A herpes simplex virus encephalitis case with no clinical response to acyclovir treatment

• Published in: Mikrobiyoloji bülteni Vol. 41; no. 4; pp. 613 - 619
• Main Authors: Cakmak Celik, Fatma, Dağdemir, Ayhan, Eroğlu, Cafer, Aydin, Omer Faruk, Incesu, Lütfi, Yilmaz, Hava
• Format: Journal Article
• Language: Turkish
• Published: Turkey 01-10-2007
• Subjects: Acyclovir - therapeutic use; Antiviral Agents - therapeutic use; Brain - pathology; Cerebrospinal Fluid - cytology; Cerebrospinal Fluid - virology; DNA, Viral - cerebrospinal fluid; Drug Resistance, Viral; Encephalitis, Herpes Simplex - cerebrospinal fluid; Encephalitis, Herpes Simplex - diagnosis; Encephalitis, Herpes Simplex - drug therapy; Erythrocyte Count; Female; Glucose - cerebrospinal fluid; Humans; Infant; Magnetic Resonance Imaging; Simplexvirus - drug effects; Simplexvirus - genetics; Simplexvirus - isolation & purification; Treatment Failure
• ISSN: 0374-9096
• DOI: 10.5578/mb.66921

In spite of high rates of morbidity and mortality in herpes simplex virus (HSV) encephalitis, however, it is one of the exceptional viral infections with specific and effective therapy. In this report a HSV encephalitis case who was clinically unresponsive to acyclovir treatment, has been presented. An 11 months old girl patient has been brought to our clinic with the complaints of high fever and focal convulsions. Analysis of cerebrospinal fluid (CSF) revealed decreased glucose level and abundant red blood cells, despite it was not traumatic. The other CSF biochemical findings were found normal. Viral serology performed with CSF yielded negative result for HSV-1 IgG, positive result for HSV-2 IgG, and negative result for HSV-1/2 IgM, however, antibody index could not be estimated since it was not possible to obtain a simultaneous serum sample. Cranial magnetic resonance imaging (MRI) showed contrast material enhancement on bilateral temporal lobes. There was no growth in the CSF cultures. Acyclovir therapy (30mg/kg/day) was started with the prediagnosis of herpes encephalitis. In the third week of therapy CSF analysis was repeated because of the presence of partial paroxysmal attacts and absence of sufficient clinical improvement. In this CSF sample HSV-1 DNA was found positive by real-time polymerase chain reaction. Since CSF findings were still abnormal and the clinical picture worsened despite 21 days of therapy, the dose of acyclovir was increased to 60 mg/kg/day (3 weeks) with a possible drug resistance problem. Control brain MRI showed contrast enhancement on bilateral temporal lobes, with more intensivity in left, and encephalomalacia. Valproic acid and haloperidol were given to the patient for the treatment of permanent partial paroxysms and orofacial dyskinesis, developing in the follow-up period, respectively. After getting these complications under control, the patient was discharged and taken into follow-up. As a result, although it could not be possible to confirm the drug resistance by molecular methods, it was thought that this might be both a clinical and virological resistance phenomenon, because of the detection of HSV-DNA in the CSF sample during the period of severity of the illness.