What does this research mean for the field?

Metagenomic sequencing of cerebrospinal fluid can successfully diagnose West Nile Virus neuroinvasive disease in immunocompromised patients when standard serological testing is falsely negative. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To report a case of Guillain-Barré Syndrome due to West Nile Virus in an immunocompromised patient treated with rituximab.

May 20, 2026

C50-32 West Nile Virus Presenting as Guillain-Barré Syndrome in an Immunocompromised Patient: A Diagnostic Challenge

Key Points

To report a case of Guillain-Barré Syndrome due to West Nile Virus in an immunocompromised patient treated with rituximab.
Detailed clinical evaluation of a 63-year-old woman with progressive weakness and respiratory failure.
Cerebrospinal fluid analysis and metagenomic sequencing were performed to identify pathogen.
Imaging studies including MRI of the brain and spine were conducted to assess CNS involvement.
Metagenomic sequencing detected West Nile Virus RNA in cerebrospinal fluid on day 12 after inconclusive serologies.
Cerebrospinal fluid showed albumin-cytologic dissociation but was negative for pathogens.
Patient required intubation due to respiratory distress and experienced no clinical improvement despite five plasmapheresis sessions.

Abstract

Abstract 1). Introduction West Nile Virus (WNV) neuroinvasive disease (NID), including encephalitis, meningitis, myelitis, and acute flaccid paralysis, occurs in less than 1% of infected individuals, with increased risk and severity in older or immunocompromised adults. WNV-associated Guillain-Barré Syndrome (GBS) is rare, with an annual incidence of 0.6/100,000. We report a case of a patient with mantle cell lymphoma (MCL) on rituximab who developed progressive weakness and respiratory failure due to WNV-associated GBS. 2). Case Presentation A 63-year-old woman with MCL on rituximab presented with rapidly progressive bilateral weakness of all extremities for two days. She denied numbness, fever, headache, or recent travel. On arrival, she was alert, oriented, and hemodynamically stable. Motor strength was symmetrically reduced in all limbs, with intact reflexes, sensation, and cranial nerves. On day 3, she developed bulbar weakness and respiratory distress, requiring intubation. Differentials considered were CNS involvement due to MCL, GBS, or paraneoplastic syndrome.Blood work showed pancytopenia. Infectious workup, including WNV serologies and imaging, was unremarkable. On day 4, she developed fever, left facial droop, diminished reflexes, and shock. Cerebrospinal fluid (CSF) analysis showed albumin-cytologic dissociation but was negative for pathogens as well as WNV antibodies. Brain MRI showed scattered hyperintensities. Spine MRI revealed ventral cauda equina root enhancement, classically seen in GBS (Figure 1), and labyrinthine facial nerve enhancement, sometimes seen in the Miller Fisher variant. Paraneoplastic panels were negative. No clinical improvement was seen after five plasmapheresis sessions. Metagenomic sequencing of CSF (MSCSF) detected WNV RNA on day 12. Despite supportive care, her condition did not improve, and on day 15, the family decided to transition to comfort care. 3). Discussion This case emphasizes the diagnostic value of MSCSF in identifying CNS infections when conventional testing is inconclusive. Our immunocompromised patient presented with acute flaccid paralysis. Blood and CSF WNV serologies were negative, likely due to rituximab-induced immunosuppression. Ultimately, MSCSF detected WNV RNA, confirming neuroinvasive WNV infection-associated GBS. This highlights two key points: (1) WNV neuroinvasive disease should be considered in acute flaccid paralysis or GBS-like presentations in immunocompromised hosts.(2) MSCSF offers superior diagnostic value when standard CSF testing fails. This abstract is funded by: None

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