Cerebral toxoplasmosis is a major cause of morbidity and mortality among HIV-infected patients, particularly from developing countries. This article summarizes current literature on cerebral toxoplasmosis. It focuses on: Toxoplasma gondii genetic diversity and its possible relationship with disease presentation; host responses to the parasite antigens; host immunosupression in HIV and cerebral toxoplasmosis as well as different diagnostic methods; clinical and radiological features; treatment; and the direction that studies on cerebral toxoplasmosis will likely take in the future.

Cerebral toxoplasmosis is the most common cause of expansive brain lesions in people living with HIV/AIDS (PLWHA) and continues to cause high morbidity and mortality. The most frequent characteristics are focal subacute neurological deficits and ring-enhancing brain lesions in the basal ganglia, but the spectrum of clinical and neuroradiological manifestations is broad. Early initiation of antitoxoplasma therapy is an important feature of the diagnostic approach of expansive brain lesions in PLWHA. Pyrimethamine-based regimens and trimethoprim-sulfamethoxazole (TMP-SMX) seem to present similar efficacy, but TMP-SMX shows potential practical advantages. The immune reconstitution inflammatory syndrome is uncommon in cerebral toxoplasmosis, and we now have more effective, safe, and friendly combined antiretroviral therapy (cART) options. As a consequence of these 2 variables, the initiation of cART can be performed within 2 weeks after initiation of antitoxoplasma therapy. Herein, we will review historical and current concepts of epidemiology, diagnosis, and treatment of HIV-related cerebral toxoplasmosis.

Toxocariasis is usually manifested as visceral larva migrans. Nervous system involvement is a rare complication. In this report, we describe one case of meningoencephalitis due to Toxocara canis and review the literature. We report a previously healthy two-year-old boy who was admitted after 24 hours of severe neurologic symptoms with marked eosinophilic pleocytosis in the cerebrospinal fluid and a single subcortical lesion detected by cerebral magnetic resonance imaging. Both serum and spinal fluid tested positive for T. canis. Initial treatment with thiabendazole was ineffective. After marked improvement in clinical and laboratory results were achieved using albendazole and corticosteroids, the child was discharged.

Cerebral toxoplasmosis is the most common cerebral focal lesion in AIDS and still accounts for high morbidity and mortality in Brazil. Its occurrence is more frequent in patients with low CD4⁺T-cell counts. It is directly related to the prevalence of anti-Toxoplasma gondiiantibodies in the population. Therefore, it is important to evaluate sensitive, less invasive, and rapid diagnostic tests. We evaluated the value of PCR using peripheral blood samples on the diagnosis of cerebral toxoplasmosis and whether its association with immunological assays can contribute to a timely diagnosis. We prospectively analyzed blood samples from 192 AIDS patients divided into two groups. The first group was composed of samples from 64 patients with cerebral toxoplasmosis diagnosed by clinical and radiological features. The second group was composed of samples from 128 patients with other opportunistic diseases. Blood collection from patients with cerebral toxoplasmosis was done before or on the third day of anti-toxoplasma therapy. PCR forT. gondii, indirect immunofluorescence, enzyme-linked immunosorbent assay, and an avidity test for toxoplasmosis were performed on all samples. The PCR sensitivity and specificity for diagnosis of cerebral toxoplasmosis in blood were 80% and 98%, respectively. Patients with cerebral toxoplasmosis (89%) presented higher titers of anti-T. gondiiIgG antibodies than patients with other diseases (57%) (P< 0.001). These findings suggest the clinical value of the use of both PCR and high titers of anti-T. gondiiIgG antibodies for the diagnosis of cerebral toxoplasmosis. This strategy may prevent more invasive approaches.

AIDS-related cryptococcal meningitis continues to cause a substantial burden of death in low and middle income countries. The diagnostic use for detection of cryptococcal capsular polysaccharide antigen (CrAg) in serum and cerebrospinal fluid by latex agglutination test (CrAg-latex) or enzyme-linked immunoassay (EIA) has been available for over decades. Better diagnostics in asymptomatic and symptomatic phases of cryptococcosis are key components to reduce mortality. Recently, the cryptococcal antigen lateral flow assay (CrAg LFA) was included in the armamentarium for diagnosis. Unlike the other tests, the CrAg LFA is a dipstick immunochromatographic assay, in a format similar to the home pregnancy test, and requires little or no lab infrastructure. This test meets all of the World Health Organization ASSURED criteria (Affordable, Sensitive, Specific, User friendly, Rapid/robust, Equipment-free, and Delivered). CrAg LFA in serum, plasma, whole blood, or cerebrospinal fluid is useful for the diagnosis of disease caused by Cryptococcus species. The CrAg LFA has better analytical sensitivity for C. gattii than CrAg-latex or EIA. Prevention of cryptococcal disease is new application of CrAg LFA via screening of blood for subclinical infection in asymptomatic HIV-infected persons with CD4 counts < 100 cells/mL who are not receiving effective antiretroviral therapy. CrAg screening of leftover plasma specimens after CD4 testing can identify persons with asymptomatic infection who urgently require pre-emptive fluconazole, who will otherwise progress to symptomatic infection and/or die.