| Publication Abstract Display | | Type: Published Manuscript | | Title: Acute HIV infection presenting as fulminant meningoencephalitis with massive CSF viral replication. | | Authors: Andrade R, Torriani F, Ellis RJ | | Year: 2014 | | Publication: Neurology Clinical Practice | | Volume: 4 Issue: 3 Pages: 256-259 | | Abstract:22-year-old man presented to the emergency department with 10 days of malaise, generalized rash, sore throat, oral ulcers, headache, nausea, and vomiting. On ex- amination he had fever (101.5°F), hepatosplenomegaly, generalized maculopap- ular rash, and lymphadenopathy. He rapidly became obtunded, requiring intubation. Initial laboratory studies showed mild transaminitis, increased lactate dehydro- genase, and 4,600 leukocytes per mL with 61% bands and 18% lymphocytes. Bacterial and fungal blood cultures were negative as well as a rapid HIV test, additional serologies (including rapid plasma reagin and Treponema pallidum particle agglutination), quantita- tive PCRs (for viruses other than HIV), and urine and blood toxicology. CSF, on hospital day 4, showed a lymphocytic pleocytosis (total leukocytes: 100), high protein, borderline hypoglycorrhachia, and negative Gram stain and culture. Brain MRI revealed no meningeal enhancement or masses. EEG revealed no epileptiform activity. Flow cytometry on bone marrow biopsy and CSF found no evidence of malignancy, as did an excisional lymph node biopsy (figure 1). An immunofluorescent assay test for HIV returned inconclusive and a Western blot detected HIV gp120/gp160 bands. Quantitative HIV RNA PCR was 1.4 3 106 copies/mL in plasma and in CSF exceeded the upper limit of quantitation (107 copies/ mL) (figure 2).
The patient’s clinical status improved and he was discharged 11 days later with a diagnosis of acute HIV infection with meningoencephalitis. Eighteen days after presentation, darunavir, ritonavir, emtricitabine, and tenofovir were started. A month later, low avidity HIV-1 anti- bodies were detected and neuropsychological testing revealed mild to moderate impairment in information processing speed, verbal fluency, and motor skills. Neurologic examination showed a mild spastic paraparesis with impaired ambulation. A spinal MRI 2 months later was nondiagnostic. Six months after presentation, his gait was improved, but upper neuron signs remained. Virologic suppression in plasma and CSF was achieved 5 months after ini- tiating antiretroviral therapy (ART) (figure 2). |
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