Case Presentation: A 52-year-old man with past medical history of end-stage renal disease status post renal transplant 14 years ago, hypertension, anxiety, systemic lupus erythematosus, and hypothyroidism presented for acute kidney injury (AKI) on chronic kidney disease stage 3, from creatinine baseline of 1.3-1.5 mg/dL to 3.7 mg/dL. He was placed on IV fluids for prerenal AKI caused by diarrhea and Nephrology was consulted. Over the course of his stay, his mental status worsened. He became drowsy, delirious, and febrile, despite his creatinine improving. Neither a computed tomography scan nor magnetic resonance imaging (MRI) of his head demonstrated any acute process. Neurology and Infectious Disease were consulted, and he was initially placed on broad-spectrum antibiotics and antivirals while he underwent lumbar puncture. Cerebrospinal fluid (CSF) fluid analysis showed glucose 58, and protein elevated to 123. Given his prior history of polysubstance abuse, Psychiatry was also consulted.The patient’s mental status worsened despite treatment, necessitating intensive care unit (ICU) admission. His CSF serology eventually was positive for West Nile IgM. He was treated with IVIG for 5 days. With IVIG, the patient clinically improved, and he was able to transfer to medicine floor. On the floor, his encephalopathy improved though he continued to have intermittent episodes of agitation and delirium. The patient was eventually able to be discharged home.
Discussion: West Nile virus (WNV) is transmitted by mosquitoes, usually of the Culex species. Since its unexpected arrival in the United States in 1999, it has become an epidemic. An estimated 26% of WNV‐infected persons become symptomatic. Most symptomatic patients experience fever, headache, weakness, myalgia, and/or arthralgia. Gastrointestinal symptoms and a transient maculopapular rash also are common. Less than 1% of infected people develop neuroinvasive diseases. However, in the case of solid organ transplant patients, such as our patient, infections are often severe, with 30%-40% mortality, and infection leads to neuroinvasive disease in 70% of cases. Most cases start with unexplained fever that is unresponsive to antibiotic therapy, followed by rapid onset of neurological deficits, with the majority requiring transfer to the ICU. CSF analysis mainly demonstrates neutrophil-predominant pleocytosis. Brain MRI is frequently normal, but can show signal abnormalities in the basal ganglia, thalamus, and brainstem. Mental status problems are among the most prevalent long-term sequelae of WNV disease, especially in patients with encephalitis. Treatment usually includes supportive care, reduction of immunosuppressive therapy, and frequent intravenous immunoglobulin.
Conclusions: WNV should be considered in patients who have an onset of an unexplained febrile illness, encephalitis, meningitis, and/or flaccid paralysis during mosquito season, particularly those who have received solid-organ transplants. A very high proportion of organ transplant recipients with WNV infection presents with neuroinvasive disease. Lumbar puncture should be performed in patients with neurologic symptoms, and in immunocompromised patients, CSF should be tested for IgM antibody and viral nucleic acid in addition to serum testing.