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conferenceseries
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Volume 8, Issue 9 (Suppl)
J AIDS Clin Res
ISSN: 2155-6113 JAR, an open access journal
STD Asia Pacific 2017
October 23-25, 2017
OCTOBER 23-25, 2017 OSAKA, JAPAN
7
TH
ASIA PACIFIC
STD and Infectious Diseases Congress
Cytomegalovirus, Varicella zoster meningoencephalitis and ischemic stroke in an HIV-AIDS patient:
A case report
Monica Pia P Reyes and Ryan M Llorin
St. Luke’s Medical Center-Global City, Philippines
A
long with the increasing number of newly diagnosed Human Immunodeficiency Virus (HIV) patients per day in the
Philippines (26 new cases/day) 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). Mechanisms of ischemic stroke include HIV-associated vasculopathy, opportunistic
infections or neoplasia, cardioembolism and coagulopathy. This case report aims to present a CNS co-infection of the three
most documented viruses that causes stroke: Cytomegalovirus (CMV), Varicella zoster virus (VZV) andHIV.The inflammatory
cascade in these infections promotes atherosclerosis, plaque rupture, and thrombosis, leading to ischemic stroke. 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. Computed tomography scan revealed
acute to sub-acute infarct, left middle cerebral artery territory. 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/mm
3
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
with elevated cerebrospinal fluid (CSF) protein, low-normal CSF glucose, and pleocytosis with lymphocytic predominance.
Viral panel showed CMV viral load of 634,000 copies/mL and VZV IgG 44.4 mIU/L clinching the diagnosis of concomitant
CMV-VZV meningoencephalitis in this HIV patient. Magnetic resonance imaging and angiogram is compatible with viral
vasculopathy. The pathogenic mechanisms of VZV reactivation in the CNS include neuronal and glial direct infection and
immune-mediated lesions including vasculitis and demyelinization while CMV infection of vascular smooth muscle cells
induces production of powerful pro-inflammatory cytokines which accelerate atherosclerosis development. This might be the
first reported case of co-infection of the CMV-VZV-HIV meningoencephalitis and ischemic stroke.
monicapiareyes@yahoo.comJ AIDS Clin Res 2017, 8:9 (Suppl)
DOI: 10.4172/2155-6113-C1-021