Neurosurgery notes/Infection/Cranial infection/Viruses/HSV encephalitis

HSV encephalitis

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Viruses
I moved all these from Herpes encephalitis

Types

HSV-1

  • Numbers
    • Is the most frequent cause of sporadic encephalitis.
    • It usually affects those older than neonates, frequently involves limbic structures, and sequentially becomes bilateral.
  • Pathology
    • In the CNS, it remains relatively shielded from the host’s immune system.
    • The virus may travel from the skin to the olfactory nerve, trigeminal nerve, or trigeminal ganglion.
      • It rarely spreads haematogenously.
      • It is found in the trigeminal ganglion in 50% of normal adults
        • Reactivates after trauma or immunosuppression.
    • Enters through the eye, mouth, and genitals and reaches the CNS by the peripheral nerves.
    • In children, the virus reaches the CNS by means of the olfactory mucosa
    • In adults by means of the trigeminal ganglion to the middle fossa.
  • Findings
    • Aseptic meningitis
    • Encephalitis
    • Myelitis
    • Keratitis
    • Skin lesions
    • Haemorrhagic necrosis of the basal frontal and medial temporal lobes
  • Diagnosis
    • By PCR to detect viral nucleic acid in the CSF (must be in first few days) or biopsy and culture of the anterior inferior temporal gyrus.
    • MRI
      • Generally targets the temporal lobe
          • Because the temporal lobe has increased receptors specific allowing HSV to invade the cells like
            • TNFRSF14/HVEM and PVRL1/nectin 1 on the neurons can be attached by HSV glycoprotein D receptors
            • PILRA, MAG, and MYH9 on the neurons can be attached by HSV glycoprotein B receptors
          • Most of the damage to the temporal lobe arise from self-inflicted immune injury. That is why even in immune suppressed individuals they don't have a higher incidence of HSV encephalitis despite having been riddled with HSV in their system
          notion image
  • Pathologic examination
    • Biopsy
      • Demonstrates Cowdry type A inclusions (intranuclear eosinophilic masses with a surrounding halo found in neurons, oligodendrocytes, and astrocytes).
      • These inclusions are best seen in the first few days of the infection.
    • The CSF culture is usually negative.
  • Outcome
    • Mortality is 50–60%. Treatment is with steroids and acyclovir IV for 14 days.

HSV-2

  • Numbers
    • Occurs in 1 in 200 to 1 in 5000 births.
    • 85% are caused by HSV-2
  • Pathology
    • Encephalitis affects mainly neonates
    • Is more diffuse.
      • Global cerebral inflammation (encephalitis)
  • Transmitted transvaginally.
  • Rare early lesions cause death, chorioretinitis, and microcephaly.
  • The virus has a predilection for vascular endothelial cells and causes thrombosis and haemorrhagic stroke that develops 2–4 weeks postpartum.
  • Pathology
    • Demonstrates microglial nodules and intranuclear inclusions.
    • The infection is diffuse and causes white matter edema without the temporal localization.
  • The most frequent manifestations are skin, eye, and mouth lesions,
  • Outcome
    • If no treatment is given, the infection may disseminate with an 80% mortality (only 50% with treatment).
  • The CNS is involved in 30% and produces fever, seizures, and lethargy.

Clinical features

  • Focal neurologic findings are usually acute (<1 week in duration) and include altered mentation and level of consciousness, focal cranial nerve deficits, hemiparesis, dysphasia, aphasia, ataxia, or focal seizures

Investigation

  • CSF
    • Lymphocytic pleocytosis, increased number of erythrocytes (in 84 percent of patients), and elevated protein
    • HSV glycoprotein B antibodies
    • HSV antigen
  • Brain biopsy
    • Still has a role in patients who have clinical deterioration despite antiviral therapy or when alternative diagnoses are being considered
  • MRI
    • In early can be normal late will show cystic malacia of temporal lobe
    • Classical sign:temporal horn insular and frontal lobe
    • Patients with seizures can have postictal MRI changes
      • Transient increase in T2 signal intensity and swelling of
        • Cortical grey matter
        • Sub cortical white matter
        • Hippocampus

For anyone above that mainly HSV1 infection

Targets

  • HSV enter the CNS through three ways
    • HSV infection in the oropharynx enter Trigeminal nerve
    • Reactivation of HSV infection and the HSV travel to the brain
    • Reactivation of dormant HSV infection already in the brain
  • HSV target the temporal lobe because the temporal lobe has increased receptors specific allowing HSV to invade the cells like
    • TNFRSF14/HVEM and PVRL1/nectin 1 on the neurons can be attached by HSV glycoprotein D receptors
    • PILRA, MAG, and MYH9 on the neurons can be attached by HSV glycoprotein B receptors
  • Most of the damage to the temporal lobe arise from self inflicted immune injury. That is why even in immune suppressed individuals they don't have a higher incidence of HSV encephalitis despite having been riddled with HSV in their system