Adults Herpes Encephalitis

In adults with HSV-1, the most common early symptoms are headache and fever. Additional symptoms include intellectual impairment, aphasia, meningeal signs, seizures, and paresthesias. Early treatment is crucial to a good outcome, and empirical acyclovir therapy can be initiated before a definitive diagnosis is established.
The virus cannot be cultured routinely from CSF, though lymphocytic pleocytosis and elevations in protein concentrations are observed. CSF viral cultures are positive for HSV in fewer than 5% of patients. Anti-HSV antibodies often do not appear until 1-3 weeks after symptom onset; therefore, antibody culture is helpful only in retrospective diagnosis.
EEG also can reveal focal temporal abnormalities, which are seen in 80% of patients; a normal EEG is believed to exclude the diagnosis. Periodic lateralized epileptiform discharges also support the diagnosis, but this finding is nonspecific. Historically, a brain biopsy provided a definitive diagnosis, but this procedure is not highly sensitive and can result in complications, including hemorrhage and edema at the biopsy site.
An RNA polymerase test of CSF, polymerase chain reaction (PCR), permits a more definitive diagnosis because it is both sensitive and specific. In this test, 2 sets of oligonucleotide primers amplify gene products from HSV-1 and HSV-2. The National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group reported a sensitivity of 94% and a specificity of 98% when compared with HSV culture from brain biopsy.
After DNA amplification, a Southern blot technique can be used to identify the characteristic herpes simplex banding. The results are positive early in the disease, and the test has a turnaround time of approximately 24 hours. This test is now considered the criterion standard for the diagnosis of HSV. Rare false-positive reports result from cross-contamination.
False-negative reports have been described in neonates and young infants, perhaps because of the presence of heme or other inhibitors. In addition, false-negative assays can occur early in the disease. A repeat assay should be considered. Note that the results remain positive during the first week of antiviral therapy.
The HHV6 virus exists in 2 subtypes, HHV6A and HHV6B, with the B subtype primarily responsible for primary infection and reactivation. Diagnosis is made by PCR analysis for HHV6 DNA in samples of CSF. It has, however, been postulated that PCR detection of HHV6 DNA in patients past the age of primary infection may reflect chromosomal integration of viral DNA rather than active infection.
Prompt therapy with acyclovir inhibits the herpes simplex polymerase and stops the virus from replicating. Improved survival rates are present when treatment is started within 4 days after the onset of illness. Patients with possible HSV should receive acyclovir 10 mg/kg intravenously every 8 hours. Rapid infusion can cause crystalluria and subsequent renal failure. The dose should be given slowly over at least 1 hour by pump infusion techniques.
A therapeutic duration of 10 days is suggested, but this may result in up to a 10% relapse rate. A longer therapeutic period of 3 weeks has been proposed. Of note is that immunocompromised patients with HHV6 infection are ineffectively treated with acyclovir, although their clinical presentation is similar to that seen in patients with HSV-1. Early identification can be helpful, because patients with HHV6 infection respond to ganciclovir and foscarnet.
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