Cerebral Toxoplasmosis in a Patient with Systemic Lupus Erythematosus

Toxoplasma gondii is a globally distributed protozoan parasite that causes toxoplasmosis and is frequently associated with infections in the immune compromised and in neonates. On initial infection, the parasite enters the host through the intestinal epithelium, usually after oocysts are ingested. Additionally, vertical transmission from mother to fetus can occur as well as infection from organ transplantation. In immune competent hosts, presentation is commonly flu-like with fever, headache and lymphadenopathy. The host’s immune response typically contains the infection, limiting it to tissue cysts comprised of slowly replicating bradyzoites. In immune deficient hosts, when tissue cysts containing bradyzoites rupture, the compromised immune system is unable to halt progression of the parasite. Bradyzoites differentiate into rapidly replicating tachyzoites and as the parasite proliferates, host cell death occurs and necrotic foci develop. Most commonly, immune deficient hosts present with encephalitis, pneumonitis, and chorioretinitis [1]. We report a case of cerebral toxoplasmosis in a female patient with systemic lupus erythematosus (SLE) being treated with hydroxy chloroquine, mycophenolate mofetil and prednisone.