The synthesis and excretion of β lactamase by several strains of from different clinical sources and the ability of both the extracellular and membrane-bound enzyme to mediate penicillin resistance was studied. When β-lactamase production was maximally induced with penicillin G or ampicillin, about 50% of the β lactamase was excreted from the cells, the amount of extracellular enzyme correlating well with the degree of resistance established by an in-vitro test model. From penicillin-binding experiments it became apparent, however, that the membrane-bound β lactamase can also constitute a barrier, strong enough on its own to prevent penicillins from reaching their target. This could be of clinical relevance if, under certain conditions , the β lactamase is insufficient for full protection of the staphylococcal cells.


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