Fluorescence micrograph showing that the large ruffles that engulf the Salmonella bacteria are actin-rich. The bacteria are labeled in green and actin filaments in red; because of the color overlap, the bacteria appear yellow. (C, from Rocky Mountain Laboratories, NIAID, NIH; D, from
J.E. Galán, Annu. Rev. Cell Dev. Biol. 17:53–86, 2001. With permission from Annual Reviews.)
The protozoan Trypanosoma cruzi, which causes Chagas disease, in Mexico and Central and South America, uses two alternative invasion strategies. In a lysosome-dependent pathway, the parasite attaches to host cell-surface receptors, inducing a local increase in Ca2+ in the host cell’s cytosol. The Ca2+ signal recruits lysosomes to the site of parasite attachment, and the lysosomes fuse with the host cell’s plasma membrane, allowing the parasites rapid access to the lysosomal compartment (Figure 23–21). In a lysosome-independent pathway, the parasite penetrates the host-cell plasma membrane by inducing the membrane to invaginate, without the recruitment of lysosomes.
1. ATTACHMENT TO HOST 2. Ca2+ SIGNAL 3. FUSION OF LYSOSOMES     CELL-SURFACE RECEPTORS     RECRUITS LYSOSOMES WITH PLASMA MEMBRANE
Figure 23–20 The life cycle of the intracellular parasite Toxoplasma gondii.
After attachment to a host cell, T. gondii uses its conoid to inject effector proteins that facilitate invasion. As the host cell’s plasma membrane invaginates to surround the parasite, it somehow removes the normal host-cell membrane proteins, so that the compartment (shown in red) does not fuse with lysosomes. After several rounds of replication, the parasite causes the compartment to break down and the host cell to lyse, releasing the progeny parasites to infect other host cells (Movie 23.6).
Light micrograph of T. gondii replicating within a membrane-enclosed compartment (a vacuole) in a cultured cell. (B, courtesy of Manuel Camps and John Boothroyd.)
HOST CYTOSOL TrypanosomacruziCa2+ Ca2+ compartment derived from lysosomal membranelysosomes lysosomes early endosome 5. SECRETION OF PORE-FORMING PROTEIN REPLICATION 4. INVASION 6. LYSIS OF SURROUNDING MEMBRANE, RELEASE OF PATHOGEN INTO CYTOSOL
Figure 23–21 The two alternative strategies that Trypanosoma cruzi uses to invade host cells. In the lysosome-dependent pathway (left),
T. cruzi recruits host-cell lysosomes to its site of attachment to the host cell. The lysosomes fuse with the invaginating plasma membrane to create an intracellular compartment constructed almost entirely of lysosomal membrane. After a brief stay in the compartment, the parasite secretes a pore-forming protein that disrupts the surrounding membrane, thereby allowing the parasite to escape into the host-cell cytosol and proliferate. In the lysosome-independent pathway (right), the parasite induces the host plasma membrane to invaginate and pinch off without recruiting lysosomes; then lysosomes fuse with the endosome prior to the parasite’s escape into the cytosol.