Antimicrobial Drugs, Microorganisms, and Phagocytes

Abstract

The literature on the interaction between antimicrobial drugs, microorganisms, and phagocytes is reviewed. Critical assessment of the methods used in various studies is indispensable in the interpretation of results. The available data seldom permit firm conclusions, but a number of interactions can be postulated. Chemotaxis is influenced by beta-lactam antibiotics, which induce an increased release of chemoattractants from bacteria; inhibitors of protein synthesis (erythromycin, tetracyclines) reduce the release of chemoattractants. Rifampin and tetracyclines inhibit chemotactic activity of granulocytes. Phagocytosis is diminished by tetracyclines and bacitracin. Intracellular killing is impaired by trimethoprim and sulfamethoxazole. Antimicrobial drugs that inhibit protein synthesis alter the surface of bacteria, changing the opsonic requirements for phagocytosis. Antimicrobial agents that act on the cell wall or disrupt the organization of the outer membrane of gram-negative bacteria increase bacterial vulnerability to the lethal action of granulocytes. Cellular enzymes of granulocytes act synergistically with a variety of drugs. Synergism between monocytes and penicillins has also been shown. The degree of penetration of an antimicrobial drug into phagocytic cells is not correlated with the intracellular activity of the drug. Polymyxin B, colistin, rifampin, vancomycin, clindamycin, and quinolones kill bacteria phagocytosed by granulocytes. Penicillins, rifampin, and chloramphenicol show microbicidal activity against bacteria ingested by monocytes or macrophages.