Invasion. 

Bacteria may invade a host passively through microtraumata or macrotraumata in the skin or mucosa. On the other hand, bacteria that invade through intact mucosa first adhere to this anatomical barrier, then actively breach it. Different bacterial species deploy a variety of mechanisms to reach this end:

 — Production of tissue-damaging exoenzymes that destroy anatomical barriers.

 — Parasite-directed endocytosis, initiated by invasins on the surface of the bacterial cells, causes the cytoskeleton of the epithelial cell to form pseudopods that bring about endocytosis.

 — Phagocytosis of enteropathogenic bacteria by M cells in the intestinal mucosa (cells that can ingest substances from the intestinal lumen by way of phagocytosis).


Spread. 

— Local tissue spread beginning at the portal of entry, helped along by tissue-damaging exoenzymes (hyaluronidase, collagenase, elastase, and other proteases). 

— Cell-to-cell spread. Bacteria translocated into the intracellular space by endocytosis cause actin to condense into filaments, which then array at one end of the bacterium and push up against the inner side of the cell membrane. This is followed by fusion with the membrane of the neighboring tissue cell, whereupon the bacterium enters the new cell (typical of Listeria and Shigella). 

— Translocation of macrophage-resistant bacteria with macrophages into intestinal lymphoid tissue following their ingestion by M cells. 

— Lymphogenous or hematogenous generalization. The bacteria then invade organs for which they possess a specific tropism.