Why Do Antibiotics Stop Working?: Going Further 9–12

What an antibiotic does

An antibiotic is a medicine that kills bacteria, or stops them multiplying, without harming your own cells much. You met the first one, penicillin, in Grade 9 Grade 9: Kingdom Fungi, and in Grade 8 that antibiotics do nothing against viruses Grade 8: Negative effects.

How can a medicine tell a bacterium from your cells? Bacteria are prokaryotes, built differently from you Grade 9: Kingdom Monera. Each antibiotic attacks one part that bacteria have and your cells don’t, or that is shaped differently in them. That part is the drug’s target.

Penicillin and its relatives (amoxicillin, ceftriaxone) stop a bacterium building its cell wall. Your cells have no cell wall. A bacterium that grows without a proper wall bursts.
Azithromycin and tetracycline jam the bacterium’s ribosomes, the machines that make proteins (How does a gene make a protein?). Bacterial ribosomes are a different shape from yours.
Ciprofloxacin stops an enzyme the bacterium needs to copy its DNA.

The drug fits its target the way a key fits a lock. If the lock changes shape, the key no longer works.

A colorized electron microscope picture of a heap of golden-brown, rod-shaped bacteria on a rough surface, against a black background, with a 1 µm scale bar — **Figure 28.1** *E. coli* bacteria, photographed through an electron microscope at 10,000 times. Each rod is about 2 µm long: 500 of them end to end would span a millimeter. A few kinds of *E. coli* cause diarrhea and urine infections; most live harmlessly in your gut. Photo: Photo by Eric Erbe, digital colorization by Christopher Pooley, both of USDA, ARS, EMU., Public domain

Your friend has a cold and asks for an antibiotic “to be safe”. What is the best reply?

Pick an answer to see why.

Four ways to survive

A bacterium that survives a drug that kills others of its kind is resistant to it; one that is killed is susceptible. A hospital laboratory finds out which by spreading bacteria from a patient on a dish of jelly and laying small paper discs on it, each soaked in a different antibiotic. Where a drug kills the bacteria, a clear ring forms around its disc.

A square dish covered in a pale streaky film of bacteria, with sixteen small white paper discs in rows; around most discs is a dark clear circle with no bacteria, of different sizes, but around one the bacteria grow right up to the paper — **Figure 28.2** A test of which antibiotics work on *Staphylococcus aureus* bacteria. Each paper disc holds a different antibiotic. A clear circle means the drug stopped the bacteria. Where the bacteria grow right up to a disc (bottom row, second from left), they resist that drug. Photo: Dr Graham Beards, CC BY-SA 4.0

Resistance comes down to a few tricks, each made by a gene.

Figure 28.3 Four ways a bacterium survives an antibiotic, and how the gene for one can pass to another bacterium. Not to scale: the drug molecules and proteins are thousands of times smaller than drawn.

Break the drug. An enzyme cuts the drug molecule before it can act. Penicillinase (one of the β-lactamases) breaks open the ring in penicillin that does the damage.
Pump it out. Proteins in the cell’s membrane pump the drug out as fast as it gets in.
Change the target. A small change in the gene for the target changes its shape a little. The cell still works, but the drug no longer fits.
Keep it out. Fewer openings in the cell’s outer layer let less of the drug in.

The genes for these tricks come in two ways. A mutation, a copying error in the bacterium’s own DNA, can change a target (trick 3) or turn up a pump. And many bacteria carry small extra rings of DNA called plasmids, which they can copy and pass to a neighbor through a thin tube, even to a different kind of bacterium. A plasmid can carry the genes for several tricks at once. This is why one bacterium can become resistant to five or six drugs in a single step.

A plasmid carrying a gene for penicillinase passes from a resistant bacterium to a susceptible one. What happens?

Pick an answer to see why.

Resistant before the drug arrives

Does an antibiotic make some bacteria resistant, the way exercise makes muscles strong? Or were the resistant ones already there, by chance, before the drug arrived? In Grade 9 you saw that Darwin’s natural selection needs variation first: the giraffes’ necks already differed before the drought Grade 9: Natural selection. For bacteria, nobody knew until 1943.

A story from science

A slot machine and a broken test tube

In 1943 the Italian biologist Salvador Luria, who had fled Mussolini’s Italy and then the Nazis in France, was working at Indiana University in the USA on bacteria and the viruses that attack them. Some bacteria survived the viruses. Had the virus made them resistant, or were they resistant already?

One evening early in 1943, at a faculty dance, he was watching a colleague play a slot machine, a gambling machine that mostly pays out nothing, and now and then a jackpot. He realized that bacteria could behave the same way. If resistance happens by chance while bacteria grow, then in most flasks a resistant mutant would appear late, and leave only a few resistant descendants. But in a rare flask, a mutant would appear early, and its descendants would double and double: a jackpot. If instead the virus made bacteria resistant only when they met it, every flask would give about the same number.

He grew many separate cultures of the same bacteria, spread each on a dish with the virus, and counted the survivors. The counts were wildly uneven: many dishes had none, a few had hundreds. The physicist Max Delbrück worked out the mathematics, and their paper of 1943 showed that resistance arises by chance mutation, before the bacteria meet the virus. They shared a Nobel Prize in 1969, with Alfred Hershey. The same test, the fluctuation test, has since shown the same for antibiotics.

A black-and-white photograph of a man in glasses, a white shirt and a striped tie, talking at his desk in an office with bookshelves, a telephone and diagrams pinned to the wall — **Figure 28.4** Salvador Luria at his desk at the Massachusetts Institute of Technology, around 1969, the year of his Nobel Prize. Photo: U.S. National Library of Medicine, Public domain

Twenty cultures of the same bacteria are grown, then each is spread on a dish with the drug. Each dot is a colony grown from one resistant bacterium. Compare the two explanations, then grow new sets of cultures and see if the pattern holds.

Explanation:

A new set of 20:

Average per dish: 10.1
Fewest to most: 0 to 128
Dishes with none: 3

If mutations happen by chance while the cultures grow, most cultures get a late mutant or none, and a few get an early one that doubles and doubles: a jackpot. This is what Luria and Delbrück saw.

A model: each culture grows from one bacterium to about 134 million; with chance mutations, each division has a 1 in 100 million chance of making a resistant mutant. The other explanation is set to give about 8 per dish.

Look at the spread, not just the average. If the drug caused resistance, the dishes would differ only a little, the way coin tosses do. With chance mutations, they differ enormously. In 1952 Joshua and Esther Lederberg went further: by copying dishes of bacteria onto fresh dishes with a pad of velvet, they picked out bacteria resistant to streptomycin from a population that had never touched the drug.

So the drug doesn’t create resistance. It finds the rare bacteria that already have it.

Worked example

How many mutants, without any drug?

A mutation that makes E. coli resistant to the drug rifampicin happens roughly once in every 100 million (10⁸) cell divisions. A culture grows from a single bacterium to 1,000,000,000 (10⁹) bacteria overnight. About how many rifampicin-resistant mutations happen while it grows, without any rifampicin near it?

Answer

To go from 1 cell to 10⁹ cells takes about 10⁹ divisions (each division adds one cell).
$\text{mutations} \approx 10^{9}\ \text{divisions} \times \frac{1}{10^{8}}\ \text{per division} = 10$
About 10 resistant mutants arise, by chance, in one overnight culture. Some will have divided and left a small family of resistant bacteria. Add rifampicin, and these few families are all that grow.

Counting the change

How fast does a rare resistant bacterium take over? Count it, generation by generation.

Bacteria multiply fast. In a warm flask with plenty of food, E. coli divides about every 20 minutes; in the body usually more slowly, but still far faster than any animal breeds. You and your parents are one human generation apart, about 25 years. In 25 years, E. coli in a flask could pass through over 600,000 generations. That is why we can watch bacteria evolve.

Here is a simple model of an infection being treated, with numbers made up to be easy to follow, but in the right range:

At the start there are 1,000,000 susceptible bacteria and 1 resistant one.
Each generation, the drug kills 9 out of every 10 susceptible bacteria; the survivors divide in two. So the susceptible ones are multiplied by 0.1 × 2 = 0.2 each generation.
The resistant ones are not harmed. But resistance costs a little: making an extra pump or enzyme uses food and energy. Say they leave 5% fewer offspring, so they are multiplied by 2 × 0.95 = 1.9 each generation.

Worked example

The share of resistant bacteria, generation by generation

Using the model above, work out the number of each kind and the percentage that are resistant for generations 0, 1 and 2.

Answer

Percentage resistant = resistant ÷ (resistant + susceptible) × 100%.

Generation	Susceptible	Resistant	Resistant (%)
0	1,000,000	1	1 ÷ 1,000,001 = 0.0001%
1	1,000,000 × 0.2 = 200,000	1 × 1.9 = 1.9	1.9 ÷ 200,001.9 = 0.00095%
2	200,000 × 0.2 = 40,000	1.9 × 1.9 = 3.61	3.61 ÷ 40,003.61 = 0.009%

(Numbers like 1.9 bacteria are averages: in some infections there would be 1, in others 2 or 3.) The share is still tiny, but it is growing nearly ten times each generation. Look at the ratio of resistant to susceptible: it is multiplied each generation by 1.9 ÷ 0.2 = 9.5.

Here is the same model, with a sample of 50 of the bacteria shown above the graph. Give the drug for a few generations, then stop it, and watch how the share of resistant bacteria changes.

Antibiotic:

Time:

Generation: 0
Resistant: 1 in 1,000,001
Resistant in the sample of 50: 0

One bacterium in a million is resistant. Press Next generation and watch the share.

A model with made-up numbers: the drug kills 9 in 10 susceptible bacteria each generation; resistant ones leave 5% fewer offspring; only the shares are shown, as if there were always room for the survivors to multiply; no chance, no immune system.

The graph has the shape of a stretched letter S. For generations nothing seems to happen: one in a million, one in a hundred thousand, still too few to find in a sample. Then, within two or three generations, resistant bacteria become most of the population. Doctors often notice resistance only at this point, when a drug that worked last year suddenly fails.

Stop the drug, and the cost of resistance shows: the susceptible ones now leave a few more offspring, and the resistant share slowly falls. But far more slowly than it rose: the drug gave the resistant ones a huge advantage; without it, their disadvantage is small.

Activity

Investigate: selection with paper squares

You need: about 150 squares of paper of one color and 100 of another, all the same size (about 2 cm; cut from old exercise-book covers or colored paper), a bag or a tin you can’t see into, and a notebook.

The squares of the first color are susceptible bacteria, the second color resistant.

Put 49 susceptible squares and 1 resistant square in the bag: a population of 50.
The bacteria divide. For every square in the bag, add another of the same color from your spare pile (now 100).
The drug. Tip them out and take away half of the susceptible squares (round down). Leave every resistant one.
Room for only 50. Put them back, shake, and without looking draw out 50. These are the next generation. Put the rest back in your spare pile.
Count and write down the resistant squares in your 50, and work out the percentage. Repeat steps 2 to 5 for eight generations, then draw a graph of the percentage resistant against generation.
Now do it again with no drug: skip step 3. This is your control.

What you should see

With the drug, the number of resistant squares roughly doubles each generation at first: 1, about 2, about 4, about 7, about 12… In about six to eight generations most of your 50 are resistant, and your graph has the stretched S shape. Without the drug, the one resistant square stays rare: it may vanish by chance, or now and then become two or three, but it doesn’t take over. Compare your graph with a classmate’s: the curves have the same shape, but not exactly the same numbers, because of the chance in step 4.

In a model like the one above, the drug kills more of the susceptible bacteria each generation (the drug is stronger). What happens to the time it takes for resistant bacteria to become most of the population?

Pick an answer to see why.

If the drug kills more susceptible bacteria, they are multiplied by a smaller number each generation, so the ratio of resistant to susceptible grows faster. A stronger selection pressure means faster change, as long as there are some resistant bacteria to start with. With none at all, a strong drug wipes out the infection, which is why it matters to treat the right infection with the right drug and the right dose, as a doctor decides.

The drug in the environment

Natural selection always works the same way: where something in the surroundings, a predator, the cold, a drought, or a drug, kills some variants more than others, the share of the survivors’ genes rises. Change the surroundings, and the share changes. Antibiotics give us unusually clear evidence of this, because we know exactly where the drug is and how much.

A story from science

Bacteria on a giant dish

In 2016, Michael Baym, Roy Kishony and their team at Harvard made a dish 120 cm long and 60 cm wide, the MEGA-plate. They filled it with jelly for bacteria to live on, in nine bands. The two bands at the ends had no drug. Moving towards the middle, each band had ten times more of the antibiotic trimethoprim than the one before: 3, 30, 300 and, in the middle, 3,000 times the smallest dose that stops the original E. coli. They put the bacteria at the two ends and filmed from above.

The bacteria spread quickly across the bands with no drug, then stopped at the edge of the first band with the drug. After a while, at one or two points along the edge, a mutant appeared that could live there, and its descendants spread into the band like a fan. At the next band they stopped again, until another mutation appeared among those. In about ten days, bacteria reached the middle, living in more than a thousand times the dose that had stopped their ancestors. Sequencing their DNA, the team could trace each step to new mutations. And the bacteria leading the front were not always the most resistant: they were the ones that happened to be in the right place first.

A model of the MEGA-plate. Bacteria start at both ends. They can only move into a stronger band after a new mutation lets them live there. Watch where the mutations happen, then run it again: the steps are the same, but where and when they happen changes each time.

Strongest drug reached: 0
Mutations that broke into stronger drug: 0

Bacteria are at both ends, where there is no drug. Press Start.

A model of the real experiment, with made-up chances: bacteria spread into a patch they can live in, and a new mutation lets a few into a band one step stronger. Colors show how many resistance mutations a patch’s bacteria have.

The same thing happens outside the laboratory, with real numbers.

When a drug is used less, resistance to it falls. In Finland in the early 1990s, doctors were asked to give fewer macrolide antibiotics (erythromycin and its relatives) for throat and skin infections. Macrolide use fell from 2.40 to 1.38 doses per 1,000 people a day between 1991 and 1992, and then stayed low. The share of throat and skin streptococci resistant to erythromycin fell from 16.5% in 1992 to 8.6% in 1996.
When the drug changes, the bacteria change. In Nepal and India in the late 1980s and the 1990s, many typhoid bacteria became resistant to the old drugs chloramphenicol, ampicillin and co-trimoxazole. Doctors moved to ciprofloxacin. In the years after, typhoid resistant to the old drugs became uncommon, while resistance to ciprofloxacin rose, until the 2014 trial in Kathmandu found it failing.
Where antibiotics are used more, resistance is commoner. Hospitals, where many patients take antibiotics, have more resistant bacteria than homes do. Farms where chickens are fed antibiotics to make them grow faster have more resistant bacteria in the chickens and in the soil around them. This is why many countries, Nepal among them, have banned colistin, one of the last drugs that still work on some resistant bacteria, for farm animals.

Did you know?

How common is resistance?

In 2025 the World Health Organization (WHO) published data from 104 countries. In 2023, about 1 in 6 bacterial infections confirmed in a laboratory was resistant to antibiotics. In WHO’s South-East Asia Region, which includes Nepal and India, it was about 1 in 3; in Europe, about 1 in 10. Between 2018 and 2023, resistance rose for more than 40% of the drug–bacterium pairs the WHO tracks. A large study published in 2024 estimated that resistant bacteria directly caused about 1.14 million deaths worldwide in 2021. That is serious. But the same study found that deaths from resistant infections among children under five had fallen by more than half since 1990, thanks to vaccines, clean water and better care. Most infections are still treatable, and what people do makes a difference.

In Finland, resistance to erythromycin fell after doctors used it less. Which explanation fits natural selection best?

Pick an answer to see why.

Why two drugs at once

Tuberculosis (TB), caused by the bacterium Mycobacterium tuberculosis, is still one of the commonest serious infections in Nepal. It is never treated with one drug. Patients take a combination, usually four drugs for the first two months. The reason is a calculation of chances.

The lung of a person with advanced TB can hold a cavity containing roughly 100 million (10⁸) TB bacteria. Spontaneous mutants resistant to the main TB drugs turn up at about these rates:

Drug	Resistant mutants in an untreated population (roughly)
isoniazid	1 in 1,000,000 (10⁶)
rifampicin	1 in 100,000,000 (10⁸)
ethambutol	1 in 100,000 (10⁵)

The mutations for different drugs are in different genes, and happen independently. The chance that one bacterium has both is the product of the two chances: just as the chance of two sixes with two dice is 1/6 × 1/6 = 1/36.

Figure 28.5 How many bacteria in a TB cavity of 100 million are expected to be resistant already, before treatment starts, to each drug alone, and to two or three drugs together. Each step on the scale is ten times the one before.

When TB treatment goes wrong, with doses missed or drugs taken alone, multidrug-resistant TB (MDR-TB) can evolve: TB that isoniazid and rifampicin no longer kill. The WHO estimated that in Nepal in 2018 about 2 in every 100 new TB patients, and about 15 in 100 patients who had been treated before, had TB resistant to rifampicin. It can still be cured, but with longer treatment and harder drugs. The same reasoning about chances is why HIV is treated with three drugs at once.

Slowing it down

You can’t stop bacteria mutating. But resistance spreads only where antibiotics are used, so how we use them decides how fast it happens. The public-health messages from the WHO and Nepal’s health services:

Take antibiotics only when a qualified doctor or health worker prescribes them, and never for colds or flu, which are caused by viruses.
Take them exactly as prescribed: the right dose, at the right times, for as long as the doctor says.
Don’t share them, and don’t use leftovers. The drug for someone else’s illness may be the wrong one for yours.
Don’t buy them without a prescription. Studies in Nepal have found that between two-thirds and nearly all of the pharmacies visited would sell antibiotics without one (as of 2022).
Prevent infections, so that fewer antibiotics are needed: wash hands with soap, drink safe water, and get vaccinated. In April 2022 Nepal gave a typhoid vaccine to more than 7 million children aged 15 months to 15 years, and it is now part of every child’s routine vaccinations at 15 months.

In 2024 Nepal’s government adopted a National Action Plan on Antimicrobial Resistance (2024–2028), covering hospitals, pharmacies, farms and food together, because resistant bacteria move between all of them.

In short

Antibiotics kill bacteria by attacking a target that bacteria have and our cells don’t. Bacteria resist by breaking the drug, pumping it out, changing the target or keeping it out. The genes come from mutation, or from other bacteria on plasmids.
Resistant variants exist before the drug arrives, by chance: Luria and Delbrück’s fluctuation test showed it from the uneven spread of counts. The drug doesn’t cause resistance; it selects it.
Under a drug, the ratio of resistant to susceptible bacteria is multiplied each generation. The share rises from a tiny fraction to most of the population in an S-shaped curve, often in days, because bacteria breed so fast.
Change the environment and the shares change: resistance rises where a drug is used and can fall slowly where it is not, because resistance often has a small cost.
Combinations of drugs work because the chances of independent mutations multiply: resistance to two drugs at once is very rare.
Use antibiotics only when prescribed, exactly as prescribed; don’t share them or buy them without a prescription; prevent infections.

Questions

A patient with a bacterial infection is given an antibiotic. Which statement about the resistant bacteria in her body is correct?

Pick an answer to see why.

In a population, resistant bacteria are 1 in 1,000. Under a drug, the ratio of resistant to susceptible bacteria is multiplied by 10 each generation. About what share is resistant after 3 generations?

Pick an answer to see why.

a.

Explain, using the ideas of variation, inheritance and selection, how a population of bacteria becomes resistant to an antibiotic.

Answer

Variation: the bacteria in a population are not all the same. By chance mutation, or by receiving a plasmid, a few carry a gene that lets them survive the drug.
Inheritance: when a bacterium divides, both daughters get a copy of its DNA, so the offspring of a resistant bacterium are resistant too.
Selection: the antibiotic kills the susceptible bacteria, or stops them multiplying, while the resistant ones survive and multiply.
Generation after generation, the share of resistant bacteria rises until most of the population is resistant, and the drug no longer cures the infection. Because bacteria divide so fast, this can happen within days in one patient, and over a few years in a whole country.

b.

A student grows 10 cultures of the same bacteria, each from a few cells, then spreads each on a dish with an antibiotic and counts the resistant colonies. These are made-up numbers, in the pattern of real experiments.
Set A: 12, 9, 14, 11, 10, 13, 8, 12, 11, 10
Set B: 0, 1, 0, 3, 0, 107, 2, 0, 5, 1

a.Find the average (mean) number of colonies in each set.
b.Which set fits the idea that the antibiotic causes resistance, and which fits the idea that resistance arises by chance mutations while the bacteria grow? Explain.

Answer

a.Set A: total 110, mean 110 ÷ 10 = 11. Set B: total 119, mean 119 ÷ 10 = 11.9. The means are nearly the same.
b.Set A fits “the drug causes resistance”: if every bacterium has the same small chance of being changed when it meets the drug, every dish gets about the same number, with a small spread (8 to 14). Set B fits “chance mutations before the drug”: in most cultures a mutation happened late, or not at all, giving few or no colonies; in one, a mutation happened early, and its descendants doubled many times, giving a “jackpot” of 107. The huge spread, not the average, is the evidence. Luria and Delbrück’s real results looked like Set B.

c.

In Finland, macrolide antibiotic use fell from 2.40 to 1.38 doses per 1,000 people a day between 1991 and 1992, and stayed low. Erythromycin resistance in streptococci was 16.5% in 1992 and 8.6% in 1996.

a.By what percentage did the use of macrolides fall?
b.By what percentage did the share of resistant bacteria fall between 1992 and 1996?
c.Explain the change in resistance using natural selection.
d.Why can’t these numbers alone prove that using less of the drug caused the fall?

Answer

a.(2.40 − 1.38) ÷ 2.40 × 100% = 1.02 ÷ 2.40 × 100% ≈ 43%.
b.(16.5 − 8.6) ÷ 16.5 × 100% = 7.9 ÷ 16.5 × 100% ≈ 48%: resistance almost halved.
c.With less of the drug around, resistant bacteria had less advantage, while resistance still had a small cost. Susceptible bacteria left slightly more offspring each generation, so their share rose and the resistant share fell. The fall took years because the cost is small: selection without the drug is weak.
d.Something else might also have changed in those years, for example which strains of streptococci were spreading. A fall in resistance at the same time as a fall in use is evidence, and it fits what selection predicts, but stronger evidence would come from comparing places that cut their use with places that didn’t, or from following the same strains over time.

d.

A TB patient feels better after two weeks and starts taking only one of his four drugs, to “save money”. Using the idea of chances, explain why this is dangerous.

Answer

In a large TB infection, there are almost certainly some bacteria resistant to any one drug: for isoniazid, about 1 in a million, so about 100 in a cavity of 100 million. While all the drugs are taken together, each drug kills the bacteria that resist the others; a bacterium resisting all of them at once is so unlikely (around 1 in 10¹⁹ for three drugs) that there is almost certainly none. With one drug alone, the bacteria resistant to it survive and multiply, and the patient’s TB becomes resistant to that drug. Later, the same can happen with another drug, step by step, until he has multidrug-resistant TB, which is harder to cure and can spread to his family. (He should go back to his health worker, who can help with the cost: TB treatment in Nepal is free.)

e.

The WHO reported that in 2023 about 1 in 3 laboratory-confirmed bacterial infections in its South-East Asia Region was resistant, compared with about 1 in 10 in Europe.

a.Give two possible reasons, linked to natural selection, for the difference.
b.Only infections tested in a laboratory are counted. Why might this make the share of resistant infections look higher than it is among all infections, especially where tests are less common?

Answer

a.Possible reasons: antibiotics may be used more, or more often without a prescription, so resistant bacteria are favored more often; more infections spread through unsafe water and crowding, so resistant bacteria pass between people more; antibiotics may be used more on farms. More selection and more spread both raise the share of resistant bacteria.
b.Where laboratory tests are expensive or far away, people are often tested only when they are very ill, or when a first antibiotic has already failed. Those are exactly the infections most likely to be resistant. So the tested infections are not a fair sample of all infections, and the share of resistant ones among them may be higher than among all infections. Comparing regions needs samples chosen in the same way.

f.

The model in “Watch the share change” is simple. List three of its simplifications, and say for each how a real infection is different.

Answer

Any three of these, or others that are true:

The numbers are fixed (the drug kills exactly 9 in 10 susceptible bacteria; resistant ones always leave 1.9 offspring). In real life the drug’s level in the body rises and falls between doses, and so does how many it kills.
It has only two kinds of bacteria. Real resistance often comes in degrees, built up mutation by mutation, as on the MEGA-plate.
It ignores chance: with only one resistant bacterium at the start, in reality it might die before dividing, and the infection could be cured.
It ignores the immune system, which kills bacteria of both kinds and often finishes off a small infection.
It ignores plasmids passed between bacteria, new mutations during treatment, and bacteria arriving from other people.
It holds the population’s shares only, as if there were always room for the survivors to multiply; in the body, numbers fall as the drug works.

Think about it

Are pesticides the same?

Farmers in the Terai have found that some insect pests are no longer killed by sprays that once worked. Using what you have learned, explain how this might have happened. What would you advise, based on the same ideas as for antibiotics?

Answer

It is the same natural selection. In a large population of insects, a few have, by chance, genes that let them survive the spray (an enzyme that breaks it down, or a changed target in the nerves). Spraying kills the rest; the survivors breed and pass on the genes, and over a few seasons most of the pests are resistant. The same ideas help: spray only when needed (less selection), don’t spray the same chemical again and again (a different chemical kills the ones resistant to the first, as in combination treatment), and use other ways to control pests, such as crop rotation, resistant crop varieties and natural enemies, as in integrated pest management Grade 10: Grade 10: Chemical pesticides.

Where to go next

Why Aren’t You Exactly Like Your Brother or Sister? Where the variation that selection works on comes from: new mutations and the reshuffling of genes in every generation.
How Does DNA Show That All Life Is Related? Mutations build up over time, so the differences in DNA between living things are a record of how they are related.
How Do New Species Begin, and End? When selection works differently in two places for long enough, one species can become two.