Toxoplasmosis, caused by the obligate intracellular parasite Toxoplasma gondii, is responsible for significant morbidity and mortality throughout the world. Although it has long been recognized as a serious congenital disease, it is only with the advent of acquired immunodeficiency syndrome (AIDS) and the increased use of immunosuppressive therapy that toxoplasmosis has reached epidemic proportions.

Humans are incidental hosts in the life cycle of T. gondii. Acute infection occurs via ingestion of meats or water contaminated with tissue cysts or tachyzoites or by handling cats, the definitive host. Once the human host develops an adequate immune response, tissue cysts are formed and a chronic or latent infection ensues. Antibodies against T. gondii will be present in serum for life. When a chronically infected person becomes immunocompromised, particularly with defects in cell-mediated immunity, devastating reactivation of the latent infection may occur.

CLINICAL MANIFESTATIONS AND DIAGNOSIS

In the immunocompetent host, primary infection is often asymptomatic. Acute infection can mimic the symptoms of mononucleosis with a common manifestation of cervical or occipital lymphadenopathy. The lymph nodes usually are nontender, are nonsuppurative, and persist for less than 4 to 6 weeks. Infrequently, toxoplasmosis can lead to myocarditis, hepatitis, polymyositis, pneumonitis, and encephalitis.

Toxoplasmosis in the immunocompromised patient is most commonly manifested by toxoplasmic encephalitis (TE), usually alone but sometimes as part of a multiorgan infection. Isolated organ involvement without central ner- vous system (CNS) disease is uncommon. In the AIDS patient, TE usually develops when the CD4 lymphocyte count falls below 100/mm3, although the risk of developing overt infection begins when CD4 counts fall below 200/mm3.