Neither an enhancement of autolytic wall degradation nor an inhibition of the incorporation of cell wall material are pre-requisites for penicillin-induced bacteriolysis in staphylococci.
In contrast to what has been postulated, penicillin G at its optimal lytic concentration of 0.1 microgram per ml did not lead to a detectable activation of autolytic wall processes in staphylococci in terms of the release of uniformly labelled wall fragments from cells pretreated with the drug for 1 h. Rather a considerable inhibition of this release was observed. A similarly profound inhibition of the release of peptidoglycan fragments occurred when staphylococci pretreated for 1 h with 0.1 microgram penicillin per ml acted as a source of crude autolysins on peptidoglycan isolated from labelled normal cells of the same strain. This clearly demonstrated that the overall inhibition of autolytic wall processes caused by penicillin was mainly due to a decreased total autolysin action rather than to an altered wall structure. Furthermore, no substantial penicillin-induced inhibition of the incorporation of 14C-N-acetylglucosamine into the staphylococcal wall could be observed before bacteriolysis started, i.e., approximately during the first 80 min of penicillin action. These results are not consistent with any of the models hitherto proposed for the action of penicillin.
D001433:Bacteriolysis; D002473:Cell Wall / Q000187:drug effects / Q000378:metabolism; D010400:Penicillin G / Q000494:pharmacology*; D010457:Peptidoglycan / Q000032:analysis / Q000378:metabolism*; D013211:Staphylococcus aureus / Q000187:drug effects / Q000378:metabolism*
D010457:Peptidoglycan; D010400:Penicillin G