No abstract

Toxoplasma encephalitis (TE) is usually diagnosed in advanced stages of HIV infection when the CD4+ count is <100-200 cells/µl. A 55-year-old woman with HIV/AIDS, well controlled on antiretroviral therapy (ART), CD4+ count in the 300 cells/μl range for >1 year presented with acute onset of headache, nausea and vomiting. She had been on her current ART regimen consisting of raltegravir, co-formulated emtricitabine/tenofovir and etravirine for three years and had been off Pneumocystis prophylaxis for 10 months (trimethoprim-sulfamethoxazole). Brain MRI showed multiple ring-enhancing, supratentorial and infra-tentorial parenchymal lesions suspicious for metastases. She had no other evidence of metastatic disease in her body. The possibilities of TE and primary CNS lymphoma were considered but deemed unlikely given the high CD4+ count. A brain biopsy demonstrated Toxoplasma tachyzoites. There was no evidence of lymphoma or carcinoma. Anti-toxoplasma treatment yielded good initial clinical and radiographic responses. While on TE maintenance therapy, she developed similar symptoms. Repeat MRI showed progression of lesions. Further work-up including CSF Epstein-Barr virus PCR and SPECT Th 201 imaging was not conclusive for CNS lymphoma. The patient's clinical condition deteriorated and she died. We postulate that functional immunological dysfunction is a possible mechanism by which our patient developed TE despite demonstrating sustained immune response on ART.

Myocardial infarction with ST segment elevation (STE) on electrocardiography (ECG) is a common presentation in emergency rooms across the world. Myocardial injury and necrosis are infrequently the initial presentation in patients with thrombotic thrombocytopenic purpura (TTP). A 48-year-old woman presented with STE myocardial infarction from outside hospital for primary percutaneous coronary intervention. However, her clinical picture was not consistent. Rapid evaluation revealed symptoms associated with microangiopathic hemolytic anemia, thrombocytopenia, acute kidney injury with waxing and waning mental status. A diagnosis of TTP was made with low ADAMST-13 activity. Plasmapheresis was initiated along with intravenous steroid therapy. The patient had a full recovery and went home after full recovery of left ventricular ejection fraction and normal myocardial perfusion studies. Rapid evaluation is needed to identify infrequent causes of STE myocardial infarction. As swift protocols are activated in the emergency room and catheterization laboratories to ensure quality control, it is equally important to integrate all aspects of the patient's clinical and objective data to detect unusual disease entities.