Abstract West Nile Virus (WNV) infection can present as a self-limiting febrile illness or, in rare cases, as a neuroinvasive disease with neuromuscular involvement. Neuroinvasive West Nile disease is more commonly seen in elderly, immunocompromised patients. Concomitant hematologic abnormalities are atypical, and their co-occurrence can obscure the diagnosis. We therefore present a rare case of West Nile neuroinvasive disease complicated by respiratory failure and concomitant severe pancytopenia, highlighting the diagnostic challenges due to the varied presentation and clinical vigilance required in critically ill patients presenting with overlapping neuroinvasive/neuromuscular and hematologic findings. Case Presentation A 46-year-old female with a history of alcohol use presented with fever, nausea, vomiting, generalised weakness, poor oral intake, oro-facial rash, and weight loss. Initial laboratory investigations revealed severe pancytopenia and macrocytosis. Vitamin B12 was profoundly low. Tick-borne diseases were negative. Peripheral smear showed no schistocytes, and bone marrow flow cytometry was negative for myelodysplastic syndrome.The patient developed acute lower extremity weakness and confusion, followed by acute hypoxemic respiratory failure warranting the need for intubation with ventilatory support. A chest X-ray was performed, which showed right lower lobe atelectasis, inconsistent with the degree of hypoxemia. CSF analysis revealed elevated protein and glucose, with three oligoclonal bands, secondary to a neuroinvasive viral infection. The MRI brain was unremarkable. IgM and IgG antibodies to West Nile virus were positive in CSF, confirming neuroinvasive disease. She was treated with IVIG and B12 supplementation, with gradual neurological improvement and hematologic recovery. Eventually, she was successfully weaned off ventilatory support, the tracheostomy tube was removed, and she was discharged to rehabilitation. Discussion This case reflects on the rare co-occurrence of West Nile neuroinvasive disease, causing severe respiratory decompensation due to neuromuscular weakness in already deconditioned patients with poor pulmonary reserve and with profound B12 deficiency. The overlapping presentations complicated our judgment and led to broad differentials, including thrombotic thrombocytopenic purpura, myelodysplastic syndrome, and autoimmune aetiologies, explaining the wide array of multi-organ manifestations. WNV should be considered in patients with unexplained neuromuscular weakness and respiratory failure, especially in endemic regions during the transmission period, when alternative etiologies do not explain the full picture. Clinicians should maintain a high index of suspicion for infectious triggers in patients with acute neurological decline, particularly when initial autoimmune and metabolic workup is inconclusive. Prompt identification of concurrent contributing factors, like nutritional, infectious, or autoimmune, is essential to guide multidisciplinary management and improve outcomes. This abstract is funded by: None
Chaudhry et al. (Fri,) studied this question.