Toxoplasmosis in AIDS: Keeping the Lid On

The management of toxoplasmic encephalitis in patients with human immunodeficiency virus (HIV) infection has been a continuously evolving process. Changes in management strategies have been made largely on the basis of clinical experiences, retrospective studies, and small, uncontrolled trials [1]. Currently, HIV-infected patients with neurologic symptoms, low CD4 counts (<100 cells/mm³), and compatible radiographic scans are usually treated empirically for Toxoplasma gondii encephalitis. Acute empiric therapy is usually initiated with either pyrimethamine-sulfadiazine or pyrimethamine-clindamycin [2, 3]; evidence of clinical improvement is seen within 1 to 2 weeks in most responding patients receiving these therapies [4, 5]. Acute therapy is continued until clinical and radiographic resolution occurs, which is usually within 3 to 6 weeks [1-5].

The combination of pyrimethamine plus sulfadiazine is the regimen of choice for acute therapy because it has been associated with a lower rate of failure due to disease progression than has pyrimethamine-clindamycin, although adverse reactions requiring discontinuation of therapy are common [1-3]. Leucovorin should always be coadministered with pyrimethamine to minimize toxicities. For acute therapy, 4 to 8 g of sulfadiazine and 50 to 75 mg of pyrimethamine per day are usually administered. Whether a regimen using lower drug doses is as effective but less toxic is currently unknown. As has been shown in controlled trials, pyrimethamine-clindamycin is clearly an efficacious and acceptable alternative [2, 3]. Other regimens with some activity in treating toxoplasmosis related to the acquired immunodeficiency syndrome (AIDS) include atovaquone, trimethoprim-sulfamethoxazole, pyrimethamine-dapsone, pyrimethamine-azithromycin, and pyrimethamine-clarithromycin [6-10]. These regimens have primarily been evaluated only during acute therapy in small numbers of …