Treatment of cerebral toxoplasmosis is not simple. The most frequently used combinations are usually effective (resistance has not yet been convincingly described), but require modification in at least half the patients due to side effects - particularly allergies. Sulfadiazine and clindamycin are presumably equally effective in combination with pyrimethamine (Dannemann 1992). However, one large European study demonstrated a trend, though not significant, in favor of sulfadiazine (Katlama 1996). A loading dose for pyrimethamine during the first few days has been propagated since the first published study (Leport 1988), although sufficient comparative data is not available.
Due to the myelotoxicity of sulfonamides and pyrimethamine, which inhibits transformation of folic acid to folinic acid, it is important to substitute sufficiently with folinic acid (unfortunately expensive!) from the start. Folic acid (cheap!) itself is ineffective, as it cannot be converted in the presence of pyrimethamine (Luft 2000).
We recommend using sulfadiazine and pyrimethamine for an initial attempt as oral treatment. In cases of sulfonamide allergy, sulfadiazine should be substituted with oral or intravenous clindamycin from the beginning. All disoriented patients should receive clindamycin infusions, at least for reasons of compliance. Because of the high rate of allergies under sulfadiazine, however, some clinicians completely oppose this treatment. But clindamycin may also be problematic - consider pseudo-membranous colitis in cases of persistent diarrhea!
If allergies or intolerance to both sulfonamides and clindamycin occur, a combination of atovaquone and pyrimethamine is a possible alternative (Chirgwin 2002). Good results are also reported with intravenous co-trimoxazole, with administration of the same dosages as for PCP (Canessa 1992). A combination of azithromycin plus pyrimethamine could be another alternative (Bosch-Driessen 2002), however there is only very vague data available.
Acute therapy is of four to six weeks duration, possibly longer for the less effective reserve therapies. There is often clinical improvement within a few days. Even in these cases, a further MRI is recommended after two weeks at the earliest. Significant resolution of lesions is often only visible after four weeks. In cases of increased intracranial pressure or extensive edema, steroids are given (8 mg dexa-methasone q 6-8 h). Administration of steroids should be for a limited duration, as there is otherwise a significantly increased risk of aspergillosis. All treatment combinations require initial monitoring of blood count, glucose, transaminases and renal parameters at least three times weekly. Maintenance therapy with the reduced dose should only be initiated if lesions have resolved by at least 75 %.
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