Contains a beta lactam ring structure. Betalactam antibiotics inhibit the growth of sensitive bacteria by inactivating transpeptidase enzymes located in the bacterial cell membrane, inhibiting crosslinkage of peptidoglycans and thus impairing cell wall synthesis

bactericidal

Binds to the bacterial 30S ribosomal subunit to inhibit protein synthesis and thus bacterial growth

Inhibits Glycopeptide synthetase  prevents peptidoglycan formation in bacterial cell well
(Unlike penicillins, prevents the transfer and addition of the muramylpentapeptide
building blocks that make up the peptidoglycan molecule itself.)
May also alter membrane permeability and selectively inhibit RNA synthesis.
Antimicrobial activity Dependent on Duration above MIC, not concentration

Bacteriocidal antimicrobials that block DNA replication by blocking tropoisomerase enzymes, which are essential for the supercoiling, replication and separation of circular bacterial DNA

Bacteria produce beta lactamases, which hydrolyse and inactivate the antibiotic

Resistance
MRSA
Many Staph
-Betalactamase prod

Alteration in access to target site – membrane impermeability / transport defect in the active transport.
Lack of O2-transport channels: Anaerobes
Multiple enzymes which block gentamicin (acetytransferases, adenyltransferases, phosphotransferases)

VanA resistance – gene mutation leading to decreased affinity of peptidoglycan precursors for vancomycin.
Induced by exposure to vanc / teicoplanin
Van B resistance – similar but only induced by vancomycin; strains may remain susceptible to teicoplanin

Alteration in target enzyme – changes to the DNA binding surface of DNA supergyrase infers resistance
Alteration in drug entry – altered expression of outer membrane porin proteins that form channels for passive diffusion of ciprofloxacin
Increase in efflux of drug – expression of nonspecific energy dependent efflux pumps which remove drug