ABSTRACT
Since 1983 Toxoplasma encephalitis (TE) is the neurological disorder most frequently found in HIV/AIDS patients. It commonly develops as a reactivation, and its etiological agent is the obligatory intra-cellular protozoan Toxoplasma gondii (T. gondii). The parasite seropositive rat, with varies in different parts of the world but is significatly high in most of then, is what keeps concern about TE constantly present. The first antiretrovirals favorate the same class and were used in single terapies; they were incapable of promoting sufficient immunological recovery to avoid opportunistic diseases and, furthermore, the concept of either primary or secundary prophylaxis had not been stablished at the time. In 1996 the apparence of two new antiretroviral classes triggered a new treatment concept. The existing prophylatic procedures were associated to a Highly Active Antiretroviral Therapy (HAART), a behavior that showed its efficacy in reducing the number of cases. Toxoplasma encephalitis has recently been described with an immune reconstruction inflammatory syndrome(IRS) related to the rapid response to HAART in severely immunodepressed individuals. Reports on reactivation or relapse noted in patients with sustained immunological recovery, when it is safe to suspend prophylaxis, suggest the participation of more agressive T. gondii strains or factors inherent to the host. It is therefore necessary to carry out more wide-ranging studies to clarify the link between parasite/host and chronic/reactivated infections of cysts. Other alternatives to the treatment and prophylaxis of AIDS and TE that facilitate the adhesion of the patient to the first approach, as well as the definition of the serological status for T. gondii and the adoption of prophylatic measures related to primary infection cases, can largely contribute to reduce the number of TE cases