Powassan Virus Reaches the Brain, Lung, and Kidney in a Transplant Recipient
A fatal case of Powassan virus infection in a liver transplant recipient in Pennsylvania offers a rare, unnerving look at how a tick-borne flavivirus can spread far beyond the nervous system when host immunity is altered. The postmortem figure alone tells the story of a systemic infection: deep gray nuclei, hippocampi, brain stem, cerebellum, lungs, kidneys, and circulating mononuclear cells all showed evidence of viral involvement. In an immunosuppressed patient, the virus did not remain a localized neuroinvasive threat. It disseminated.
The imaging and tissue studies together point to a broad viral burden rather than isolated encephalitis. Magnetic resonance imaging showed T2 hyperintensity in bilateral deep gray nuclei and thalami, with additional near-symmetric involvement of the hippocampi, brain stem, and cerebellar hemispheres. Faint perivascular enhancement appeared in the deep gray nuclei, and there was faint leptomeningeal enhancement along the left cerebellum. In the setting of chronic liver dysfunction, bilateral globus pallidi also showed T1 hyperintensity from manganese deposition, a separate radiologic finding that could have complicated interpretation but did not obscure the underlying inflammatory process.
The pathology is even more striking. The cerebellum showed widespread meningoencephalitis with marked Purkinje cell necrosis, diffuse lymphoplasmacytic parenchymal inflammation, leptomeningeal inflammation, and microgliosis. Powassan virus antigen and RNA were abundant, especially in the molecular cell layer, but they were not confined there. Viral signal appeared in multiple cell types across the tissue layers, and similar histopathologic evidence extended to neurons in the pons and cerebrum. For a pathogen often framed as a cause of encephalitis, this tissue map broadens the clinical picture: the virus can occupy multiple compartments of the central nervous system at once, especially when immune control is impaired.
One sentence captures the bedside consequence plainly: this was not a brain-only infection.
Pulmonary involvement added another layer of concern. The lungs showed mild lymphocytic pneumonitis, bronchiolar epithelial denudation, and epithelial cell apoptosis. Powassan antigen and RNA were detected in bronchiolar epithelial cells, with involvement of other cell types such as pneumocytes and endothelial cells. That pattern suggests the virus reached respiratory tissues directly rather than causing only secondary inflammatory injury. In a transplant recipient, where fever, encephalopathy, and respiratory decline can all be attributed to broad infectious or noninfectious causes, such findings sharpen the differential toward disseminated viral disease.
Renal tissue reinforced that interpretation. Multifocal interstitial predominantly mononuclear peritubular infiltrates accompanied acute tubular injury, including epithelial denudation, attenuation with loss of apical cytoplasm, and pigmented casts. Powassan antigen and RNA were present in renal tubular epithelial cells. This matters because kidney injury in a critically ill transplant recipient can be dismissed as multifactorial, yet direct viral detection in tubular epithelium provides a clearer mechanistic link between systemic infection and organ dysfunction. A pathogen capable of entering renal tissue, pulmonary epithelium, and brain parenchyma is behaving as a disseminated infection, not a confined neurotropic event.
Circulating mononuclear cells carried viral antigen as well, with detection across organs including the kidneys, lungs, and liver. That finding raises the possibility that infected immune cells may have served as vehicles for spread or reflected a high-level viremic state at the tissue level. Either way, the histology argues for bloodstream dissemination and multi-organ seeding. In an immunocompromised host, reduced viral clearance likely allowed that process to continue unchecked until severe central nervous system injury and systemic organ involvement became fatal.
Powassan virus deserves attention because it is uncommon but capable of severe neurologic disease, and this case shows how transplantation can magnify that danger. Tick-borne flaviviruses are usually discussed in the context of outdoor exposure and seasonal risk, but immunosuppression changes the clinical geometry. Once the virus gains entry, impaired adaptive immunity can permit broader tissue invasion, delayed recognition, and more extensive damage before the diagnosis becomes apparent. The pathology here shows why tissue confirmation matters: brain MRI alone may suggest encephalitis, but autopsy provided proof of viral spread across distinct organ systems.
The case also strengthens the practical value of considering tick-borne pathogens in transplant recipients with unexplained encephalitis or multiorgan dysfunction. Powassan infection is rare, yet the stakes are high when neurologic symptoms intersect with respiratory or renal abnormalities. This patient’s tissue findings—meningoencephalitis, pneumonitis, acute tubular injury, and viral antigen and RNA in multiple organs—show a disease process that was biologically diffuse and clinically unforgiving.
No broad epidemiologic estimate comes from this single case, and no treatment comparison is possible here. What remains is a pathology lesson with direct clinical weight: in an immunosuppressed host, Powassan virus can move through the brain, lung, kidney, and circulating mononuclear cells before death, leaving a diffuse trail of viral antigen, RNA, and tissue destruction behind it.