A NOVEL, HIDDEN PENICILLIN-INDUCED DEATH OF STAPHYLOCOCCI AT HIGH DRUG CONCENTRATION, OCCURRING EARLIER THAN MUROSOME-MEDIATED KILLING PROCESSES

In log-phase cells of staphylococci, cultivated under high, ''non-lyti c'' concentrations of penicillin G, there occurred a novel killing pro cess hitherto hidden behind seemingly bacteriostatic effects. Two even ts are essential for the appearance of this ''hidden death'': (i) the failure of the dividing cell to deposit enough fibrillar cross-wall ma terial to be welded together, and (ii) a premature ripping up of incom plete cross walls along their splitting system. ''Hidden death'' start ed as early as 10-15 min after drug addition, already during the first division cycle. It was the consequence of a loss of cytoplasmic const ituents which erupted through peripheral slit-like openings in the inc omplete cross walls. The loss resulted either in more or less empty ce lls or in cell shrinkage. These destructions could be prevented by rai sing the external osmotic pressure. In contrast, the conventional ''no n-hidden death'' occurred only much later and exclusively during the s econd division cycle and mainly in those dividing cells, whose nascent cross walls of the first division plane had been welded together. The se welding processes at nascent cross walls, resulting in tough connec ting bridges between presumptive individual cells, were considered as a morphogenetic tool which protects the cells, so that they can resist the otherwise fatal penicillin-induced damages for at least an additi onal generation time (''morphogenetic resistance system''). Such welde d cells, in the virtual absence of underlying cross-wall material, los t cytoplasm and were killed via ejection through pore-like wall openin gs or via explosions in the second division plane and after liberation of their murosomes, as it was the case in the presence of low, ''lyti c'' concentrations of penicillin. Bacteriolysis did not cause any of t he hitherto known penicillin-induced killing processes.