Journal of the Louisiana State Medical Society
Figure 3: Fused PET-CT images at the same level as Figure 1 show no hypermetabolism in the region of the dominant mass (m). The smaller lesions in Figure 2 also were not hypermetabolic.
component in the left frontal lobe. There was a midline shift of 6 mm from the midline to the right. The patient was initially admitted to the medical inten- sive care unit. He was started on dexamethasone to decrease the cerebral edema, levetiracetam for seizure prophylaxis, and empiric treatment with leucovorin, sulfadiazine, and pyrimethamine for possible toxoplasmosis. Of note, he had a positive toxoplasma serology five years prior. MRI of the brain demonstrated multiple heterogeneously contrast- enhancing lesions throughout both cerebral hemispheres. The largest of these lesions measured 4.1 cm x 4.0 cm x 3.5 cm in the left frontal lobe. The lesion and its associated edema resulted in a mass effect with sulcal effacement and intimal shift of the midline to the right side (Figures 1, 2). Rapid plasma regain and serum cryptococcal antigen were negative. A lumbar puncture was not performed due to the increased risk of herniation. After 10 days of treatment with antitoxoplasmosis ther- apy, he had no change in his neurologic exam. A subsequent positron emission tomography of the brain did not show any significant changes and no areas of increasedmetabolic activity (Figure 3). A brain biopsywas performed. The tissue specimens were consistent with toxoplasmosis (Figures 4, 5). With the biopsy demonstrating toxoplasmosis, the pa- tient was discharged to complete a course of pyrimethamine, sulfadiazine, and leucovorin. Antiretroviral therapy was to be initiated as an outpatient. DISCUSSION Epidemiology and Etiology Toxoplasmosis, an infection with a worldwide distri- bution, is caused by the intracellular protozoan parasite, Toxoplasma gondii . Feline cats are the only animals in which T. gondii can complete its reproductive cycle. 2 Following feline ingestion of any form of T. gondii , the parasite infects the gut epithelial cells and reproduces. The feline then ex- cretes infectious oocysts in feces. When non-felines, includ- ing humans, ingest T. gondii oocysts, the organisms invade intestinal epithelium and disseminate throughout the body. They then encyst in any type of nucleated cell and can lie dormant within tissues for the life of the host. There are four means of acquiring toxoplasmosis in humans: ingestion of infectious oocysts from the environment (usually from soil contaminated with feline feces); ingestion of tissue cysts in meat from an infected animal; through vertical transmission froman infectedmother to her fetus; or via blood transfusion or organ transplantation from an infected donor. 2 Immunocompetent persons with primary infection are usually asymptomatic, but latent infection can persist for the lifetime of the host. 3 Seroprevalence rates of toxo- plasmosis vary substantially among different countries (eg, approximately 15% in the United States to more than 50% in certain European countries). 4 AmongHIV-infected patients, seroprevalence of antibodies to T. gondii mirror rates of seropositivity in the general population. 5 In patients with
Figure 4: Anti- toxoplasma immunohisto- chemistry highlighting the toxoplasma oocyst (60x).
Figure 5: Toxoplasma oocyst with encysted toxoplasma bradyzoites (40x).
42 J La State Med Soc VOL 166 January/February 2014
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