Antimicrobial resistance

Based on Wikipedia: Antimicrobial resistance

In the hedgerows of Europe, an arms race has been quietly underway for millions of years. Hedgehogs carry a fungus on their skin that naturally produces antibiotics—chemicals that kill bacteria. The bacteria that live alongside these hedgehogs faced a choice: evolve or die. They evolved. Long before Alexander Fleming noticed mold killing bacteria in a petri dish in 1928, long before the first human patient received penicillin, bacteria living on hedgehogs had already developed resistance to these natural antibiotics.

This is the unsettling truth at the heart of antimicrobial resistance: we are not fighting a new enemy. We have simply accelerated an ancient process to catastrophic speed.

What Antimicrobial Resistance Actually Means

Let's be precise about terms, because confusion here costs lives.

Antimicrobials are drugs that kill or stop the growth of microbes—the tiny organisms that can cause infections. This category includes antibiotics (which target bacteria), antivirals (which target viruses), antifungals (which target fungi), and antiparasitics (which target parasites). When we talk about antimicrobial resistance, we mean that microbes have developed the ability to survive exposure to drugs that previously killed them.

Here's a crucial distinction that many people get wrong: a person cannot become resistant to antibiotics. The bacteria infecting that person become resistant. This isn't a semantic quibble. It matters because it means resistance doesn't stay with one patient—it spreads. A resistant bacterium can move from person to person, from animals to humans, from soil to food. The resistance belongs to the microbe, and the microbe travels.

In surveys across Europe, Asia, and North America, researchers found that while 70 percent of people had heard of antibiotic resistance, 88 percent of those people thought it meant some kind of physical change in the human body. It doesn't. It means the bacteria have changed, and our drugs no longer work against them.

The Scale of the Crisis

Nearly five million people die each year from infections involving antimicrobial-resistant organisms. In 2019 alone, resistant infections directly killed 1.27 million people globally—more than HIV/AIDS or malaria. Another 3.68 million deaths that year were associated with resistant infections, meaning resistance was a contributing factor even if not the sole cause.

One in five of those who died were children under the age of five.

The World Health Organization considers antimicrobial resistance one of the greatest threats to global public health. Without dramatic intervention, projections suggest we could see ten million deaths annually by 2050. To put that in perspective, that would make antimicrobial resistance deadlier than cancer is today.

In Europe, the numbers tell a grim story of their own. In 2015, antibiotic-resistant bacteria caused nearly 672,000 infections in the European Union and European Economic Area, killing more than 33,000 people. Most of these infections were acquired in healthcare settings—the very places people go to get well. By 2019, deaths from resistant infections in Europe had climbed to 133,000.

How Resistance Develops

Bacteria reproduce with astonishing speed. Some species can divide every twenty minutes, meaning a single bacterium can produce millions of descendants in a day. Each division carries a small chance of genetic mutation. Most mutations are neutral or harmful to the bacterium. But occasionally, a mutation provides an advantage—like the ability to survive an antibiotic.

When antibiotics are present, they kill susceptible bacteria while leaving resistant ones alive. These survivors reproduce, passing their resistance genes to their offspring. This is natural selection in action, the same process Darwin described, operating on a timescale we can observe in days rather than millennia.

But here's where it gets more complicated. Bacteria can also share genes with each other directly, without reproduction, through a process called horizontal gene transfer. Imagine if you could hand your neighbor a gene for blue eyes and they could instantly have blue eyes. That's essentially what bacteria do with resistance genes.

There are three main ways this happens. In conjugation, bacteria connect through a tiny tube and pass genetic material between them. In transduction, viruses that infect bacteria accidentally carry resistance genes from one bacterium to another. In transformation, bacteria pick up free-floating genetic material from their environment—including from dead bacteria that have burst open.

This means resistance can spread not just from parent to offspring, but between completely unrelated bacteria. A harmless soil bacterium might develop resistance and then transfer that resistance to a dangerous pathogen. The genes move through bacterial communities like gossip through a small town.

Why This Is Happening Now

Antimicrobial resistance is natural. It has always existed. What's changed is the pace.

The primary driver is overuse and misuse of antimicrobials. Studies in the United States have found that up to one in three antibiotic prescriptions in outpatient settings are unnecessary. Of the approximately 154 million antibiotic prescriptions written annually, as many as 46 million are inappropriate for the condition being treated. In one French intensive care unit study, between 30 and 60 percent of prescribed antibiotics were unnecessary.

When antibiotics are prescribed correctly, doctors choose a specific drug matched to a specific infection, at the right dose, for the right duration. When this process goes wrong—wrong drug, wrong dose, treatment stopped too early—bacteria get exposed to antibiotics without being killed. This is the perfect training ground for resistance.

Consider what happens when someone stops taking antibiotics because they feel better. The initial doses have killed the most susceptible bacteria, which is why symptoms improve. But less susceptible bacteria may remain. Without completing the full course, these hardier survivors can multiply and cause a relapse—now with a population that's more resistant than before.

Self-medication makes this problem dramatically worse. In many countries, particularly those with limited healthcare access, people buy antibiotics without prescriptions and treat themselves. In the Indian state of Punjab, 73 percent of the population treats minor health issues through self-medication. Globally, self-medication rates in low- and middle-income countries range from 8 to 93 percent depending on the region.

People self-medicate for understandable reasons: they can't afford a doctor, can't take time off work, or live far from healthcare facilities. But without proper diagnosis, they often take the wrong antibiotic, at the wrong dose, for conditions that may not even be bacterial infections. Each misuse accelerates resistance.

The Problem with Superbugs

When a microbe develops resistance to multiple drugs, we call it multidrug-resistant. The popular term is "superbug," though this makes them sound like comic book villains rather than the mundane killers they actually are.

The reality of a superbug infection is grimly ordinary. You might catch what seems like a routine urinary tract infection. Normally, a course of simple antibiotics would clear it up in days. But if the bacteria are resistant to first-line treatments, doctors must try alternatives. These backup drugs are often more expensive, may have worse side effects, and sometimes require intravenous administration in a hospital rather than pills at home.

And if the bacteria are resistant to those alternatives too? Options narrow. Treatment becomes experimental. Some infections become essentially untreatable.

We are approaching what some researchers call the "post-antibiotic era"—a return to conditions resembling those before Fleming's discovery, when a simple cut could lead to a fatal infection. Common procedures we take for granted—surgery, organ transplants, cancer chemotherapy, care for premature infants—all depend on our ability to prevent and treat bacterial infections. Without effective antibiotics, these medical advances become far more dangerous.

A Conspiracy of Silence

Antimicrobial resistance has a strange relationship with public attention. It kills more people than many diseases that receive far more funding and media coverage. Yet it remains in the background, a slow-motion crisis that lacks the dramatic arc of a pandemic or the emotional immediacy of cancer.

Part of this is the nature of the threat. Resistance doesn't cause a specific disease with a recognizable name. It makes existing diseases harder to treat. A child who dies of resistant pneumonia is recorded as dying from pneumonia, not from antimicrobial resistance. The statistics are there, but they're hidden within other categories.

The COVID-19 pandemic actually worsened the situation in two ways. First, it redirected scientific attention and resources away from antimicrobial resistance research. Second, the widespread fear of infection led to increased antibiotic prescriptions—even though COVID-19 is caused by a virus, against which antibiotics are useless. Doctors prescribed antibiotics to prevent secondary bacterial infections or simply because anxious patients demanded something, anything. Each unnecessary prescription added fuel to the resistance fire.

The One Health Approach

Antimicrobial resistance cannot be solved by medicine alone because the problem doesn't exist in medicine alone.

Antibiotics are used extensively in agriculture—not just to treat sick animals, but to promote growth and prevent disease in healthy ones. Worldwide, more antibiotics are used in animals than in humans. These drugs enter the environment through animal waste, contaminate water supplies, and create reservoirs of resistant bacteria that can transfer their genes to human pathogens.

Resistance also moves through the environment in other ways. Pharmaceutical manufacturing waste, hospital sewage, and agricultural runoff all contribute to a global pool of resistance genes. Bacteria in soil, water, and wildlife carry and exchange these genes, creating pathways we're only beginning to understand.

The "One Health" approach recognizes that human health, animal health, and environmental health are interconnected. Solving antimicrobial resistance requires coordinated action across all three domains. This means limiting antibiotic use in farming, improving sanitation to reduce infection transmission, monitoring resistance patterns across species, and developing new drugs while preserving the effectiveness of existing ones.

What Can Be Done

Prevention remains the most effective strategy. Every infection prevented is an antibiotic course not needed, a selection pressure not applied, a resistance opportunity not created.

Better hygiene—handwashing, sanitation, clean water—reduces infections at the source. Vaccines prevent diseases that might otherwise require antibiotic treatment. Hospital infection control protocols, when properly followed, dramatically reduce the spread of resistant organisms in healthcare settings.

When antibiotics are necessary, using them wisely matters enormously. This means prescribing narrow-spectrum antibiotics that target specific bacteria rather than broad-spectrum drugs that affect many species. It means diagnostic tests to confirm bacterial infection before prescribing. It means completing full courses of treatment. It means doctors resisting pressure from patients who demand antibiotics for viral infections.

Surveys of physicians in the United States found that only 63 percent considered antibiotic resistance a problem in their own practice, while 23 percent believed aggressive prescribing was necessary to avoid inadequate care. This disconnect between individual decisions and collective consequences lies at the heart of the problem. Every doctor may feel justified in their prescribing, yet the cumulative effect accelerates resistance for everyone.

We also desperately need new antibiotics. The pipeline has been drying up for decades. Pharmaceutical companies have limited incentive to develop drugs that are used sparingly (as new antibiotics should be) and that bacteria may quickly develop resistance to. Public investment, new economic models for drug development, and international cooperation are all necessary to ensure new treatments reach patients.

Beyond new antibiotics, alternative approaches are under investigation. Bacteriophages—viruses that infect and kill bacteria—offer one possibility. These are much more specific than antibiotics, attacking particular bacterial species while leaving others unharmed. Other researchers are exploring ways to disarm bacteria without killing them, removing their ability to cause disease while reducing the selection pressure for resistance.

A Global Challenge

Antimicrobial resistance respects no borders. A resistant strain that emerges in one country can spread worldwide within weeks. Yet the resources to combat resistance are distributed unevenly.

In wealthy nations, the challenge is often overuse—too many prescriptions, too much antibiotic use in industrial agriculture, too little attention to completing treatment courses. In poorer nations, the challenge is often access—people dying from treatable infections because they can't get antibiotics at all, while others self-medicate with whatever they can obtain.

Both problems feed resistance. Overuse creates resistant strains. Undertreatment allows infections to spread and persist, creating more opportunities for resistance to develop and transmit. Any global solution must address both.

There have been calls for international treaties on antimicrobial resistance, similar to agreements on climate change or nuclear weapons. Such frameworks could coordinate surveillance, regulate antibiotic use in agriculture, fund research into new treatments, and ensure access to essential medicines in developing countries. So far, these efforts have produced declarations and guidelines but little binding action.

The Race We Cannot Lose

Alexander Fleming's original penicillin—the natural form he discovered growing on bread mold—rapidly lost effectiveness against human infections. None of the natural penicillins originally identified (scientists eventually catalogued varieties called F, K, N, X, O, U1, and U6) are used clinically today. They all fell to resistance.

We developed synthetic modifications and entirely new antibiotic classes. For decades, we stayed ahead. But the pace of bacterial evolution has been catching up to the pace of human innovation. Common infections—respiratory infections, urinary tract infections, sexually transmitted diseases, tuberculosis—are becoming harder to treat. Some strains of gonorrhea are now resistant to almost all available antibiotics.

The hedgehog's bacteria evolved resistance over millions of years. We have accelerated that process by many orders of magnitude. Every antibiotic prescription, every dose fed to farm animals, every wastewater discharge adds to the selection pressure driving bacteria toward resistance.

We cannot stop evolution. But we can stop making it worse. We can use the tools we have more carefully, develop new ones more urgently, and recognize that the miracle of antibiotics was never a permanent victory—only a temporary advantage in an ongoing war.

The microbes are watching. They are waiting. And they are adapting.