Herpes Simplex (HSV) Encephalitis, Non-congenital

Background Gross Pathology Histopathology & Immunohistochemistry Congenital HSV encephalitis

BACKGROUND AND CLINICAL INFORMATION: Head

Incidence of 1 case per 500,000 persons per year in the U.S.A.

Clinical features:

May suggest space occupying lesions in the brain.
The only common form encephalitis that occurs sporadically throughout the year. This is the most common sporadic acute viral encephalitis.
Can be found in all parts of the world.
Motality and morbidity with treatment is about 20%.
Most cases are caused by type I virus but can be caused by type II virus in neonates and in immunesuppressed patients

CSF: The CSF is typically hemorrhagic and a lymphocytic pleocytosis is usually seen in repeated lumbar puncture.

Dectection of the virus by PCR of CSF is the most sensitive method. The diagnostic test is identification of virus by culture of the CSF. Brain biopsy has been used to make the diagnosis but is being replaced by PCR of CSF.

GROSS PATHOLOGY: Head

Location:

Characteristic widespread, bilateral but asymmetrical involvement. Necrosis, particularly in the temporal lobe and the hippocampus.
Cingulate gyrus may also be involved.
The brain stem is rarely involved.
Latent viral particles brain stem and trigerminal ganglions.

Gross Pathology: HSV encephalitis usually presents as bilateral necrotic lesion of the temporal lobes.

HISTOPATHOLOGY AND IMMUNOHISTOCHEMISTRY: Head

Essentially acute necrotizing encephalitis with typical inclusion bodies. It is essentially an acute necrotizing vasculitis.

The range of inflammatory cells infiltration can vary from intense to light. In the later case, the histologic picture may suggest infarction. Identification of viral inclusions and immunostaining are very helpful. Imaging and clinical history are also very important.

Necrosis may be extensive enough to mimic infarct. However, perivascular cuffing of inflammatory cells, focal aggregation of mesenchymal cells in the form of neuronophagic nodules or as classic microglial nodules should raise the question of viral infection.

Intranuclear inclusion bodies can be seen, though not easy, and best detected by immunostaining. On HE stain, the inclusion bodies appaear as homogenous wine red glassy nuclei with 3M characteristics: Multinuclei, Molding, Margination of chromatin under basement membrane.

Viral antigen may not be detectable in patients died three weeks after the encephalitis or treated with acyclovior.

May cause necrotic lesions in the liver, kidneys, adrenals, and other organs.