Pathogenesis of septicaemia: aspects of cellular defence mechanisms

In the secondary defence line against bacterial invasion, the phagocytic cell systems serve as effector mechanisms of specific and unspecific immunity. In bacterial infections including septicaemia the outcome of the host-parasite interaction is determined by the ability of the mono- and polymorphonuclear phagocytes to recognize and kill the invading organisms in the presence of humoral and lymphocytic factors. The quantitative aspects of phagocytic deficiency is well recognized, in general and the risk of bacterial infection in a given patient is related directly to the duration of granulocytopenia and inversely to the number of circulating granulocytes. Reduced numbers of monocytes or, as in the splenectomized patient, lack of tissue macrophages may also add to increase suseptibility to infection with certain bacteria. Functional defects in phagocytosis in the presence of normal peripheral neutrophil and monocyte counts become increasingly important with the sophisticated procedures of modern medicine. In reviewing the functional capacity of the phagocytes it is convenient to consider four interrelated phases: 1) the vascular phase characterized by amrgination, adherence and diapedesis of the cells, 2) the chemotaxis of the directed movement of the cells to site of microbial invasion, 3) the phagocytosis or ingestion of microorganisms, and 4) the cellular factors involved in the killing and decomposition of the microorganisms. Enhanced susceptibility to infection has been related to defects in any of these functions, and the basic types of inborn or acquired abnormalities are reviewed. The problems of iatrogenic defects in antimicrobial host resistance may, hopefully, be reduced by an increasing knowledge in pathophysiology and the various steps involved in the cellular defence mechanisms.