A-Z Index × Submit A-Z Index × Submit A-Z Index Search Dropdown × Submit Facebook Twitter LinkedIn Syndicate Emerging Infectious Disease journal ISSN: 1080-6059 Disclaimer: Early release articles are not considered as final versions. Any changes will be reflected in the online version in the month the article is officially released.
We describe histopathologic findings from a fatal case of Powassan virus lineage 2 (deer tick virus) in an immunosuppressed liver transplant patient in Pennsylvania, USA. We confirmed infection in postmortem brain, lung, and kidney by immunohistochemistry, in situ hybridization, and reverse transcription PCR, demonstrating infection of pulmonary and renal tissues.
Powassan virus (POWV) is a tickborne flavivirus that causes severe encephalitis. Cases are increasing annually; 60 cases and 9 deaths were confirmed in the United States during 2024 ( 1 ). Neuroinvasive disease occurs in 94% of confirmed cases and 98% of fatalities ( 1 ). We describe novel histopathologic findings of disseminated POWV infection with multiorgan involvement in a liver transplant recipient in Pennsylvania, USA.
Figure . Magnetic resonance imaging and microphotographs for detection of POWV lineage 2 (deer tick virus) in postmortem tissues from a liver transplant patient with fatal infection and histopathological features of formalin-fixed,...
The patient was a 38-year-old woman in southeastern Pennsylvania, USA, who had alcohol-associated cirrhosis and remote preexposure prophylactic rabies vaccination 16 years earlier. She had undergone orthotopic liver transplant 6 weeks before seeking care at an emergency department for malaise, headache, fever, and leukocytosis. After admission, she had multiple generalized seizures. Magnetic resonance imaging revealed hydrocephalus with rapidly progressive enhancement of the cerebellum, brainstem, white matter, cortex, leptomeninges, and spinal cord ( Figure , panels A–E). Cerebrospinal fluid (CSF) studies were consistent with viral encephalitis ( Appendix Table 1). We ruled out autoimmune and other causes of viral encephalitis. Brain biopsy demonstrated lymphocytic encephalitis without features of a specific infectious etiology. We noted necrotic tissue intraoperatively, and the procedure was complicated by hemorrhage. The patient’s neurologic status deteriorated further, and she died after being transitioned to comfort care. CSF reverse transcription PCR testing for POWV was positive for lineage 2 (deer tick virus) the day before her death. POWV serum IgM test result was positive after her death ( Table ). Of note, CSF metagenomic sequencing on an earlier sample was negative for POWV ( Appendix Table 1), which might reflect low viral load or testing detection limits.
Because of the patient’s rapid neurologic decline and imaging findings, rabies was initially suspected because other common causes were ruled out. Testing was expeditiously conducted for the safety of other organ recipients. Antemortem serum and CSF indirect immunofluorescent antibody rabies testing detected IgG, but not IgM. A rapid fluorescent focus inhibition test detected high serum rabies antibody titers and low CSF titers. Presence of rabies IgG in the CSF, although atypical, was attributed to previous vaccination and might have resulted from serum antibody spillover secondary to leaky blood–brain barrier from severe meningoencephalitis. Results of additional antemortem and postmortem rabies test results, including immuno…