Herpes Simplex Virus1 Infection

Herpes simplex virus-1 infection is the major cause of sporadic and malignant encephalitis, chiefly in adults and young subjects. The infection is acquired by exposure to contaminated saliva or respiratory secretion. The virus initially causes a nasopharyngitis. By retrograde axonal transport, it reaches the trigeminal ganglia, where it becomes latent. Reactivation of the virus produces herpes vesicles on the lips (cold sore) or oral mucosa. The brain is infected by spread of the virus along the trigemi-nal nerve roots or dural nerves to the meninges and then to the frontal and basal temporal regions. Alternatively, it is suggested that a nasopharyngeal infection spreads along the olfactory nerves to the frontobasal and temporal regions, evoking an acute encephalitis.

Clinical Features

The onset is acute, presenting with meningeal symptoms and signs combined with behavioral changes, hallucinations, altered states of consciousness, and focal neurologic deficits. The course is fulminant, and the mortality is high, about 50% to 70%. Early diagnosis and the initiation of antiviral therapy are imperative, but even treated cases are often left with neurologic and psychiatric sequelae varying from personality changes, Korsakoff syndrome, and language and cognitive deficits, to a persistent vegetative state.

Herpes simplex virus-specific DNA is identified in the CSF using PCR. Neuroimaging adds to the diagnosis. CT scan during the early course of the disease shows bilateral, often asymmetrical, low densities in the orbital and temporomesial areas, mixed with hyper-dense hemorrhages. On MRI, the lesions are hypoin-tense on T1- and hyperintense on T2-weighted images. Electroencephalogram (EEG) may show periodic sharp and slow wave discharges at 2- to 3-seconds intervals. In a few cases, brain biopsy is performed to establish the diagnosis; immunofluorescent stain is a quick diagnostic tool to identify the viral antigen.

Pathology

The pathology is characterized by a hemorrhagic necrotizing encephalitis, typically confined to the fronto-orbital cingular and temporomesial regions (Fig. 6.10). Grossly, the brain is swollen and the blood vessels congested. Petechial hemorrhages are scattered throughout the leptomeninges and cerebral cortex of the affected regions.

FIGURE 6.10

Herpes simplex-1 encephalitis (HSE). A. Schematic drawing shows the distribution of the lesions in the fronto-orbital and temporal regions. B. Perivascular hemorrhages in the subarachnoid space and cerebral cortex. C. Neuronophagia. D. Cortical necrosis (HE).

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The histology is characterized by (a) perivascular and diffuse infiltrations with lymphocytes, some neutro-phils, and macrophages in the leptomeninges and cerebral cortex; (b) pericapillary hemorrhages; (c) paren-chymal necrosis; (d) neuronophagia and neuronal destruction; and (e) eosinophilic intranuclear inclusions in residual neurons and glial cells (see Fig. 6.10). In chronic cases, the brain shows atrophy, cystic necrosis, and gliosis in the frontotemporal regions.

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