[Status febrilis: humoral and cellular factors]

Clinical fever seems clearly associated with those diseases in which inflammation, in one form or other, plays a dominant role. The actual contribution of the various listed factors to the febrile response associated with any specific disease may, of course, be complex. For instance in a gram-positive infection, inflammatory cells may be activated to produce endogenous pyrogen at the site of bacterial multiplication by any or all of the following mechanisms, most of which have been demonstrated experimentally: phagocytosis of bacteria, chemotactic factors produced by bacteria or released from injured tissue of complement activation, immune reactions (either cellular or antibody-mediated) in a previously sensitized host, and toxins, e.g. endotoxins which may activate phagocytic cells directly.