In infections with pathogens such as streptococci and staphylococci, phagocytosis is the most important defense mechanism of the host, a function restricted to a few specialized cell types, the polymorphonuclear leukocytes and the monocytes of the blood and the macrophages of the tissues. However, in infections caused by pathogens that multiply inside of host cells, this is not true at all. For one thing, phagocytosis is not a mechanism of host resistance against intracellular parasites, it is an opportunity for them to reach the environment in which they multiply. For another, many intracellular parasites are taken up by and multiply within host cells not usually thought of as being phagocytic. The growth of the tranchoma agent is conjunctival epithelia and the growth of typhus rickettsiae in the endothelial cells lining small blood vessels are good examples. If phagocytosis is the evolutionary response of the host to the threat of invasion by pathogenic microorganisms, then intracellular parasitism is the counter-response of the would-be invader. It is the evolution of mechanisms for turning the host's weapon of phagocytosis against itself. The host cell is the walled city of Troy, and phagocytosis is the wooden horse that carries the intracellular parasites through the open city gates. How intracellular parasites get into host cells has been a neglected subject of investigation, but with growing appreciation of the importance of intracellular parasitism in the total infectious disease picture, phagocytosis of intracellular parasites is now receiving more attention. In today's lecture, I will tell you how recent work in my own and in other laboratories has provided the first tentative and incomplete answers to two questions. How do intracellular parasites get inside host cells? Are they phagocytosed like other microorganisms or do they have special mechanisms of entry? How do intracellular parasites avoid being killed and digested by host cells?