Q.75 Which one of the following is NOT correct about antibiotic resistance mechanism
in microbes?
(A) Mycoplasma is naturally resistant to penicillins due to presence of R plasmid.
(B) Gram–negative bacteria are impermeable to penicillin G.
(C) β–lactamases of bacteria can cleave penicillins.
(D) Selective microbes can efflux penicillins entering the cell and develop resistance.

Option (A) is NOT correct.

Mycoplasma exhibits natural resistance to penicillins due to the complete absence of a cell wall, rendering these antibiotics—which target cell wall synthesis—ineffective. This resistance is intrinsic and unrelated to R plasmids, which typically carry acquired resistance genes like those for β-lactamases in other bacteria.

Option Analysis

(A) Mycoplasma and R Plasmids

Mycoplasma lacks a cell wall, so penicillins cannot inhibit peptidoglycan synthesis, providing inherent resistance. R plasmids mediate transferable resistance via enzymes or efflux but are not the basis for Mycoplasma’s penicillin resistance, as this trait stems from its biology, not plasmids.

(B) Gram-Negative Impermeability

Gram-negative bacteria possess an outer membrane with porins that limits penicillin G entry, especially hydrophobic forms, contributing to intrinsic resistance. Reduced permeability via porin loss or modification further enhances this effect.

(C) β-Lactamase Action

Bacterial β-lactamases hydrolyze the β-lactam ring in penicillins, inactivating them and conferring resistance, a common enzymatic mechanism.

(D) Efflux Pumps

Certain bacteria use efflux pumps to expel intracellular penicillins, reducing effective concentrations and developing resistance, particularly in Gram-negatives.

Antibiotic resistance mechanisms in microbes pose major challenges in treating infections, especially with penicillins. This article breaks down a key CSIR NET-style MCQ on Mycoplasma penicillin resistance and related bacterial strategies, helping students master concepts like cell wall absence, impermeability, enzymatic cleavage, and efflux for competitive exams.

Core Mechanisms

Penicillins target penicillin-binding proteins (PBPs) to disrupt cell wall synthesis, but microbes evade this through:

• Intrinsic lack of cell wall in Mycoplasma, making penicillins irrelevant.

• Outer membrane barriers in Gram-negatives restricting entry.

• Hydrolytic enzymes like β-lactamases cleaving the β-lactam ring.

• Active efflux pumping out the drug.

Why Option A Fails

Mycoplasma’s penicillin resistance arises from no peptidoglycan target, not R plasmids, which spread acquired traits like β-lactamase genes in walled bacteria. This distinction is crucial for exam questions on natural vs. acquired resistance.

Exam Relevance

For CSIR NET Life Sciences, understanding these differentiates intrinsic (e.g., Mycoplasma) from acquired resistance (e.g., plasmids, mutations). Gram-negative porin alterations and efflux amplify resistance in pathogens like Pseudomonas.