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Antibiotic Resistance Evolution Lab

Watch natural selection play out inside a bacterial infection. The antibiotic kills the susceptible bacteria, while resistant survivors and new mutants multiply and take over. Change the dose, the treatment course, the starting resistance, the mutation rate, and the fitness cost, then run the simulation to see whether the infection is cleared or resistance evolves.

Guided Experiment: No treatment: who wins, susceptible or resistant?

Without any antibiotic, will the resistant strain or the susceptible strain dominate the population? Think about the fitness cost of resistance.

Write your hypothesis in the Lab Report panel, then click Next.

Bacterial Population Over Time

Line chart of susceptible and resistant bacteria over time with antibiotic concentration overlaid11001e41e61e81e90h12h24h36h48h60h72hTime (hours)Bacteria (log scale, cells)
Susceptible Resistant Total Antibiotic
Population compositionno bacteria
Population cleared

Controls

Time 0 / 72 h
x MIC
%
%

Current Readings

Press Run Experiment to start the simulation

Data Table

(0 rows)
#Dose(x MIC)CourseStart resistant(%)Final totalFinal resistant(%)Outcome
0 / 500
0 / 500
0 / 500

Reference Guide

Natural Selection and Antibiotic Resistance

Antibiotic resistance is evolution in action. A bacterial population is not all the same. A few cells may already carry genes that let them survive a drug. When an antibiotic is used, it kills the cells that cannot resist and spares the ones that can.

The survivors reproduce and pass their resistance to the next generation. Over time the resistant cells make up more and more of the population. The antibiotic did not create the resistance. It selected for cells that already had it.

Step 1Variation in the population Step 2Antibiotic kills susceptible cells Step 3Resistant cells survive Step 4Resistant cells multiply and spread

Susceptible vs Resistant and the Fitness Cost

Susceptible bacteria are killed by normal doses of an antibiotic. Resistant bacteria can survive much higher concentrations because of a protective trait, such as a pump that removes the drug or an enzyme that breaks it down.

Resistance is not free. Making those extra proteins costs energy, so resistant cells often grow more slowly than susceptible cells when no antibiotic is present. This fitness cost is why resistance usually stays rare until a drug gives the resistant cells an advantage.

No antibioticSusceptible grows faster With antibioticResistant survives Fitness costSlower resistant growth ResultResistance rare until selected

Why Finishing the Full Course Matters

Doctors stress finishing a full course of antibiotics for a reason. The first cells to die are the most susceptible. The hardier and partly resistant cells take longer to kill. If you stop early, those tougher survivors are still alive.

Once the drug clears from the body, the survivors rebound. The infection can return, and the bacteria that grow back are the ones that were hardest to kill in the first place. A full course keeps the drug present long enough to finish the job.

Full courseClears survivors Stopped earlySurvivors rebound Low doseSelects for resistance Right dose and timeBest chance of cure

Mutation, MIC, and How Resistance Spreads

New resistance can also appear by random mutation as bacteria copy their DNA. Most mutations do nothing or are harmful, but a rare one can protect against a drug. The more cells divide, the more chances there are for such a mutation to appear.

The minimum inhibitory concentration, or MIC, is the lowest drug level that stops a strain from growing. Resistant strains have a much higher MIC. Resistance genes can also pass between bacteria directly, which lets it spread quickly through a population.

MICDose that stops growth Resistant MICMuch higher than normal MutationRandom source of resistance Gene transferSpreads resistance fast

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