mechanisms of antibiotic resistance in bacteria

Overview

further characterize resistance as a global health emergency, noting that resistance has been detected to all antibiotics currently in clinical use.

How Resistance Is Acquired

Bacteria may be innately resistant or may acquire resistance. Giedraitienė et al. (2011) identify the main routes of acquired resistance:

• Chromosomal mutation, leading to cross-resistance
• Horizontal gene transfer via plasmids (conjugation or transformation), transposons (conjugation), integrons, and bacteriophages (transduction)

This finding is corroborated for E. coli specifically: the most prevalent mechanism continues to be the acquisition of resistance genes through horizontal gene transfer, facilitated by mobile genetic elements such as plasmids and transposons .

Peterson & Kaur (2018) add an environmental dimension, noting that resistance genes are not confined to the clinic but are widely prevalent in environmental bacterial populations. Their transfer to plasmids and integrons in pathogenic bacteria can translate into a problem of large proportions .

Biochemical Resistance Mechanisms

Once resistance genes are acquired, bacteria deploy several biochemical strategies :

In E. coli, extended-spectrum β-lactamases (ESBLs) and carbapenemases play a prominent role in conferring resistance to β-lactam antibiotics, while efflux pumps and porin mutations mediate resistance to fluoroquinolones and aminoglycosides .

Plasmid-Mediated vs. Mutation-Driven Resistance

Zhang et al. (2025) investigate how the type of resistance mechanism shapes treatment outcomes. Their findings suggest that antibiotic treatments with fixed dosing schedules are more likely to be effective when resistance arises exclusively through plasmid-mediated transmission . In contrast, when treatment fails, mutation-driven mechanisms tend to favor selection of fully resistant bacterial strains .

Biofilm-Based Resistance

Biofilm communities represent a distinct resistance context. Hall & Mah (2017) describe biofilms as surface-attached microbial groups encased in an extracellular matrix that are significantly less susceptible to antimicrobials than planktonic cells. Contributing mechanisms include interaction of antimicrobials with biofilm matrix components, reduced bacterial growth rates, and specific genetic determinants of resistance and tolerance . Individually, each mechanism only partially accounts for the increased recalcitrance; acting together, they ensure survival even under aggressive treatment regimens . E. coli further employs adaptive strategies including biofilm formation and persister cell formation .

Environmental and Sublethal Exposure Contributions

Sublethal antibiotic or antimicrobial exposure can also drive resistance. Kaweeteerawat et al. (2017) found that bacteria (E. coli and S. aureus) pre-exposed to sublethal doses of silver nanoparticles exhibited increased resistance toward antibiotics, with IC50 values elevated by 3–13-fold, along with elevated MIC and MBC values across antibiotics with diverse mechanisms of action. Peterson & Kaur (2018) further note that selective pressure from human activities results in enrichment of resistance determinants in bacterial populations .

Path Forward

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