However, there is no evidence to support the routine prescribing of antiepileptic drugs in patients with toxoplasmosis. HIV patients with a CD4 count of <200 cells/μL and positive toxoplasma serology require prophylaxis against toxoplasma encephalitis (category IIb recommendation). Although there are no randomized clinical trials of toxoplasma prophylaxis per se, trials of PCP prophylaxis have demonstrated efficacy
of TMP-SMX and dapsone plus pyrimethamine against toxoplasma encephalitis [90,91]. Various doses can be used but TMP-SMX 480–960 mg/day is the preferred regimen. Dapsone 50 mg/day and weekly pyrimethamine 50 mg is reserved for individuals who are allergic to TMP-SMX. Atovaquone mTOR inhibitor may also be considered. In addition, all HIV-seropositive individuals should be advised to avoid the ingestion of undercooked red meat, to wash their hands http://www.selleckchem.com/products/CAL-101.html after any contact with soil, and to avoid emptying cat litter trays. If this is not feasible, emptying cat litter trays daily and ensuring that hands are washed after all disposal of cat excreta must be advised. Primary and secondary prophylaxis can be discontinued when the CD4 count is repeatedly above 200 cells/μL (level
Ib recommendation). HAART has lessened the incidence of toxoplasma encephalitis. HAART has been associated with a decline in toxoplasma encephalitis and should be initiated as soon as the patient is clinically stable (usually approximately 2 weeks after commencing acute treatment of toxoplasma encephalitis to lessen the likelihood of IRIS). There have been
a number of reports of IRIS associated with toxoplasma encephalitis . After the initiation of HAART, primary prophylaxis maybe discontinued after successful suppression of HIV viral replication and restoration of the CD4 counts to >200 cells/μL for 3 months . After HAART, maintenance therapy may be discontinued after 6 months of successful suppression of HIV viral replication and elevation of CD4 count to >200 cells/μL Methisazone [69,94,95]. First identified as a clinical entity in 1958, progressive multifocal leukoencephalopathy (PML) was subsequently characterised to be an opportunistic infection (OI) in 1971 when virus particles were identified from a patient with underlying Hodgkin disease (named JC virus after the patient initials). This was later further identified as being a double-stranded DNA 40-nm icosahedron virus belonging to the subfamily of Polyoma viruses. Asymptomatic seroconversion occurs predominantly in childhood although seroprevalence continues to increase until old age and over 70% of the population are seropositive . The exact mechanism of transmission is ill-understood but is probably by respiratory secretions and via the tonsillar tissues. Following primary infection, the virus disseminates and sets up latent infection in several organs (spleen, bone marrow, kidneys and B-lymphocytes).