## Why option 1 is correct The structure marked **B** — tissue cysts containing bradyzoites — represents the latent form of Toxoplasma gondii. In immunocompetent individuals, these cysts remain dormant and asymptomatic. However, when CD4 count falls below 100 cells/μL in HIV patients, reactivation of these latent cysts occurs, releasing bradyzoites that transform into rapidly dividing tachyzoites. This reactivation causes cerebral toxoplasmosis, the most common cause of mass lesions in the CNS in AIDS patients. The multiple ring-enhancing lesions in the basal ganglia with perifocal edema are the classic radiologic hallmark of this reactivation disease (Harrison 21e Ch 226). ## Why each distractor is wrong - **Option 2**: Acute primary infection typically presents with mononucleosis-like illness and lymphadenopathy in immunocompetent hosts, not focal CNS lesions. Moreover, the patient's CD4 count of 65 cells/μL indicates severe immunosuppression; reactivation of latent infection is far more common than primary infection in this setting. - **Option 3**: Free tachyzoites (marked **A** in the diagram) are the acute, rapidly dividing form that cause tissue damage during primary infection. Chronic persistent tachyzoite infection does not occur in immunocompetent hosts because the immune system controls acute infection and forces conversion to the latent cyst form. The clinical picture here is reactivation from cysts, not persistent tachyzoite infection. - **Option 4**: Congenital toxoplasmosis presents in infancy with the classic TORCH triad (hydrocephalus, intracranial calcifications, chorioretinitis). A 28-year-old presenting with new CNS lesions and severe immunosuppression has reactivation of acquired latent infection, not congenital disease. **High-Yield:** Bradyzoites in tissue cysts = latent toxoplasmosis; reactivation when CD4 < 100 cells/μL in HIV = cerebral toxoplasmosis with multiple ring-enhancing basal ganglia lesions. [cite: Harrison 21e Ch 226]
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