Page 917 - Veterinary Immunology, 10th Edition

genital infections of humans, Trichomonas vaginalis stimulates a local
VetBooks.ir IgE response. This allergic reaction increases vascular permeability,

permitting IgG antibodies to reach the site of infection and
immobilize and eliminate the organisms.

In babesiosis, the sporozoites invade red blood cells and the
infected red cells incorporate Babesia antigens into their membranes.
These antigens induce antibodies that opsonize the red cells and
cause their removal by phagocytosis. Macrophages and cytotoxic

lymphocytes recognize the Babesia antigen-antibody complexes on
the surface of infected red cells and destroy them by antibody-
dependent cell-mediated cytotoxicity.
Intracellular parasites use many strategies to invade cells and

avoid destruction. Most gain entry by employing host-mediated
processes such as phagocytosis. Apicomplexans such as Toxoplasma
and Cryptosporidium, however, actively penetrate cells. Once inside,
they persist within specially modified vacuoles. Protective

immunity against apicomplexan protozoa, such as Cryptosporidium,
Eimeria, Neospora, Plasmodia, and Toxoplasma, is generally mediated
by Th1 responses. For example, T. gondii is an obligate intracellular
parasite whose tachyzoites live within cells, especially macrophages

(Fig. 28.2). They penetrate these cells by “gliding” through
molecular junctions in the cell membrane and so do not trigger
phagosome formation. Toxoplasma tachyzoites are therefore not
destroyed since their “parasitophorous vacuoles” do not mature

and fuse with lysosomes. Toxoplasma can thus persist inside cells in
an environment free of antibodies, oxidants, or lysosomal enzymes.
The parasites eventually produce perforin-like molecules that
permeabilize the cell membrane and permit the tachyzoites to

escape and invade other cells. Antibodies and complement can
destroy extracellular Toxoplasma and prevent its spread between
cells (Fig. 28.3). Antibodies, however, have little or no influence on
the intracellular forms of the parasite. These intracellular organisms

can only be destroyed by a Th1 response.

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