Toxoplasma gondii, an intracellular protozoan that lies dormant in infected individuals and rarely reemerges unless there are significant deficits in cell-mediated immunity.
Toxoplasma gondii is an intracellular protozoan parasite. Transmission can occur through the ingestion of oocysts from cat feces or infected meat, direct transmission between a mother and fetus, or from organ transplantation, which leads to invasion followed by dissemination of the parasite where it typically lies dormant. It is a ubiquitous organism and nearly 10% of individuals will be seropositive for T. gondii, but the parasite does not usually cause severe disease in immunocompetent individuals. In patients with HIV infection and CD4+ cell counts less than 100 cells/mm3, however, reactivation can occur with several distinct clinical syndromes of which cerebral toxoplasmosis results in the most morbidity. Cerebral toxoplasmosis typically presents with multiple ring-enhancing lesions within the substance of the cerebral cortex, most commonly the frontal and parietal lobes, although single lesions can occur. It is commonly associated with cerebral edema, which may result in mass effect and shifting of adjacent structures. Seizures, focal neurologic deficits, and systemic symptoms are common, as are signs of increased intracranial pressure. Patients with HIV and positive toxoplasma IgG antibodies are typically treated empirically with a sulfonamide and pyrimethamine if cerebral toxoplasmosis is suspected. If necessary, the confirmatory diagnosis occurs through a brain biopsy, which will demonstrate a dense infiltrate of lymphocytes, macrophages, and plasma cells, along with the presence of the T. gondii organisms. Cerebral toxoplasmosis is an AIDS-defining disease.
Although toxoplasmosis may affect multiple organ systems (eg, pulmonary, ocular), encephalitis is by far the most common manifestation.
| Symptoms (encephalitis) | • Headache • Confusion • Fever • Focal neurologic deficits/seizures | | --- | --- | | Diagnosis | • AIDS with CD4 count <100/mm3 • Positive Toxoplasma gondii IgG • MRI: Multiple ring-enhancing brain lesions (with a preference for the basal ganglia) | | Treatment | • Sulfadiazine & pyrimethamine (plus leucovorin to prevent hematologic side effects) for several weeks • Antiretroviral initiation within 2 weeks if not on it already (once patients are clearly tolerating toxoplasma therapy) • Prophylaxis: TMP-SMX (CD4 count <100/mm3) |
There is no reliable test for toxoplasmic encephalitis. The diagnosis is generally made by the presence of suspicious clinical symptoms, positive T gondii IgG serology, and characteristic central nervous system findings on MRI.
Primary prophylaxis against toxoplasmosis is highly effective at preventing the condition in those with advanced AIDS. Therefore, all patients with HIV undergo laboratory evaluation (T gondii IgG testing) for exposure; those with positive serology who have a CD4 count <100/mm3 require primary prophylaxis with trimethoprim-sulfamethoxazole (TMP-SMX), which reduces the risk of toxoplasmosis to 0%-2%.
Patients on antiretroviral treatment can usually discontinue TMP-SMX prophylaxis when their CD4 count is >200/mm3 for 3 months (and there is adequate viral suppression). TMP-SMX is also used for primary prophylaxis against Pneumocystis pneumonia for those with a CD4 count <200/mm3.
No improvement after bactrim raises the concern for lymphoma
Lymphoma (Choice C) of the CNS is a rare form of non-Hodgkin lymphoma that occurs in immunocompromised patients. Patients may present with focal neurologic deficits, vision changes, neuropsychiatric symptoms, and increased intracranial pressure. Neuroimaging will show ring-enhancing lesions similar to those in toxoplasmosis. Toxoplasmosis is more common than CNS lymphoma and should be the presumptive diagnosis for this patient with multiple ring-enhancing lesions. If symptoms do not improve with sulfadiazine or pyrimethamine therapy, CNS lymphoma should be considered.