Case Presentation: A 73-year-old male presented with three days of vertigo, headache, tinnitus and vomiting, following recent exposure to a viral upper respiratory tract infection. Initial imaging was unremarkable, and laboratory studies showed mild thrombocytopenia. By day three, he developed fever, confusion, and respiratory failure requiring ICU admission and intubation. Lumber puncture resulted in White Blood Count 7 (neutrophils 9%), RBC 2, protein 95, and glucose 56. CSF testing revealed positive for West Nile virus IgG. By day 20, the patient developed progressive bilateral lower-extremities (LE) weakness with absent reflexes; Motor strength was 5/5 in upper extremities and 2/5 in the LE. Tone and proprioception were reduced, though sensations remained intact. MRI of the spine with contrast showed increased enhancement of the ventral cauda equina nerve roots, consistent with Guillain- Barré Syndrome (GBS). He was treated with intravenous immunoglobins (IVIG) and demonstrated clinical improvement, later being transferred to inpatient rehabilitation for continued recovery.
Discussion: West Nile virus (WNV) infection remains an important public health concern and presents a wide clinical spectrum, ranging from asymptomatic infection to severe neuroinvasive disease. Approximately 80% of infected individuals remain asymptomatic, 20% developed self-limited febrile illness, and about 1% progressed to neuroinvasive disease (4). Several host-related factors-including advanced age, hypertension, immunosuppression, and impaired immune response-are associated with increased risk of severe outcomes (1). According to CDC data from 1999 to 2024, 16,992 WNV infections were reported, of which 31,806 involved neuroinvasive cases. In 2024 alone, 1,791 cases were recorded, including 1,335 neuroinvasive cases and 164 deaths, nearly all attributable to neuroinvasive complications. Guillain-Barré syndrome (GBS) is uncommon, with an incidence of approximately 1 to 2 cases in 100,000 individuals (3). While most cases follow respiratory and gastrointestinal infections, WNV is a recognized but rare trigger. Prior CDC data suggest approximately 13% of WNV infections with neurological involvement may develop GBS. Diagnosis relies heavily on thorough neurological examination, electrodiagnostic testing, and exclusion of alternative causes. Neuroinvasive WNV disease (WNND) carries high morbidity and long-term consequences. In a long-term follow-up cohort of 26 patients with WNND, 15% died during acute hospitalization, 23% died during medium-term follow-up. Although 80% of survivors eventually achieve functional independence with prolonged rehabilitation, many are unable to return to their prior cognitive level (5).
Conclusions: The incidence of WNV fever has increased over the past two decades, emphasizing the need for heightened awareness, particularly during summer and early fall and among individuals with high risk factors exposures (2). Early recognition, patient education, and close monitoring in both outpatient and inpatient settings can reduce morbidity and hospital length of stay. Because initial symptoms may be nonspecific, timely differentiation is essential. As neuroinvasive cases continue to rise, incorporating WNV antibody testing into respiratory viral panels may improve early detection and management.