Neuroinvasive disease due to West Nile virus: Clinical and imaging findings associated with a re-emerging pathogen.

The West Nile virus (WNV) is an arbovirus than can infect human beings and cause severe neuroinvasive disease. Taking the outbreak that occurred in Spain in 2020 as a reference, this article reviews the clinical and imaging findings for neuroinvasive disease due to WNV. We collected demographic, clinical, laboratory, and imaging (CT and MRI) variables for 30 patients with WNV infection diagnosed at our center. The main clinical findings were fever, headache, and altered levels of consciousness. Neuroimaging studies, especially MRI, are very useful in the diagnosis and follow-up of these patients. The most common imaging findings were foci of increased signal intensity in the thalamus and brainstem in T2-weighted sequences; we illustrate these findings in cases from our hospital.

Initial Seronegative West Nile Virus Encephalitis in an Immunocompromised Child.

We present a case of initial seronegative West Nile virus encephalitis in an immunocompromised child due to B-cell acute lymphoblastic leukemia. Although diagnostic guidelines for West Nile virus infection exist, we highlight that these may not be met in immunocompromised patients who may have a delayed immune response.

West Nile virus neuroinvasive disease associated with rituximab therapy.

West Nile virus neuroinvasive disease (WNVND) manifests with meningitis, encephalitis, and/or acute flaccid paralysis. It represents less than 1% of the clinical syndromes associated with West Nile virus (WNV) infection in immunocompetent patients. Immunosuppressive therapy is associated with increased risk of WNVND and worse prognosis. We present a patient with WNVND during therapy with rituximab, and a review of the literature for previous similar cases with the goal to describe the clinical spectrum of WNVND in patients treated specifically with rituximab. Our review indicates that the most common initial complaints are fever and altered mental status, brain magnetic resonance imaging often shows bilateral thalamic hyperintensities, and cerebrospinal analysis consistently reveals mild lymphocytic pleocytosis with elevated protein, positive WNV polymerase chain reaction, and negative WNV antibodies. Treatment is usually supportive care, with intravenous immunoglobulins (IVIG) plus corticosteroids and WNV-specific IVIG also used. The disease is usually fatal despite intervention. Our patient's presentation was very similar to prior reports, however demonstrated spontaneous improvement with supportive management only. WNVND is a rare and serious infection with poor prognosis when associated with rituximab therapy. Diagnosis is complicated by absent or delayed development of antibodies. The presence of bilateral thalamic involvement is a diagnostic clue for WNVND. There is insufficient evidence to recommend the use of corticosteroids or IVIG.

Longitudinally extensive transverse myelitis in a patient infected with West Nile virus.

Until now, longitudinally extensive transverse myelitis (LETM) was reported in association with various viral infections. We describe the case in which a diagnosis of LETM was established as a clinical manifestation of West Nile virus (WNV) infection. We report a 39-year old man with WNV infection and LETM. In neurological examination, there was a left periscapular hypotrophy, moderate weakness of left arm, decreased left brachioradialis reflex, tandem instability and gait ataxia. Cervical spine MRI showed enhancing intramedullary lesion extending from C3-C7 level. According to the neurological, EMG and MRI findings, a diagnosis of LETM, with affection of anterior horn cells of the cervical spinal cord, induced by WNV infection was established. The patient was treated with antibiotics, acyclovir and high dose-steroids, methylprednisolone (MP) 1 g/daily in intravenous infusion, for 5 consecutive days, followed by tapering doses of prednisone during the next four months. Six weeks after onset of symptoms, previously described lesion on cervical spine MRI resolved, and the patient gradually clinically improved.

West Nile Neuroinvasive Disease Presenting as Elsberg Syndrome.

INTRODUCTION: Elsberg syndrome (ES) is a rarely recognized cause of cauda equina syndrome and lower thoracic myelitis, mainly linked to reactivation, or occasionally primary, infection with herpes simplex virus type 2. West Nile virus neuroinvasive disease is rarely considered in the differential diagnosis of patients with ES. CASE REPORT: A 63-year-old man with pancreatic cancer in remission and polymyalgia rheumatica on low-dose prednisone presented with a 10-day history of low-back pain and a viral-type illness with low-grade fever, nausea, and vomiting. Days later, he developed left leg monoparesis, neurogenic bladder, and bowel. Magnetic resonance imaging of the lumbar spine revealed a hyperintense signal abnormality within the central spinal cord and conus medullaris with mild swelling of the conus. Cells, proteins, and glucose in cerebrospinal fluid were 67/mm, 70 mg/dL, and 58 mg/dL, respectively. Serology was positive for West Nile virus IgM. Nerve conduction studies and electromyography showed an acute motor neurogenic process affecting left lumbosacral segments. CONCLUSIONS: West Nile virus neuroinvasive disease is an uncommon condition that should be considered in patients with ES. Determining the etiology of ES in the acute setting may avoid unnecessary diagnostic investigations and treatments.

Significant cardiomyopathy secondary to West Nile virus infection.

West Nile virus (WNV) myocarditis has been documented pathologically in birds and mammals, but has rarely been reported in human clinical syndromes. Severe cardiomyopathy as a consequence of WNV has not yet been reported.

West Nile virus encephalitis with thalamic involvement in an immunocompromised child.

West Nile virus has been an increasingly important pathogen in the United States since it was first reported in 1999. Neuroinvasive West Nile virus has been infrequently reported in the pediatric population. We report a case of severe West Nile virus encephalitis with cranial magnetic resonance imaging findings not yet described in children.

Clinical findings of West Nile virus infection in hospitalized patients, New York and New Jersey, 2000.

Outbreaks of West Nile (WN) virus occurred in the New York metropolitan area in 1999 and 2000. Nineteen patients diagnosed with WN infection were hospitalized in New York and New Jersey in 2000 and were included in this review. Eleven patients had encephalitis or meningoencephalitis, and eight had meningitis alone. Ages of patients ranged from 36 to 87 years (median 63 years). Fever and neurologic and gastrointestinal symptoms predominated. Severe muscle weakness on neurologic examination was found in three patients. Age was associated with disease severity. Hospitalized cases and deaths were lower in 2000 than in 1999, although the case-fatality rate was unchanged. Clinicians in the Northeast should maintain a high level of suspicion during the summer when evaluating older patients with febrile illnesses and neurologic symptoms, especially if associated with gastrointestinal complaints or muscle weakness.