Abstract
Herpes simplex-1 virus encephalitis (HSE) is the most commonly recognized cause of sporadic encephalitis in the United States. Historically HSE has been considered extremely detrimental given the associated relentless neurological deterioration secondary to cerebral edema and status epilepticus. With recent advances in antiviral therapeutics in past decades, the majority of complications can be managed effectively although the associated morbidity and mortality still remains high. The key modifiable factor determining recovery is the rapid initiation of antiviral therapy. We discuss the case of a 19-year-old female with HSE who received standard acyclovir therapy. Despite using recommended dosage and duration of acyclovir, her clinical condition worsened significantly and subsequently required multiple antiviral therapeutics and steroid therapy.
Highlights
Herpes simplex virus (HSV) infection is the leading cause of necrotizing viral encephalitis in developed countries [1,2]
About 90% of herpes simplex virus encephalitis (HSE) cases in adults and children are related to type-1 HSV [3]
Herpes simplex-1 virus encephalitis (HSE) is believed to result from reactivation of latent HSV-1 in dorsal root ganglia that subsequently spreads to the central nervous system (CNS) predominantly affecting temporal lobes [2,3]
Summary
Herpes simplex virus (HSV) infection is the leading cause of necrotizing viral encephalitis in developed countries [1,2]. We describe the case of an immunocompetent female who presented with complaints of headaches, altered mental status, and short-term memory loss and was diagnosed as having severe HSE. Her clinical condition deteriorated despite early acyclovir therapy requiring deviation from standard antiviral therapy. She had a known history of hypothyroidism and had been non-compliant with her thyroid medication for over one year. The patient’s mental status improved, she developed severe genital labial swelling as an adverse effect of the foscarnet She remained on acyclovir at 10 mg/kg/dose every eight hours for a total of 30 days. At the time of discharge after 17 days of hospitalization (~22 days from symptom onset), neurological deficits were short-term memory loss, hyperorality, and irritability
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