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ISSN: 2329-6879
Occupational Medicine & Health Affairs
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Zika Virus Encefalitis

Luis González Z*, José Vergara C and José Jáuregui S

Department of Critical Medicine, Universidad Espíritu Santo, Ecuador

*Corresponding Author:
Luis González Zambrano, MD
Intensivist Clinic, Head of Intensive Therapy, HLV
Universidad Espíritu Santo, Ecuador
Tel: 0999613478
E-mail: [email protected]

Received date: September 11, 2017; Accepted date: September 14, 2017; Published date: September 24, 2017

Citation: Luis González Z, José Vergara C, José Jáuregui S (2017) Zika Virus Encefalitis. Occup Med Health Aff 5:306. doi: 10.4172/2329-6879.1000306

Copyright: © 2017 Luis González Z, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Clinical Image

A Male, 23 years old, pancreatitis and cholecystectomy 1 month ago, presented to our ED with a history of 6 days of fever, dizziness and confusion. He reported no headache, neck stiffness or seizures. Physical examination the patient was somnolent, with reactive isochoric pupils, quadriparetic with hyporeflexia. He became stuporous with shock and leukocytosis. Treatment with meropenem and vancomycin were initiated empirically. Magnetic resonance imaging (MRI) of the brain revealed hyper intense lesions in the brain stem, fornix and bilateral thalamus (Figures 1A and 1B) with no midline shift. The CSF analysis results were non-specific with mild protein elevation. CSF molecular biology testing with PCR RNA for Zika virus was positive. A diagnosis of acute disseminated Zika virus encephalitis was made. Immunomodulatory therapy with IVIG was initiated. Follow-up MRI of the brain showed progression of lesions to midbrain, basal ganglia and brain cortex (Figures 1C and 1D). He had no response to 5 days of IVIG therapy and subsequently the patient died.


Figure 1(A,B): MRI brain (FLAIR) at beginning, there are bilateral simetri hyper intense lesions incuad rigeminal tuberculosis, periacue ductal gray matter and fornix.


Figure 1(C,D): Brain MRI follow-up at 4 days shows bilateral extending basal ganglia (putamen) and brain cortex hyper intense lesions with accentuation in cuadrigeminal tuberculosis and thalamus.

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