The preceding discussion makes it clear that there are multiple determinants, related to the microorganism, the host defense cell, and the presence of activating T cell stimuli that must be considered when examining at the cellular level how and why intracellular pathogens are able to cause infection. From the standpoint of the interaction of the mononuclear phagocyte's antimicrobial mechanisms with T gondii, L donovani, and C psittaci, the determinants which appear to influence directly the outcome of intracellular infection include: a. the magnitude of the phagocyte's respiratory burst capacity; b. the ability to respond specifically and effectively to microbial ingestion with the generation of O2- and H2O2; c. susceptibility to H2O2; and d. the presence of and susceptibility to oxygen-independent mechanisms. T cell dependent enhancement of the mononuclear phagocyte's antimicrobial mechanisms is a particularly critical element in cellular resistance to infection, and thus, host defense. If the activated state is not properly achieved, the macrophage remains susceptible to and perpetuates intracellular infections.