A 32‐year‐old man experienced several days of hallucinations and strange behavior. He was brought in by a coworker from an industrial ship that had sailed from India. He had been in bed for the past few days with fever and sweats. The patient appeared anxious, had difficulty answering questions, and was oriented only to place. He was febrile, tachycardic, and tachypneic. He had mild, bilateral ataxia of his upper extremities and an impaired tandem gait but was otherwise normal. The patient had a microcytic anemia, no leukocytosis, a sodium of 128 mmol/L, an AST of 230 units/L, an ALT of 170 units/L, a creatinine kinase of 7100 units/L, and an arterial oxygen of 77 mm Hg. Computerized tomography of the chest revealed multiple pulmonary emboli. MRI of the brain showed diffuse cortical atrophy without specific lesions. Cerebrospinal fluid had a normal cell count. However, fluid analysis was positive for West Nile virus antibody.
West Nile virus (WNV) is a multiorgan infection that infects neurons and spreads through the body. It can lead to motor or sensory deficits and personality changes. It is important for the internist to recognize encephalitis because many laboratory tests and imaging techniques may be inconclusive. In our patient with a recent travel history, altered mental status, ataxia, and hallucinations, this was an important diagnosis to consider. West Nile virus was originally confined to South Asia and Africa, but it has spread through North America, making its recognition important to the American internist. WNV, a flavivirus and member of the arthropod‐borne viruses (arbovirus), is asymptomatic in more than 80% of cases. However, of those patients with symptomatic infection, most require hospitalization and develop West Nile fever, which is characterized by the acute onset of fever, malaise, headache, muscle pain, and weakness.
Patients should be empirically treated while awaiting diagnostic results. Diagnosis of WNV can be performed by detection of IgM or IgG WNV immunoglobulins. However, IgG detection may indicate a past, rather than a current, infection. Microsphere immunoassays are a newer and potentially more accurate method. Finally, the virus can be detected in cerebrospinal fluid, serum, or tissues by isolation or nucleic‐acid amplification tests. Neuroimaging such as MRI can be helpful in detecting herpes simplex virus, abscess, and fungal etiologies. Our patient exhibited several symptoms of encephalitis, including transaminitis and rhab‐domyolysis. The cortical atrophy noted on MRI was a result of a separate chronic disease process that may have predisposed him to more serious symptoms related to the virus. The severity of the disease in this case likely caused him to be bedridden and placed him in a hypercoagulable state, causing pulmonary emboli. Treatment for West Nile virus is largely supportive care. Pharmacotherapy with interferon and ribavirin has shown mild efficacy in vitro but has not yet been tested in clinical trials.
N. Shah ‐ none; J. Hambley ‐ none; M. Glass ‐ none
To cite this abstract:Shah N, Hambley J, Glass M. The Nile Ain't Just a River. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 388. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/the-nile-aint-just-a-river/. Accessed January 19, 2020.