Toxoplasma Encephalitis in an Allogeneic Hematopoietic Stem Cell Transplant Recipient in Korea

To the Editor, Toxoplasma gondii is an intracellular protozoan parasite. Immunocompetent persons with primary infection are usually asymptomatic, but latent infection can persist for the life of the host [1]. In immunocompromised patients, however, a risk exists of reactivating the infection, which may become life-threatening [1]. Toxoplasmosis appears to be a rare opportunistic infection after hematopoietic stem cell transplantation (HSCT). The most frequently involved organ was the central nervous system (CNS), with 48% of patients having isolated cerebral infection and 76% of patients with disseminated disease showing brain involvement. Little is known about toxoplasmosis after HSCT in Korea. Here, we describe a Korean patient with isolated cerebral toxoplasmosis following allogeneic HSCT. A 37-year-old woman was admitted because of headache, myalgia, and fever. She had been well until 1 week before admission, when her headache developed. Myalgia and fever occurred 5 days before admission and her headache worsened. Fifty days prior to admission, she had undergone HLA-matched sibling, non-T cell-depleted allogeneic HSCT for aplastic anemia. Her conditioning regimen included cyclophosphamide (50 mg/kg a day for 4 consecutive days) and antithymocyte immunoglobulin (3 mg/kg a day for 3 consecutive days), and prophylaxis against graft-versus-host disease (GVHD) consisted of short-course methotrexate (15 mg/ m on day 1 and 10 mg/m on days 3, 6, and 11) and cyclosporine (4 mg/kg beginning 1 day before transplant). The pre-transplant T. gondii serostatus of both donor and recipient was not known, but the recipient had been treated with clindamycin for toxoplasma uveitis 10 years previously, at which time she was initially positive for toxoplasma IgM and negative for IgG, but became IgG-positive 5 months later. Soon after HSCT (day 40, 2 weeks before admission), she developed grade II acute GVHD of the skin, and immunosuppressive therapy (i.e., methyl prednisone 48 mg) was started. At the same time, gancyclovir (10 mg/ kg/day) therapy was initiated because she was cytomegalovirus (CMV) antigenemia-positive (41/200,000 white blood cells). Fluconazole and acyclovir were administered as prophylaxis against candidiasis and herpes simplex infection, and pentamidine nebulizer was administered once monthly as prophylaxis against Pneumocystis jirovecii. On admission (day 57), her blood pressure was 124/84 mmHg, her pulse was palpable at 94 beats per minute, and her temperature was 38.8°C. At admission, she had a white blood cell count of 1,200/mm with an absolute neutrophil count of 880/mm, a hemoglobin level of 9.2 g/dL, a hematocrit of 30.6%, a platelet count of 59,000/ mm, and a C-reactive protein concentration of 4.29 mg/dL. She took methyl prednisone 6 mg, which had been tapered from the initial dose of 48 mg, for treatment of acute GVHD. Brain magnetic resonance imaging (MRI) revealed focal high signal intensity (SI) in the right caudate nucleus and right thalamus on T2 weighted images and combined subtle ring-enhancement of the lesions (Fig. 1A and 1B). Toxoplasma serology revealed an equivocal IgG titer (7 IU/mL) and negative IgM titer on hospital day (HD) 1. She was negative for serum galactomanan. A lumbar puncture yielded clear cerebrospinal fluid (CSF) with a white blood count of 2/ mm, including 3% neutrophils and 63% lymphocytes,