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serologic tests are positive and the CD4 lymphocyte count is <200/µL, then prophylaxis with
trimethoprim-sulfamethoxazole may be useful.[208]
Toxoplasma gondii encephalitis produces necrotizing abscesses with acute and chronic
inflammation, macrophage infiltration, and vascular proliferation. These lesions can be large
and widespread; they usually are found in cerebral cortex, subcortical white matter, and deep
gray nuclei. The numerous free tachyzoites at the periphery of necrotizing lesions are very
destructive, and there is a significant inflammatory response with a variety of inflammatory cell
types to them. True cysts or pseudocysts containing T gondii bradyzoites may not have
accompanying inflammation until the wall of the cyst ruptures. Cysts may not be numerous.
Often there is vasculitis, thought to be an allergic response, and endothelial proliferation in some
blood vessels has been observed.
Toxoplasma gondii lesions may organize and contain numerous lipid-laden macrophages.
A fibrous capsule with collagen, typical for brain abscess, can often be identified in surgical
biopsies, along with a lymphoplasmacytic infiltrate. At autopsy, a fibrous capsule is less
commonly seen and inflammation may be sparse, with scattered neutrophils. Healing may
continue to form small less than 0.5 cm cystic lesions with macrophages and surrounding gliosis.
Organizing and cystic lesions contain few detectable organisms. Immunohistochemical staining
with antibody to T gondii helps to reveal the tachyzoites.[778]
Therapy with a combination of oral pyrimethamine and sulfadiazine results in a response
for most patients with cerebral toxoplasmosis. Complications of skin rash and nephrotoxicity,
usually from the sulfadiazine, occur in less than half of patients. Bone marrow toxicity of
pyrimethamine can be ameliorated by concomitant folinic acid therapy. An alternative therapy
consists of clindamycin with pyrimethamine. Treatment with leucovorin is often effective.
Clindamycin and clarithromycin have also been used. Relapses are common, and mean survival
is less than a year.[775,776] Life-long maintenance of pyrimethamine therapy (with or without
sulfadiazine) is needed to prevent relapses. The lack of a response to antitoxoplasma therapy in
1 to 2 weeks may suggest the need to search for another diagnosis.[746]

CRYPTOCOCCUS NEOFORMANS.-- Cryptococcal leptomeningitis and encephalitis
are seen in less than 5% of patients with AIDS at autopsy.[758] The lack of extensive
inflammatory cell reactions to C neoformans from the immunocompromised status of AIDS
patients may be the reason for lack of meningeal signs. The most common presenting features of
CMV meningitis in AIDS include malaise, fever, nausea, vomiting, and headache.
Encephalopathic features of lethargy, altered mentation, personality changes, and memory loss
may occur.[452] Cranial nerve palsies, psychiatric abnormalities, and seizures are less frequent
findings.[746] A subgroup of patients infected with C neoformans var gattii have multiple
enhancing lesions by computed tomography, high cryptococcal antigen titers, papilledema, and a
worse prognosis, though this variant is more likely to be seen in patients who are not
immunocompromised.[779]
By computed tomographic (CT) imaging, cerebral cryptococcosis may have high or low
attenuated lesions with or without contrast enhancement. By magnetic resonance imaging (MRI)
scans, lesions appear hypointense and discrete when T1 weighted, but they appear as
hyperintense “soap bubbles” most often in the basal ganglia and thalamus that are well-
circumscribed without edema when T2 weighted. The lesions are non-enhancing with contrast
by MRI. Meningeal involvement may produce T2 hyperintensity, but the lack of a marked
inflammatory response may make leptomeningeal involvement difficult to detect, but meningitis