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Biography

Monica Pia P. Reyes, MD is a licensed physician since 2013. She is currently a 3rd year Internal Medicine.Resident at St. Luke’s Medical Center- Global City, Philippines and is planning to subspecialize in Infectious Diseases. She is currently the Resident Head of the Committee on Internal Academics and Research. Her interest in research got her to present oral cases and posters in some specialty conventions in Manila.

Abstract

Background: Along with the increasing number of newly diagnosed patients with Human Immunodeficiency Virus (HIV) per day in the Philippines (26 new cases/day)1 is an increasing number of HIV patients diagnosed with Central Nervous System Infection (CNSI) and Stroke. A study shows that the risk of ischemic stroke was higher among those with HIV infection compared with uninfected people (hazard ratio 1.17)2. Mechanisms of ischemic stroke include HIV-associated vasculopathy, opportunistic infections or neoplasia, cardioembolism and coagulopathy3. Methods: Presented is a 35-year-old male with HIV who is non-compliant with anti-retroviral therapy and who had recent untreated Shingles was brought in with decreased sensorium, signs of meningeal irritation and right-sided neurologic deficit. This case report presents a CNS co-infection of the three most documented viruses that causes stroke: Cytomegalovirus (CMV), Varicella Zoster Virus (VZV) and HIV. The inflammatory cascade in these infections promotes atherosclerosis, plaque rupture, and thrombosis, leading to ischaemic stroke4. Results: Computed Tomography scan revealed Acute to Subacute Infarct, Left Middle Cerebral Artery Territory (Figure 1). He was admitted and started empirically on Vancomycin, Ampicillin, Cefepime and Ganciclovir for Central Nervous System Infection. HIV work-up revealed a CD4 of 11 cells/mm3 and HIV-1 RNA of 1,124,215 copies/mL. CMV IgG is positive at 65 U/mL. Lumbar tap done had an elevated opening pressure 17.4 cm with elevated cerebrospinal fluid (CSF) protein of 120.9 mg/dL (NV: 15- 45), low-normal CSF glucose of 42. 0 mg/dL (NV: 40-70), and pleiocytosis of 1,880 cells/uL with lymphocytic predominance. Viral panel showed CMV viral load of 634,000 copies/mL and VZV IgG 44.4mIU/L clinching the diagnosis of concomitant CMV-VZV meningoencephalitis in this HIV patient. Magnetic Resonance Imaging and Angiogram is compatible with viral vasculopathy. CMV chorioretinitis, the most common clinical manifestation of CMV end-organ disease in HIV patients, was also diagnosed based on hazy media, relative afferent pupillary defect and vitreous opacities on ultrasound of the right eye. He was given Intravenous Ganciclovir for 3 weeks and Intravenous Acyclovir for 2 weeks. He was sent home with oral Valganciclovir to be taken until CD4 counts >100 cells for at least 3 months. Antiretrovirals were also started. The pathogenic mechanisms of VZV reactivation in the CNS include neuronal and glial direct infection and immune-mediated lesions including vasculitis and demyelinization5 while CMV infection of vascular smooth muscle cells induces production of powerful pro-inflammatory cytokines which accelerate atherosclerosis development6. Conclusion: Opportunistic infections are an emerging cause of stroke in patients in HIV. This might be the first reported case of co-infection of the three most documented viruses that causes stroke: Cytomegalovirus, Varicella Zoster Virus and Human Immunodeficiency Virus.