problem shared by human, animal and environmental health.

Pharmacology's answer

β-lactamase inhibitors (clavulanic acid, tazobactam, avibactam, vaborbactam) protect a partner β-lactam from some enzymes; each covers a different set, and metallo-β-lactamases such as NDM escape most of them. Newer agents (cefiderocol) and older drugs brought back (colistin) treat some carbapenem-resistant infections, at the cost of toxicity. These are WHO Reserve antibiotics, kept for confirmed or strongly suspected resistant infections.

Surveillance and stewardship

WHO's Global Antimicrobial Resistance and Use Surveillance System (GLASS) helps countries collect and share comparable resistance and use data. In the Americas, PAHO runs the Latin American and Caribbean Network for Antimicrobial Resistance Surveillance (ReLAVRA+) and issues epidemiological alerts, for example on new combinations of carbapenemases in Enterobacterales. Locally, laboratory data become the hospital antibiogram that guides empirical choices.

  • Prescribe only when needed, with the narrowest effective drug and shortest effective course
  • Hand hygiene, isolation and screening limit spread in hospitals
  • Vaccination prevents infections and so reduces antibiotic use
  • Report unusual resistance to the laboratory and to public health

Test yourself

Think of the answer, then tap the question to see it.

How do MRSA strains resist β-lactams?

They carry mecA, which encodes an altered penicillin-binding protein (PBP2a) with low affinity for most β-lactams.

Why do carbapenemase genes spread so quickly?

They are often carried on plasmids and other mobile elements that pass between bacteria, including between different species.

What is the role of a β-lactamase inhibitor such as tazobactam?

It inactivates some β-lactamases so that the partner β-lactam (piperacillin) is not destroyed; it has little antibacterial action of its own.

What is GLASS?

WHO's Global Antimicrobial Resistance and Use Surveillance System, which helps countries collect, analyse and share comparable data on resistance and antimicrobial use.

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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: Antimicrobial resistance (World Health Organization (WHO), 2026); Global Antimicrobial Resistance and Use Surveillance System (GLASS) (World Health Organization, 2026); Antimicrobial Resistance - PAHO/WHO | Pan American Health Organization (Pan American Health Organization (PAHO), 2026); First Detection of the Plasmid-Mediated Class A Carbapenemase KPC-2 in Clinical Isolates of Klebsiella pneumoniae from South America (Antimicrobial Agents and Chemotherapy (PMC), 2006).

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