If the link between inhibition of cell wall synthesis and production of autolysins which cause the ninks is broken, bacteria are not killed. This may be one mechanism of resistance. Note the implication that the beta-lactams are effective in growing and dividing organisms. In this case, the drugs inhibit formation of the cross-wall which divides an elongating organism into two organisms. This results in abnormally elongated, grotesque, worm-like bacilli and the process is not completely understood.
Many antibacterials produce a post-antibiotic effect that is incompletely understood.
This effect, of varying duration depending on the drug and degree of damage done, helps explain why one may allow the concentration of cidal drugs like the beta-lactams to drop below the MIC for a target organism for a short time during each dose interval. The peptidoglycan transpeptidases may be thought of as one of the penicillin binding protein referred to in discussions of bacterial resistance elsewhere in this lecture. The beta-lactam must bind to these enzymes to be active. If the enzymes are modified in some way so that they do not bind the beta-lactam, the organism will be resistant to the drug. Although the beta lactam antibiotics are similar in many respects, there are differences among them with respect to pharmacokinetics, toxicity, and antibacterial activity.