SUMMARY. The ability of aminoglycoside antibiotics and rifampicin to kill that had been ingested by blood polymorphonuclear leukocytes (PMNs) was investigated. Gentamicin and streptomycin failed to kill intracellular staphylococci, possibly because they could not penetrate PMNs or were inactivated by the low intraphagolysosomal H. Rifampicin accumulated within the leukocytes in a form that killed staphylococci in a cell-free medium, but the bactericidal activity of intracellular rifampicin against ingested staphylococci was much less than that in a cell-free system. Investigations with granules isolated from PMNs, at various H-values, revealed that the impairment of rifampicin activity was a result of limitation of the staphylococcal growth rate by a low H. These observations indicate that the inhibition of intraphagocytic bacterial growth by the low intraphagolysosomal H and other phagolysosomal bacteristatic factors determines the antimicrobial activity of accumulated antibiotics.


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