2399 West Nile Encephalitis in a Post-Liver Transplant Patient

Abstract

INTRODUCTION: West Nile Virus (WNV) is a neurotropic flavivirus that is transmitted from animals to humans by the bite of the Aedes, Anaphales, or Culex mosquito, with disease incidence peaking in the late summer and early fall. It is the leading cause of arboviral illness in the U.S. While many infected with WNV are asymptomatic, 25% of patients develop fever, and less than 1% of patients will develop neurologic symptoms. Age over 75-years old and immunosuppressed state are risk factors for developing neuroinvasive disease. CASE DESCRIPTION/METHODS: A 65-year old woman with a history of HCV cirrhosis complicated by HCC status post successful orthotopic liver transplantation (OLT) in 2016 compliant with tacrolimus and everolimus immunosuppression (ISP) presented with painless jaundice and acute transaminemia. Liver biopsy revealed severe acute cellular rejection (ACR), so steroids and thymoglobulin were started. Tacrolimus was increased and everolimus was changed to mycophenolate mofetil. Clinically, she appeared well and her LFTs responded to treatment. Suddenly, she developed fever to 103º associated with bilateral hand tremors. Infectious workup was obtained, and she was started on broad-spectrum antibiotics. Initially, symptoms were attributed to changes in ISP and treatment of ACR. However, she developed progressively worsening dyskinesia and encephalopathy eventually requiring intubation. Given initial negative infectious workup, lumbar puncture was obtained; see Table 1. HSV, VZV, and Lyme PCR as well as VDRL in the CSF were negative. Given clinical symptoms, positive WNV IgM in the CSF, and MRI Brain concerning for WNV neuroinvasive disease, patient was treated with IVIG for 5 days. WNV IgG became positive as well on repeat lumbar puncture 2 weeks later. Patient’s encephalopathy improved, and she was able to be extubated. DISCUSSION: There may be a delay in diagnosis and treatment of WNV encephalitis in post-liver transplant patients as neurologic symptoms may be attributed to ISP or as in this patient, to the treatment of acute cellular rejection. West Nile encephalitis must remain on the differential diagnosis when neurologic symptoms are present in a post-liver transplant patient, especially in endemic areas during the summer and fall months. A change in this patient’s ISP for the treatment of ACR may have caused the development of a more severe, neuroinvasive response to WNV infection and ISP management in such patients should be studied further.