Antibiotic Resistance in a Hospital Outbreak
A hospital reports an outbreak of a bacterial infection. Culture shows a strain that is resistant to the first-line antibiotic but sensitive to a second-line drug. Reviewing records, clinicians find the first-line antibiotic was used heavily in the ward for two years. A colleague argues the bacteria "learned" to resist because they were exposed to the drug and that the second-line drug will eventually teach them to resist it too. Another colleague says the resistance allele was already present at low frequency before the drug was introduced and that the drug simply changed which bacteria survived. The team must decide how to use the second-line drug to slow resistance.
1. Evaluate the two colleagues' explanations and explain how natural selection produced the resistant population.
Read the worked answer
The second colleague is correct. Resistance arises from pre-existing genetic variation - for example, a mutation or a plasmid-borne gene - that existed at low frequency before the antibiotic was used. When the first-line drug is applied, it kills susceptible bacteria while resistant ones survive and reproduce. The drug is the selective pressure, not a teacher. The first colleague's "learning" idea is Lamarckian and wrong: bacteria do not acquire resistance because they were exposed; exposure only changes allele frequencies. The heavy use of the drug over two years increased the proportion of resistant cells through directional selection. This is observable as a rise in the frequency of the resistance allele in the population, not a change in any individual bacterium.
2. Recommend a strategy for using the second-line drug and justify it in terms of selection pressure and fitness cost.
Read the worked answer
Use the second-line drug only when needed and, where possible, combine it with other agents or rotate drug classes rather than using it continuously. Continuous single-drug exposure creates strong directional selection for any rare resistant variants, so the same process that produced first-line resistance will repeat. Combination therapy presents multiple independent targets, so a bacterium would need several resistance mutations at once, which is far less likely. Reserving the drug limits the time selection acts. Also consider that resistance often carries a fitness cost when the drug is absent; reducing drug pressure can allow susceptible strains to outcompete resistant ones, though this is not guaranteed if compensatory mutations arise. Monitor susceptibility over time so the strategy can be adjusted.