VZV encephalitis: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
The causative agent for VZV encephalitis is [[varicella zoster virus]] (VZV), a double-stranded [[DNA virus]] within the [[Herpesviridae ]] family of viruses. The [[immune system]] eventually eliminates the virus from most locations, but it remains dormant (or [[viral latency|latent]]) in the [[ganglion|ganglia]] adjacent to the [[spinal cord]] (called the [[dorsal root ganglion]]) or the ganglion semilunare (ganglion Gasseri) in the base of the skull.
The exact pathogenesis of VZV encephalitis is not fully understood. It is known that VZV encephalitis is the result of the [[varicella zoster virus]], a double-stranded [[DNA virus]] within the [[Herpesviridae]] family of viruses.<ref name=Mandell1> M.D. JE, Dolin R, Blaser MJ. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, Expert Consult Premium Edition. Saunders; 2014.</ref> The [[immune system]] eliminates the virus from most locations, but it remains [[viral latency|latent]] in the [[dorsal root ganglion]] and the [[trigeminal]] ganglion near the base of the skull. Initial infection by VZV presents as [[chickenpox]], often in children between 1-9. VZV reactivation, which presents as [[shingles]] in adults, is the result of a decline in the frequency of VZV-specific [[T cell]]s.<ref name="pmid9300702">{{cite journal| author=Sadzot-Delvaux C, Kinchington PR, Debrus S, Rentier B, Arvin AM| title=Recognition of the latency-associated immediate early protein IE63 of varicella-zoster virus by human memory T lymphocytes. | journal=J Immunol | year= 1997 | volume= 159 | issue= 6 | pages= 2802-6 | pmid=9300702 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9300702  }} </ref> The molecular basis of reactivation remains unknown.<ref name=Mandell1> M.D. JE, Dolin R, Blaser MJ. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, Expert Consult Premium Edition. Saunders; 2014.</ref> Some histopathologic studies suggest of a postinfectious [[demyelinating]] process, while other findings cite direct viral cytopathology.<ref name="pmid6326714">{{cite journal| author=Bauman ML, Bergman I| title=Postvaricella encephalitis. | journal=Arch Neurol | year= 1984 | volume= 41 | issue= 5 | pages= 556-8 | pmid=6326714 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6326714  }} </ref><ref name="pmid4311227">{{cite journal| author=McCormick WF, Rodnitzky RL, Schochet SS, McKee AP| title=Varicella-Zoster encephalomyelitis. A morphologic and virologic study. | journal=Arch Neurol | year= 1969 | volume= 21 | issue= 6 | pages= 559-70 | pmid=4311227 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4311227  }} </ref><ref name="pmid582251">{{cite journal| author=Takashima S, Becker LE| title=Neuropathology of fatal varicella. | journal=Arch Pathol Lab Med | year= 1979 | volume= 103 | issue= 5 | pages= 209-13 | pmid=582251 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=582251  }} </ref>


==Causes==
==Causes==

Revision as of 14:19, 16 February 2016

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Anthony Gallo, B.S. [2]

Synonyms and keywords: Varicella zoster virus encephalitis; Herpes zoster encephalitis; Varicella zoster encephalitis; Varicella encephalitis;

Overview

Classification

Based on the duration of symptoms, VZV encephalitis may be classified into either acute or chronic.

Pathophysiology

The exact pathogenesis of VZV encephalitis is not fully understood. It is known that VZV encephalitis is the result of the varicella zoster virus, a double-stranded DNA virus within the Herpesviridae family of viruses.[1] The immune system eliminates the virus from most locations, but it remains latent in the dorsal root ganglion and the trigeminal ganglion near the base of the skull. Initial infection by VZV presents as chickenpox, often in children between 1-9. VZV reactivation, which presents as shingles in adults, is the result of a decline in the frequency of VZV-specific T cells.[2] The molecular basis of reactivation remains unknown.[1] Some histopathologic studies suggest of a postinfectious demyelinating process, while other findings cite direct viral cytopathology.[3][4][5]

Causes

VZV encephalitis may be caused by either varicella (chickenpox) or herpes zoster (shingles).

Differentiating VZV Encephalitis from Other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications, and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT

MRI

Treatment

Medical Therapy

Prevention

References

  1. 1.0 1.1 M.D. JE, Dolin R, Blaser MJ. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, Expert Consult Premium Edition. Saunders; 2014.
  2. Sadzot-Delvaux C, Kinchington PR, Debrus S, Rentier B, Arvin AM (1997). "Recognition of the latency-associated immediate early protein IE63 of varicella-zoster virus by human memory T lymphocytes". J Immunol. 159 (6): 2802–6. PMID 9300702.
  3. Bauman ML, Bergman I (1984). "Postvaricella encephalitis". Arch Neurol. 41 (5): 556–8. PMID 6326714.
  4. McCormick WF, Rodnitzky RL, Schochet SS, McKee AP (1969). "Varicella-Zoster encephalomyelitis. A morphologic and virologic study". Arch Neurol. 21 (6): 559–70. PMID 4311227.
  5. Takashima S, Becker LE (1979). "Neuropathology of fatal varicella". Arch Pathol Lab Med. 103 (5): 209–13. PMID 582251.