Toxoplasma gondii is an obligate intracellular protozoan, found worldwide. It is now the most common cause of CNS mass lesions in patients with AIDS, occurring in 5-10% of AIDS patients. Toxoplasmosis may also cause eye disease (chorioretinitis) and congenital infection with multiple neurologic sequelae. The vast majority of patients with cerebral toxoplasmosis have severe immunosupression, most commonly AIDS. Symptoms and signs are those of an enlarging mass lesion. Headache, alteration of behavior, and fever are the most common signs. Most patients also display focal neurologic signs on examination (hemiparesis, ataxia, aphasia, etc.). Symptoms and signs usually evolve subacutely over 1-4 weeks. Brain imaging shows ring-enhancing lesions, most commonly in the basal ganglia and at the cortical gray-white junction. Multiple lesions are seen in 70% of patients. Serum toxoplasma (IgG) titres are usually, but not always, positive. CSF may be normal, or show changes consistent with aseptic meningitis. Detection of toxoplasma DNA in the CSF by PCR is very specific for cerebral toxoplasmosis, but not very sensitive. For these reasons, CSF is rarely obtained in suspected toxoplamosis.

Toxoplasma lesions have a clinical and radiographic presentation similar to that of brain abscesses and primary CNS lymphoma (PCNSL). PCNSL, which develops in 2% of AIDS patients, is particularly likely to be confused with toxoplasmosis. The diagnosis is often made by an empiric trial of antitoxoplasma therapy. Improvement should be seen in 10-14 days. If not, other diagnoses are more likely, and brain biopsy may be considered. Biopsy is often considered as a first step for single lesions in patients with negative toxoplasma titres, a situation where PCNSL is the likely diagnosis. If antitoxoplasma treatment is effective, it is continued for six weeks. Even after successful treatment, lifelong prophylaxis is required.

While commonly referred to as abscesses, toxoplasmal lesions are actually areas of coagulative necrosis which are secondarily infested with organisms. Thus, the central region is composed of coagulated brain parenchyma, and the organisms are found in the surrounding tissue. The coagulative necrosis is initiated by vascular damage caused by the organisms. As toxoplasmal cysts may (at least theoretically) be dormant within the brain, we always search for free tachyzoiites to confirm that the toxoplasma organisms are actually responsible for the parenchymal damage.