Antibiotic Resistance and Genetic Plasticity (2B)
Help Questions
MCAT Biological and Biochemical Foundations of Living Systems › Antibiotic Resistance and Genetic Plasticity (2B)
A clinician notices that a patient’s Klebsiella isolate becomes resistant to two unrelated antibiotics during therapy. Genome sequencing reveals no new chromosomal mutations but identifies a newly acquired plasmid carrying two resistance genes. The plasmid is readily transferred to a lab strain during co-culture, but transfer is blocked when cell-to-cell contact is prevented using a membrane that allows diffusion of small molecules but not bacteria. Which mechanism best explains the observed resistance?
Translation errors creating transient resistance proteins without genetic change
Conjugation requiring direct contact to transfer a multi-resistance plasmid
Transduction mediated by bacteriophages that diffuse through the membrane
Transformation by uptake of naked plasmid DNA diffusing across the membrane
Explanation
The skill being tested is identifying conjugation as a contact-dependent resistance transfer mechanism. Conjugation involves pilus-mediated plasmid transfer between touching cells, often carrying multiple resistance genes, and is blocked by preventing contact. In this Klebsiella case, a new plasmid with two resistance genes is acquired, transferable in co-culture but not across a contact-preventing membrane. Choice A is correct as it fits the direct contact requirement for plasmid transfer. Choice B fails because transformation uses free DNA, which diffuses through the membrane, but transfer was blocked. To verify, use membrane separation experiments in similar setups. Confirm plasmids via sequencing and test for multiple resistance linkage.
A bacterium becomes resistant to rifampin, which targets bacterial RNA polymerase. Sequencing shows a single nucleotide change in rpoB (RNA polymerase beta subunit). In vitro transcription assays show normal transcription rate but rifampin no longer inhibits the enzyme. Based on the data, which genetic change is most consistent with the resistance observed?
Deletion of the rpoB gene that forces the cell to use eukaryotic RNA polymerase
A synonymous mutation in rpoB that reduces translation of RNA polymerase
A missense mutation in rpoB that alters the rifampin binding site without abolishing function
A frameshift mutation in rpoB that truncates RNA polymerase and prevents transcription
Explanation
The skill being tested is recognizing missense mutations in target genes for resistance. Missense mutations change amino acids, altering drug-binding sites in essential proteins like RNA polymerase without losing function. Here, a single rpoB nucleotide change allows normal transcription but prevents rifampin inhibition. Choice B is correct as it describes a missense mutation modifying the binding site while preserving enzyme activity. Choice C is incorrect because a frameshift would truncate and inactivate the polymerase, halting transcription. In similar analyses, classify mutation types via sequencing. Test functionality with in vitro assays to ensure viability.
A lab compares two E. coli populations exposed to the same antibiotic. Population X is grown at a single high concentration and shows few survivors. Population Y is exposed to gradually increasing concentrations over several days and becomes highly resistant. Sequencing of Population Y reveals multiple mutations, including one in the drug target. What outcome is most likely given the adaptation described?
Population Y becomes resistant because antibiotics are metabolized into mutagens that specifically edit the target gene
Gradual exposure can allow stepwise selection of mutants with increasing resistance, leading to a more resistant population
Population Y becomes resistant because sensitive cells convert resistance proteins into DNA and pass them to offspring
High-dose exposure increases mutation rate in survivors in a directed way, producing identical resistant genotypes
Explanation
The skill being tested is comparing selection strategies in resistance evolution. Gradual antibiotic exposure enables stepwise accumulation of mutations, selecting increasingly resistant variants over time. In this E. coli comparison, Population Y's gradual exposure yields highly resistant mutants with multiple changes, including in the target. Choice A is correct as it explains stepwise selection leading to greater resistance. Choice B is incorrect because mutations are not directed; high-dose survivors show fewer adaptations. For analogous experiments, sequence genomes at intervals. Assess resistance levels via MIC to quantify evolution.
A bacterium becomes resistant to an antibiotic that binds a specific cell wall enzyme. Researchers find that resistant cells produce the same amount of enzyme as sensitive cells, but the enzyme’s amino acid sequence differs by one residue. The antibiotic concentration inside the cell is unchanged. Which mechanism best explains the observed resistance?
Epigenetic silencing of the enzyme gene, preventing the antibiotic from finding its target
Acquisition of a plasmid encoding a porin that increases antibiotic efflux
A point mutation causing an amino acid substitution that lowers antibiotic binding to the enzyme
Gene duplication of the enzyme locus, diluting the antibiotic among more targets
Explanation
The skill being tested is recognizing target modification via mutation in resistance. Point mutations can substitute amino acids in enzymes, reducing antibiotic binding without changing expression or intracellular levels. Here, resistant cells have one amino acid difference in the cell wall enzyme, with unchanged production and drug concentration. Choice B is correct as it explains lowered binding via substitution. Choice A fails because enzyme amounts are the same, not duplicated. For related problems, compare protein sequences and binding affinities. Measure expression and drug levels to rule out alternatives.
A lab strain gains resistance to chloramphenicol. The resistant strain carries a new plasmid encoding an acetyltransferase that chemically modifies chloramphenicol. When the plasmid is cured (lost), the strain becomes sensitive again, and no chromosomal mutations are detected. Which outcome is most consistent with this system?
Resistance will be lost when the plasmid is removed because the resistance determinant is plasmid-encoded
Resistance will persist because acetyltransferase activity is an irreversible environmental adaptation
Resistance will persist because plasmid genes automatically integrate into the chromosome during curing
Resistance will increase because plasmid loss triggers compensatory meiosis to generate resistant spores
Explanation
The skill being tested is distinguishing plasmid-mediated from chromosomal resistance. Plasmid-encoded resistance, like acetyltransferase modifying chloramphenicol, is lost upon plasmid curing, reverting sensitivity without chromosomal changes. Here, resistance is plasmid-linked and lost after curing, with no mutations detected. Choice A is correct as it explains loss due to plasmid removal. Choice B fails because plasmids do not automatically integrate; resistance reverts. To confirm, perform plasmid curing and sensitivity tests. Sequence chromosomes to exclude mutations.
A lab evolves Pseudomonas in the presence of an antibiotic that targets a specific enzyme. Resistant colonies arise at low frequency even when the antibiotic is absent, and their frequency increases only after antibiotic exposure. Sequencing shows different single-base substitutions in the enzyme gene across independent resistant colonies. Which mechanism best explains the observed resistance?
Bacteria acquire resistance by meiosis generating new allele combinations under stress
Resistant colonies arise because the antibiotic provides a carbon source that supports growth
Antibiotic exposure causes the same adaptive mutation to occur in every cell that encounters the drug
Random point mutations pre-exist, and antibiotic selection enriches mutants with reduced drug binding
Explanation
The skill being tested is explaining the role of pre-existing mutations in antibiotic resistance evolution. Random mutations occur independently of selection, and antibiotics enrich resistant variants by killing sensitive cells, as seen in fluctuation tests. In this Pseudomonas experiment, resistant colonies with varied enzyme gene mutations appear at low frequency without antibiotic, increasing post-exposure. Choice B is correct as it describes selection of pre-existing mutations reducing drug binding. Choice A is incorrect because antibiotics do not cause identical adaptive mutations in all cells; variations in mutations indicate randomness. For related questions, perform fluctuation tests to detect pre-existing mutants. Sequence multiple isolates to confirm mutational diversity.
A donor bacterium carrying a resistance plasmid is separated from a recipient bacterium by a filter that prevents cells from passing but allows small molecules and free DNA to diffuse. After incubation, the recipient remains sensitive. However, when donor and recipient are mixed without the filter, recipients become resistant. Which mechanism best explains the observed resistance?
Selection of resistant recipients caused by antibiotic molecules diffusing through the filter
Transformation by diffusion of plasmid DNA through the filter into the recipient
Conjugation requiring direct cell-to-cell contact for plasmid transfer
Transduction by bacteriophages that cannot cross the filter due to their small size
Explanation
The skill being tested is recognizing contact dependency in conjugation. Conjugation transfers plasmids via direct cell-to-cell contact, blocked by filters preventing bacterial passage but allowing DNA or small molecules. Here, resistance transfers only when mixed without filter, not when separated. Choice C is correct as it requires contact for transfer. Choice B fails because free DNA diffuses through the filter, but no transfer occurred. To verify, use filter separation experiments. Confirm by detecting plasmids in recipients post-mixing.
A bacterial population is exposed to an antibiotic that targets a metabolic enzyme. Resistant mutants carry a single base change that slightly reduces enzyme efficiency but prevents antibiotic binding. In antibiotic-free media, resistant mutants grow more slowly than wild-type. What outcome is most likely in a mixed culture without antibiotic over many generations?
Both genotypes will be eliminated because the enzyme mutation prevents any metabolism
Resistant cells will fix in the population because resistance mutations are always beneficial
Resistant cells will convert wild-type cells by secreting the mutated enzyme as a genetic template
Wild-type cells will tend to increase in frequency because they have higher fitness without antibiotic
Explanation
The skill being tested is understanding fitness trade-offs in mixed populations. Resistance mutations often carry costs, reducing growth in drug-free conditions, allowing wild-type to increase via competition. In this mixed culture without antibiotic, resistant mutants grow slower due to enzyme inefficiency. Choice D is correct as it explains wild-type frequency increase from higher fitness. Choice B fails because costly mutations do not fix without selection. For similar scenarios, compete genotypes in drug-free media. Monitor frequencies over generations to observe dynamics.
A researcher tests whether antibiotic resistance in a bacterial isolate is due to a chromosomal mutation or a plasmid. The isolate is resistant, but after several passages at high temperature (which destabilizes some plasmids), resistance is lost. Whole-genome sequencing shows no changes in the antibiotic target gene. Which mechanism best explains the observed resistance?
Resistance was due to a stable chromosomal point mutation that reverted because heat directly repairs DNA
Resistance was plasmid-mediated and was lost when the plasmid was cured during high-temperature passage
Resistance was caused by increased antibiotic concentration at high temperature selecting for sensitivity
Resistance was caused by permanent changes in membrane lipids that are inherited independently of DNA
Explanation
The skill being tested is differentiating plasmid from chromosomal resistance stability. Plasmids can be destabilized and lost (cured) by high temperature, reverting plasmid-mediated resistance without chromosomal alterations. In this isolate, resistance is lost after high-temperature passages, with no target gene changes. Choice A is correct as it explains curing of the resistance plasmid. Choice B fails because heat does not repair DNA; chromosomal mutations would persist. To confirm, use curing agents and sequence for plasmids. Test sensitivity pre- and post-treatment.
A bacterial isolate shows resistance to an antibiotic that targets DNA replication. Enzyme assays show the drug inhibits wild-type enzyme but not the resistant enzyme. Sequencing reveals a single nucleotide substitution in the replication enzyme gene; plasmid screening is negative. Which mechanism best explains the observed resistance?
Acquisition of a resistance gene by conjugation that replaces the replication enzyme with a eukaryotic homolog
Transformation by uptake of antibiotic molecules that act as mutagens to create resistance
Increased transcription of the replication enzyme that chemically degrades the antibiotic
A point mutation in the replication enzyme that reduces antibiotic binding while retaining activity
Explanation
The skill being tested is identifying target mutations in replication inhibitors. Point mutations in replication enzymes like gyrase can reduce antibiotic binding, conferring resistance while maintaining enzyme activity, without plasmids. Here, a nucleotide substitution in the enzyme gene prevents drug inhibition but allows normal function, with negative plasmid screens. Choice B is correct as it describes the mutation reducing binding. Choice A fails because no eukaryotic homolog replacement occurs; resistance is mutational. For related resistance, assay enzyme inhibition and sequence genes. Rule out plasmids via screening.