Table 1 Mode of action of antibiotics and mechanisms of bacterial antibiotic resistance

β-lactams

Cell wall synthesis inhibitors. Binds trans peptidase also known as penicillin binding proteins (PBPs) that help form peptidoglycan

Beta-lactamase production primarily - bla genes

Expression of alternative PBPs

[20,21,22]

β-lactamase inhibitors

Inactivates the enzyme; beta-lactamase

Hydrolysis of the beta-lactam ring

Production of extended spectrum beta-lactamases (ESBLs)

Fluoroquinolones

Binds DNA-gyrase or topoisomerase II and topoisomerase IV; enzymes needed for supercoiling, replication and separation of circular bacterial DNA.

Target modification

Decreased membrane permeability

Efflux pumps

[23]

Macrolides, Lincosamides and Streptogamin (MLS)

Binds the bacterial 50S ribosomal subunits; inhibit protein synthesis

Target site modification

Active drug efflux

[24]

Aminoglycosides

Bind to the bacterial 30S ribosomal subunit thus inhibit bacterial protein synthesis

Target site modification (via the action of 16S rRNA methyltransferases (RMTs))

Enzymatic Drug Modification (adenylation, acetylation and phosphorylation), Efflux systems

[25]

Tetracycline

Bind reversibly to the 30S ribosomal subunit as such blocks the binding of the aminoacyl-tRNA to the acceptor site on the mRNA-ribosome complex

Efflux systems, Target modification, Inactivating enzymes, Ribosomal protection

[26, 27]

Sulfonamides (Folate pathway inhibitors)

Inhibit the bacterial enzyme dihydropteroate synthetase (DPS) in the folic acid pathway, thereby blocking bacterial nucleic acid synthesis

Excessive bacterial production of dihydrofolate reductase (DHFR)

Reduction in the ability of the drug to penetrate the bacterial cell wall

Production of altered forms of the dihydropteroate synthetase (DPS) enzyme with a lower affinity for sulfonamides

Hyperproduction of para-amino benzoic acid (PABA), which overcomes the competitive substitution of the sulfonamides

[28, 29]