A substance that kills susceptible bacteria or inhibits their growth through a biological target such as cell wall synthesis or translation. The effect depends on organism and exposure; growth inhibition, killing and selection of resistant survivors are different experimental outcomes.
A cephalosporin antibiotic in the beta-lactam family. It inhibits bacterial cell wall synthesis; organism susceptibility depends on more than the drug’s chemical class alone.
A tetracycline-family antibiotic that interferes with bacterial protein synthesis. Activity depends on entry, target interaction and resistance mechanisms rather than the drug name alone.
A beta-lactam antibiotic whose activity involves inhibition of bacterial cell wall synthesis. Penicillin also names a broader chemical family, so a particular formulation or derivative should be specified when its properties matter.
An aminopenicillin antibiotic acting on bacterial cell wall synthesis. Susceptibility can be altered by beta-lactamase activity and other mechanisms, separating target chemistry from whole-organism response.
Reduced killing under antibiotic exposure without a corresponding increase in the concentration inhibiting growth. It differs from growth-based antibiotic resistance.
Survival of a subpopulation during bactericidal exposure while the broader population remains susceptible. Regrown survivors can recover the original susceptibility; persistence is not synonymous with every persistent infection.
A cell that transiently survives a bactericidal antibiotic exposure without necessarily carrying inherited resistance. Its descendants can regain the original susceptibility, connecting physiological state with bacterial persistence rather than a changed growth-inhibition threshold.[ref]
Bacterial persistence as a phenotypic switch by Nathalie Q. Balaban and others. Phenotypic switching
The lowest tested antimicrobial concentration preventing defined visible growth under specified conditions. It measures an organism-level response, not just the catalytic efficiency of an isolated resistance enzyme.
A cephalosporin antibiotic in the beta-lactam family. Its substituents affect interactions with bacterial targets and resistance enzymes; susceptibility to beta-lactamase hydrolysis therefore depends on the particular enzyme rather than the family name alone.
A penicillin antibiotic, also called benzylpenicillin, that acts on bacterial cell wall synthesis. It is used as a reference substrate in some beta-lactamase measurements, separating an enzyme’s activity on one substrate from activity on the entire drug family.
The ability of a microorganism to grow under antibiotic exposure that inhibits a susceptible comparison, often reflected in an increased minimum inhibitory concentration. Survival alone does not establish resistance: antibiotic tolerance and bacterial persistence concern killing and survival without necessarily changing that growth threshold.
An aminoglycoside antibiotic that interferes with bacterial protein synthesis. Resistance can provide a selectable marker in molecular genetics, as in the 1973 plasmid construction experiment; survival under selection identifies a phenotype rather than every detail of the inserted DNA.
An antibiotic that interferes with bacterial protein synthesis. Its resistance markers have been used in molecular genetics, including the 1973 plasmid construction experiment, linking an experimentally selectable growth trait with carriage of a genetic construct.
