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TOXOPLASMA GONDII INFECTIONS
Toxoplasmosis is an uncommon infection that, before the AIDS epidemic, was rarely
seen in adults. It is more common in warm humid climates, and this distribution may influence
its appearance in AIDS. Toxoplasmosis can occur perinatally as a congenital infection in the
absence of HIV infection.[475] Ingestion of poorly cooked meat (usually pork) is a principle
form of transmission in adults, though ingestion of food or water contaminated with T gondii
oocysts is also an important route of infection.[476]
T gondii can invade virtually all tissues of the body, but in AIDS patients, the organ
system distribution of T gondii infection is generally not widespread. The central nervous
system is involved in most cases. Extracerebral toxoplasmosis is more likely to occur later in the
course of AIDS with a greater degree of immunosuppression when the CD4 lymphocyte count is
low. Extracerebral sites for T gondii in AIDS are most often eye and lung, with heart and
gastrointestinal tract involved much less often. Other organs are infrequently involved, with
reticuloendothelial tissues occasionally affected (Table 5).[477]
The clinical appearance of toxoplasmosis is typically that of altered mental status from
central nervous system involvement. Headaches, fever, and focal neurologic deficits may occur.
Diagnosis may be suggested by elevated serologic titers, but many persons have antibodies to T
gondii because of subclinical infection. Serologic titers give no indication of dissemination. The
presentation of cerebral toxoplasmosis may appear quite similar to that for non-Hodgkin
lymphoma, and stereotaxic brain biopsy may be useful for diagnosis. Extracerebral
toxoplasmosis may sometimes be diagnosed by bronchoalveolar lavage or endoscopic
biopsy.[477]
The gross appearance of toxoplasmosis is not distinctive. In the brain, the diagnosis is
suggested by finding multiple small areas of necrosis or cystic change, while in the heart, a
patchy parenchymal myocarditis with tan to white irregular infiltrates may occur in severe cases.
In other organs, there are no specific features and grossly visible lesions may not be apparent.
In biopsy material, diagnosis is best made by finding characteristic cysts filled with the
organisms--dubbed bradyzoites in this location. The cysts may be "true" cysts formed only by
the T gondii, or they may be "pseudocysts" that form within an existing cell and use the cell wall
as a cyst wall. Cysts average 50 microns in size. Free T gondii organisms, called tachyzoites,
are 2 to 3 microns wide and are often difficult to distinguish, with hematoxylin-eosin staining,
from background cellular debris.[401] The sexual cycle of T gondii occurs in the definitive host,
the cat, where oocysts form in the intestine and are excreted into the environment to be ingested
by other animals or man.[476]
Encysted T gondii usually produce no or minimal inflammatory reaction, but serologic
titers may increase. However, rupture of the cysts with release of T gondii as free tachyzoites
does produce a host response. The tachyzoites are too small to be morphologically distinctive by
hematoxylin-eosin staining in most tissue sections. Immunohistochemical staining may aid in
finding not only the cysts, but also in identifying free tachyzoites.[475]
The inflammation that accompanies the cysts and free tachyzoites is usually mixed, with
neutrophils, lymphocytes, macrophages, and plasma cells in varying proportions. These mixed
inflammatory cell infiltrates occur in a patchy pattern within involved organs. Even though
inflammation may be extensive, finding cysts is still difficult, though the greater the degree of