The results of four studies described in this paper support the idea that pneumococcal autolysin (N-acetylmuramyl-L-alanine amidase) plays a key role in generating the pneumococcal purpura-producing principle (PPP) from the bacterial cell wall. This conclusion is based on the observation that (i) concentrates of pneumococcal cell-free extracts prepared at a pH which is inhibitory to autolysin activity contained significantly less PPP activity than extract concentrates prepared at a pH which is optimal for autolysin activity; (ii) PPP activity was not detectable in concentrates of cell-free extracts prepared from cells which contained ethanolamine in the cell wall, but a normal amount of activity was found in extract concentrates derived from cells containing choline in the cell wall; (iii) PPP activity was not detectable in concentrates of cell-free extracts prepared from an autolysin-defective mutant, but a normal amount of activity was found in extract concentrates derived from the wild-type strains; and (iv) incubation of purified wild-type strain cell walls with pneumococcal autolysin resulted in a significant increase in the amount of purpurogenic activity in the supernatant fluids of the incubation mixtures.
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Chetty et al. (1981) studied this question.
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