west nile virus

Based on the epidemiological and clinical features, the most likely cause of this patient’s presentation among the available options is West Nile (WN) virus.

Since its initial identification in the United States in 1999, WN virus has become the leading cause of arboviral disease in the continental United States. The virus has been identified in all US states, but the highest incidence is reported in Arizona, Texas, Colorado (as in this patient’s case), California, and Nebraska. Infection also follows a seasonal pattern, with the vast majority of cases occurring between June and October, with a peak in late August and early September.

People are typically infected with WN virus through a mosquito or tick bite, and most have no symptoms or have a self-limited, nonspecific viral syndrome. However, some patients develop a neuroinvasive form of the disease that is characterized by acute onset of fever with encephalitis and flaccid paralysis. The acute flaccid paralysis syndrome has similarities to poliomyelitis, as the virus affects the anterior horn cells of the spinal cord. A key feature of the weakness associated with WN virus is that it is asymmetric (as in this patient’s case). The estimated mortality of neuroinvasive WN virus disease is approximately 10%, and the degree of functional recovery among survivors is highly variable. Other neurologic presentations include meningitis (which is more common in children), seizures, tremors, and myoclonus. The CSF profile in this case is typical for WN virus, including pleocytosis with lymphocyte predominance and no RBCs. With neuroinvasive WN virus, the CSF WBC count is typically moderately elevated (<500/µL [<0.5 × 109/L]), with moderately elevated protein levels (above the upper limit of normal but <150 mg/dL) and normal glucose levels. In patients with clinical presentations consistent with WN virus infection, diagnosis is confirmed by detecting WN virus IgM antibody in the serum and/or CSF by using IgM antibody capture enzyme-linked immunosorbent assay. The standard approach to managing this condition is supportive care alone, as there is no specific antiviral or other evidence-supported therapy.

Herpes simplex virus (HSV)-1 is not the most likely cause of this patient’s presentation. Patients with HSV-1 encephalitis characteristically present with fever and encephalopathy (as in this case), but the neurologic manifestations classically include cranial nerve deficits and seizures. The asymmetric flaccid weakness in this case is more characteristic of WN virus than HSV-1 disease. The CSF profile in HSV-1 typically demonstrates an increased WBC count and lymphocytosis (as in this case), but the majority of patients also have an elevated RBC count (absent in this case). Most patients with HSV-1 encephalitis also have MRI abnormalities, including temporal lobe lesions (absent in this case). HSV-1 does not have a typical seasonal pattern or a specific geographic distribution in the United States.

Rickettsia rickettsii causes Rocky Mountain spotted fever (RMSF) and is not the most likely cause of this patient’s presentation. This rickettsial infection typically occurs in the spring and early summer, and patients often present with fever, nausea, vomiting, and headache. RMSF also causes a maculopapular rash that typically starts 48 to 96 h after fever onset. Patients with RMSF also characteristically have thrombocytopenia, leukopenia, and elevated transaminase levels (all absent in this case) and have lower-level elevation of WBCs in the CSF (typically <100/μL [<0.1 × 109/L]) with a higher elevation of protein (100-200 mg/dL).

Cryptococcus neoformans is also not the most likely cause of this patient’s presentation. Most patients who develop cryptococcal meningitis are immunocompromised (eg, from HIV, glucocorticoids, history of solid organ transplant, hematologic malignancy). Other common features of cryptococcal meningitis include a subacute presentation over 1 to 2 weeks (unlike the acute presentation in this case), meningeal signs (headache, neck stiffness, photophobia), and elevated intracranial pressure with elevated opening pressure during lumbar puncture (absent in this case). The CSF profile of cryptococcal meningitis is characterized by lower-grade pleocytosis (<50/μL in patients with HIV [<0.05 × 109/L] and <200/μL [<0.2 × 109/L] in patients without HIV) and low glucose levels.123456

Footnotes

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  4. Perfect JR, Dismukes WE, Dromer F, et al. Clinical practice guidelines for the management of cryptococcal disease: 2010 update by the infectious diseases society of america. Clin Infect Dis. 2010;50(3):291-322. PubMed ↩

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