Table 1.
Bacterial resistance mechanisms against antibiotics.
| Antibiotic Resistance Mechanism | Characteristics | Example | Ref. |
|---|---|---|---|
| Target modification or mutation | Mutation or modification of bacterial site will interfere with target matching, thus affecting the effect of antibiotics | Modifying PBPs in MRSA, production of β-lactamases or carbapenemases in genus Klebsiella; fluoroquinolone-resistant S. aureus Mycobacterium tuberculosis resistance to rifampicin is mainly caused by the mutation of the rpoB gene and vancomycin-resistant Enterococcus (VRE) |
[29] |
| Reduced permeability | Deletion or damage of Omps is a source of bacterial resistance | Loss of porin D2 from outer cell wall in imipenem-resistant P. aeruginosa | [30] |
| Inactivating enzymes | Inactivating enzymes produced by bacteria, such as antibiotic hydrolases or similar enzymes, can hydrolyze or modify antibiotics inside the cell, rendering their inactivation before reaching the target site | Production of penicillin-inactivating β-lactamase by penicillin-resistant S. aureus, Haemophilus influenzae, and Escherichia coli bacteria, gentamicin-resistant enterococci via enzymatic inactivation of aminoglycosides and carbapenem-producing Enterobacteriaceae | [31] |
| Efflux pumps | Pumping of harmful molecules out of the bacterial cell | Increased efflux of tetracycline, macrolides, clindamycin, or fluoroquinolones in S. aureus | [32] |
| Metabolic enhancement or auxotrophy | Core genome mutations change metabolic pathways and induce antibiotic resistance | The genome of clinically pathogenic E. coli | [33,34] |
| Community cooperative resistance | Most bacteria coexist in communities, collectively resisting antibiotic effects; bacterial biofilms are efficiently protective of biofilm-forming bacterial species | P. aeruginosa, S. aureus, S maltophilia, and other bacteria | [35] |
| Target protective proteins (TPPs) | Bacterial synthetic protein protects antibiotic targets from antibiotics, eliminating their bacteriostatic effects | Clinically isolated S.aureus and other staphylococcus resistance to fusidic acid due to the level acquisition of genes encoding the FusB-type protein | [36] |
| Cell morphology changes | Modulating the body’s relative area via absorption efficiency changes can lead to the dilution of antibiotics entering the bacterial cell | Cells of the commonly used model organism Caulobacter crescentus | [37] |
| Self-repair systems | The multiple antibiotic resistance operon of enteric bacteria manipulates DNA repair and outer membrane integrity, enhancing antibiotic resistance | E. coli multiple antibiotic resistance (mar) loci was recognized as a determinant for cross-resistance to tetracyclines, quinolones, and β-lactams | [38] |
AR, antibiotic resistance; Ref., reference; MLSB = macrolide, lincoside, streptogramin; PB, penicillin-binding.