Q.32 Plasmid mediated antibiotic resistances in bacteria are acquired by
(A) hydrolysis by β-lactamase (penicillin resistance).
(B) expression of aminoglycoside modifying enzyme (kanamycin resistance).
(C) mutation in DNA gyrase (quinolone resistance).
(D) overproduction of dihydrofolate reductase (trimethoprim resistance).
Plasmid Mediated Antibiotic Resistance in Bacteria: MCQ Solved
Plasmid-mediated antibiotic resistances enable bacteria to acquire resistance genes via horizontal transfer, primarily through enzymatic inactivation or target protection. The correct answer to the question is both (A) and (B), as these involve plasmid-encoded enzymes for penicillin and kanamycin resistance, while (C) and (D) typically involve chromosomal mutations or other mechanisms.
Option Analysis
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(A) Hydrolysis by β-lactamase (penicillin resistance): Correct. β-lactamase enzymes, encoded by plasmids like those carrying TEM or AmpC genes, hydrolyze the β-lactam ring in penicillin, inactivating it. This is a classic plasmid-mediated mechanism observed in Enterobacteriaceae and Neisseria.
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(B) Expression of aminoglycoside modifying enzyme (kanamycin resistance): Correct. Plasmids encode aminoglycoside-modifying enzymes (AMEs) such as acetyltransferases (AAC), phosphotransferases (APH), or nucleotidyltransferases (ANT) that chemically modify kanamycin, preventing ribosomal binding.
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(C) Mutation in DNA gyrase (quinolone resistance): Incorrect for plasmid mediation. Quinolone resistance primarily arises from chromosomal mutations in gyrA/gyrB genes of DNA gyrase; plasmid mechanisms like qnr genes protect gyrase but do not involve mutations.
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(D) Overproduction of dihydrofolate reductase (trimethoprim resistance): Incorrect as stated. Plasmids typically encode drug-insensitive DHFR variants (e.g., dfrA genes), not overproduction of the chromosomal enzyme; overproduction is a rarer chromosomal mechanism.
Plasmid mediated antibiotic resistance in bacteria poses a major challenge in treating infections, as these extrachromosomal DNA elements facilitate rapid gene transfer among bacterial populations. This SEO-optimized guide breaks down the key mechanisms—hydrolysis by β-lactamase for penicillin resistance and expression of aminoglycoside modifying enzymes for kanamycin resistance—while clarifying why DNA gyrase mutations and dihydrofolate reductase overproduction are not primarily plasmid-based. Ideal for CSIR NET Life Sciences aspirants studying bacterial genetics and biotechnology.
Key Mechanisms
Plasmids carry resistance genes (R-plasmids) that confer advantages like antibiotic inactivation through enzymes. Common plasmid-mediated types include:
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β-lactamase production hydrolyzing penicillin’s β-lactam ring.
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Aminoglycoside modifying enzymes (e.g., AAC for kanamycin) adding acetyl, phosphate, or nucleotide groups to block ribosomal action.
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Efflux pumps or target protection (e.g., qnr for quinolones), though less common for the listed options.
These spread via conjugation, transforming sensitive bacteria into resistant ones quickly.
Clinical Implications
Plasmid mediated antibiotic resistance drives multidrug-resistant (MDR) pathogens like ESBL-producing E. coli. Unlike chromosomal mutations, plasmids enable inter-species transfer, accelerating global AMR crises. Strategies include plasmid-curing agents and novel inhibitors targeting transfer machinery.
